&EPA
           United States
           Environmental Protection
           Agency
            Environmental Criteria and
            Assessment Office
            Research Triangle Park, NC 27711
EPA-600/8-84-020aF
   August 1986
           Research and Development
Air Quality
Criteria for
Ozone and Other
Photochemical
Oxidants
           Volume I of V

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                       EPA-600/8-84-020aF
                               August 1986
   Air Quality Criteria
  for Ozone and Other
Photochemical Oxidants

       Volume I of V
   Environmental Criteria and Assessment Office
  Office of Health and Environmental Assessment
     Office of Research and Development
     U.S. Environmental Protection Agency
      Research Triangle Park, N.C. 27711

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                                  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.

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                                   ABSTRACT


     Scientific information is presented and evaluated relative to the health
and welfare effects associated with 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 health and welfare effects are emphasized, but additional infor-
mation is provided for understanding the nature of the oxidant pollution pro-
blem and for evaluating the reliability of effects data as well as their
relevance to potential exposures to ozone and other oxidants at concentrations
occurring in ambient air.  Information is presented on the following exposure-
related 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, chem-
istry, 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 epidemio-
logical 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.
                                      m

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                        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 Epidemic!ogical 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

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                               TABLE OF CONTENTS
LIST OF TABLES	      1x
LIST OF FIGURES	      . x
LIST OF ABBREVIATIONS 	      xi
AUTHORS, CONTRIBUTORS, AND REVIEWERS	,      xv

1.  SUMMARY AND CONCLUSIONS	     1-1
     1.1  INTRODUCTION	     1-1
     1.2   PROPERTIES, CHEMISTRY, AND TRANSPORT OF OZONE AND OTHER
           PHOTOCHEMICAL OXIDANTS AND THEIR PRECURSORS 	     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
                   Including 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.
                   1.2i3.3   Atmospheric Reactions of PAN, H202,
                             and HCOOH ...-.'		     1-8
           1.2.4   Meteorological and Climatological Processes 	     1-9
                   1.2.4.1   Atmospheric Mixing		.	....     1-9
                   1.2.4.2   Wind Speed and Direction	     1-11
                   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
                  , 1.2.4.5   Stratospheric-Tropospheric 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 Models	     1-20
                   1.2.6.3   Box Models 	     1-20
                   1.2.6.4   Validation and Sensitivity Analyses
                             for Dynamic Model s	     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

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                          TABLE OF CONTENTS
                             (continued)
              1.3.1.1   Quality Assurance and Sampling 	
              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
                        Homo! ogues	     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
1.4   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 Concentrations 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
1.5   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 Analysis	     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

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                          TABLE OF CONTENTS
                             (continued)
      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 Plant 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 Dosimetry 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   Central 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

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                          TABLE OF CONTENTS
                             (continued)
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 Pol 1utant Mixtures 	     1-164
      1.11.5  Identification of Potentially At-Risk
              Groups				     1-164
1.12  REFERENCES 	     1-166

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                                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 mobile laboratory  	    1-152
                                     IX

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                                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

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                             LIST OF ABBREVIATIONS
AChE
avg
BAKI
Be (7Be)
C
°C
CA
CC
CHSC(0)02
cm
CNS
CO
C02
COLD
cone., concn.
CV
dbh
DN'PH
ECD
EDU
EKMA
FEF
Fe2(S04)3
FEV
FEV1
FID
fR
FTIR
FVC
G-6-PD
GC
GPT
acetylcholinesterase
average
boric acid buffered potassium iodide
beryllium (radioactive isotope of beryllium)
carbon, concentration
degrees Celsius
chromotropic acid
closing capacity
acetylperoxy radical
centimeter
central nervous system
carbon monoxide
carbon dioxide
chronic obstructive lung disease
concentration
closing volume
diameter at breast height
2,4-di nitropheny1hydrazi ne
electron-capture detector
ethylenediurea
Empirical Kinetic Modeling Approach
forced expiratory flow
ferric sulfate
forced expiratory volume
forced expiratory volume in 1 sec
flame ionization detector
respiratory frequency
Fourier-transform infrared
forced vital capacity
glucose-6-phosphate dehydrogenase
gas chromatography
gas-phase titration

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                             LIST OF ABBREVIATIONS
                                  (continued)
GSH
HC
HCOOH
HN03
HN04
HO
H02
MONO
HPLC

HPPA
hr
hr/day
HRP
H2Q2
H2S04
I
I"
1C
I/O
IR
KI03
km
LAAPCD
LCV
LDH
L/min
M
ra
MBTH
mi
glutathione
hydrocarbon(s)
formic acid
nitric acid
peroxynitric acid
hydroxy
hydroperoxy
nitrous acid
high-pressure liquid chromatograpy; high-performance
liquid chrotnatography
3-(p_-hydroxyphenyl)propionic acid
hour(s)
hours per day                                     ;
horseradish peroxidase
hydrogen peroxide
sulfuric acid
impact
iodide ion
inspiratory capacity
ratio of indoor to outdoor ozone concentrations  '
infrared
potassium iodate
ki 1ometer                    .
Los Angeles Air Pollution Control District    ';
leuco crystal violet
lactate deyhydrogenase
liters per minute ,   ..-.  .   ••.
molar       .••.    •         : .
meter(s). .  ,  •;    -..,	>••-
3-methyl-2-benzothiazolinone hydrazone
mile(s)                 •

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                             LIST OF ABBREVIATIONS
                                  (continued)
NADPH                  nicotinamide adenine dinucleotide phosphate
NAPBN                  National Air Pollution Background Network
NBKI                   neutral buffered potassium iodide
(NH4)2S04              ammonium sulfate
NF                     National Forest
nm                     nanometer(s)
NMHC                   nonmethane hydrocarbons
NMOC                   nonmethane organic compounds
NO                     nitric oxide
NQ2                    nitrogen dioxide
N03                    nitrogen trioxide
NO                     nitrogen oxides
  r\
AN2                    nitrogen washout
NPSH                   non-protein sulfhydryls
NR                     natural rubber
N20                    nitrous oxide
OH                     hydroxyl group (or radical)
Q2                     oxygen
03                     ozone
OZIPP     .     ,        Ozone Isopleth Plotting Package
PAN                    peroxyacetyl nitrate
PA02                   alveolar partial pressure of oxygen
 M                      »
PBzN                   peroxybenzoyl nitrate
PEFR                   peak expiratory flow rate
pH                     negative log of H ion concentration
PPN                    peroxypropionyl nitrate
ppb                    parts per billion
ppm                    parts per million
rad                    radiation absorbed dose
RBC                    red blood cell
RV                     residual volume
                                    xm

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                             LIST OF ABBREVIATIONS
                                  (continued)
Sa02
SAROAD
SBR
sec
SGaw
SNAAQS
S02
S04
S0x
SRaw
SRM
SURE
T
TF
Tg/yr
TGS-ANSA

TLC
TSH
pg/m3
pm/hr
UV
voc
ZnS04
arterial oxygen saturation
Storage and Retrieval of Aerometric Data
styrene-butadiene rubber
second(s)
specific airway conductance
Secondary National Ambient Air Quality Standards
sulfur dioxide
sulfate
sulfur oxide(s)
specific airway resistance
Standard Reference Material
Sulfate Regional Experiment Sites
time, temperature
tropopause-folding events
teragrams per year
triethanolamine, guaiacol(£-methoxyphenol),  sodium
metabisulfite; and 8-anilino-l-naphthalene sulfonic acid
total lung capacity
thyroid stimulating hormone
microgram(s) per cubic meter
micrometer(s) per hour
ultraviolet
tidal volume
minute ventilation; expired volume per minute
volatile organic compounds
zinc sulfate
                                    xiv

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                    .AUTHORS, CONTRIBUTORS, AND REVIEWERS
Authors:
Dr.  Richard M.  Adams
Department of Agricultural and Resource Economics
Oregon State University
Con/all is, OR  97331

Dr.  Donald E. Gardner
Northrop Services, Inc.
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
BatteHe, 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

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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

                                      xv i

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Contributing Authors:
Dr.  Robert Frank
Department of Environmental Health Sciences .
Johns Hopkins School of Hygiene and Public Health
615 N. Wolfe 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
                                     xv

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                            SCIENCE ADVISORY
                    CLEAN AIR SCIENTIFIC ADVISORY COMMITTEE
     The substance of this document was reviewed by the Clean Air Scientific
Advisory Committee of the Science Advisory Board in public sessions.
                             SUBCOMMITTEE ON OZONE
                                   Chai rman

                              Dr. Morton Lippmann
                                   Professor
                     Department of Environmental Medicine
                      New York University Medical Center
                            Tuxedo, New York  10987
                                    Members
Dr. Mary 0. Amdur
Senior Research Scientist
Energy Laboratory
Massachusetts Institute of Technology
Cambridge, Massachusetts  02139

Dr. Eileen G. Brennan
Professor
Department of Plant Pathology
Martin Hall, Room 213, Lipman Drive
Cook College-NJAES
Rutgers University
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.  Robert Frank
Professor of Environmental  Health
  Sciences
Johns Hopkins School of Hygiene
  and Public Health
615 N. Wolfe Street
Baltimore, Maryland  21205

Professor A. Myrick Freeman II
Department of Economics
Bowdoin College
Brunswick, Maine  04011

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 POA1EO

Dr.  Jay S. Jacobson
Plant Physiologist
Boyce Thompson Institute
Tower Road
Ithaca, New York  14853
                                     xvm

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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 El 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 Biostatisties
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 Health 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

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                         PROJECT TEAM FOR DEVELOPMENT
                                      OF
        Air Quality Criteria for Ozone and Other Photochemical Oxidants
Ms. Beverly E. Til ton, 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. Chi Ids
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. Thomas B. McMullen
Environmental 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

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                          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 deriva-
tion of  National  Ambient Air Quality 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,  experi-
mental 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 photochemical  oxidants  in  ambient air
consist mainly of  ozone, peroxyacetyl nitrate,,and nitrogen dioxide,  and  of.
considerably  lesser  amounts of other  peroxyacyl  nitrates, hydrogen peroxide,
alkyl hydroperoxides, nitric and nitrous acids, and formic acid.  Other••oxida'nts
suspected to  occur  in ambient air but only in trace amounts include peracids
and ozonides.  Only  data on ozone, peroxyacyl nitrates,..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, peroxy-
acetyl 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

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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.
Generally, 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 we!fare-related chapters met other selection
criteria, including the appropriate use and satisfaction of statistical 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 upm. 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 pre-
sented 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

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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 OtherPhotochemical Oxidants
   '  Ozone  (03)  and  other photochemical oxidants occurring at low concentra-
tions  in  ambient air,  such as peroxyacetyl  nitrate  (PAN),  hydrogen peroxide
(HpOp), 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,
H2Q2/H2Q  (Weast, 1977).   No standard potential for  peroxyacetyl nitrate in
neutral or buffered  aqueous systems,  such as  those  that occur  in biological

                                    1-3

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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, especi-
ally in the  laboratory,  is its thermal instability.   Its explosiveness dic-
tates 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 abili-
ty.  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.  All three pollutants of most concern in this document (0-,,  PAN,
and HpOp)  must be generated j_n situ for the calibration of measurement tech-
niques.   For  ozone  and  H?®?'  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 (NO ),  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 emissions 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 hydrocar-
bons (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

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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  a!.,  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 haloe-
thenes 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 (N0?) 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 acetyl-
peroxy radicals  to  form peroxyacetyl  nitrate,  a phytotoxicant and  a lachryma-
tor.  Although ubiquitous, nitrous oxide (N-O)  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 precursors  to  ozone from predominantly
manmade  sources;  photochemical reactions that  take place  during the disper-
sion and  transport of these precursors; and scavenging processes  that reduce
the concentrations of both 0^  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

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increasingly well-character!zed.   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, nonbio-
logical materials,  and such phenomena as visibility degradation and acidifica-
tion of cloud and rain water.
1.2.3.1    Formationand Transformation of Ozone and OtherPhotochemical  Oxi-
dants.  In the troposphere, ozone is formed through the dissociation of N02 by
sunlight to yield an oxygen atom, which then reacts with molecular oxygen (0?)
to produce an 0, molecule.  If  it  is  present,  NO can  react rapidly with  03  to
form NOp and an 02 molecule.  In the absence of competing reactions, a steady-
state or  equilibrium concentration  of 03 is soon established between 03,  N02,
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 03 begins depends  heavily on the initial
N0/N09 and NMOC/NOV ratios (National Research Council, 1977).
     £m            /\
     The major role played by organic compounds in smog reactions  is attribut-
able 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  a!.,  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 0~ itself.  Other free  radicals, such as hydro-
and alkylperoxy radicals and the nitrate (NO,,) radical play important roles in
photochemical air pollution.
     The  presence of organic  compounds, oxides of nitrogen,  and sunlight does
not mean  that the photochemical  reactions will  continue indefinitely.  Termi-
nation reactions gradually  remove  NOp from the reaction mixtures, such  that
the photochemical cycles  slowly come to an end unless fresh NO and N02 emis-
sions are  injected  into  the atmosphere.  Compounds containing nitrogen,  such
as PAN, nitric  acid (HN03), and peroxynitric acid (HWL),  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  a!.,  1979;  Atkinson et  al.,  1985).   The
                                    1-6

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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 under-
stood.
     In the  presence  of NO ,  natural hydrocarbons  (i.e.,  those organic com-
                           x\
pounds emitted from  vegetation) can also undergo photooxidation reactions to
yield 0~,  although most naturally emitted hydrocarbons are olefins and are
scavengers as  well as producers of  0~  (e.g.,  Lloyd et al., 1983;.Atkinson
et al.,  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 certain cases, with  N03  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 well as photolysis, in the case of aldehydes and other
oxygenated organics.  Only for organics whose ozone  reaction rate constants
                      *5™f    *3           "1     "1
are  greater  than  -10    cm  molecule    sec   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
                                                                           — 1 Q
with cyclic  alkenes.  The  rate  constants  for these reactions range  from ~10
       —14.    3         —i     "~"i
to ~10     cm  molecule    sec   (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  photochemical 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 (Atkinson 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

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     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 NCL  radicals  (Carter et a!.,  1981a;  Atkinson  et  al.,
1984d) predominate.
     For oxygen-containing organic compounds, especially those without carbon-
carbon 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 (Atkinson and Carter, 1984).
     Certain reactions  of ozone  other than  its  reactions  with  organic com-
pounds are important in the  atmosphere.  Ozone reacts rapidly with NO to  form
NOg, and subsequently with  N02 to produce the nitrate  (NO,)  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 S02 to H2$Q4, both indirectly
in the gas phase  (via formation of  OH  radicals  and Criegee biradicals) and
directly in aqueous droplets.
1.2.3.3  Atmospheric Reactions of  PAN, Hg02, and HCOQH.   Because PAN  is  in
equilibrium with acetyl  peroxy radicals and N02,  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
lower  temperatures,  PAN will persist-, in  the atmosphere (Wallington et al.,
1984; Aikin et  al.,  1983) and contribute to the long-range transport of NO .
                             !                                    "          X
     Although hydrogen,( peroxide;formed  in Ithe^gas  phase from the reactions of
hydroperoxyl radicals plays  ,a role-in HOY chemistry  in the,; troposphere,  and
                   *       -     '          y^
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 H202  will be.taken up in
aqueous  droplets.   Over the  past decade, evidence  has  accumulated that H,
                                    1-8

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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 S02 to H^SO^
(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 N0? dissolved in aqueous
droplets, although relevant data are limited and additional  research is required
(see, e.g., Gertler et a!., 1984).   Substantial  uncertainties remain concerning
the quantitative role of H^O^ in acidification of aqueous particles and droplets
(Richards 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 remains concerning the
quantitative role of HCOOH and the higher organic acids, they, potentially play
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  found 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,- and the seasonality of incursions of stratospheric ozonek
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 pollu-
tant at  the receptor.   The rate at which atmospheric mixing proceeds  and the
                                    1-9

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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 inver-
sions  (base at ground  level) and  elevated  inversions  (the entire  layer is
above the surface)  are both common  (Hosier,  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  solar  radiation but break-
ing  up  by about mid-morning as the result of  surface heating by  the sun (Hosier,
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  (Hosier, 1961; Holzworth,  1964; Robinson,
1952).   In coastal  areas generally, such as  the New  England coast (Hosier,
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
~200 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 poten-
tial 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

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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 determi-
nants 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,
light winds  can  result in high oxidant levels  even  if the mixing  layer  is
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  (  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 followed 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 lead to the stagnation type of air  pollution episodes.   The Northeast
states  are  highly  susceptible  to pollutant plume transport effects, although
some notable stagnation episodes have  also  affected  this area (e.g.,  Lynn
et al.j  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 a!., 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 dis-
tribution.   Intensity  varies diurnally, seasonally, and with latitude, but the
effect  of  latitude  is strong only in  the winter.  Experimental studies have
verified the effects on  oxidant  formation of Tight intensity (Peterson, 1976;
Demerjian  et a!.,  1980) and its  diurnal  variations  (Jeffries  et a!., 1975;
1976),  as well as  on the overall  photooxidation process  (Jaffee et  a!., 1974;
Winer et al., 1979).
                                    1-11

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     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 concen-
trations (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 is 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) in-
jection 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 cri-
teria document for ozone  and other photochemical  oxidants (U.S. Environmental
Protection Agency, 1978).   In that document, transport phenomena were classi-
fied into three categories, depending upon transport distance:   urban-scale,
mesoscale, and synoptic-scale.   In urban-scale transport,  maximum concentra-
tions of 0, are  produced about 20 miles or so (and about 2 to 3 hours)  down-
wind from the  major  pollutant source areas.   In mesoscale transport, 0, 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, characteris-
tic 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

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Wolff  et  al.,  1977a).   Simple  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 tropo-
sphere, where  it forms a more  or less uniformly mixed  background concentra-
tion,  has been  known  in  various degrees of detail  for many years (Junge,
1963).   It is  widely  accepted  that  the  long-term  average tropospheric back-
ground concentration of about 30 ppb  to  50 ppb results  primarily,  though  not
                                     1-13

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exclusively, from  the  transfer of stratospheric ozone  into the upper tropo-
sphere, 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 trans-
tropopause movement of ozone-rich air into the troposphere (Johnson and Viezee,
1981).
1.2.4.6   Stratospheric 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 is  based on  the  assumption  that beryllium-7  ( Be) is a
unique tracer for air parcels of stratospheric origin.   Calculated correlations
between surface  ozone and  Be 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

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concluded that "the  experimental  technique involving a  Be/0- ratio to esti-
mate the daily stratospheric  component of ground-level Q~  is  unverified and
considered to be  inadequate for air quality  applications"  (p. 1009).   This
group of investigators  have suggested, however, that  Be may  be used, under
appropriate meteorological  conditions, as  a qualitative tracer for air masses
of  stratospheric  origin (Johnson  and  Viezee, 1981; Viezee et a!.,  1979).
     Other methods used to  attempt to  quantify the  stratospheric component  of
surface ozone include aircraft observations of TF events coupled with calcula-
tions of downward  ozone  flux,  and examination of surface ozone data records.
From such data,  Viezee et al.  (1983) concluded that direct ground-level contri-
butions  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).
1.2.4.7  Background Ozone from Photochemical Reactions.   Whereas stratospheric
ozone  is thought by  many  investigators  to be the  dominant contributor to
background  levels  of ozone,  as  discussed  above,  other  investigators  have
concluded that as much as  two-thirds of  the annual  average  background  concen-
trations may  result 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.
     /\
     Studies on the  role of NO   in  nonurban  ozone  photochemistry  have shown
                               /\
that  ozone  formation at  many  of  the  locations  is  not NO -limited,  but  depends
                                                       s\
on  VOC reactions, as well (e.g., Martinez and Singh, 1979; Kelly et al., 1984;
                                    1-15

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Liu et al., 1984).  Background NO  concentrations at most remote, clean "loca-
                                 J\
tions range from  <0.05  ppb upward.   Mean concentrations of  NO  at nonurban
                                                               J\
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  are  higher  than previously thought  (see,
e.g., Singh et  al.,  1980;  Kelly et  al.,  1984,  regarding global models and
assumed reservoirs of NO-)-
                        X
     The contributions  of  biogenic VOC to background ozone, although a matter
of controversy in recent years,  appear not to be significant under most atmos-
pheric 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
(NOV), emitted by manmade  and by natural sources; and on suitable conditions
   
-------
biogenic emissions  of organic  compounds  in the  United States are highly
inferential but data  suggest that the yearly rate  is the same  order of magni-
tude 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  in the United States were estimated at 19.4 Tg/yr
                            x>.
for 1983.  Retrospective  estimates  show that manmade NO  emissions rose from
                                                        x>.
about 6.8 Tg/yr in 1940 to about 18.1 Tg/yr in 1970 (U.S.  Environmental  Protec-
tion Agency,  1986).   Annual  emissions of manmade  NO   were some 12 percent
                                                    s\
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   emissions are based  on uncertain  extrapolations
                          x>.
from very  limited  studies,  but appear to be about an order of magnitude less
than manmade NO  emissions.
               s\
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~  to C-.Q molecular-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 generally 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

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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,  ri-butane,  iso-pentane,  and ri-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 ,  like hydro-
                                                                 Ps,
carbon concentrations,  tend  to peak in urban areas  during  the early morning,
when atmospheric  dispersion  is limited and automobile traffic is dense.  Most
NO   is emitted as nitric oxide (NO),  but  the NO is  rapidly converted to N0~,
  />                                                                         £-
initially by thermal oxidation and subsequently by  ozone and peroxy radicals
produced in atmospheric photochemical  reactions.  The relative concentrations
of NO  versus  N02 fluctuate  day-to-day,  depending  on diurnal  and day-to-day
fluctuations in ozone  levels and photochemical  activity.
     Urban NO   concentrations  during the 6:00 to 9:00  a.m.  period in 10 cities
             /tr\
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 a!., 1979),  although concen-
trations two  to  three times  higher  occur in cities  such  as Los Angeles.
Concurrent  NMHC measurements for these 10 cities showed that NMHC/NO   ratios
                                                                     J\
ranged from 5 to  16.
1.2.5,2.4   Nitrogen  oxides in  nonurban areas.   Concentrations of NO  in clean
           '::::::::::::::--":   "•'•	'"" -»----^-"'==-::-    •:--::.•::-..:.                                       ^
remote environments  are  usually  <0.5 ppb (Logan,  1983).   In exceptionally
clean  air, NO   concentrations  as low as 0.015 ppb have been recorded (Bellinger
             *>
et al., 1982).   Concentrations of NO  at  nonurban  sites in the northeastern
                                     y\
United States  appear to be  higher than  NO  concentrations in the west by a
                                           J\
factor of  ten  (Mueller and  Hidy,  1983).  From the limited amount  of  data
available, NO   concentrations  in unpopulated  nonurban  areas  in the west average
             f{
<1 ppb; but in nonurban  northeastern  areas  average NO  can  exceed 10 ppb.
*"""
                                     1-18

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1.2,6  Source-Receptor (Oxldant-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 atmos-
pheric 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 chemical  and  physical  processes influencing air pollution forma-
tion  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  Eulerian, 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  simplest form  of, trajectory model  is the empirical  kinetic modeling
approach  (EKMA),  This approach was developed from earlier efforts (Dimitriades,
1972)  to  use smog chamber  data.to develop  graphical  relationships between
morning NMOC and NO   levels and afternoon-maximum concentrations of ozone.   In
                   }\
applying  EKMA,  the Ozone  Isopleth  Plotting  Package  (OZIPP) (Whitten and Hogos
1978)  is  used to  generate ozone  isop!eths 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

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     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/NO  concentration ratios, reductions in NO  will
                                s\                                       /\
decrease ozone  formation; (2) at moderate  NMOC/NO   ratios, reductions  in  NMOC
                                                 /\
and NO  will  decrease  ozone formation; and  (3)  at  very low NMOC/NO  ratios,
      /\                                                             /\
increases in NO will  inhibit ozone formation.  These predictions  cannot be
                /\
assumed to apply to all 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 forma-
tion of controlling NMHC and NO  (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 present-
ly available  source-receptor models require a degree  of  simplifying assump-
tions to deal with practical limitations imposed by existing computer capabil-
ities, 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

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experimental data from ambient air measurements or environmental chamber runs.
Reliability and  applicability also  depend on the quality  of the chemical
kinetics mechanisms used to define the Oo~HC~NO  relationship,
                                        O      j\
     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,  recom-
mended 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 OT 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 instrumen-
tation  (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

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quality control (U.S. Environmental Protection Agency, 1977b).  Design criteria
for DO 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  Qxidants and Ozone.   Techniques for the
continuous monitoring  of  total  oxidants and 03 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,

                         03 + 3I~ + H20 •» I3~ + 02 + 20H~             (1-1)

is measured  by ultraviolet  absorption in colorimetric  instruments and by
amperometric means  in  electrochemical  instruments.  The  term "total  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 immedi-
ately 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  (NOp) and
sulfur dioxide (SOp)  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 concentra-
tions 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

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                                                  TABLE 1-1.  SUMMARY OF OZONE MONITORING TECHNIQUES
l\5
CO
Principle
Continuous
colon metric
Continuous
electrochemical
Chemi 1 uai neseence
Chemi 1 umi nescence
Ultraviolet
photometry
Reagent
10(20)% KI
buffered at
pH = 6.8
2% KI
buffered at
pH =6.8
Ethyl ene,
gas-phase
Rhodamine-B
None
Response
Total
oxidants
Total
oxidants
Q3~specific
03-specific
03-specific
Minimum
detection limit
0.010 ppn
0.010 ppm
0.005 ppin
0.001 ppat
0.005 ppra
Response
tine, 90% FSa
3 to 5 minutes
1 minute
< 30 seconds
< 1 minute
30 seconds
Major
interferences
N02(+20%, 10%KI)
S02(-100%)
N02(+6%)
so2(-ioo%)
Noneb
None
Species that
absorb at 254 nn
References
Littman and Benoliel (1953)
Tokiwa et al. (1972)
Brewer and Mil ford (1960)
Mast and Saunders (1962)
Tokiwa et al. (1972)
Nederbragt'et al. (1965)
Stevens and Hodgeson (1973)
Regener (1960, 1964)
Hodgeson et al. (1970)
Bowman and Horak (1972)
    aFS = full  response.

     A signal enhancement of 3 to 12% has been reported for measurement of 03 in humid versus  dry  air  (California Air  Resources  Board,  1976).

     No significant  interferences have been reported in routine ambient air monitoring.   If abnormally high  concentrations  of  species that
     absorb  at  254 ran  (e.g., aromatic hydrocarbons and mercury vapor) are present, some positive response  may  be expected.   If high  aerosol
     concentrations  are  sampled, inlet filters must be used to avoid a positive response. •

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designated as a  reference  method if it is based on the same principle as the
reference method and meets performance specifications.  An acceptable equiva-
lent 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 absorp-
tion 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 pro-
duces chemiluminescence, the  intensity  of which is directly proportional to
ozone concentration.
1.3.1.3  Calibration Methods.   All  the  analyzers  discussed above  must be
calibrated periodically with  ozonized air  streams, in  which the ozone concen-
tration 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 contami-
nation.
     A primary ozone calibration system  consists of a  clean air source, ozone
generator, sampling manifold, and means for measuring absolute ozone concentra-
tion.  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 a!., 1972).   Once the output of the generator has
been calibrated  by a primary  reference method,  it  may  be  used to calibrate 0,,
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

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                                                  TABLE  1-2.   OZONE  CALIBRATION TECHNIQUES
Method
1% NBKI
2% NBKIC
11 Unbuffered
KI
UV photometry
\—>
i
en Gas-phase
titration (GPT)
1% BAKI
Reagent
1% KI,
phosphate buffer
pH = 6.8
2% KI
phosphate buffer
pH = 6.8
1% KI
pH = 7
None
Nitric oxide
standard reference
gas
1% KI,
boric acid buffer
pH = 5
Primary standard3
Reagent grade
arsenious oxide
Reagent grade
potassium biiodate

03 absorptivity at
Hg 254 nm emission
line
Nitric oxide SRM
(50 ppm in N2)
from NBS
Standard KI03g
solutions
Organization
and dates
EPA
1971-1976
CARB
until 1975
LAAPCD
until 1975
All
1979-present
EPA, States
1973-present
EPA
1975-1979
Bias,
Purpose [03]./[03]
Primary reference 1.12 ± 0.05
procedure
Primary reference 1. 20 ± 0.05
procedure
Primary reference 0,96
procedure
Primary reference
procedure
Alternative reference 1,030 ± 0,015
procedure (1973-1979)
Transfer standard (1979-present)
Alternative reference 1.00 ± 0.05
procedure
 In the case of the iodometric methods,  the primary standard is  the  reagent used to prepare or standardize iodine solutions,
 The uncertainty limits represent the range of values obtained in several  independent studies.
cPre-humidified air used for the ozone source.
 Only one study available (DeMore et al.,  1976).
p
 UV photometry used as reference method by CARB since 1975.   This technique used as an interim, alternative reference procedure by
 EPA from 1976 to 1979.'
 This is the value reported in the latest  definitive study (Fried and  Hodgeson,  1982).   Previous studies reported biases ranging from
 0 to 10 percent (Burton et al., 1976; Paur and McElroy,  1979),
^This procedure also recommended a standard I3  solution  absorptivity  to  be used instead of the preparation of standard iodine solutions.

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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  inter!aboratory 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 a!., 1977),  nor in a KI procedure
that used boric  acid  as buffer (Flamm, 1977).  A summary of results of these
prior studies was  presented  in  the previous criteria document (U.S.  Environ-
mental 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 proce-
dures 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 CU 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,
analyzers.   Examples of transfer  standards  that  have been  used are commercial
O.j 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  com-
plicated by  the  relative scarcity of  simultaneous data, the presence of both
positive (N02) and negative  (S02) interferences  in total oxidants measurements

                                    1-26

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of ambient air,  and  the change in the basis of calibration.  In particular,
the presence  of NOp  and  SCL interferences prevent the  establishment  of a
definite quantitative relationship between ozone and oxidants data.   Neverthe-
less,  some  interesting conclusions 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 NOp 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)  in  1974,  1976,  and 1978.  The maximum hourly data pairs 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 03 + 0.005
                         (Correlation coefficient = 0.92)             (1-2)

The oxidant data were uncorrected for NOp and SQp interferences, and on individ-
ual days maximum oxidant  averages were both higher than and  lower than ozone
averages.
     In summary, specific ozone measurements agree fairly well with total oxi-
dants corrected  for  NOp and SQp interferences, and in such corrected total
oxidants measurements ozone  is the dominant contributor.  Indeed, it is diffi-
cult  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  a-ir quality.
1.3.1.5    Methods for Sampling and Analysis of Peroxyacetyl  Nitrate and Its
Homologues.   Only  two analytical  techniques have  been  used to obtain signifi-
cant data on ambient peroxyacetyl nitrate (PAN) concentrations.   These are gas
chromatography with  electron capture  detection  (GC-ECD)  and long-path  Fourier
                                    1-27

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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 a!.,
1963; Stephens, 1969),   With  carbowax or SE30  as  a stationary phase, PAN,
peroxypropionyl nitrate  (PPN),  peroxybenzoyl  nitrate (PBzN), and other homo-
logues (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-ml  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 auto-
matic 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 humidifi-
cation 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  in-
frared 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 Wiliner, 1983; Holdren and Spicer, 1984) permit
the quantitative analysis of PAN without calibration standards.  The absorptiv-
                 w. ~\
ity of the 990  cm   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

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pathlengths up to 2 km for ambient measurements of PAN and other trace constit-
uents.  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 internal 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  available   !
and must be prepared.  Earlier methods used to synthesize PAN have been summa-
rized 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
violently  explosive  and  should  be  handled behind explosion  shields using
plastic  full-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 alkyl  nitrates (Hendry and  Kenley,
1977; Kravetz et al. , 1980; Nielsen  et al., 1982; Holdren and  Spicer, 1984).
After the nitration  is  complete, the  hydrocarbon fraction  containing  PAN
concentrations of  2  to 4  mg/ml  can  be stored at -20°C  for periods  longer than
a  year  (Holdren and  Spicer,  1984).
                                    1-29

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     The most direct  method for absolute analysis of these PAN samples is by
infrared absorption,  using  the  IR absorptivities mentioned earlier.   Conven-
tional IR instruments and 10-cm gas cells can analyze gas standards of concen-
trations >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 proce-
dure (Stephens, 1969).   The favored  procedures now use ion chromatography to
analyze for nitrite (Nielsen et a!.,  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~C(Q)Og,
                                                                        >J     £.
and its decomposition products rapidly oxidize nitric oxide (NO) to NGp with a
stpichiometry that has been experimentally determined.
1.3.1,6   Methodsfor Sampling and Analysis of Hydrogen Peroxide.    Hydrogen
peroxide (H202) 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 SO,   and in the acidification of rain (Penkett et al.,  1979; Dasgupta,
1980a,b; Martin and Damschen, 1981; Overton and Durham, 1982).
     One of  the major problems,  however,  in assessing the role  of  atmospheric
HpOp has been a lack of adequate measurement methodology.  Earlier measurements
(Gay and Bufalini, 1972a,b; Bufalini  et al., 1972; Kok et al., 1978a,b) reporting
HLOg concentrations of 0.01 to 0.18 ppm are now believed to be far too high,
and to be  the  result  of  artifact H?02 formation  from reactions  of  absorbed Q~
(Zika and  Saltzman, 1982; Heikes et  al.,  1982;  Heikes,  1984).   Maximum tropo-
spheric H202 concentrations predicted by  modeling calculations  (Chameides and
Tan, 1981;  Logan  et al., 1981)  and  observed in  recent  field  studies  (Das et
al., 1983) are on the order of 1 ppb.                             .:.
     Almost  all of  the methods used for  the measurement of atmospheric  hLOg
have used  aqueous  traps for sampling.  Atmospheric 03, however, which  is also
absorbed at  concentrations  much higher than H202, 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 substantially

                                    1-30 , , ,.

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reduce this interference (Zika and Saltzman, 1982; Das et al., 1983).   Another
problem identified with aqueous sampling is that other atmospheric species (in
particular, SCL) may  interfere with the generation of H_Q2  in aqueous traps •
and also react with collected HJD? to reduce the apparent concentration measured
(Heikes et al., 1982).
     Of the techniques  that  have  been used  for the measurement of aqueous and
gas-phase HpO?, 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).                                                .        V:
     Hydrogen peroxide in the atmosphere may be detected at  low concentrations
by the chemiluminescence obtained from copper(ID-catalyzed  oxidaton of luminol
(5-amino-2,3-dihydro-l,4-phthalazinedione)  by H^O^  (Armstrong and Humphreys,
1965; Kok et al., 1978a,b).  This technique as initially employed suffered the
interferences from 0- and SQ2 discussed above for aqueous traps.  Das et al.
(1982) employed a static version of the method of Kok et al. (1978a) to measure
H202 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 luminol-
based H^O* 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 substrates
by H^Op.  The production or decay of the fluorescence intensity of the substrate
or  reaction product  is measured as it is oxidized by HpO,,,  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_-hydroxy-
phenyl)propionic  acid (HPPA)  (Zaitsu  and Okhura, 1980);, and leuco crystal
violet (LCV) (Mottola et al., 1970).
     The decrease in  the fluorescence intensity of scopoletin is measured as a
function of HuQ9  concentration.   Detection limits have  been reported to be
             -.11
quite  low  (10     M).   The chief  disadvantage  of  this approach  is that  the
concentration-  of  H?0? must be within a  narrow  range  to  obtain an accurately

                                    1-31

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measureable  decrease  in fluorescence.  Oxidation of  LCV  produces intensely
                                                                       5  ~1
colored crystal violet,  which has a molar absorption coefficient of 10  M
  ••II
on   at the  analytical  wavelength,  596 nm.   The detection limit reported was
  **8
10   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 a!., 1983; Dasgupta and Hwang,  1985).  The measurement of the fluores-
cence intensity of the product  dimer  provides  a quite sensitive means  for the
assay of H202.
     As with 03, ti?®? calibration standards are not commercially available and
are  usually  prepared at  the time  of use.  The  most convenient method for pre-
paring aqueous  samples containing micromolar concentrations  of H?0p is simply
the  serial dilution of  commercial grade 30 percent HyQ-  (Fisher Analytical
Reagent).   Techniques for the convenient generation of gas-phase standards are
not  available.  A  technique  often used for generating ppm concentrations of
H«0« in air  involves the injection of micro!iter quantities of 30 percent HpO«
solution into a metered  stream of air that flows into a Teflon bag.   Aqueous
and  gas-phase samples are  then  standardized by conventional  iodometric proce-
dures (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.  These methods,
still in use for analysis of total nonmethane organic compounds, are essentially
organic carbon analyzers, since the response of the FID detector  is 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  detectqfiihas been
utilized both as   a stand-alone  continuous detection  system (non-speciation
                                    1-32

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analyzers have indicated an overall poor performance of the commercial instru-
ments 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 a!., 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  ^system 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 preconcen-
tration  techniques  in  present use  are  cryogenic  collection and the  use of
solid adsorbents  (McClenny et  al., 1984;  Jayanty  et a!., 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.s  1981),  the 3-methyl~2-benzo-
thiazolene  (MBTH)  technique for total aldehydes (e.g., Sawicki et al., 1961;
Mauser  and Cummins, 1964),  Fourier-transform  infrared  (FTIR)  spectroscopy
(e.g., Hanst et al., 1982; Tuazon et al., 1978, 1980, 1981a), and high-perfor-
mance liquid chromatography employing 2»4-dim"trophenyl-hydrazine  derivatiza-
tion  (HPLC-ONPH) for aldehyde speciation  (e.g., Lipari and  Swarin, 1982; Kuntz
et al.5  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 jji  situ analysis of  ambient  air.  These advantages are offset, however,
by the  relatively  high cost and lack of  portability  of  the instrumentation.
                                    1-33

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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 ^substi-
tuted 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 hydro-
carbons with oxides of nitrogen, CU, and hydroxyl radicals will  produce signi-
ficant 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 (Qsman et al.} 1979; Westberg et a!., 1980).   Additional
research efforts should focus on this area.
1,3.2.2  Nitrogen Oxides.  Aside from the essentially unreactive nitrous oxide
(NgO), only two  oxides of nitrogen occur in ambient air at appreciable concen-
trations:   nitric oxide (NO)  and nitrogen dioxide  (N02).   Both compounds,
together designated as NO  , 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 measuring NO and N02 is
the chemiluminescence  method  (F.R.,  1976).   The measurement principle is the
gas-phase  chemiluminescent reaction of  0-  and NO (Fontijn  et  a!.,  1970).
While NO is determined directly in this fashion, NO^ is detected indirectly by
first reducing  or thermally  decomposing the gas quantitatively to NO with a
converter.  The  reaction of NO and 0_ forms excited N0« 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 NQ2 converter.  The magnitude of these interferences
is dependent  upon the type of converter  used (Winer et a!.,  1974; Joshi and
                                    1-34

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Bufalini, 1978).  The detection  limit of commercial chemiluminescence instru-
ments for N02 measurement is 2.5 ug/m3 (0.002 ppm) (Katz, 1976).
     Development of an  instrument  based on the chemiluminescent reaction of
NQ2 with luminol (5-amino-2, 3-dihydro-l,  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 Q3 have been achieved.
     Other acceptable methods  for measuring ambient N0?  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 = triethanolamine, guaiacol (o-methoxyphenol), sodium metabisulfite,
and 8-anilino-1-naphthalene sulfonic  acid].   The  sodium arsenite method and
the TGS-ANSA method were designated as equivalent methods in 1977.   For descrip-
tions of these  methods,  the reader is  referred to the  EPA criteria document
for nitrogen  oxides  (U.S.  Environmental Protection Agency, 1982).  While 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 NO  measurements.   The U.S. Environmental Protection Agency
                     A
(1975) has issued a technical assistance document that describes in detail the
two acceptable calibration methods for NO  :  (1) the use of  standard reference
                                         "
materials (SRMs) and (2) gas-phase titration (GPT) of NO with Og.   The SRM for
NO  is  a  cylinder of compressed  NO in  N-;  the mixture  is  both accurate and
stable (Hughes,  1975).   The SRM for N0£ is the N02 permeation tube (O'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 Oo  t
to  form N02 plus 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

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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 indoor-
outdoor gradients  for exposure analyses;  (4) assessing whether the concentra-
tions 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 Stat-
istical 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; Phila-
delphia,  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).  Second-
highest 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,  respectively.   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

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   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 REGIONS3
Division
and region
SMSA
population,
SMSA millions
Second-highest
1983 03
concn. , ppm
Northeast

  New England
Boston, MA
  .Middle Atlantic  Buffalo, NY
                   Nassau-Suffolk, NY
                   Newark, NJ
                   New York, NY/NJ
                   Philadelphia, PA/NJ
                   Pittsburgh, PA
South
  South Atlantic
South

  West South
   Central
North Central

  East North
   Central
  West North
   Central
Atlanta, GA
Baltimore, MD
Ft. Lauderdale-Hollywood,
Miami, FL
Tampa-St. Petersburg, FL
Washington, DC/MD/VA
Dallas-Ft. Worth, TX
Houston, TX
New Orleans, LA
San Antonio, TX
Chicago, IL
Detroit, MI
Cleveland, OH
Cincinnati, OH/KY/IN
Milwaukee, WI
Indianapolis, IN
Columbus, OH
                                             FL
St. Louis, MO/IL
Minneapolis-St. Paul
Kansas City, MO/KS
  >2

1 to <2
  >2
1 to <2
  >2
  >2
  >2
  >2
  >2
1 to <2
1 to <2
1 to <2
  >2
  >2
  >2
1 to <2
1 to <2
                                         MN/WI
  >2
  >2
1 to <2
1 to <2
1 to <2
1 to <2
1 to <2
  >2
  >2
1 to <2
0.18

0.12
0.17
0.25
0.19
0.10
0.14
0.17
0.19
0.10
0.12
0.14
0.17
0.16
0.28
0.12'
0.12
0.17
0.17
0.15
0.15
0.18
0.14
0.12
0.18
0.13
0.13
                                    1-37

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 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 REGIONS9
Division
and region
West
Mountai n

Pacific










SMSA

Denver-Boulder, CO
Phoenix, AZ
Los Angeles- Long Beach, CA
San Francisco-Oakland, CA
Anaheim-Santa Ana-
Garden Grove, CA
San Diego, CA
Seattle- Everett, WA
Riverside-San Bernardino-
Ontario, CA
San Jose, CA
Portland, OR/WA
Sacramento, CA
SMSA Second-highest
population, 1983 Og
millions concn. , ppm

1 to <2
1 to <2
>2
>2

1 to <2
1 to <2
1 to <2
I to <2

1 to <2
1 to <2
1 to <2

0.14
0.16
0.37
0.17

0.28
0.2Q
0.10
0.34

0.16
0.12
0.15
 Standard 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 transpor-
tation  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 03; populations of 1  to 2 million,  0.14 ppm
03; and populations of 0.5 to 1 million, 0.13 ppm 03-  As noted above, however,
coincident meteorology favorable for oxidant formation undoubtedly contributes
to the apparent  correlation between population and ozone levels.
     Among all  stations  reporting  valid ozone data  ( 0.28 ppm.
                                    1-38

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     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 respites
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 :throtigh 1981).  A -con-
centration  of  >0.18 ppm was recorded  at that site  on only 2  single 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 concentra-
tions of ozone.                                     .

1.4.2.   Trends  in Nationwide Ozone Concentrations                   .         V
     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  derivation  of
recent trends  in  ozone  concentrations and the interpretation  of.those, trends  ;
is  complicated  by  two  potentially significant  factors  that  have affected', ;
aerometric  data since  1979:   (1) the promulgation  by  EPA.  in  1979 of  a  new  ,,K
calibration procedure for ozone  monitoring (see  Chapter 4);. ,and (2) the intro-
duction 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  changes  -
in  meteorology  or  in  precursor emission  rates that  may  have occurred  over the <
same time span.                      .              .          • ,       ,,
     The nationwide trends  in  ozone concentrations  for a  9-year period, 1975 •
through  1983:,  are  shown in  Figure 1-1 (U.  S.  Environmental Protection  Agency,--\
1984).   The data given  are  trends as  gauged by the  composite, average  of  the
                                    1-39.

-------
    0.18
    0,17
E
ex
Q.
o

<
oc
t-
z
Ul
o
z
o
o
U!
z
o
M
o
0.16
0.15
0.14
    ,0.13
    0.12
                                                       CA (27 Stations) _
                                                                   f
D (MAMS STATIONS (62)


T 95% CONFIDENCE

1 INTERVALS


CALL STATIONS (176)

"95% CONFIDENCE

X INTERVALS
              A CALIFORNIA STATIONS (27)


              V ALL STATIONS EXCEPT

                CALIFORNIA (149)

               I      I       I      I
                                            I
              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).
                                    1-40

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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, concen-
trations  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 0,  concentrations at predominantly  urban
stations aggregated for 1979, 1980, and 1981, as well as the  highest 1-hour 03
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

-------
no
O


I

z

O
z
O
O
UJ
z
O
N
O
                  3359

                0.45
                0.40
                0.35
                0.30
                0,25
                0,20
                0.15
                0.10
                0.05
99.9 99,8
                       99  98   95   SO
60  70  60  50 40  30  20
TO
1  0.5  0,2 0.1 0.05  0.01
                                         Mill
               HIGHEST


               2nd-HIGHEST


               3rd-HIGHEST

               HIGHEST, NAPBN SITES
                         1  I   1   1   1   i
                                1   I   I   I   I    I     II     I
                                                                                    _LL
                   0.01  0.05 0.1 0.2  0.5  1   2    5   10    20  30  40  SO  60  TO  80    90   95   98  99    99.8 99.9    99.99


                             STATIONS WITH PEAK 1-hour CONCENTRATIONS < SELECTED VALUE, percent



                    Figure 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).
                    Source; U.S. Environmental Protection Agency (1980,1981,1982).

-------
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 concentra-
tions measured in  1980 at Kisatchie National Forest (NF), Louisiana; Custer
NF5 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 concen-
trations 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 concen-
tration 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 al., 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

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1.4.4.  Diurnal and Seasonal Patterns in Ozone Concentrations
     Since the photochemical reactions of precursors that result in ozone for-
mation are driven by  sunlight, as well 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 simultaneous processes:  (1) downward 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 concen-
trations 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

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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 to  the  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
(in  the third quarter).   The data also 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  least  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  health  and welfare.   Averaging
times must correspond to, or be  related in  a consistent manner to, the pattern
of exposure that elicits untoward responses.
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1.4.5  SpatialPatterns 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 concen-
trations 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 concentra-
tions  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 varia-
tions  1th in the timing and the magnitude of the peak concentrations, and, in
the case  of transported ozone,  are  related to the temporal  variations between
urban  and  nonurban areas  discussed above.   Data from urban, suburban, rural,
uid remote sites (see, e.g., SAROAD, 1985a-f; Martinez and Singh, 1979; Lefohn,
1984   Evans,  1985;  respectively) corroborate  the  conclusion drawn in  the 1978
c'iuHa  document  (U.S.   Environmental  Protection Agency,  1978)  that ozone
;_,nce»,trations can  sometimes  be higher in some suburban or even  rural areas
jowwtnd  of urban plumes than in the urban areas themselves; and, furthermore,
, at higher concentrations can  persist longer in  rural and remote  areas,
iarge1:1 because  of the  absence  of nitric oxide (NO) for chemical scavenging.
          onurban areas downwind of urban plumes,  peak concentrations can
  air, as  the result of transport,  at virtually any hour of the  day or night,
df -ending  upon many factors, such as the  strength of the  emission source,
i'ldvtvion time, scavenging, and  wind speed (travel  time) and other meteorological
far-.IKS.  The dependence of the  timing of peak exposures upon these transport-
related factors  is well-known and is illustrated here by two studies.  Evans

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ozone concentrations occurred  at  distances of 10 to  70  km (ca.  6 to 43 mi)
north-northeast of the  urban  center.   Consequently, it would be possible for
peak ozone concentrations  to  occur in the late 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 concen-
trations 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, especially  since  the aerometric data  for nonurban areas are
far from abundant.
1.4.5.2  Geographic, Vertical, and AltitudinalVariations in OzoneConcentrations.
Although of  interest  and concern  when estimating global  ozone budgets, demon-
strated 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.,
Seller and  Fishman,  1981;  Gal bally  and  Roy,  1980;  Oltmans, 1981, cited  in
Logan et al., 1981).  The most pertinent vertical and altitudinal gradients in
                                    1-47

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ozone concentrations are:   (1)  increases in concentration with height above
the surface of the ground (regardless of altitude); (2) increases in concentra-
tion 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 ground-
level emissions of NO or by deposition on reactive surfaces such as vegetation.
Data  illustrative of the near-surface gradient were reported by Pratt 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 considera-
tion 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; Seller 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).
     Increases 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
      J»
of exposures and the accurate derivation of dose-response functions, especially
for forests and other vegetation.
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     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/day  of concentrations >0.10 ppm  at the station at
817 m (2860 ft) was probably the result of contact of that zone of the mountain-
side 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, respec-
tively  (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
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possible occurrence  of  nighttime peak concentrations of ozone, the occurrence
of multiple peaks  in a  24-hour period, or the persistence of elevated concen-
trations 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  varia-
tions are  important  for exposure assessments for human populations.   Indoor-
outdoor 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 a!., 1973; Thompson et a!., 1973; Peterson and Sabersky,  1975).   Ozone  reacts
with surfaces inside buildings, so that decay may occur fairly rapidly,  depending
upon the nature of interior surfaces and furnishings (e.g.,  Davies et a!., 1984;
Content et al., 1985).  Ratios of indoor-to-outdoor (I/O) ozone concentrations
are quite variable,  however, since cooling and ventilation systems, air infil-
tration or exchange  rates, interior air circulation rates,  and the composition
of  interior  surfaces all  affect indoor  ozone  concentrations.   Ratios (I/O,
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
(Sabersky et al., 1973) in an air-conditioned office building (but with 100 per-
cent  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-conditioned 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  City
(Smith, 1981), and for Detroit (Kelly et al., 1986).  Such gradients should be
taken into consideration, where possible, in exposure assessments.
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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),
peroxypropionyl  nitrate  (PPN), and hydrogen peroxide (Hp02).  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 a!., 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
Taylor,  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  a!., 1981a;
Grosjean,  1983;  respectively).   The only published 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

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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 concentra-
tions 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 concentra-
tions at the respective sites for the more recent data ranged from 0.05 ppb at
Denver and  Pittsburgh  to 0.7 ppb mt  Los Angeles in 1979  (Singh et a!., 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 concentra-
tions by a factor of 3 to 4.
     The concentrations  of  H^O/j 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 HpO? in ambient air, even in the high-oxidant atmosphere of the
Los Angeles area.   (The limit of detection for a 1-ktn-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).
1.4.6.2  Patterns.  The patterns  of formic acid  (HCOOH),  PAN, PPN, and ^9
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 I-LQo (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/03  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.
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     Indoor-outdoor data on  PAN  are limited to one report (Thompson et a"!.,
1973), which confirms  the  pattern to be expected from the known chemistry of
PAN; that is,  it  persists  longer indoors than  ozone.   Data  are lacking on
indoor-outdoor ratios for the other non-ozone oxidants.

1.4.7  RelationshipBetweenOzone and Other Photochemical Qxidants
     The relationship  between  ozone concentrations and the concentrations of
PAN, PPN, tiyOy, 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 concentra-
tions 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 potentially  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  also result in the  control of
the other four oxidants.
     Control!ed-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 locations 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

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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
are 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,
HgOg, 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 docu-
ment.
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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 CL  injury.   The effects of 03 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 03 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  03 diffuses  from the  ambient
air into the leaf through  the  stomata,  which can  exert some control  on 0-
uptake, to  the  active sites within the  leaf.  Ozone injury will  not occur if
(1) the rate of  0» uptake  is low  enough  that the plant can detoxify or metab-
olize  0-, 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 SO,  (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, will  not  limit
plant  growth if the process impacted by u\ is  not or does not become rate-
limiting.   This  implies that not  all effects of  03 on plants are reflected in
growth  or   yield  reductions.   These  conditions  also  suggest that there  are
combinations of 03 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 0, are present.
The occurrence of injury  indicates that additional  studies should be conducted
in areas  where  vegetation shows foliar injury to  assess the risk of  0- to
vegetation and to determine if the intended use or value of the plants is being
impaired.

1.5.1  Linn ting Values of Plant Response to Ozone
     Several approaches  have  been used to estimate the 0« 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 0~ concentrations and exposure
durations that would induce specific amounts of visible injury involves exposing
plants to a range of 03 concentrations and exposure durations, and then evalua-
ting 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 03 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         5 OR 20 PERCENT INJURY TO VEGETATION
                       GROWN UNDER SENSITIVE CONDITIONS3
                                     (ppm)
Ozone concentrations that may produce
Exposure
time, hr
0.

1.

2.

4.

8.
5

0

0

0

0
Sensitive plants
0.
(0.
0.
(0.
0.
(0.
0.
(0.
0.
35 -
45 -
15 -
20 -
09 -
12 -
04 -
10 -
02 -
0.50
0.60)
0.25
0.35)
0.15
0.25)
0.09
0.15)
0.04
Intermediate
0.
(0.
0.
(0.
0.
(0.
0.
(0.
0.
55 -
65 -
25 -
35 -
15 -
25 -
10 -
15 -
07 -
0.
0.
0.
0.
0.
0.
0.
0.
0.
plants
70
85)
40
55)
25
35)
15
30)
12
5% (20%)
injury:
Less
sensitive plants
£0.

SO.

W.

£0.

£0.
70 (0.

40 (0.

30 (0.

25 (0.

20 (0.
85)

55)

40)

35)

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 concen-
trations 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~ on crop yield or  intended use.
     The concept of limiting  values also was used to estimate the 0~ concen-
trations 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~ 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 0,  concentration of  0.05 ppm  for several  hours  per  day for exposure
periods greater than  16  days.  At 10 days the 0,, 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~
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 0,  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 field,  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 03  (Heck  et  a!., 1982).   The primary  objectives of
NCLAN were:

     1.   To define the relationships between yields of major agricultural
          crops and 03 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 Oq>
     3.   To advance  understandng of the cause and effect relationships that
          determine crop responses to pollutant exposures.
                                   1-58

-------
    1.0
       -I  I    III
                            1      I    II  I  1111
E
a
a.


O
oc


Ul
o

O
O
ui

O
N
O
    0.1
   0.01
—  \    44* 19OM8 *45


                DO17 Q31


                1514  30   59
         40*  010  ft)   •

          \  1213     41    AC
           \     26       *8
                     CD 29
                                      21Q  11D
                                    146       •48-52
                                              ,10
              VO24

               \
                           39
7QD20


 • 42430D9


   5«   33

      54 «• 55, 56

           3*
                                                        58
                      \
                                                      57
                                            53
            EXPOSURE, hr/day

              A < 1.99

              D   2 TO 3.99

              O   4 TO 5.99

              • > 6

            NOS. = REF. NOS. ON TABLE 11-4
                  ll
                             I      I    I   II  I  I  I I
                8  10
                            20        40    60  80 100


                             EXPOSURE PERIOD, days
                                                    200
                                 400
           Figure 1-3. Relationship between ozone concentration,
           exposure duration, and reduction in plant growth or yield (see
           Table 6-18; also U.S. EPA, 1978).


           Source: U.S. Environmental Protection Agency (1978).
                                   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 CL concentrations  and sufficient repli-
cation to permit the  development of exposure-response models.  In the NCLAN
studies, plants were  exposed to a range of 0, concentrations.   Chambers  were
supplied with either charcoal-filtered  air  (control), ambient air, or ambient
air supplemented with 0- to provide concentrations three or four levels greater
than ambient.  Consequently,  the CL exposures were coupled to the ambient 03
level; days  with the highest  ambient CL  were also the  same  days  when the
highest concentrations  occurred in  a specific treatment  in a chamber.  As the
ambient 03 varied  from  day-to-day,  the base to which additional 03 was added
also varied.  This  coupling of the 0.,  exposures  to the ambient environment
means that high  03 concentrations occurred in the chambers when the environ-
mental and air  chemistry  conditions,  in the ambient air, were  conducive for
producing elevated  ambient 0»  levels.   The plant  response data  have been
analyzed using regression approaches.   The exposures were typically character-
ized by a 7-hr  (9:00 a.m. to  4:00 p.m.) seasonal mean 03 concentration.  This
is the time period when 0,, was added to the exposure chambers.
                         »5

1.5.3  Estimates ofOzone-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 composi-
tion, 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 injury 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 limiting 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 0,, 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 analyze the  data:   (1) studies that
developed predictive equations relating 03 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, 03 was
added to either charcoal-filtered  or  ambient air to  create  a  range  of 03
concentrations.   In  summarizing  the data, 0~-induced yield loss  was  derived
from a comparison  of the performance of the plants in charcoal-filtered air,
although other reference concentrations  have been used.  Various regression
techniques  have  been used to derive exposure-response functions.   The use of
regression  approaches  permits  the estimation of the CL 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- 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,  concen-
tration.  Both approaches have been  used  to  summarize  the data on crop responses
to 03  using the  Weibull function (Raw!ings  and  Cure,  1985).   As an  example of
response, the 0~ 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, concentration exceeded
0.04  to  0.05 ppm.    Concentrations  of  0.028 to 0.033  ppm were  predicted  to
                                    1-61

-------
    6000
   6OOO
19
.C
O
LU
2  3000
w
   2000
   1000
W
                    SOYBEAN (DAVIS)
                    RALEIGH. 1981 AND 1 982
  1981(Ol
  y " ES93'1'
                 I
           _L
                         °-872
                         _L
J_
        0  0.02 0.04 0.06 0.08 0.1  0.12 0.14

             Oa CONCENTRATION, ppm
   6000
   BOOO
S 4000
O
ui
O
ui
   3000
   2000
   1000
                             WHEAT (ABE)
                             ARGONNE,
                             1982 AND 19S3
           1§82(O)
            1983 (A)

            y = B873-«V°'10B»14'4
        0  0.020.040.060.080,1 0.120.14
                                         6000
                                                   6000
                                       o

                                       I
                                                   4000
                                          3000
                                                   2000
1000
                       fBjV  SOYBEAN (WILLIAMS)
                         * XBELTSVIIIF un ioni
                                                               BELTSVILLE, MD, 1981 AND 1982
                                                             1981JO)
                                                             1982(A|
                                                                              I
                                                                                   I
                                              0 0.020.040.060,080.1  0.120.14

                                                    O3 CONC5ENTRATION. ppm


                                            6000
                                                      5000
                                          * 4000
                                          O
                                          ui
                                            3000
                                            2000
                                            1000
                                                   (D)
                                                              WHEAT (ARTHUR 71)
                                                              ARGONNE, 1982 AND 1883
                                                     1982(0)
                                                     y = 4B13-(0,/0.146)2-BB

                                                  -  1983 |A|
                                                 0  0.02 0.04 0.06 0.08 0.1 0,12 0.14
             O3 CONCENTRATION, ppm                            Oa CONCENTRATION, ppm
           Figure 1 -4. Examples of the effects of ozone on the yield of soybean and wheat
           cultivars. The O3 concentrations are expressed as 7-hr seasonal mean concentrations.
           The cultivars were selected as examples of O3 effects and of year-to-year variations in
           plant response to O3.

           Source: Soybean data from Hecket al. (1984); wheat data from Kress etal. C1985).
                                          1-62

-------
    6000


    5500


    5000


|   4500

3

!g   4000
Q
UJ
UJ
V)   3500
Q
z

£   3000
3

    2500


    2000


    1500
    (A)
COTTON (SJ-2)
SHAFFER. CA. 1981 AND 1982
                 1981 (0)
                  = 6546-<°3/0.199)1-228
                    1982(A)
0 0.02 0.04 0.06 0.08 0.1 0.12 0.14 0.16 0.18 0.2

      O3 CONCENTRATION, ppm
     34

     33

     32

     31

S    30
*a
o    29

>    28


I    -

     26

     25

     24

     23
n TOMATO (MURIETTA)
  TRACV. CA, 1981 AND 1982
                                                     1981 (O)
                                                      = 329-(0,/0.142)3-807

                                                              \
                                                     1982(A)
                                                     y = 32.3-l3-06
                                                        I     t    II    I    111     I
                                       0  0.02  0.04  0.06 0.08  0.1  0.12  0.14 0.16

                                               O3 CONCENTRATION, ppm
                 a.
                 o>
                 UJ
                 SE
                 S
                 O
         16

         15

         14

         13

         12

         11

         10

          9

          8

          7

          6

          5

          4

          3

          2

          1
                                         TURNIP (TOKYO CROSS)
                                         RALEIGH, 1979 AND 1980
                                           1980(A)
                                           y=16.25-«V0.094)3-94
                             I
                                                     I
                                                         I
                         0   0.02  0.04 0.06  0.08  0.1  0.12  0.14  0.16

                               O3 CONCENTRATION, ppm
    Figure 1 -5. Examples of the effects of ozone on the yield of cotton, tomato, and
    turnip. The O3 concentrations are expressed as 7-hr seasonal mean concentrations.
    The species were selected as examples of O3 effects and of year-to-year variations in
    plant response to O3.

    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 PREDICTED
  TO OCCUR AT 7-hr SEASONAL MEAN OZONE CONCENTRATIONS OF 0.40 and 0.06 ppm
03 concentrations, ppm,


Species
Legume crops
Soybean, Corsoy
Soybean , Davis (81)
Soybean, Davis (CA-82)
Soybean, Davis (PA-82)
Soybean, Essex
Soybean, Forrest
Soybean, Williams
Soybean, Hodgson
Bean, Kidney
Peanut, NC-6
Grain crops
Wheat, Abe
Wheat, Arthur 71
Wheat, Roland
Wheat, Von a
Wheat, Blueboy II
Wheat, Coker 47-27
Wheat, Holly
Wheat, Oasis
Corn, PAG 397
Corn, Pioneer 3780
Corn, Coker 16
Sorghum, DeKalb-28
Barley, Poco
Fiber crops
Cotton, Acala SJ-2 (81)
Cotton, Acala SJ-2 (82)
Cotton, Stone vi lie
Horticultural crops
Tomato, Murrieta (81)
Tomato, Murrieta (82)
Lettuce, Empire
Spinach, America
Spinach, Hybrid
Spinach, Viroflay
Spinach, Winter Bloom
Turnip, Just Right
Turnip, Pur Top W. G.
Turnip, Shogoin
Turnip, Tokyo Cross
predicted to
yield losses
10%

0.048
0.038
0.048
0.059
0.048
0.076
0.039
0.032
0.033
0.046

0.059
0.056
0.039
0.028
0.088
0.064
0.099
0.093
0.095
0.075
0.133
0.108
0.121

0.044
0.032
0.047

0.079
0.040
0.053
0.046
0.043
0.048
0. 049
0.043
0.040
0.036
0.053
aThe yield losses are derived from Weibull
cause
of;
30%

0.082
0.071
0.081
0.081
0.099
0.118
0.093
0.066
0.063
0.073

0.095
0.094
0.067'
0.041
0.127
0.107
0.127
0.135
0.126
0.111
0.175
0.186
0.161

0.096
0.055
0.075

0.108
0.059
0.075
0.082
0.082
0.080
0.080
0.064
0.064
0.060
0.072
equations
Percent yield
to occur at
losses predicted
7-hr seasonal
mean Os concentration of;
0.04 ppm

6.4
11.5
6.4
2.0
7.2
1.7
10.4
15.4
14.9
6.4

3.3
4.1
10.3
28.8
0.5
2.2
0.0
0.4
0.3
1.4
0.0
0.0
0.0

8.3
16.1 '
4.6

0.8
10.3
0.0
6.8
2.6
6.0
5.8
7.7
10.1
13.0
3.3
and are based
0.06 ppm

16.6
24.1
16.5
10.4
14.3
5.3
18.1
18.4
28
19.4

10.4
11.7
24.5
51.2
2.8
8.4
0.9
2.4
1.5
5.1
0.3
2.7
0.5

16.2
35.1
16.2

3.7
,31.2
16.8
17.2
9.2
16.7
16.5
24.9
26.5
29.7
15.6
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 0, 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 03 concentrations predicted to
cause  a  10 percent yield  loss  (Table  1-5)  is  given in  Figure  1-6  to  help
illustrate the  range of concentrations  and  their relative frequency of occur-
rence.   The data  in Figure 1-6 are based on  37 species or cultivar yield-
response functions developed from studies in open-top field 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.il  percent of the species  or  cultivars would
display a  10  percent  loss  at 7-hr  seasonal  mean  concentrations below 0.035
ppnij suggesting that these plant types  are  very sensitive to On-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~.  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 0^, 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 0,.
     Several exposure-response  models,  ranging from simple linear to complex
nonlinear  models,  have  been  used to describe  the  relationship  between plant
yield  and 0- exposure.   When exposure-response models  are used, it is important
for the fitted equations not to show systematic deviation from the data points
                                            2
and for  the  coefficient of determination (R )  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

-------
9-
| o
3
e
OT 7 —
CC
1 6~
CC S~
o
05
O
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to 3—
0.
o
CC 2-
0 *
1-
0-


10.8%
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10.8%
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13.S%
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21,6%
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0



                                               I
<0.035         |     0.040-0.044     |      0.050-0.059     I      _>0.080
          0.035-0.039           0.045-0:049          0.060-0.079
                          7-hr SEASONAL MEAN
                      OZONE CONCENTRATIONS, ppm
 Figure 1 -6. Number and percentage of 37 crop species or cuitivars 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

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                                                                       o
the  equations  have  moderate-to-high coefficients  of  determination (R ). ,
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.s  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~.
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 03  on  crop yield.   These  studies
were designed  to  test  whether specific 0., 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, concentration that signi-
ficantly 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 Q~  concentrations of  0.10 ppm  (frequently the lowest concentration used
in  the  studies)  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 CL  concentration was required to cause an effect than
was estimated  from the regression studies, it should be noted that the concen-
trations derived  from  the  regression studies were based on a 10  percent yield
loss,.while 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.    Chemical
protectants (antioxidants) have been used to estimate the impact of ambient 0,,
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 chemical
protectants are  used,  care must be  used  in interpreting the data because the
chemical itself  may alter  plant growth.  The  chemical  may  not be effective
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
                                   1-67

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TABLE 1-6.  OZONE CONCENTRATIONS AT WHICH SIGNIFICANT YIELD LOSSES HAVE BEEN NOTED FOR
       A VARIETY OF PLANT SPECIES EXPOSED UNDER VARIOUS EXPERIMENTAL CONDITIONS
Plant species
Alfalfa
Alfalfa
Pasture grass
Ladino clover
Soybean
Sweet corn
Sweet corn
Wheat
Radish
Beet
Potato

Pepper
Cotton
Carnation
Coleus
Begonia

Ponderosa pine
Western white
pine
Loblolly pine
Pitch pine
Poplar
Hybrid poplar
Hybrid poplar
Red maple
American
sycamore
Sweetgum
White ash
Green ash
Willow oak
Sugar maple
Exposure duration
7 hr/day, 70 days
2 hr/day, 21 day
4 hr/day, 5 days/wk, 5 wk
6 hr/day, 5 days
6 hr/day, 133 days
6 hr/day, 64 days
3 hr/day, 3 days/wk, 8 wk
4 hr/day, 7 day
3 hr
2 hr/day, 38 days
3 hr/day, every 2 wk,
120 days
3 hr/day, 3 days/wk, 11 wk
6 hr/day, 2 days/wk, 13 wk
24 hr/day, 12 days
2 hr
4 hr/day, once every 6 days
for a total of 4 times
6 hr/day, 126 days
6 hr/days, 126 days

6 hr/day, 28 days
6 hr/day, 28 days
12 hr/day, 5 mo
12 hr/day, 102 days
8 hr/day, 5 day/wk, 6 wk
8 hr/day, 6 wk
6 hr/day, 28 days

6 hr/day, 28 days
6 hr/day, 28 days
6 hr/day, 28 days
6 hr/day, 28 days
6 hr/day, 28 days
Yield reduction,
% of control
51, top dry wt
16, top dry.wt
20, top dry wt
20, shoot dry wt
55, seed wt/plant
45, seed wt/plant
13, ear fresh wt
30, seed yield
33, root dry wt
40, storage root dry wt
25, tuber wt

19, fruit dry wt
62, fiber dry wt
74, no. of flower buds
20, flower no.
55, flower wt

21, stem dry wt
9, stem dry wt

18, height growth
13, height growth
+1333, leaf abscission
58, height growth
50, shoot dry wt
37, height growth
9, height growth

29, height growth
17, total dry wt
24, height growth
19, height growth
12, height growth
Q3 concentration,
pptn
0.10
0.10
0.09
0.10
0.10
0.10
0.20
0.20
0.25
0.20
0.20

0.12
0.25
0.05-0.09
0.20
0.25

0.10
0.10

0.05
0.10
0.041
0,15
0.15
0.25
0.05

0.10
0.15
0.10
0.15
0.15
Reference
Neely et al. (1977)
Hoffman et al. (1975)
Horsman et al. (1980)
Blum et al. (1982)
Heagle et al. (1974)
Heagle et al. (1972)
Oshima (1973)
Shannon and Mulchi (1974)
Adedipe and Ormrod (1974)
Ogata and Haas (1973)
Pell et al. (1980)

Bennett et al. (1979)
Oshinia et al. (1979)
Feder and Campbell (1968)
Adedipe et al. (1972)
Reinert and Nelson (1979)

Wilhour and Neely (1977)
Wilhour and Neely (1977)

Wilhour and Neely (1977)
Wilhour and Neely (1977)
Wilhour and Neely (1977)
Patton (1981)
Patton (1981)
Dochinger and Townsend (1979)
Kress and Skelly (1982)

Kress and Skelly (1982)
Kress and Skelly (1982)
Kress and Skelly (1982)
Kress and Skelly (1982)
Kress and Skelly (1982)

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an objective method  of  assessing the effects of CU 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
(Table 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  fromAmbient  Exposures.    A  number  of
research studies  have demonstrated that ambient 0- 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~) 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 yield (Table
1-8).   Over several  years,  bean yields varied from a 5 percent increase to a
22 percent  decrease  in  response to 0, 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~ 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).  Field  studies in  the San Bernardino National Forest
showed that during the last 30 years ambient 0- 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).  Calcula-
tions  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  YieldLoss  Summary.  Several  general  conclusions can  be  drawn from
the various approaches  used to estimate  crop  yield loss.   The data  from the
comparisons of  crop yield in charcoal-filtered and  unfiltered air (ambient
exposures) clearly show that  ambient levels  of G~ 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 0,  occurrences greater than 0.08 ppm.
                                   1-69

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                                       TABLE 1-7.  EFFECTS OF OZONE ON CROP YIELD   .
                                    AS DETERMINED BY THE USE OF CHEMICAL PROTECTANTSC
 I

o
                  Species
               Beans (green)
\ield reduction,
 % of control
   03 exposure,
       ppm
     Reference
      41
Onion
Tomato
Bean (dry)
Tobacco
Potato
38
30
24
18
36
>0.08 for total
of 27 hr over
3.5 months

>0.08 on 5 days out
of 48

>0.08 on 15 days '
over 3 months

>0.08 on 11 days
(total of 34 hr)
over 3 months

>0.08 on 14 days
during the summer

>0.08 ppm on 18 days
(total of 68 hr)
over 3 months
               Potato
      25
Manning et al. (1974)
                                                                          Wukasch and Hofstra (1977b)
                                                                          Legassicke and Ormrod (1981)
                                                                          Temple and Bisessar (1979)
                                                                          Bisessar and Palmer (1984)
                                                                          Bisessar (1982)
                        Clarke et al. (1983)
               aAll the  species were treated with  the  antioxidant, EDU, except the bean study by
                Manning  et al. (1974) which used the systemic fungicide, benomyl.

                Yield  reduction was determined  by  comparing the yields of plants treated with
                chemical  protectants (control)  to  those  that were not treated.

               GThis study was run over 2 years when the 03 doses were 65 and 110 ppm-hr,
                respectively, but the yield loss was similar both years.

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                                 TABLE 1-8,   EFFECTS Of AMBIENT OXIDANTS  ON  YIELD  OF SELECTED CROPS
Plant species
Tomato
(Fireball 861 VR)
Bean
(Tendergreen)
os
concentration,
ppm
0.035
(0.017-0.072)
0.041
(0.017-0.090)
Exposure duration
99 day average
(6:00 a.m. - 9:00 p.m.)
43 day average
(6:00 a.m. - 9:00 p.m.)
Yield, %
reduction
from control
33, fruit fresh
wt
26, pod fresh wt
Location
of study
New York
Reference
MacLean and
Schneider (1976)
Snap bean (3 cultivars:
  Astro, BBL 274,  BBL
  290)

Soybean (4 cultivars:
  Cutler, York,  Clark,
  Dare)
Forbs, grasses,  sedges
Sweet corn
  (Bonanza)
 0.042
>0.05
 0.052


 0.051


 0.035



>0.08
3 mo average
(9:00 a.m.  - 8:00 p.m.)
31% of hr between
8:00 a.m. - 10:00 p.m.
from late June to mid-
September over three
summers; 5% of the time
the concentration was
>0.08 ppm

1979, 8 hr/day average
(10:00 a.m. - 6:00 p.m.),
April-September
1980, 8 hr/day average
(10:00 a.m. - 6:00 p.m.),
April-September
1981, 8 hr/day average
(10:00 a.m. - 6:00 p.m.),
April-September

58% of hr (6:00 a.m.
 9:00 p.m.),
 1 July-6 September
1, pod wt
20, seed wt
32, total above-
 ground biomas

20, total above-
 ground biomass

21, total above-
 ground biomass
9, ear fresh wt
Mary!and
Maryland
Virginia


Virginia
California
Heggestad and
Bennett (1981)
Howell et al.
(1979); Howe11
and Rose (1980)
Duchelle et al.
(1983)
Thompson et al.
(1976a)
  (Monarch Advance)
>0.08
                               28, ear fresh wt

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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, concentra-
tion (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/culti-
vars tested were predicted to display a 10 percent yield loss at 7-hr seasonal
mean 0- 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-  effects, although  a  specific value cannot be  derived from the
discrete treatment studies.

1.5.4  Effectson CropQua!ity
     Based on  results  of the few studies  that  have  been conducted, 03 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 On-induced alterations in quality are decreased oil
in soybean seeds  (Howell  and Rose,  1980;  Kress  and Miller, 1983);  decreased
p-carotene, vitamin C,  and carbohydrates in alfalfa (Thompson et al., 1976b;
Neely et al.s  1977);  and increased  reducing sugars that  are  associated with
undesirable darkening  when  potatoes are used to make  potato  chips (Pell et
al., 1980).

1.5.5  Statistics Used to Characterize Ozone Exposures
     The characterization and representation  of plant exposures to 0~  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 mean  0,,  concentra-
tions, although  various  averaging times have been used.   Some studies have
also  used  cumulative 03  dose.  The difficulty of selecting  an  appropriate
statistic to  characterize plant  exposure has been summarized by Heagle and
Heck (1980).   Ambient  and experimental 03 exposures  have been presented as
                                   1-72

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seasonal, monthly, weekly, or daily means; peak hourly means; number of hours
above a  selected concentration; or the number of hours above selected concen-
tration  intervals.   None of these  statistics adequately  characterize  the
relationships among  03 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-> are equally effec-
tive in  causing plant responses and (2) minimizes  the  contributions  of the
peak concentrations  to the resonse.  The  mean  treats low-level,  long-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 multiplied 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~
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 03 and SCL on soybeans.   The "impact (I)" is calculated similarly
to total  dose, except the concentration  is raised to an exponent greater  than
          W
one  (I = C   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~ 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 equally
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

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     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~ concentration was substantially more important than exposure
duration  in  causing  foliar  injury  (Tonneijck, 1984).   In  beans,  foliar  injury
                                                          2
occurred when  the  internal  0~ flux exceeded 115  umoles/m 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
Og 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~  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 Heagle,  1982),  tobacco (Heagle and
Heck, 1974), and  bean (Runeckles and Rosen, 1977) showed that plants exposed
to a low level of 03 for a few days became more sensitive to subsequent 0-
exposures.   In  studies with tobacco, Mukammal  (1965)  showed  that a  high Oj
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 03 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, concentration for the same total  exposure
period.   Walmsley et al.  (1980) continuously exposed radishes to 03 for several
weeks and found that the plants acquired  some  0~ 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 Og.  The newer leaves also displayed a slower
rate of senescence.   The observations by  Elkiey  and Ormrod (1981) that  the 0,
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 G*3  exposure  is also  important;  i.e. whether  the exposure  is  at a  constant
or  variable  concentration.    Musselman  et al.  (1983)  recently  showed that
constant  concentrations  of  03 caused the  same types  of plant  responses  as
                                    1-74

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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»  in open-top exposure
                                                    **»
chambers showed that significant yield reductions occurred when the maximum CL
                                                                             «5
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~ exposure profiles that gave the equivalent
total 0~ 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 concentra-
tion; 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 SOg  also  showed that plants exposed to variable  concentrations
exhibited a greater plant response than those exposed to a constant concentra-
tion (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 foliar 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  loss  (Heagle et al.,  1974; Oshima  et al.s  1975).   The relative
sensitivities  of  two potato cultivars were reversed  when judged by  foliar
injury versus  yield reductions (Pell et  al.,  1980).   In field corn, foliar
injury occurred at a lower 0»  concentration than  yield reductions; but as  the
03  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 0~-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 uptake, assimila-
tion, biosynthesis,  and trans!ocation.   An impairment in these processes  may
lead to reduced plant yield if the process  is  limiting.
                                   1-75

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     For plant growth to occur, plants must assimilate C02 and convert it into
organic substances; an  inhibition  in carbon assimilation may be reflected in
plant growth or yield.   In several  species 03 (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 03  (0.12 ppm  for  2
hr)  inhibited  an enzyme  that catalyzes the assimilation  of  CO,,  (Pell  and
Pearson, 1983).
     Ozone, in addition to decreasing  the  total  amount of  COy  that is assimi-
lated, alters that pattern by which the reduced amount of assimilate is parti-
tioned throughout the plant.   There is generally less photosynthate translo-
cated 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,  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 0, impairs the fertilization process in plants.
This  suggestion  has  been  confirmed in tobacco  and corn  studies  using low
concentrations of 0, (0.05 to 0.1.0  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
Oo-induced  yield  reduction  has been attributed.to premature senescence.   The
premature  leaf drop  decreases the  amount  of photosynthate that 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
Oo.  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

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some have  researched  the physiological  basis for  the  influences.  The  para-
meters studied  include  environmental  factors, biological factors, and inter-
actions with other air pollutants.
1.5.8,1  Environmental Conditions.  Environmental conditions before and during
plant exposure are more influential 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.,  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 tempera-
           tures, 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 CL at high
           humidity than at  low humidity.  It  is  generally accepted that plants
           in  the  eastern United  States  are injured by lower concentrations  of
           CL .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 0-, (U.S. Environmental Protec-
           tion  Agency,  1978).  The  reduced 03 sensitivity is apparently related
           to  stomatal closure, which reduces 0~ uptake (U.S.  Environmental
           Protection  Agency,  1978; Olszyk and Tibbitts, 1981; Tingey et  a!.,
           1982).  Water stress does not confer  a  permanent tolerance to 0~;

                                    1-77

-------
          once the water  stress  has been alleviated, the plants regain their
          sensitivity to 03 (Tingey et a!., 1982).

1.5.8.2  Interaction with Plant Diseases.  Ozone can affect the development of
disease in plant populations.   Laboratory evidence suggests that 0., (at ambient
concentrations or greater  for 4 hr or more) inhibits infection by pathogens
and subsequent disease development (Laurence, 1981; Heagle, 1982;  U.S.  Environ-
mental Protection Agency, 1978).   Increases, however, in diseases  from "stress
pathogens"  have  been noted.   For example, plants exposed to  03  were  more
readily injured  by  Botrytis than plants not exposed to 03 (Manning et a!.,
1970a,b; Wukasch and Hofstra, 1977a,b; Bisessar, 1982).   Both field and labora-
tory studies have confirmed that the roots and cut stumps of 03-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;  Miller et a!.,  1982).  Studies in the San  Bernardino
National Forest  showed  that 0.,-injured trees were predisposed  to attack by
bark beetles  and that  fewer bark beetles were required to kill an 0~-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 0- with  SOp.   They showed that Bel W-3 tobacco plants exposed to CU (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 SOp on plant response to
0-3 at ambient  and higher concentrations in several  plant  species:   soybean
(Heagle et al., 19835; Reich and Amundson,  1984), beans (Qshima, 1978; Heggestad
and Bennett, 1981), and potatoes (Foster et al., 1983).  In these studies, G3
altered plant yield but  SCL had no significant  effect and did not interact
with On  to  reduce plant  yield unless the SO,, exposure concentrations and
frequency of occurrence were  much  greater than  the  concentrations  and fre-
quencies 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 03 and SQp 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).  Co-
occurrence 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_
and SOp)  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 03 when combined with
pollutants other  than SOp,  and no clear  trend  is available.  Preliminary
studies using three-pollutant mixtures (03, SOp,  NQp) showed that the additions
of SOp  and NOp  (at low concentrations)  caused a  greater growth  reduction  than
DO alone.

1.5.9  Economic Assessment of Effects of Ozone on Agriculture
     Evidence  from the plant science literature clearly demonstrates that fl-
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 welfare.  The plausibility of this premise has resulted
in numerous  attempts  to  assess,  in monetary  terms, the losses from ambient 0~
or the  benefits of Q~ control  to agriculture.  Many  of these  assessments  have
been  performed since publication  of the  1978  03 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
      *s
assessments is not  appropriate  here,  it is  instructive to highlight certain
key issues.   First,  the  evidence on crop response  to  03  should reflect how
crop yields  will  respond  under actual field conditions.  Second,  the air
quality data  used to frame current or  hypothetical  effects  of CL on  crops
                                                                 O
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™
air quality;  and (2) ideally, should accurately reflect institutional  considera-
tions, such as regulatory programs, that may result in  market distortions.
     The assessments of 0^ damages to  agriculture  found in the literature
display a  range of  procedures for  calculating  economic  losses,  from  simple
monetary calculation procedures  to  more complex economic assessment methodol-
ogies.  The  simple   procedures  calculate monetary  effects  by multiplying
predicted  yield or  production changes  resulting from  exposure to 0.,  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 proce-
dure may be  badly  biased, leading to potentially incorrect policy decisions.
     Most of the post-1978 economic assessments focus on 03 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,
                                   1-80

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                                      TABLE 1-9.   SUMMARY OF ESTIMATES OF  REGIONAL  ECONOMIC CONSEQUENCES OF OZONE  POLLUTION
   Reference and
   study region
                    Crops
Annual benefits
  of control,
  $ million
                                                               Evaluation of critical data and assumptions
 Plant response data
Aeronetric data
Economic model data
Additional comments
   Adams et al.   12 annual crops:     $45 (in 1976
   (1982);
   Southern
   California
               beans,  broccoli,
               cantaloupes,
               carrots,  cauli-
               flower, celery,
               lettuce,  onions,
               potatoes, tomatoes
               cotton, and sugar
               beets.
  dollars)
Inadequate; uses Larsen-   Adequate;  exposure
Heck (1976) foliar injury  measured as cumu-
models converted to yield lative seasonal
losses.                     exposure in
                           excess of Cali-
                           fornia standard
                           (0.08 ppn), from
                           hourly data col-
                           lected for sites
                           closest to produc-
                           tion regions.
                    Adequate; a price endo-
                    genous mathematical
                   (quadratic) programming
                    model reflecting agro-
                    nomic, environmental,
                    and economic conditions
                    in 1976.
                          Economic effect measured as a
                          change in economic surplus (sum
                          of consumers and producers'
                          surpluses) between base case
                          (actual Oa levels in 1976)'
                          aftd economic surplus that
                          would be realize.d if all
                          regions were in compliance with
                          1971 photochemical oxidant
                          standard of 0.08 ppm.
 i
00
Lueng et al.    9 crops:  lemons,     $103 (in 1975
(1982);        oranges (Valencia   dollars)
Southern       and Navel),  straw-
California     berry,  tomato,
               alfalfa,  avocado,
               lettuce,  and celery.
                   Inadequate;  03-yield
                   response functions
                   estimated from second-
                   ary data on  crop  yields.
                           Adequate for some
                           regions; exposure
                           measured in aver-
                           age monthly con-
                           centration in ppm
                           for 12 hr period
                           (7:00 a.m.  to
                           7:00 p.m.).   Data
                           from 61 Calfornia
                           Air Resources
                           Board monitoring
                           sites.
                    Adequate on demand side;
                    economic model is
                    composed of linear
                    supply and demand
                    curves for each crop
                    estimated with data
                    from 1958-1977, but
                    ignores producer-level
                    adjustments.
                          Economic effect is measured as
                          a change in economic surplus
                          between base case (1975) and a
                          clean air environnent reflecting
                          zero 03.
Howitt et al. 13 crops: alfalfa, From $35 (bene-
(1984a,b); barley, beans, fit of control
California celery, corn, to 0.04 ppm) to
cotton, grain sor- $117 (loss for
ghum, lettuce, Increase to
onions, potatoes, 0.08 ppm) (in
rice, tomatoes, 1978 dollars).
and wheat.





Adequate for some crops; Adequate; Califor- Adequate; economic model Economic effects measured as
most response functions nia Air Resources similar to Adams et al. changes in economic surplus
derived from NCLAN data Board data for (1982) but includes some across three 03 changes fron
through 1982. Surrogate monitoring sites perennial crops and re- 1978 actual levels. These
responses used for celery, closest to rural fleets 1978 economic and include changes in ambient 03
onions, rice and potatoes production areas. technical environment.
are questionable. Exposure measured
as the seasonal
7-hr average in
each production
area for compati-
bility with NCLAN
exposure.
to 0.04, 0.05, and 0.08 ppm
across all regions.







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TABLE 1-9 (cont'd).  SUMMARY OF ESTIMATES OF REGIONAL ECONOMIC CONSEQUENCES OF OZONE POLLUTION

Reference and
study region
Rowe et al.
(1984);
San Joaquin
Valley In
California






h- '
1
00
J^J
Adaas and
MeCarl
(1985);
Corn Belt














Annual benefits
of control ,
Crops $ million
14 annual and $43 to $117
perennial crops: depending on
alfalfa, barley, degree of
beans, carrots, control,
corn, cotton, nteasured in
grain sorghum, 1978 dollars.
grass hay, grapes,
pasture, potatoes,
saf flower,
tomatoes and
wheat.


3 crops: corn, $668 (in 1980
soybeans, and dollars)
wheat.



















Evaluation of critical data and assumptions3
Plant response data
Adequate for $om crops;
response functions based
on both experimental and
secondary data, Host
crops from NCLAN data.
Responses for the remain-
ing crops were based on
surrogate responses of
similar crops in the
data set.



Adequate; 03 yield
response information
from NCLAN "for 3 yr
(1980-1982). Yield
adjustments estimated
from Weibull response
models.











Aerometric data
Adequate; 4 expo-
sure levels were
tested. The aver-
age hourly concen-
tration was used
in roost functions
to predict changes.
All data were froi
California Air
Resources Board
monitoring sites in
predominantly rural
areas.
Adequate except
for linkage of
7-hr seasonal
mean to hourly
standards. Data
are interpolated
from SAROAD
monitoring sites
by Krigingb
procedure ,
measured as
1980 seasonal
7-hr average.
Regulatory
analysis assumes
that 03 is log-
normally
distributed.
Economic model data
Adequate; sane as in
Howitt et al.
(1984a,b).










Adequate; economic
estimates are generated
by a mathematical pro-
gramming model of U.S.
agriculture reflecting
1980 conditions. Farm-
level response is
portrayed by 12
individual "represen-
tative" farm models
to generate supply
adjustments used in
the national-level
model .




Additional comments
Economic effects Measured as the
change in economic surplus be-
tween the 1978 base case and three
increasingly stringent control
scenarios: (1) a 50% reduction in
in no. of hr >0.10 ppm; (2)
meeting the current standard of
0.10 ppm; and (3) meeting an 03
standard of 0.08 ppm.




Economic estimates represent
changes in economic surplus
(sum of consumers' and pro-
ducers' surpluses) between
current (1980) 03 levels and
increases and decreases in
ambient 03 levels. Reduction
to a uniform ambient level of
0,04 ppm across all regions
results in benefits of $668
million.








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                                  TABLE 1-9 (cont'd).  SUMMARY OF ESTIMATES OF REGIONAL ECONOMIC CONSEQUENCES OF OZONE POLLUTION
 i
00
CO

Reference and
study region Crops
Hjelde et al, 3 crops: corn,
(1984); soybeans, and
Illinois wheat.











Page et al. 3 crops: corn,
(1982); soybeans and
Ohio River wheat.
Basin









Annual benefits
of control ,
$ million
Ranges from
$55 to $220
annually for
period 1976
to 1980.









$7.022 measured
as present
value of pro-
ducer losses
for period
1976 to 2000.
Annual i zed
losses are
approx. $270
in 1976
dollars.






Evaluation of critical data and assumptions3
Plant response data
Adequate when cross*
checked against NCLAN
data; responses are
estimated from secon-
dary (non-experimental)
data on actual farmer
yield, input, and 03
concentrations. Results
are translated into yield
effects and compared to
NCLAN data from Illinois.



Inadequate; crop losses
provided by Loucks and
Armentano (1982);
responses derived by
synthesis of existing
experimental data.




•*


Aerometric data
Adequate; same
Kn'ged data set as
used in Adams and
HcCarl (1985),
except only for
Illinois and
cover 5 yr
(1976-1980).
Exposure is mea-
sured as seasonal
7-hr average to
facilitate compa-
rison with NCLAN
response estimates.
Inadequate; dose
measured as cumu-
lative seasonal
exposure for a
7-hr period
(9:30 a.m. to
4:30 p.m.)
Monitoring sites
at only 4 loca-
tions were used
to characterize
the regional
exposure.
Economic model data
Adequate at producers
level; economic model
consists of a series
of annual relationships
on fanners' profits
These functions).
These functions are
adjusted to represent
changes in 03 (±25X)
for each year. Model
does not include consumer
(demand) effects.


Inadequate; the econo-
mic model consists of
• regional supply curves
for each crop. The
predicted changes in
production between
"clean air" case and
each scenario are used
to shift crop supply
curves. The analysis
ignores price changes
from shifts in supply.

Additional comments
The estimates represent increases
in farmers' profits that could
arise for a 25% reduction in 03
for each year (1976-1980). Years
with higher ambient levels have
highest potential increase in
profits for changes.







Losses are measured as differ-
ences in producer surplus across
the various scenarios. Since
prices are assumed fixed (In
real terms) over the period,
no consumer effects are
measured.







-------
                               TABLE 1-9 (cont'd).   SUMMARY OF ESTIMATES  OF  REGIONAL  ECONOMIC CONSEQUENCES  OF OZONE  POLLUTION
Reference and
study region
Crops
Annual benefits
  of control,
  $ Million
                                           Evaluation of critical  data and assumptions
                                                        Plant response data
Aerometric data
EconoMic node! data
Additional comments
    Benson et al.  4 crops: alfalfa,   $30.5 (measured  Inadequate; but innova-
    (1982);        wheat, corn, and    in 1980 dollars) tive crop loss models
    Minnesota      potatoes.  Cultivar                  estimated using experi-
                  believed to be                       mental yield-03 data
,_,                limited to one per                   from other researchers.
 i                 crop.                                Crop loss modeling
2                                                     includes both chronic
                                                       and espisodic response
                                                       and crop development
                                                       stage as factors in
                                                       yield response, by
                                                       regressing yield on 03
                                                       exposures for various
                                                       time windows, during the
                                                       growing season.
                                                                              Adequate;  air
                                                                              quality  data are
                                                                              for  state  of
                                                                              Minnesota  for
                                                                              1979 and 1980.
                                                                              Exposure measured
                                                                              several  ways but
                                                                              generally  as a
                                                                              daily exposure  sta-
                                                                              tistic reflecting
                                                                              either sun of hourly
                                                                              averages or the mean
                                                                              hourly average.
                                                                               Adequate on demand side;
                                                                               The economic estimates
                                                                               are derived from a
                                                                               comprehensive economic
                                                                               model  calibrated to
                                                                               1980 values.
                                                                                            The economic effect measured
                                                                                            in terms of short-run profit
                                                                                            changes for Minnesota producers.
                                                                                            If yields are assumed to change
                                                                                            only in Minnesota then losses to
                                                                                            Minnesota producers are $30.5
                                                                                            million.  If yields change in
                                                                                            Minnesota and the rest of U.S.,
                                                                                            then producers gain $67 million
                                                                                            as a result of increases in crop
                                                                                            prices.
 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, aerometric, or economic information and models currently available.

 Kriging is a spatial  interpolation procedure that has  been used to generate 03  concentration  data  for  rural  areas in  which  no monitoring sites  have
 been established.   See Heck et al.  (1983b).

-------
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 interdependences
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 level.   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 03 levels on agriculture.
     In the first  of these studies, Kopp et al.  (1984) measured the national
economic effects  of  changes in ambient air 0.,  levels  on the  production 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
03~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., 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

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TABU 1-10.   SWHftRY OF ESTIMATES OF NATIONAL  ECONOMIC CONSEQUENCES OF OZONE POLLUTION

Annual benefits



of control, Evaluation of critical data and assumptions3
Study Crops
Ryan at al. 16 crops: alfalfa,
(1981) beets, broccoli,
cabbage, corn
(sweet and field),
hay, Una beans,
oats, potatoes,
sorghun, soybeans,
spinach, tobacco,
tomatoes, and
wheat.






i — » 	
i Shriner et al. 4 crops: corn,
g (1982) soybeans, wheat,
and peanuts.
Multiple cultivars
of all crops but
peanuts.





Adams and 3 crops; corn,
Crocker (1984) soybeans, and
cotton. Two corn
cultivars, three
soybean, two
cotton.







$ billion Plant response data
$1.747 (in 1980 Inadequate; yield-response
dollars). information derived fron
a synthesis of 5 yield
studies in the literature
prior to 1980. Synthe-
sized response functions
estimated for both chronic
and acute exposures
for six crops. For
the remaining 10 crops
surrogates are used.
Yield changes are based
on reductions in Q3 to
meet 1980 Federal stan-
dard of 0.12 ppm In non-
compliance counties.
$3.0 (in 1978 Adequate; analysis uses
dollars). NCLAN response data for
1980. Functions esti-
mated in linear fora.
Yield changes reflect
difference between 1978
ambient 03 levels of
each county and assumed
background of 0.025 ppm
concentration.

$2.2 (in 1980 Adequate; analysis uses
dollars). NCLAN 03-yield data for
1980 and 1981. Functions
estimated in linear form.
Yield changes measured
between 1980 ambient
levels and an assumed 03
concentration of 0.04 ppm
across all production
regions.



Atroaetric data
Inadequate; dose
measured in sev-
eral ways to
correspond to
underlying
response function.
Qa data derived
froa National
Aeroisetric
Data Bank and
from Lawrence
Berkeley
Laboratory, for
period 1974-1976.


Unknown; exposure
may be measured as
highest 7-hr.
average, rather
than 7-hr NCLAN
average. Rural
ambient concen-
trations for 1978
tconoaic node! data
Inadequate; naive econo-
mic model. Monetary
impact calculated by
multiplying changes in
county production by
crop price in 1980.
Measures impact on
producers only.








Inadequate; same as Ryan
et al. (1981) except
uses 1978 crop prices.





Additional comments
Dollar estimate Is for the 531
counties exceeding the
Federal standard of 0.12 ppm.
This study is essentially an
updated version of Benedict
et al. (1971) reported in 1978
criteria document.









Dollar estimates are for all
counties producing the four
crops. As with Ryan et al.
(1981), estimates are for
for producer level effects
only.


estimated by Kriging0
procedure applied
to SAROAD data.
Adequate; 1980
ambient Q3 levels
estimated by
Kriging of SAROAD
monitoring sites,
translated into a
seasonal 7-hr
average.







Adequate on demand side;
inadequate on modeling
producer behavior; eco-
nomic model consists of
crop demand and supply
curves. Corresponding
price and quantity
adjustments result in
changes in economic
surplus. No producer
level responses
modeled; only measures
aggregate effects.


Economic estimate measured in
terms of changes in consumer
and producer surpluses associated
with the change in 03.










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                                  TABLE 1-10 (cont'd).   SUMMARY OF ESTIMATES OF NATIONAL ECONOMIC CONSEQUENCES OF OZONE POLLUTION
Study
Adams et al.
(1984a)
Annual benefits
of control ,
Crops $ billion
4 crops: corn, $2.4 (in 1980
soybeans, wheat, dollars).
and cotton. Two
cultivars for corn
and cotton, three
for soybeans and
and wheat.
Evaluation of critical data and assumptions3
Plant response data Aerometric data
Adequate; analysis uses Adequate; same
NCLAN 03-yield data for as Adams and
1980 through 1982. Yield Crocker (1984).
changes measured between
1980 ambient levels and
25% reduction in
Oa across all regions.
Functions estimated in
both linear and quadratic
form.
Economic model data
Inadequate producer
model; same as Adams
and Crocker (1984),
except that analysis
examines range of
economic estimates
reflecting variability
in yield predictions
resulting from sample
size and functional
form.
Additional comments
Same as Adams and Crocker (1984).
Linear functions result in higher
yield losses and hence higher
economic loss estimates.
Reported estimate ($2.4 billion)
is for quadratic response
function.
   Kopp et al,
   (1984)
 i
co
5 crops; corn,
soybeans, wheat,
cotton, and
peanuts.  Multiple
cultivars of each
crop except peanuts.
$1.2 (in 1978
dollars).
Adequate; analysis uses
NCLAN Os yield response
data for 1980 through
1982.  Yield losses (for
estimates reported here)
measured as the differ-
ence between ambient 1978
03 and a level assumed to
represent compliance with
an 0.08 ppin standard.
Adequate; same as
Adams and Crocker
(1984) and Adams
et al. (1984b)
but for 1978
growing season.
Adequate; economic model
consists of producer-
level models, by crop,
for numerous production
regions.  Predicted
yield changes are used
to generate supply
shifts for each region/
crop combined with crop
demand relationships
to estimate producer
and consumer surpluses.
In addition to measuring the
change in economic surplus for
various assumed 03 levels, the
analysis also includes an exam-
ination of the sensitivity of
the estimates to the nature of
the demand relationships used
in the model.
   Adams et al.
   (1984b)
6 crops: barley,
corn, soybeans,
cotton, wheat, and
sorghum.  Multiple
cultivars used for
each crop except
barley and grain
sorghum; two for
cotton, three for
wheat, two for corn,
and nine for soybean.
$1.7 (in 1980
dollars).
Adequate; analysis uses
NCLAN 03 yield response
data for 1980 through
1983.  Yield changes
reflect changes from
1980 ambient 03 of 10
and 40% reduction and
a 25% increase for each
response.
Adequate; same as
above but for 1980
and 1976 through
1980 periods.
Adequate; economic model
consists of two compo-
nents: a series of farm-
level models for each of
55 production regions
and a national model
of crop use and demand.
Yield changes are used
to generate regional
supply shifts used in
national model.
Consumer surplus estimated
for both domestic and foreign
markets; producer surplus
nationally and by region.  The
analysis includes a range of
economic estimates reflecting.
changes in response and 03
data and assumptions.
    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, aerometric, or economic information and models currently available.
            is a spatial interpolation procedure that has been used to generate 03 concentration data for rural areas in which no monitoring sites have
    been established.  See Heck et al. (1983b).

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an increase  in  0^  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. agricul-
tural 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., adjustments are sub-
stantial, but  make up a relatively  small  percentage  of total agricultural
output (about 4 percent).   Specifically,  in this analysis,  a 25 percent reduc-
tion 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 defen-
sible 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, particu-
larly Q~~moisture  stress  interactions,  in many of the response experiments.
Also, the 0, 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- 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 bene-
fits 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
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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 signifi-
cantly would require  that  their sensitivities to 03 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 substan-
tial 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 03~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.   Uncertain-
ties 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  literature 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- 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 03 formation and transport processes for
use  in formulating rural 03 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, concentra-
tions  in ambient air.   For a cost-benefit analysis to be complete, the annual-
ized estimated benefits  to agriculture that would result from 0, control would
have to  be combined with benefits  accruing  to other sectors and then  compared
with the overall annualized compliance costs.
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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,.   Both CL
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, 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 Affecting  PlantResponse 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^ tended to reduce PAN injury (Nouchi et al., 1984).
1.5.10.2   LimitingValues 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  dura-
tions 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
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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 a!., 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 a!., 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 a!., 1950) for which the foliage is
the marketable portion.  After severe  PAN damage, entire crops may be unmarket-
able 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 THEIR 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, espec-
ially  "stress  pathogens"  (National  Research  Council,  1977;  U.S.  Environmental
Protection Agency, 1978; this document, Chapter 6).  The responses elicited by
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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).  Ozone-
induced 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-);
sweetgum, 29 percent  (0.10 ppm 03);  green ash, 24 percent (0.10 ppm); willow
oak, 19 percent  (0.15 ppm 0~); 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; Kress 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
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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-  (with a 1-hr
daily maximum of 0.126 ppm 0,) and 0.076 ppm 0_ (with a  1-hr daily maximum of
0.094 ppm 03).
     Field studies  on  the  Cumberland Plateau (near Oak Ridge,  TN) have shown
reductions in growth in eastern white pine exposed to ambient air 0., concentra-
tions >0.08 ppm (1-hr)  (Mann  et  a!., 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 ozone-
sensitive.    In  the Blue Ridge Mountains  of Virginia,  Benoit et al.  (1982)
found reductions in radial growth of sensitive eastern white pine in  a multi-
year study in which 1-hr 0~ concentrations were generally 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 species  in which stomates remain open  at  night, such as eastern white
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.   All 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,
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1981; Benoit et al., 1982).  In addition, the age of the plant and its develop-
mental 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 CL stress.  Needles  of sensitive eastern
white pine usually exhibit injury symptoms within a few days after exposure to
high CL 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 0, over a period of 10 to 20 years (Miller and Elderman, 1977; Miller
et al.,  1982;  Mclaughlin  et al., 1982;  Benoit et al.,  1982).   Decline 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 successional 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 arid Jeffrey
pines (see Section 1.6.4 below).
     Marked morphological deterioration of the common lichen species, Hypogymm'a
enteromorpha, was  documented  in areas of the San Bernardino Mountains having
high oxidant  concentrations.   A comparison of the  species of lichens found

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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 critical  importance of examining pollutant-pathogen  and poll ant-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.

1.6.4  Effects 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
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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 micro-
flora 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-hr-
average  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 green-
houses,  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 accumula-
tion of  litter under stands with the most severe needle injury and by defolia-
tion,  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 interac-
tions, 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
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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  03 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,  03-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.  Duchelle
et al. (1983) found reductions in the growth and productivity of graminoid and
forb vegetation  in  the  Shenandoah National Park,  where 1-hr ozone concentra-
tions ranged from   0.08  to  0.10 ppm  in the 3-year study period,  with 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.

1.6.5  Economic Valuation 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
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(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.  Theo-
retically, 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 expo-
sure 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.
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     The formation of  cracks  and the depth of cracking in elastomers are re-
lated 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 propor-
tionately 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 um/hr for hot SBR.  When antiozonants were added to the com-
pounds, 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 per-
cent-strain.   Under 20-percent strain, the mean cracking rate for 0.08 ppm was
1.94 um/hr.  From these and other data, they estimated that at the ozone stan-
dard of the  time (0.08 ppm, 1-hr average), and at the annual NO  standard of
                                                                X
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 atmos-
pheric pressure,  humidity,  sunlight,  and other atmospheric  pollutants.   Veith
and  Evans (1980) found a 16-percent difference in cracking rates reported from
laboratories 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 prob-
lem  worsened at  higher relative humidities.   When fast-blooming waxes  and
antiozonants or other  antioxidants were added, only the combination of protec-
tive measures allowed  good adhesion and afforded  protection  from  ozone and
sunlight  attack.  Wenghoefer  (1974)  showed that  ozone (up to  0.15 ppm),  espe-
cially  in combination  with high relative  humidity  (up to 90 percent), caused
greater adhesion  losses  than  did  heat  and N02 with or without  high relative
humidity.
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     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 N02>   Subsequent work by Schmitt (I960,  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  cottons  nylon, and acrylic fibers have  greater but varying
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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 Toss 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 in 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 are now out-
dated  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 esti-
mates 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 merely made  bold assumptions
in  this regard,  most of which  remain  unverified through the present  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
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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 confi-
dently.
     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 mate-
rials  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:
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     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 sampling 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 CU have been studied extensively in animals and
a wide array  of toxic effects have been ascribed to 0- inhalation.   Although
much has been accomplished to  improve the  existing  data base,  refine the  con-
centration-response relationships  and  interpret better the mechanisms of 0-
effects, many of  the  present data were not  accumulated  with the idea that
quantitative comparisons  to man would be drawn.   In many cases, only qualita-
tive comparisons can be made.  To maximize the extent that animal  toxicological
data can be  used  to estimate the  human health  risk of exposure  to 03, the
qualitative as well as quantitative similarities between the toxicity of 0~ to
animals and man must  be considered more carefully in the future.  Significant
advances have been made in understanding the toxicity of 03 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,.
     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 presen-
ted below:
                                                    /
1.   Studies have  been cited when the reported effects are clearly due to 0^
     exposure.  Effects due  to mixtures of 0, with  other pollutants have  been
     summarized in  a  separate figure and table.  Studies involving exercise,
     diet deficiencies, or other possible modifiers of response to Og have not
     been included.
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2.   Cited studies report  the  effects of 03 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
maerophage function"  includes  such diverse  endpoints as  measurements of  lyso-
somal and  phagocytic  activity, maerophage 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 concen-
trations which did and did not cause these effects.

1.8.2  Regional Dosimetry  in the Respiratory Tract
     The amount  of 0, acting at a given site  in the lung  is related to the
airway luminal concentration at that level.   As a result, 0, 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- is quite reactive chemically.  Reactions with components
of this  layer cause an increase in total absorption of Q~ in the upper airways
and  in  a reduction of the amount  of 0,  reaching sensitive  tissues.  The site

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at which uptake and subsequent interaction occur and the  local dose (quantity
of 0, 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 dissimilari-
ties 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- and other oxidants in humans.
     The animal  studies that  have been conducted on  ozone  absorption are
beginning to  indicate  the  quantity and site of 03 uptake in  the  respiratory
tract.   Experiments on the nasopharyngeal  removal  of  03  in  animals suggest
that the fraction of 0^ 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,
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, absorption, mathematical  models  have
been developed to simulate the processes involved  and  to  predict 0., 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, 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 models  have been developed  to  simulate  lower respiratory  uptake
(McJilton et  al.,  1972; Hiller et  al.,  1978b, 1985).   These  models are  very
similar in their treatment of 03 in the airways (taking into account convection,
diffusion, wall  losses,  and ventilatory patterns)  and in  their use  of  morpho-
logical data  to  define the dimensions of the airways and  liquid  lining.  The
models  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-
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
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reactions, as well as in the fact that the newer model includes chemical  reac-
tions of Og 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,)  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 know-
ledge 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, 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  CL 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  CU.   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 0- in man.  Since animal studies
are  the  only available approach  for investigating the full  array  of  potential
disease  states induced by  exposure to 0,, quantitative use of animal data is
in  the  interest  of better establishing 03 levels to  which  man can safely  be
exposed.
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1.8.3  Effects of Ozone on the Respiratory Tract
1.8.3.1  Morphological Effects.   The morphological changes which follow exposure
                      o
to less than 1960 ug/m  (1.0 ppm) 0,, are very similar in all species of labora-
tory mammals studied.   Of the many specific cell types found in the respiratory
system, two types,  ciliated cells and type 1 alveolar epithelial cells, are
the cells most damaged morphologically following 03 inhalation. Ciliated 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 03 exposure of experi-
mental animals,  damaged  ciliated cells have been  reported in all of  these
conducting  airways  (Schwartz  et  a!.,  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 I alveolar epithelial cells are shed (sloughed)
from the tissue surface and are  replaced by multiplication of other cell types
less damaged by 0»  (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  hyperplastic
(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  a!.,. 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
                         3
of  0~  as low as  392  ug/m   (0.2  ppm).  Damage to  centriacinar type 1 alveolar
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epithelium in rats has been well documented as early as 2 hours after exposure
                                3
to 03 concentrations  of 980 ug/m   (0.5 ppm)  (Stephens  et al., 1974a).  In the
same publication the  authors  report damage to centriacinar  type  1 alveolar
                                                    3
epithelial cells after 2  hours exposure to  392 ug/m   (0.2 ppm) 03, 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
                                      3
occurs following exposure  to  980 ug/m  (0,5 ppm) 03 for 2 hours (Stephens et
al., 1974a).  Damage  to  ciliated cells has  been  seen  following exposure of
                                 3
both rats and monkeys to 392 ug/m  (0.2 ppm) 0-,  8 hr/day for 7 days (Schwartz
et al., 1976; Castleman  et al., 1977).  Centriacinar  inflammation has been
                                                       3
reported as early as 6 hours after exposure to 980 ug/m  (0.5 ppm) 0., (Stephens
                                                      •a             3
et al., 1974b) and 4 hours after exposure to 1568 ug/m  (0.8 ppm) 03 (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
    3
ug/m  (0.5 ppm) 03, 8 hr/day  (Eustis et al.s  1981)  and in rats exposed to 980
ug/m3 (0.5 ppm)  03, 24 hr/day for 180 days (Moore and Schwartz, 1981).  Damage
to centriacinar type  1 cells  was reported  following exposure of young rats  to
490 ug/m3 (0.25 ppm)  0~, 12 hrs/day  for 42 days  (Barry et al.s 1983;  Crapo  et
                                                                       3
al., 1984).   Changes  in type  1 cells were  not detectable after 392 ug/m  (0.2
                                                                       3
ppm) 03,  8 hr/day  for 90 days but  were seen  in rats exposed  to 980 ug/m  (0.5
ppm) for  the  same period (Boorman et al.,  1980).   Centriacinar  inflammatory
                                                            3
changes persist during 180-day exposures of rats to 980 ug/m  (0.5 ppm) 03, 24
hr/day (Moore and  Schwartz,  1981)  and one-year  exposures of monkeys  to 1254
ug/m3 (0.64 ppm) 03, 8 hr/day (Fujinaka et al., 1985).
     Remodeling of  distal  airways  and centriacinar regions  occurs following
long-term exposures to  CU.   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 respiratory 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 a!., 1984a;  Fujinaka  et al., 1985).  Three
studies provide morphological evidence of mild fibrosis  (i.e.,  local  increase
of collagen)  in centriacinar interalveolar septa following exposure to < 1960
    3
|jg/m  (< 1  ppm)  of 03 (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 a!., 1980;  Moore and Schwartz,  1981).
     While morphometry of small pulmonary arteries  is not commonly studied in
0-~exposed animals, pulmonary artery  walls  thickened by muscular hyperplasia
                                                      3
and edema were reported in rabbits exposed to 784 n9/m  (Q.4 ppm) 03, 6 hr/days
5 days/week  for 10 months (P'an et  al., 1972).  Thickened intima and  media in
                                                                  3
pulmonary arterioles were reported in monkeys exposed to 1254 |jg/m  (0.64 ppm)
03, 8 hr/day for 1 year (Fujinaka et al.,  1985).
     Several of the effects of 03 inhalation persisted after the Qg inhalation
ended and the animals  breathed only filtered air several days or weeks. Lungs
from rats exposed  to  1568 (jg/m  (0.8 ppm) 03 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
                                                      3
in monkeys 7 days after 50 hours exposure to 1568 [jg/m  (0.8 ppm) 0-  (Castleman
                                                                       3
et al.,  1980)  and  in  mice 10 days after a 20-day exposure to 1568 [jg/m  (0.8
ppm) DO,  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 (jg/m3 (0-5 ppm) 03> 24 hr/day (Moore and Schwartz, 1981).
     While not all  species of laboratory mammals have been studied following a
single 0- 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 cell  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  Q~ 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.  Duration  of centriacinar inflammation during 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 pul-
monary 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, 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~ 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).
1.8.3.2  Pulmonary 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., 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
                                                       3
exposure for 2  hr to  concentrations of 431  to  980  |jg/m   (0.22 to 0.5 ppm)
produces rapid,  shallow  breathing  and increased pulmonary resistance  during
exposure (Murphy  et al.,  1964;  Yokoyama,  1969;  Watanabe et  a!., 1973; Amdur
et al., 1978).   The onset of these effects is rapid and the abnormal breathing
pattern usually  disappears within  30 min after cessation of 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

-------
                               «e°
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0.6-

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          Figure 1 -7. Summary of morphological effects in experimental animals
          exposed to ozone. See Table 1-11 for reference citations of studies

          summarized here.

-------
         TABLE 1-11.  SUMMARY TABLE:  MORPHOLOGICAL EFFECTS OF OZONE
                            IN EXPERIMENTAL ANIMALS
  Effect/response
03 concentration, ppm
         References
Damaged ciliated
  and type 1 cells
Proliferation of non-
  ciliated bronchiolar
  and type 2 cells
Centriacinar
  inflammation
 [0.2], 0.5, 0.8
 0.2, 0.5, 0.8
 0.2, 0.35
 0.25
 0.25
 0.26, 0.50, 1.0
 0.5
 0.5
 0.5
 0.5, 0.8
 0.5, 0.8
 0.54, 0.88
 0.8
 0.8
 0.85

 0.2, 0.35
 0.35, 0.50, 0.70,
  0.75, 1.0
 0.5
 0.5
 0.5
 0.5, 0.8
 0.54, 0.88
 0.64
 0.7
 0.8
 0.8
 0.8
 1.0

 [0.2], 0.5, 0.8
 0.2
 0.2, 0.5, 0.8
 0.25
 0.25
 0.35
 0.5
 0.5
 0.5, 0.8
 0,5, 0.8
 0.5, 0.8
 0.54, 0.88
 0.54, 0.88
 0.64
 0.8
 1.0
Boorman et al. (1980)
Schwartz et al. (1976)
Castleman et al.  (1977)
Barry et al. (1983)
Crapo et al. (1984)
Boatman et al. (1974)
Stephens et al. (1974b)
Moore and Schwartz (1981)
Evans et al. (1985)
Eustis et al.  (1981)
Mellick et al. (1975, 1977)
Stephens et al. (1974a)
Castleman et al.  (1980)
Plopper et al. (1978)
Stephens et al. (1978)

Castleman et al.  (1977)
Evans et al. (1976b)

Evans et al. (1985)
Zitnik et al.  (1978)
Moore and Schwartz (1981)
Eustis et al.  (1981)
Freeman et al. (1974)
Fujinaka et al. (1985)
Evans et al. (1976a)
Castleman et al.  (1980)
Lum et al. (1978)
Ibrahim et al. (1980)
Cavender et al. (1977)

Boorman et al. (1980)
Plopper et al. (1979)
Schwartz et al. (1976)
Barry et al. (1983)
Crapo et al. (1984)
Castleman et al.  (1977)
Stephens et al. (1974b)
Moore and Schwartz (1981)
Mellick et al. (1975, 1977)
Brummer et al, (1977)
Last et al. (1979)
Stephens et al. (1974a)
Freeman et al. (1974)
Fujinaka et al. (1985)
Castleman et al.  (1980)
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            [0.2], 0.5, 0.8          Boorman et al.  (1980)
  remodeling             0.2, 0.5, 0.8            Schwartz et al.  (1976)
                         0.5                      Moore and Schwartz (1981)
                         0.64, 0.96               Last et al. (1984a)
                         0.64                     Fujinaka et al.  (1985)
                         1.0                      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- 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 M9/m3 (0.56  to  0.85  ppm)  of Oj  (Lee et  al., 1979,
1980).  Aerosolized  ovalbumin caused  an increased incidence of anaphylaxis in
                                   o
mice preexposed to 980 or 1568 ug/m  (0.5 or 0.8 ppm) of 0- continuously for 3
                 >,                                         O
to 5  days  (Osebold et al., 1980).   In  addition, increased airway sensitivity
to histamine or  cholinomimetic  drugs  administered by aerosol or  injection has
                                                                 2
been  noted  in several  species after exposure to 980  to 5880 ug/m  (0.5 to 3.0
ppm)  of  03  (Easton and Murphy, 1967; Lee et al., 1977; Abraham et al.5 1980,
1984a,b; Gordon  and  Amdur,  1980; Gordon et al., 1981, 1984; Roum and Murlas,
1984).  The mechanism responsible for 0~-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 respon-
siveness to  bronchoconstrictors by altering sensitivity of the airway smooth
muscle directly  or through released cellular mediators (Gordon et al.s 1981,
1984; Abraham et al.,  1984a,b).  In  some  species,  increased airway hyperreac-
tivity 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 bronchoeon-
strictors (Abraham et al., 1984a).
     The time  course  of airway hyperreactivity after exposure to 980 to 5880
|jg/m (0.5 to 3.0 ppm) of  0.,  suggests a possible association with  inflammatory
cells and pulmonary  inflammation  (Holtzman et a!., 1983a,b; Sielczak et a!.,
1983; Fabbri et  al.,  1984; O'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  demon-
strate increased collateral  resistance  following 30 min local exposure of 0™
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 0,  in  the airways but  also  on the extent  of penetration  of
ozone into the lung periphery.
     The effects  of  short-term  exposures to 0™ 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).
                                                                           3
     Exposures of  4  to  6 weeks to  ozone concentrations  of 392 to 490 ug/m
(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 ug/m  (0.4 to
0.8 ppm) for up  to 180 days (Moore  and  Schwartz,  1981;  Costa et al.,  1983;
                                                                        o
Martin et al., 1983).   Exposure to 0- concentrations of 980 to 1568 ug/m  (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

-------
E
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                 Figure 1 -8. Summary of effects of short-term ozone exposures on

                 pulmonary function in experimental animals. See Table 1-12 for

                 reference citations of studies summarized here.

-------
          TABLE 1-12.          TABLE:  EFFECTS ON PULMONARY FUNCTION
           OF SHORT-TERM EXPOSURES TO OZONE IN EXPERIMENTAL ANIMALS
  Effect/response       03 concentration, ppm
                            References
Increased breathing
  frequency
0.22, 0.41, 0.8
0.34, 0.68, 1.0
0.5
Amdur et al.  (1978)
Murphy et al.  (1964)
Yokoyama (1969)
Decreased tidal volume     0.34, 0.68, 1.0      Murphy et al. (1964)
Decreased lung
  compliance
Increased residual
  volume (RV),
  closing capacity
  (CC), and closing
  volume (CV)

Decreased diffusion
  capacity
[0.22], 0.41, 0.8
0.26, 0.5, 1.0
1.0

0.24 - 1.0
Amdur et al. (1978)
Watanabe et al. (1973)
Yokoyama (1974)

Inoue et al. (1979)
0.26, 0.5, 1.0
Watanabe et al. (1973)
Increased pulmonary
resistance


Increased airway
reactivity



[0.22]
0.26, 0.5, 1.0
0.5
1.0
[0.1]-0.8
[0.1]-0.8, 1.0
0.5, 1.0
0.7
1.0
Amdur et al. (1978)
Watanabe et al. (1973)
Yokoyama (1969)
Yokoyama (1974)
Gordon and Amdur (1980)
Gordon et al. (1981, 1984)
Abraham et al. (1980, 1984a,b)
Lee et al. (1977)
Holtzman et al. (1983a,b)
1.8.3.3  Biochemical Effects.   The  lung is metabolically active, and several

key steps in metabolism have been studied after 03 exposure.  Since the proce-

dures 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, gluta-

thione)  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

-------
                                                                       £>U
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 a
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c
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0.1_
0.2-

0.3-
0.5-
0.6-
0.7_
0.8_
0.9-
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         Figure 1-9. Summary of effects of long-term ozone exposures on

         pulmonary function in experimental animals. See Table 1-13 for

         reference citations of studies summarized here.

-------
          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
Increased pulmonary
  resistance
Decreased lung
  compliance

Decreased inspiratory
  flow

Decreased forced
  expiratory volume
  (FEV,) and flow
  (PEP)
   [0.08], [0.12], 0.25
   0.2
   [0.2], 0.8
   0.4

   0.2, 0.8
   0.5, 1.0
   0.64
   0.64

   0.5, 0.8
   0.64

   [0.08], 0.12, 0.25
   0.2, 0.8
   0.64
Raub et al.  (1983)
Bartlett et al.  (1974)
Costa et al.  (1983)
Martin et al.  (1983)

Costa et al.  (1983)
Yokoyama et al.,  1984
Wegner (1982)
Kotlikoff et al.,  1984

Eustis et al.  (1981)
Wegner (1982)

Raub et al.  (1983)
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 On  since exposure  to  ozone causes numerous effects on lung struc-
ture,  function, and biochemistry.   Acute exposure  to high  ozone  levels
          3
(2920 ug/m , 2 ppm) typically decreases antioxidant metabolism,  whereas repeated
                                                     3
exposures to  lower  levels (between 272 and 1568 (jg/m  ,  0.2 and 0.8 ppm)  in-
creases this metabolism (DeLucia et al.,  1975b).   In rats maintained on normal
diets, this response has been observed after a week of continuous or intermit-
tent exposure to 392 ug/m3 (0.2 ppm) 03 (Mustafa, 1975; Mustafa and Lee,  1976;
Plopper et al., 1979).   Similar responses are seen in monkeys and mice, but at
                                3
higher concentrations  (980 ug/m ,  0.5  ppm)  (Fukase et al.,  1978; Mustafa and

Lee, 1976).
     The effects of 0, 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

-------
                               3
high ozone  levels (> 3920 |jg/m ;  >  2  ppm)  decreases metabolism (and thus,
                                                                   3
oxygen consumption);  repeated exposure to lower levels (> 1568 jjg/m ,  0.8 ppm)
increases oxygen  consumption (Mustafa et al., 1973;  Schwartz  et a!,,  1976;
Mustafa and  Lee,  1976).   Effects  in rats on  normal  diets  have been observed
                                                                3
after  a  short-term exposure to ozone  levels  as  low as 392 |jg/m   (0.2 ppm)
(Schwartz et al.,  1976; Mustafa et al., 1973;  Mustafa and Lee,  1976).   Monkeys
                                                 3
are affected at a higher level of ozone (980 pg/m , 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; Ghow et al., 1974; Schwartz et  al.,
1976; Mustafa et al., 1973).  Rats on a vitamin E-deficient diet experience an
                                          o
increase in  enzyme activities at  196  ng/m   (0-1 ppm) ozone as compared  to
        3
392 jjg/m  (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  effects  from continuous  versus  intermittent
exposure; this, along with concentration-response data, suggests that the con-
centration 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? 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 respon-
siveness 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
                                                                 3
substrate  and  the enzyme.  Acute  exposure to 1470 to  1960 ug/m  (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 E-
                                                            3
deficient  rats  receiving a short-term exposure  to  196  ug/m (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 frequent-
ly 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
                                                      o
been shown in the lungs of rats exposed to > 1372 ug/m   (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 ijn vivo  or i_n vitro exposure  to ozone (Hurst et al.,
1970; Hurst and Coffin, 1971).
     As discussed  previously, long-term exposure to  high 0- 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
                       2
observed, with 980 |jg/m  (0-5 ppm) 03 being the minimally effective concentra-
tion 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
                  o
392  and  1568 |jg/m (0.2  and 0.8  ppm) 0, after an  intermittent exposure for 62
days.
     The effects  of  03  on  increasing collagen  content may be progressive;
i.e., after a  6-week  intermittent exposure of rats  to 0.64 or 0.96 ppm 0,
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  03  to initiate peroxidation  of  unsaturated fatty
acids ijn 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  altera-
tions, 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
                                                            2
sensitive techniques were  developed,  lower levels (510 ug/m , 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 interpre-
tation was that edema had occurred.  This  effect was more pronounced several
hours after  exposure  ceased.   At  higher  concentrations,  a  loss  of carrier-
mediated 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  fl-
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 |jg/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, 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 vari-
ables that can influence  the determination  of  the lowest effective concen-
tration 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

-------
IX)
00
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                                   Figure 1-10. Summary of biochemical changes in experimental animals
                                   exposed to ozone. See Table 1-14 for reference citations of studies
                                   summarized here.

-------
               TABLE 1-14.  SUMMARY TABLE:  BIOCHEMICAL CHANGES
                   IN EXPERIMENTAL ANIMALS EXPOSED TO OZONE
  Effect/response
 03 concentration, ppm
   References
Increased Og
  consumption
Increased lysosomal
  enzyme activities
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

Increased GSH
 metabolism
[0.1], 0.2
[0.1], 0.2, 0.35, 0.5, 0.8
0.2, 0.5, 0.8
0.2, 0.5, 0.8
0.45
0.8
0.8

[0.2], [0.5], 0.8
0.7, 0.8
0.7, 0.8

[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
[0.1], 0.26,
[0.25], 0.5,
0.6, 1.0
1.0
[0.1]
[0.5], 0.8
0.8
0.51, 1.0
1.0
0.2, 0.35, 0.8
0.2, 0.5, 0.8
0.2, 0.5, 0.8
[0.1]
0.1, 0.2
0.2, 0.35, 0.5.
0.2, 0.5r 0.8
0.2, 0.5, 0.8
0.2, 0.5, 0.8
0.2, 0.5, 1.0
0.32
0.45
0.5
                                      0.8
Mustafa (1975)
Mustafa and Lee (1976)
Mustafa et al. (1973)
Schwartz et al.  (1976)
Mustafa et al. (1982)
Chow et al, (1976)
Elsayed et al. (1982a)

Chow et al. (1974)
Oil lard et al. (1972)
Castleman et al,  (1973a,b)

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)

Hu et al. (1982)
Alpert et al. (1971a)
Williams et al.  (1980)
Reason et al. (1979)

Chow et al. (1981)
Chow et al. (1977)
Chow and Tappel  (1973)

Mustafa and Lee (1976)
Schwartz et al.  (1976)
DeLucia et al. (1972, 1975a,b)
Chow et al. (1981)
Plopper et al. (1979)
Mustafa and Lee (1976)
Chow et al. (1974)
DeLucia et al. (1972, 1975a,b)
Schwartz et al. (1976)
Fukase et al.  (1975)
Moore et al. (1980)
Mustafa et al. (1982)
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
                      0.7,  0.75,  0.8
                           Fukase et al. (1978)
                           Chow and Tappel (1972, 1973)





Increased NPSH



Decreased
unsaturated
fatty acids
0.8

0.8
0.9
0.9
0.1, 0.2
0.2, 0.5, 0.8
0.45
0.8
0.5


. Elsayed et al, (1982a,b;
1983)
Chow et al. (1976)
Tyson et al. (1982)
Lunan et al. (1977)
Plopper et al, (1979)
DeLucia et al. (1975b)
Mustafa et al. (1982)
Chow et al . (1976)
Roehm et al . , 1972


     Ciliated cells are  damaged  by 03 inhalation, as  demonstrated  by major
morphological changes  in  these  cells including necrosis and ploughing 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 non-
viable particles  from  the lung.   Rats exposed  to  784,  1568,  I960,  or 2352
    3
|jg/m  (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  particles,  and the decreased  short-term clearance  is an
anticipated  functional result predicted from morphological observations.  The
mucous glycoprotein production of  the  trachea  is  also altered  by 0~ exposure.
Mucous glycoprotein  biosynthesis,  as measured  ex  vivo  in  cultured  trachea!
explants from exposed rats, was  inhibited by short-term continuous exposure to
1568 |jg/m3  (0.8 ppm)  of 0, 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 trachea!  mucus was
                                   1-125

-------
                                                            q
significantly reduced following a 2 hr exposure to 1960 [ig/m  (1.0 ppm) (Abraham
et al.» 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 0, 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 respira-
tory 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 organ-
isms responsible  for the  respiratory infections  in  a community  still requires
further investigation.
     Ideally, studies of  pulmonary liost 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 know-
ledge 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, 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 CL 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  CL  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 CL 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  CL will protect
against the effects of subsequent exposure to lethal doses and the development
of lung edema  (Stokinger et a!., 1956;  Fairehild,  1967;  Coffin and Gardner,
1972a; Chow, 1984).  The prolongation of mucociliary clearance reported for CL
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-,, 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 CL.  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 CL exposures.
These investigators  suggest that during  continuous exposure to CL 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 CL  as
the pre-exposed counterpart (Plopper  et al., 1978).  This information is an
important observation because  it implies that the  decrease in susceptibility
to CL  persists  only  as  long as  the  exposure to CL  continues.   The biochemical
studies of Chow et al.  (1976) support this conclusion.
                                   1-127

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

                                         in experimental animals. See Table 1-15 for reference citations of

                                         studies summarized here.

-------
        TABLE 1-15.   SUMMARY TABLE:   EFFECTS OF OZONE ON HOST DEFENSE
                      MECHANISMS IN EXPERIMENTAL ANIMALS
  Effect/response
                03  concentration,  ppm
                            References
Delayed mucociliary
  clearance; accelerated
  alveolar clearance,
  ciliary beating
  frequency
Inhibited bactericidal
  activity
Altered macrophage
  membrane
Decreased macrophage
  function
Altered
  cells
no.  of defense
[0.1]
0.4, 0.8, 1.0
[0.5]
[0.5], 1.0
0.8
1.2

0.4
0.4
0.5
0.62
0.7
0.7
0.99

0.1, 1.0
0.5
0.5
0.5, 1.0

0.25, 0.5

0.5
0.5, 0.67
0.5, 0.67
0.8
1.0
1.0

0.2
0.2, 0.35, 0.5, 0.8
0.2, 0.35
0.2, 0.5, 0.8
0.25
0.5
0.5, 0.88
0.5
0.5, 0.88
0.5, 0.8
0.54, 0.88
0.8
1.0
1.0
Grose et al.  (1980)
Kenoyer et al.  (1981)
Friberg et al.  (1972)
Abraham et al.  (1980)
Phalen et al. (1980)
Frager et al. (1979)

Coffin and Gardner (1972b)
Goldstein et al.  (1972)
Friberg et al.  (1972)
Goldstein et al.  (1971b)
Bergers et al.  (1983)
Warshauer et al.  (1974)
Goldstein et al.  (1971a)

Gardner et al.  (1971)
Dowel 1 et al. (1970)
Hadley et al. (1977)
Goldstein et al.  (1977)

Hurst et al. (1970)
Hurst and Coffin (1971)
Alpert et al. (1971b)
Coffin et al. (1968)
Coffin and Gardner (1972b)
Schwartz and Christman (1979)
Shingu et al. (1980)
McAllen et al.  (1981)

Plopper et al.  (1979)
Dungworth et al.  (1975)
Castleman et al.  (1977)
Boorman et al.  (1977, 1980)
Barry et al. (1983)
Zitnik et al. (1978)
Stephens et  al. (1974a)
Last et al.  (1979)
Brummer et al. (1977)
Eustis et al. (1981)
Freeman et al. (1974)
Castleman et al. (1980)
Freeman et al. (1973)
Cavender et  al. (1977)
                                    1-129

-------
   TABLE 1-15 (continued).  SUMMARY TABLE:  EFFECTS OF OZONE ON HOST DEFENSE
                      MECHANISMS IN EXPERIMENTAL ANIMALS
Effect/response
Increased suscepti-
bility to infection









Altered immune
activity




03 concentration, ppm
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
0.1
0.5, 0.8
0.5, 0.8
0.59

0.8
References
Coffin et al . (1967)
Miller et al . (1978a)
Ehrlich et al. (1977)
Aranyi et al. (1983)
11 ling 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)
Aranyi et al . (1983)
Osebold et al . (1979, 1980)
Gershwin et al. (1981)
Campbell and Hilsenroth
(1976)
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 toler-
ance 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 nonrever-
sible pulmonary changes.
     Tolerance may  not  be long-lasting.   During 0, 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).

1.8.4  Extrapulmonary Effects of Ozone
     It is still believed  that 03,  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-  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 CMS.   Ozone exposure
also produces  effects on  animal  behavior that may  be  caused by pulmonary
consequences of  0~,  or by nonpulmonary (CMS) mechanisms.   The  mechanism by
which 03 causes  extrapulmonary changes is  unknown.   Mathematical models  of 0~
dosimetry predict  that  very  little  0, penetrates  to  the blood of the alveolar
capillaries.   Whether these effects result from 0, or a reaction product of 0,
which penetrates to the blood and is transported is the subject of speculation.
1.8.4.1  Central Nervous System and Behavioral  Effects.   Ozone significantly
affects the  behavior of  rats during exposure  to concentrations  as  low as
        3
235 (jg/m  (0.12  ppm)  for 6 hr.  With  increasing concentrations  of  0~, 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  0- exposure concentra-
               3
tions (490 pg/m  ,  0.25 ppm),  an increase in activity is observed after exposure
                                          3
ends. ^Higher  0- concentrations (980 (jg/m , 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~, 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, prompt-
ing Weiss et al. (1981) to suggest  that 03 impairs the inclination to respond.
Two  studies  indicate  that mice will respond to  remove themselves from an
                                            3
atmosphere containing greater than 980 (jg/m  (0.5 ppm)  (Peterson  and Andrews,
1963, Tepper et  al. ,  1983).   These studies  suggest  that  the aversive effects
                                   1-131

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of 0- 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
0- concentrations.
1.8.4.2  Cardiovascular Effects.  Studies on the effects of 03 on the cardio-
vascular system  are few, and to date there  are no  reports of attempts to con-
firm these studies.   The  exposure of rats to 0Q alone or in combination with
                  3                            3
cadmium (1176 ug/m ,  0.6 ppm 0~)  resulted in measurable  increases in systolic
                              •3                                            s
pressure and  heart  rate  (Revis  et al., 1981).  No additive  or antagonistic
response was  observed with  the  combined exposure.   Pulmonary capillary blood
                                                                      3
flow and PaOy decreased  30  min following exposure of dogs to  588 (jg/m  (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 0- on the hematological  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 differ-
ences in various components of the serum.
     Effects  of  03  on the circulating RBCs can be readily identified by exa-
mining  either morphological and/or biochemical endpoints.   These  cells are
structually  and  metabolically well understood and  are available  through rela-
tively  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
                                               3
RBCs isolated from monkeys exposed to 1470 (jg/m  (0.75 ppm) of 03 4 hr/day for
4 days  (Clark et al.,  1978).   A single 4-hr  exposure to 392 (jg/m3  (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
                                        Q
following  a  4-hr exposure  to 1666 (jg/m  (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
                                                           3
biochemical  effects.   RBCs  of monkeys exposed to  1470 ug/m  (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,.   The RBCs from
these animals, after  being exposed to 0-, had a significant increase in the
activity of GSH peroxidase, pyruvate kinase,  and lactic dehydrogenase,  but had
                                                 3
a decrease  in  RBC GSH after exposure to 1568 |jg/m   (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,
                                                    3
or catalase activities.  At a  lower  level  (980 ug/m ,  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
        3
980 ug/m  (0.5 ppm).  These effects were not observed in vitamin E-supplemented
rats.  Mice on a vitamin E-supplemented diet and those  on  a deficient diet
                                                                   3
showed an increase in G-6-PD activity after an exposure of 627 ug/m  (0.32 ppm)
of Q~  for  6 hr.   Decreases observed in AChE activity occurred in both groups
(Moore et al., 1980).
     Other  blood  changes  are attributed to 0~.  Rabbits  exposed for 1  hr to
        3
392 ug/m  (0.2 ppm) of 0,  showed a significant drop in total blood serotonin
                                                                    3
(Veninga, 1967).  Six- and 10-month exposures of rabbits to 784 ug/m  (0.4 ppm)
of 0~  produced an increase in serum protein  esterase  and in serum trypsin
inhibitor.   This  latter  effect may be a  result  of  thickening of the small
pulmonary 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 0, but was not affected when the exposure was intermittent (8 hr/day,
                                                            3
7 days).  The 03 concentration in both studies was  1568 ug/m  (0.8 ppm) of 0~.
     Short-term  exposure  to low concentrations  of  0~  induced an  immediate
                                                     •5                   -
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
0, have also been seen following in vitro exposure  of RBCs from humans (Freeman
 J                               —— ——~~~~~~~
and  Mudd,  1981;  Menzel  et al., 1975b; Verweij  and  Van Steveninck, 1981).  A
common  effect  observed  by a number  of  investigators is  that 0«  inhibits the
membrane ATPase activity of RBCs (Koontz and Heath, 1979; Kesner et al., 1979;
                                   1-133

-------
Kindya and  Chan,  1976;  Freeman eta"]., 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 jr» 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 0« reaching the RBC cannot be determined with any accuracy.
1.8.4.4  Cytogenetic and Teratogem'c Effects.   Uncertainty still exists regard-
ing possible  reproductive,  teratogenic, and mutational  effects  of exposure to
ozone.  Based  on  various  _1n 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 jni vitro exposure concentra-
tions 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 j_n
vitro to ozone may result  in chemical  reactions between ozone and culture
media that might not occur iji 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  03 (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 unlimited 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.
1.8.4.5  Other Extrapulmonary Effects.  A  series  of studies was conducted to
show that Q~  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 MQ/m3 (1-0 ppm), effects were observed after 1,  2, and 3
days of exposure.   As the  concentration of O™ was reduced,  increasing  numbers
of daily 3-hr exposures were required to produce a significant effect.   At the
                                       3
lowest concentration studied  (196  \ig/m ,  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 mechanistic 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-  toxicity.   Most of these studies were designed to
investigate the hypothesis that the  survival rate of  mice and  rats  exposed  to
lethal concentrations  of 0-  could be increased by use of  various  thyroid
blocking agents or by thyroidectomy.  To follow up these findings, demons and
Garcia (1980a,b) and demons and Wei  (1984)  investigated  the effects of a
                           3
24-hr exposure to 1960 |jg/m  (1.0 ppm) of 0, 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 concen-
tration of thyroid  stimulating  hormone (TSH), in circulating thyroid hormones
(T, and T.) and in protein-bound iodine.  No alterations were observed in many
other hormone levels measured.   Thyroidectomy prevented the effect of 0~ on
TSH and T. and hypophysectomy prevented effects on T«, unless the animals were
supplemented  with T-  in their drinking water.  The thyroid gland itself was
altered (e.g., edema)  by 03>   The authors hypothesyzed that 03 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,  exposure in
combination with  N02 have been described for  increased  susceptibility to
bacterial infection (Ehrlich et al., 1977, 1979; Ehrlich,  1980, 1983),  morpho-
logical  lesions (Freeman  et  al.,  1974), and increased antioxidant metabolism
(Mustafa et al.,  1984).   Additive or possibly synergistic effects from  exposure
to 0~  and  HUSO,  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 03
and (NH^Op SO- had  synergistic  effects  on collagen synthesis and  morphometry,
including percentage of fibroblasts (Last et al., 1983, 1984a).
     Combining 0,  with other  particulate pollutants  produces  a  variety of
responses, depending  on  the endpoint measured.   Mixtures  of 0,,  Fe^SO-)^
HpSO-, and (NH^^SO* produced the same effect on clearance rate as exposure to
Q~ alone.  However,  when  measuring changes in host defenses,  the combination
of 03 with N02 and ZnS04 or 03 with S02 and (NH4)2S04 produced  enhanced effects
that can not be attributed to 03 only.
     However, since  these issues  are complex, they must be addressed experi-
mentally using exposure regimens for combined pollutants that are more represen-
tative of ambient ratios of peak concentrations, frequency, duration, and time
intervals between events.
     The interactive  effects  of 0,, 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 03 and  PAN are examined and compared, it is obvious that the

                                    1-136

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                                                                                  X
                                                                                         *
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--J
0.1 _
0.2-
E 0.3-
a
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c 0.4^
.2
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S 0.5-
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e
8 0.6-
0)
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5 0.7-
0,8-

0.9_
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                                        Figure 1-12. Summary of extrapulmonary effects of ozone in
                                        experimental animals. See Table 1-16 for reference citations of studies
                                        summarized here.

-------
           TABLE 1-16.  SUMMARY TABLE:  EXTRAPULMONARY EFFECTS OF OZONE
                              IN EXPERIMENTAL ANIMALS
Effect/response 03 concentration, ppm
CNS effects 0.05, 0.5
0.1 - 1.0
0.12 - 1.0
0.2, 0.3, 0.5, 0.7
0.5
0.5
0.5
0.6
1.0
1.0
References
Konigsberg and Bachman (1970)
Weiss et al. (1981)
Tepper et al. (1982)
Murphy et al. (1964)
Tepper et al. (1983)
Reynolds and Chaffee (1970)
Xintaras et al . (1966)
Peterson and Andrews (1963)
Fletcher and Tappel (1973)
Trams et al. (1972)
Hematological effects
Chromosomal, reproduc-
  tive, teratological
  effects
Liver effects
Endocrine system
  effects
0.06, 0.12, 0.48
0.2
0.2, 1.0

0.25, 0.32, 0.5
0.4
0.4
0.5
0.64
0.75
0.8
0.8
0.85
0.86
1.0
1.0
1.0

0.1
0.2
0.24, 0.3
0.43
0.44
1.0

0.1, 6.25, 0.5, 1.0

0.82
1.0

0.75
0.75
0.75
0.75
1.0
1.0
Calabrese et al. (1983)
Brinkman et al,  (1964)
Veninga (1967, 1970)
Veninga et al. (1981)
Moore et al. (1980; 1981a,b)
Jegier (1973)
P'an and Jegier (1972, 1976)
Menzel et al. (1972)
Larkin et al. (1983)
Clark et al. (1978) .
Chow and Kaneko (1979)
Chow et al. (1974)
Menzel et al. (1975a)
Schlipkoter and Bruch (1973)
Dorsey et al. (1983)
Mizoguchi et al. (1973)
Christiansen and Giese (1954)

Brinkman et al.  (1964)
Veninga (1967)
Zelac et al. (1971a)
Tice et al. (1978)
Kavlock et al. (1979)
Kavlock et al. (1980)

Graham (1979)
Graham et al. (1981, 1982a,b)
Veninga et al. (1981)
Gardner et al. (1974)

Atwal and Wilson (1974)
Atwal et al. (1975)
Atwal and Pernsingh (1981, 1984)
Pernsingh and Atwal (1983)
demons and Garcia (1980a,b)
demons and Wei (1984)
                                     1-138

-------

E
Q.
a
 «.
c
o
0)
o


o
o

0!


O
N

O
'
0.1-
0.2-
0.3-
0,4-

0.5-
0.6-
0.7-
0.8-
0.9-

1.O






c
4


<
i

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3

0
3 • * (
t I

t
'
I

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I

             Figure 1 -13. Summary of effects in experimental animals exposed to

             ozone combined with other pollutants. See Table 1-17 for reference

             citations of studies summarized here.

-------
    TABLE 1-17.  SUMMARY TABLE:  INTERACTION OF OZONE WITH OTHER POLLUTANTS
                           IN EXPERIMENTAL ANIMALS
Effect/response
Pollutant concentrations
  References
Increased
pulmonary
lesions
Increased
pulmonary
sensitivity

Increased anti-
oxidant metabolism
and D£ consumption

Altered mucus
secretion

Increased collagen
synthesis
Increased
susceptibility to
respiratory
infections
   [0.25 ppm 03
     +2.5 ppm N02]
   [0.5 ppm 03
     + 1  mg/m3 H2S04]
   [0.5 ppm Q3
     + 10 mg/m3 H2S04
   0.64, 0.96 ppm 03
     + 5 mg/m3 (NH4)2 S04
   0.9 ppm 03
     +0.9 ppm N02
   1.2 ppm 03
     + 5 mg/m3 (NH4)2S04

   0.5 ppm 03
     + 1 mg/m3 H2S04
   0.45 ppm 03
     +4.8 ppm N02
   0.5 ppm 03
     +1.1 mg/m3 H2S04

   [0.5], [0.8], 1.5 ppm 03
     + 5 mg/m3 (NH4)2S04
   0.5 ppm 03
     + 1 mg/m3 H2S04
   0.64, 0.96 ppm 03
     + 5 mg/m3 (NH4)2S04

   0,05 ppm 03
     + 3760 Mg/m3 (NH4)2S04
   0.05 ppm Q3
     + 100-400 Mg/m3 N02
     +1.5 mg/m3 ZnS04
   0.1 ppm Q3
     +0.9 mg/m3 H2S04
     (sequential exposure)
   0.1 ppm 03
     +4.8 mg/m3 H2S04
   0.1 ppm 03
     + 940 Mg/m3 N02
   0.1 ppm 03
     +13.2 mg/m3 S02
     +1.0 mg/m3 (NH4)2S04
Freeman et al.  (1974)

Moore and Schwartz (1981)

Cavender et al. (1978)

Last et al. (1984a)

Freeman et al.  (1974)

Last et al. (1983)


Osebold et al.  (1980)



Mustafa et al.  (1984)



Last and Cross (1978);
Last and Kaizu (1980)

Last et al. (1983)

Last et al. (1983)

Last et al. (1984a)
Ehrlich et al. (1977, 1979);
Ehrlich (1980)
Ehrlich (1983)
                                                     Gardner et al. (1977).


                                                     Grose et al. (1982)

                                                     Ehrlich (1980)

                                                     Aranyi et al. (1983)
                                   1-140

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         TABLE 1-17 (continued).   SUMMARY TABLE:   INTERACTION OF OZONE
                           WITH OTHER POLLUTANTS

Effect/response       Pollutant concentrations         Referencest

Altered upper            [0.1 ppm 03                 Grose et al. (1980)
respiratory                +1.1 mg/m3 H2S04]
clearance                  (sequential exposure)
mechanisms               0.4 ppm 03                  Goldstein et al. (1974)
                           +7.0 ppm N02
                         0.5 ppm 03                  Last and Cross (1978)
                           + 3 mg/m3 H2S04
                         [0.8 ppm 03                 Phalen et al.  (1980)
                           +3.5 mg/m3
                             (Fe2(SQ4)3
                              + H2S04
                              + (NH4)2S04}]
test animals  must be  exposed  to  concentrations  of  PAN much  greater  than  those
needed with 0- to 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 concen-
trations 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^O^ toxicity have involved
concentrations much higher than those found in the ambient air, or the investi-
gations were conducted by using  various jin vitro techniques for exposure.
Very limited  information  is available on the health significance of inhalation
exposure to  gaseous  \\JSy.  Because H^Og is  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 of  HpOx  when using isolated cells  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 epidemiologies!  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 pro-
duced 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 eta!., 1972; Hueter etal., 1966).  Certain
other biological responses were observed in both treatment groups, including a
decrease in spontaneous  activity,  a  decrease  in  infant  survival  rate,  fertil-
ity, 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 SO  showed significant pulmonary functional abnormalities that
                  *\
had relatively good correlation with structural changes (Hyde 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  did  not  interact  in  any synergistic or additive
                          y\
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^
exposure  (Table 1-18).   In most of the studies  reported, greatest  attention
has been accorded decrements in FEV-, „, 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 03),  the observed decrements in FEV^ Q primarily
reflect FVC decrements  of similar magnitude, with  little or  no contribution
from changes in resistance.

                                   1-142

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                                                      TABLE 1-18.  SUMMARY TABLE:  CONTROLLED HUMAN EXPOSURE TO OZONE
CO
Ozone® k
concentration Measurement ' Exposure
ug'/i3
HEALTHY
627
1960
980
980
1470
ppm method duration
ADULT SUBJECTS AT REST
0.32 HAST, NBKI 2 hr
1.0
0.5 CHEM, NBKI • 2 hr
0.50 CHEM, NBKI 2 hr
0. 75
Activity*1
level (Vr) Observed effects(s)

R Specific airway resistance increased with
acetylcholine challenge; subjective symptoms
in 3/14 at 0.32 ppm and 8/14 at 1.0 ppm.
R (10) Decrement in forced expiratory volume and
flow.
R (8) Decrement in forced expiratory volume and
flow.
No. and sex
of subjects Reference
v
13 nale Konig et al., 1980
1 female
40 male Folinsbee et al,,
(divided into four 1978
exposure groups)
8 male Horvath et al.,
7 female 1979
EXERCISING HEALTHY ADULTS
235
353
470
588
784
314
470
627
353
470
588
784
392
686
0.12 CHEM, UV 2.5 hr
0.18
0.24
0.30
0.40
0.16 UV, UV 1 hr
0.24
0.32
0.18 CHEM, UV 2.5 hr
0.24
0.30
0.40
0.20 UV, UV 1 hr
0. 35 (mouth-
piece)
IE (65) Decreient in forced expiratory volume and
i 15-nin intervals flow suggested at 0.12 ppm with larger
decrements at >_ 0, 18 ppm; respiratory
frequency and specific airway resistance
increased and tidal volume decreased at
>_ 0.24 ppm; coughing reported at all
concentrations, pain and shortness of
breath at S 0.24 ppm.
CE (57) Small decrements in forced expiratory
volume at 0.16 ppm with larger decrements
at >0,24 ppa; lower-respiratory symptoms
increased at >0. 16 ppm.
IE (65) Individual responses to Os were highly
915-nin intervals reproducible for periods as long as 10
months; large intersubject variability
in response due to intrinsic responsiveness
to Os.
IE (77.5) @ vari- Decrement in forced expiratory volume and
able competitive flow with IE and CE; subjective symptoms
intervals increased with 03 concentration and may
CE (77.5) limit performance; respiratory frequency
increased and tidal volume decreased with
CE.
135 male McDonnell et al.,
(divided into six 1983
exposure groups)
42 male Avol et al,, 1984
8 female
(competitive
bicyclists)
32 male McDonnell et al.,
1985a
10 male Adams and Schelegle,
(distance runners) 1983

-------
TABLE 1-18 (continued).   SUWiARY TABLE:   CONTROLLED  HUMAN EXPOSURE TO OZONE
Ozonta
concentration
Mg/»4
392
823
980
392
490
412
,_, 490
i
*" 588
980
. 725
980
1470
784
784
pp«
0.2
0.42
0.50
0.20
0.25
0.21
0.25
0.3
0.5
0.37
0.50
0.75
0.4
0.4
Measurement * Exposure Activity
tiethod duration level (Vc)
UV, UV 2 hr IE (30 for male,
18 for female
subjects)
@ 15-min intervals
UV, UV 2 hr IE (68)
(4) 14-min periods
UV, UV 1 hr CE (81)
UV, UV 1 hr CE (63)
CHEM, NBKI • 2 hr R (10), IE (31,
50, 67)
@ 15-rain intervals
MAST, NBKI 2 hr R (11) & IE (29) .
@ 15-inin intervals
UV, NBKI 2 hr IE (2xR)
@ 15-rain intervals
CHEM, NBKI & 3 hr IE (4-5xR)
HAST, NBKI
Observed effects(s)
Repeated daily exposure to 0,2 ppm did not
affect response at higher exposure concen-
trations (0.42 or 0.50 ppm); large inter-
subject variability but individual
pulmonary function responses were highly
reproducible. «
Large intersubject variability in response;
significant concentration-response relation-
ships for pulmonary function and respiratory
symptoms.
Decrement in forced expiratory volume and
flow; subjective symptoms may limit per-
formance.
Increased responsiveness to 03 lasts for
24 hr, may persist in some subjects for
48 hr, but is generally lost within 72 hr.
Decrement in forced expiratory volume and
flow; the magnitude of the change was
related to 03 concentration and VV.
Total lung capacity and inspiratory
capacity decreased with IE (50, 67); no
change in airway resistance or residual
volume even at highest IE (67). No-
significant changes in pulmonary function
were observed at 0.1 ppn.
Good correlation between dose (concen-
tration x VV) and decrement in forced
expiratory volume and flow.
Specific airway 'resistance increased with
histamlne challenge; no changes were
observed at concentrations of 0.2 ppm.
Decrement in forced expiratory volume and
SG was greatest on the 2nd of 5 exposure
days; attenuated response by the 4th day
of exposure.
No. and sex
of subjects
8 male
13 female
20 male
6 male
1 female
(distance cyclists)
19 male
7 female
40 male
(divided into four
exposure groups)
20 male
8 female (divided into
six exposure groups)
12 male
7 female
(divided into three
exposure groups)
10 male
4 female
Reference
Gliner et al. , 1983
Kulle et al., 1985
Folinsbee et al. ,
1984
Folinsbee and
Horvath, 1986
Folinsbee et al. ,
1978
Silverman et al, ,
1976
Dimeo et al., 1981
Fa'rrell et al., 1979

-------
                                               TABLE  1-18  (continued).  SUMHARY TABLE:  CONTROLLED HUMAN EXPOSURE TO OZONE
en
Ozone .
concentration Measurement ' Exposure
ug/nr1 ppm nethod duration
784 0.4 CHEH, UV 3 hr
784 0.4 CHEM, UV 2.5 hr
823 0.42 'UV, UV 2 hr
882 0.45 UV, UV 2 hr
921 0.47 UV, NBKI 2 hr
980 0.5 MAST, NflKI 6 hr
1176 0.6 UV, NBKI 2 hr
(noseclip)
1470 0.75 HAST, NBKI 2 hr
Activity
level (VE)
IE (4-5xR)
for 15 lain
IE (71)
S> 15-min intervals
IE (30)
IE (27)
@ 20-min intervals
IE (3xR)
IE (44) for two
15-m'n periods
IE (2xR)
i 15-min intervals
IE (2xR)
1 15-min intervals
Observed effects(s)
Decrement in forced expiratory volume was
greatest on the 2nd of 5 exposure days;
attenuation of response occurred by the
5th day and persisted for 4 to 7 days.
Enhanced bronchoreactivity with ;
methacholine on the first 3 days;
attenuation of response occurred by
the 4th and 5th day and persisted
for > 7 days.
Atropine pretreatment prevented the
increased R w observed with Oa exposure,
partially blocked the decreased forced
expiratory flow, but did not prevent the
Da-induced decreases in FVC and TLC,
changes in exercise ventilation, or
respiratory symptoms.
Decrement in forced expiratory volume and
flow greatest on the 2nd of 5 exposure
days; attenuation of response occurred by
the 5th day and persisted for < 14 days with
considerable intersubjeet variability.
Increased responsiveness to Oa was found
with a 2nd Oa challenge given 48 hr after
the initial exposure.
Decrement in forced expiratory volume and
flow greatest on the 2nd of 4 exposure
days; attenuation of response occurred by
the 4th day and persisted for 4 days.
Small decrements in forced expiratory
volume and specific airway conductance.
Specific airway resistance increased in 7
nonatopic subjects with histamine and
methacholine and in 9 atopic subjects
with histaaine.
Decrements in spirometric variables
(20&-55SQ; residual volume and closing
capacity increased.
No. and sex
of subjects '
13 male
11 female
(divided intd two
exposure groups)
8 male
24 male
1 male
5 female
8 male
3 female
19 male
1 female
11 male
5 female (divided
by history of atopy)
12 male
Reference 7
Kulle et al., 1982
Beckett et al.
1985 '
Horvath et al., 1981
8ed1 et al., 1985
Linn et al., 1982b
Kerr et al., 1975
Holtzman et al. ,
1979
Hazucha et al . ,
1973

-------
                                           TABLE 1-18.  (continued)  SUHHARY TABLE:  COHTMLLED B1WSH EXPOSURE TO OZONE
Ozone • ,
concentration Measurement '
pgTI3 pp »ethod
Exposure
duration
Activityd
level (VE)
Observed effects(s)
Ko. and sex
of subjects
Reference
EXERCISING HEALTHY CHILDREN
235 0.12 CHEH, UV
2.5 hr
IE (39)
tlS-nrin intervals
Small decrements in forced expiratory
volune, persisting for 24 hr. No subjec-
tive symptoms.
23 male
(8-11 yrs)
McDonnell et al.,
1985b,c
ADULT ASTHMATICS
392 0.2 CHEH, NBKI
490 0.25 CHEK, NBKI
2 hr
2 hr
IE (2xR)
@ 15-ain intervals
R
No significant changes in pulmonary func-
tion. Snail changes in blood biochemistry.
Increase in symptom frequency reported.
No significant changes in pulmonary func-
tion.
20 male
2 feaale
5 nales
12 female
Linn et al., 1978
Silverman, 1979
ADOLESCENT ASTHMATICS
V 235 0.12 UV
i— «
.p.
cr,
SUBJECTS WITH CHRONIC OBSTRUCTIVE
235 0.12 UV, NBKI
353 0.18 UV, NBKI
490 0.25
392 0.2 CHEH, NBKI
588 0.3
784 0.41 UV, UV
1 hr
(mouthpiece)
IUNS DISEASE
1 hr
1 hr
2 hr
3 hr
R

IE (variable)
8 15-min intervals
IE (variable)
@ 15-min intervals
IE (28) for
7.5 min each
half hour
IE (4-5xR)
for 15 Bin
No significant changes in pulmonary function
or symptoms.

No significant changes in forced expiratory
performance or symptoms. Decreased arterial
oxygen saturation during exercise was
observed.
No significant changes in forced expiratory
performance or symptoms. Group mean arterial
oxygen saturation was not altered by Oa
exposure.
No significant changes in pulmonary function
or symptoms. Decreased arterial oxygen
saturation during exposure to 0.2 ppm.
Small decreases in FVC.and FEVa.0.
4 male
6 female
(11-18 yrs)

18 male
7 feiale
15 male
13 feiale
13 male
17 sale
3 female
Koenig et al., 1985

Linn et al., 1982a
Linn et al., 1983
Solic et al., 1982
Kehrl et al., 1983,
1985
Kulle et al., 1984
 Ranked by lowest observed effect level.
 Measurement method:   HAST = Kl-Coulometric  (Hast neter); CHEH = gas phase chenriluminescence; UV = ultraviolet photometry.
cCalibration method:   NBKI = neutral  buffered  potassium  iodide; UV = ultraviolet photometry.
 Minute ventilation reported in L/min or as  a  multiple of resting ventilation.  R = rest; IE = intermittent exercise; CE = continuous exercise.

-------
     Results from studies of at-rest exposures to 0,  have demonstrated decre-
                                                                             3
merits in  forced expiratory volumes and  flows  occurring at and above  980 ug/m
(0.5 ppm) of 03 (Folinsbee et a!., 1978; Horvath et al., 1979).   Airway resis-
tance is  not clearly affected at these  0~  concentrations.   At  or below 588
    3
pg/m  (0.3  ppm) of  Q3, changes in pulmonary  function do not occur during  at
rest exposure  (Folinsbee et al.,  1978),  but the  occurrence  of some 0,,-induced
pulmonary symptoms has been suggested (Kb'nig 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
    3
(jg/m  (0.30 ppm)  of 03 (Folinsbee et  al.,  1978).   With heavy  intermittent
exercise  (V^ = 65 L/min),  pulmonary symptoms are present and  decrements  in
forced expiratory volumes and flows are suggested  to occur following 2-hr
                      3
exposures to 235  pg/m  (0.12 ppm) of  0_ (McDonnell et al., 1983).   Symptoms
are present and decrements  in forced expiratory volumes and flows definitely
                        3
occur at 314 to 470 ug/m  (0.16 to 0.24 ppm) of 0™ following 1 hr of continuous
heavy exercise at a  Vp of 57  L/min (Avol  et al., 1984) or very  heavy exercise
at a V£  of  80  to  90  L/min (Adams  and Schelegle,  1983; Folinsbee  et al.,  1984)
and following  2 hr  of intermittent heavy exercise  at a VV  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; Parrel! et al.,
                                                                             3
1979) or even with heavy exercise while exposed at levels as high as 980 |jg/m
(0.50 ppm)  03  (Folinsbee  et al.,  1978;  McDonnell et al., 1983).   Increased fR
and decreased  VT, while maintaining the  same VV, occur with prolonged heavy
exercise  when  exposed at  392  to 470 ug/m3 (0.20  to  0.24 ppm) of 03 (McDonnell
et al.,  1983;  Adams and ScheTegle, 1983).  While an  increase in RV  has  been
                                              3
reported  to result  from exposure to 1470 ug/m   (0.75 ppm)  of 0_ (Hazucha  et
al., 1973), changes  in RV have not been  observed following exposures to 980 jjg/
m   (0.50 ppm) of 0-, or  less,  even with  heavy exercise  (Folinsbee et al.,
1978).  Decreases in TLC and 1C have been observed to result from exposures to
        3
980 ug/m  (0.50 ppm) of 03 or less, with  moderate and heavy exercise (Folinsbee
et al., 1978).
     Recovery  of  the lung from the effects of 03 exposure consists  of return
of pulmonary function (FVC,  FEV,, and  SR ) to preexposure levels.  The time
course of this recovery is related to the magnitude of the 03~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 03 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^,  the
simple product of Qg concentration,  VV, and exposure duration  (Silverman  et
al . , 1976),  The relative contribution  of these  variables to pulmonary decre-
ments is  greater for  0~ concentration than for VV.   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  03 (Horvath et al., 1981;  Gliner  et al , 1983; McDonnell
et al., 1983; Kulle et al., 1985).  Individual  responses to a given 0- concen-
tration have been shown to be quite reproducible (Gliner et al., 1983; McDonnell
et al,, 1985a)j indicating that some individuals are consistently more respon-
sive to Og than are others.  No  information  is available to account for these
differences.   Considering the  great  variability in  individual  pulmonary re-
sponses to Q~ exposure, prediction equations that only use some form of effec-
tive dose are not adequate for predicting individual responses to 0^,
     In addition to overt changes in pulmonary function, enhanced nonspecific
bronchial reactivity has been observed  following exposures to 0- concentrations
         ~                  •                                   o
>588 fjg/m  (0.3 ppm) (Holtzman et al.,  1979; Konig et al., 1980; Dimeo et al.,
~~
                            3
1981).  Exposure to 392 pg/m  (0.2 ppm) of 0,, with intermittent light exercise
does not affect nonspecific bronchial reactivity (Dimeo et al., 1981).
     Changes in forced expiratory volumes and flows resulting from 0- 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 03 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   and FVC  (McDonnell
                                                      sw
et al . , 1983).   The increased  responsiveness  of  airways  to histamine and
methacholine  following 03 exposure  most  likely results from  an  Qg-induced
increase in airways permeability or from an alteration of smooth muscle charac-
teristics.
                                   1-148

-------
     Decrements in pulmonary  function  were not observed for adult asthmatics
exposed for  2 hours  at  rest (Silverman, 1979) or  with intermittent light
                                                             3
exercise (Linn et a!., 1978)  to CL concentrations of 490 |jg/m   (0.25 ppm)  and
less.  Likewise,  no significant changes in pulmonary function or symptoms were
found in adolescent  asthmatics  exposed for 1  hr  at rest to 235 ug/m  (0.12
ppm) of 03 (Koenig et al., 1985).   Although these results indicate that asthma-
tics are not more responsive to 03 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 Q~
                           Q                                                  a
concentrations of 588 |jg/m  (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
           q
to 804 |jg/m   (0.41 ppm)  (Kulle  et al., 1984).   Small decreases in Sa02  have
also been  observed  in some of these studies but  not in others;  therefore,.
interpretation of these decreases and their clinical significance  is uncertain.
     Many variables have not been adequately addressed  in the available clini-
cal  data.  Information  derived  from Oq exposure of smokers and nonsmokers  is
sparse  and somewhat  inconsistent,  perhaps partly  because  of  undocumented
variability in smoking histories.   Although some degree of attenuation appears
to occur  in  smokers,  all current results 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 differ-
ences in  response  to CL 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 compari-
son with adult males  exposed  under identical conditions has  indicated that  the
effects of 0™ on  lung spirometry were  very similar  (McDonnell et  al.,  1985c).
While a few  studies  have  investigated sex differences, they have  not conclu-
sively  demonstrated  that men and women respond differently  to 0~,  and consid-
eration 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 following 0^ 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 03, decrements in pulmonary function
are greatest on the second exposure day (Parrel! et a!., 1979; Horvath et al.,
1981; Kulle et al.,  1982;  Linn et al., 1982b); thereafter, pulmonary respon-
siveness to CL  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.s  1982b) to  7  (Horvath et al., 1981)  days.   Repeated
daily exposures to a given low effective dose of 03 does not affect the magni-
tude of decrements in pulmonary function resulting from exposure at a higher
effective dose of 03 (Gliner et al., 1983).
     There is some evidence suggesting that exercise performance may be limited
by exposure to  CU,  Decrements in forced  expiratory flow occurring with 03
exposure during  prolonged heavy exercise  (V>  =  65  to 81 L/min) along with
increased fR and decreased VT might be expected to produce ventilatory limita-
tions at near maximal exercise.  Results  from  exposure to ozone during high
exercise levels (68 to 75 percent of max VOp) indicate that discomfort associ-
ated with maximal  ventilation may be an important factor in limiting perfor-
mance (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~  concentrations  as high  as
                3
784 to 1176 ug/m   (0.4 to 0.6 ppm).   Chromosome or chromatid aberrations would
therefore be unlikely at lower 03 levels.   Limited data have indicated that 03
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,  N02,  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 simultaneous effect of PAN and 0~; however, there are not
enough data to evaluate the significance of  this effect.  Further studies are
also required to  evaluate  the relationships between 0~ 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 popula-
tions  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 environ-
mental  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,  includ-
ing determination of individual  activity patterns and adequacy of number and
location  of  pollutant monitors;  difficulty in identifying oxidant  species
responsible for observed effects;  and characteristics  of the populations  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 con-
trol led-exposure studies.   In  addition,  the measured  responses in  ambient air
can be  compared to  clean, filtered air without pollutants or to filtered air
containing artificially-generated  concentrations  of 03 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 demon-
strated that  respiratory effects  in  Los Angeles  area  residents are related  to
03  concentration  and  level  of exercise.  Such effects include:   pulmonary
                                   1-151

-------
                    TABLE 1-19.  SUMMARY TABLE:  ACUTE EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS IH FIELD STUDIES WITH A MOBILE LABORATORY3
en
IX)
Mean ozone
concentration
ug/mj ppi»
282 0.144
300 0,153
306 0,156
323 0.165
341 0.174
Measurement >c
Method
UV,
UV
UV,
UV
UV,
NBKI
UV,
NBKI
UV,
NBKI
Exposure Activity
duration level (Vg) Observed effect(s)
1 hr CE{32) Siall significant decreases in FVC (-2.11), FEV0 75
(-4.0X), FEVt.0 (-4.2%), and PEFR (-4.4X) relative
to control with no recovery during a 1-hr post-
exposure rest; no significant increases in
symptoms.
1 hr CE(53) Hi Id increases in lower respiratory symptom scores
and significant decreases in FEVi (-5.3%) and
FVC; mean changes in ambient air were not statisti-
cally different from those in purified air contain-
ing 0.16 ppm Os.
1 hr CE(38) No significant changes for total symptom score or
forced expiratory performance in normals or
asthmatics; however, FEVi remained low or
decreased further (-31) 3 hr after ambient air
exposure in asthmatics.
1 hr CE(42) Small significant decreases in FEV, (-3.3X) and
FVC with no recovery during a 1-hr postexposure
rest; TLC decreased and M\z increased slightly.
2 hr IE(2 x R) Increased symptom scores and small significant
@ 15-rain decreases in FEVi (-2.4%), FVC, PEFR, and TLC
intervals in both asthmatic and healthy subjects however,
25/34 healthy subjects were allergic and "atypi-
cal ly" reactive to 0$.
No.
of subjects
59 healthy
adolescents
(12-15 yr)
50 healthy
adults (compe-
titive bicy-
clists)
48 healthy
adults
50 asthmatic
adults
60 "healthy"
adults
(7 were
asthmatic)
34 "healthy"
adults
30 asthmatic
adults
Reference
Avol et al., ISBSa.b
Avol et al., 1984, 1985c
Linn et al,, 1983;
Avol et al., 1983
Linn et al., 1983;
Avol et al., 1983
Linn et al., 1980, 1983
    Ranked by lowest observed effect level for 03 in ambient air.
    Measurement method:  UV = ultraviolet photonetry.
   cCalibratlon method:  UV = ultraviolet photonetry standard; NBKI = neutral buffered potassium iodide.
   Tlinute ventilation reported In L/min or as a multiple of resting ventilation.  CE = continuous exercise, IE = intermittent exercise.

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                                                           3
function decrements  seen  at 03 concentrations of  282  |jg/m  (0.144 ppm) in
exercising healthy adolescents; and increased respiratory symptoms and pulmonary
function decrements  seen  at 0- concentrations  of 300 jjg/m  (0.153 ppm) in
                                                                3
heavily exercising athletes and at 0, concentrations of 341 |jg/m   (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  normal, 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 0~ than "non-allergic" normal  subjects.   Concerns raised
about the  relative contribution to untoward  effects in these field studies by
pollutants other  than 0,  have been diminished by direct comparative findings
in exercising  athletes  (Avol  et al., 1984,   1985c) showing  no  differences in
response between chamber exposures to oxidant-polluted ambient air with a mean
                             3
CL concentration  of  294 yg/m  (0.15 ppm) and purified air  containing  a con-
                                                  3
trolled concentration of  generated 03 at 314 (jg/m  (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 epidemiclogical literature  on  photochemical  oxidants.  Inves-
tigative approaches  comparing communities  with high 0,  concentrations and
communities with  low 0~ 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.
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     Studies of effects  associated with  acute exposure that are considered to
be qualitatively useful for standard-setting purposes include those on irrita-
tive 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- 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- 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, meteoro-
logical variables, and non-environmental factors in the analysis.   Although 0,,
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 a!.,  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 a!.,  1967;
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.,.  Although  several
additional  studies  have shown respiratory irritation  apparently  related to
exposure to ambient  0~ or oxidants in  community populations,  none of these
epidemiologies! 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 03 concentrations ranging from 20 to 274 ug/m
(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
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quantitative data on  acute  effects  of CL because of methodological 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-
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 a!.,
1985a,b) which have shown small decreases in forced expiratory volume and flow
            o
at 282  ug/m  (0.144  ppm) of 03 in the ambient air;  and with the results from
the controlled  human  exposure  studies in exercising children  which have shown
                                                         3
small decrements  in  forced  expiratory volume at 235 pg/rn   (0.12  ppm)  of 0,
(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 medica-
tions,  the  absence of records  for all days  on which symptoms could  have oc-
curred, and the possible 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, 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 03  and tempera-
ture.   All  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 03  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 photochemical  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
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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,, 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 03 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 03  lasting  2 to 4 hr
have demonstrated decrements in forced expiratory volume and flow occurring at
and above 0.5 ppm of 03 (Chapter 10).  Airway resistance was not significantly
changed at these  Q3 concentrations.   Breathing 03 at  rest  at concentrations
< 0.5 ppm did  not significantly  impair pulmonary  function although  the occur-
rence of  some  03-related  pulmonary symptoms  has been suggested  in a number of
studies.
     One  of  the  principal modifiers  of the  magnitude  of response  to 03  is
minute  ventilation (VV),  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 VV 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  (VV > 35  L/min), since the mode of breathing changes at that
VV 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  QS with light exercise (VV < 23 L/min);
     2.   At >0.30 ppm  Q3 with moderate exercise  (V£ = 24-43 L/min);
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     3.   At >0.24 ppm 03 with heavy, exercise (VE = 44-63 L/min); and
     4.   At >0.18 ppm On with very heavy exercise (VV > 64 L/min).

Note, however, that data from specific individual studies indicate that pulmo-
nary function  decrements  occur with very heavy exercise in healthy adults at
0.15 to  0.16  ppm Q3 (Avol et  a!.,  1984) and suggest that  such effects may
occur  in  healthy adults at levels  as  low as 0.12 ppm 0., (McDonnell et a"L,
1983).   Also, pulmonary function decrements  have been observed  in children and
adolescents at concentrations  of 0.12 and  0.14 ppm 03 with  heavy  exercise
(McDonnell et  a!.,  1985b;  Avol et  a!.,  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 signi-
ficance.
     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  FEV-,  to illustrate the
effects  of  intermittent exercise and 0-  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™ 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  FEF2c_75^) are
consistent with  FEV.,  and,  therefore, are not depicted here.  It  is important
to  note,  however, that any predictions of average pulmonary function responses
to  03  only  apply 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 a!., 1984; Avol et a!.,  1984, 1985c) but the differences
between  intermittent and continuous  exercise are  not clearly established.
More experimental  data are needed  to make  any  quantitative evaluation of 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

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                        110
                     8  100
                     a
                     a

                     UJ
                     S
                     D
                         90
en
oo
                     tc.
                     o
0.
X
UJ

Q
UJ
O
tc.
O
u.

O
UJ
U)
                         80
                         70
                         60
                                                                VERY HEAVY

                                                                EXERCISE
 ••-.  LIGHT EXERCISE
    MODERATE

     EXERC|SE
                                                0.2                 0.4


                                                        OZONE CONCENTRATION, ppm
0.6
                                                                                       0.8
                              Figure 1-14. Group mean decrements in 1 -sec forced expiratory volume during 2-hr ozone

                              exposures with different levels of intermittent exercise: light (V"E < 23 L/min); moderate

                              (VE = 24-43 L/min); heavy (Vg = 44-63 L/min); and very heavy (V"E > 64 L/min).

                              (Concentration-response curves are taken from Figures 12-2 through 12-5 in Chapter 12,

                              Volume V.)

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within 24 hr.   In some individuals, an enhanced responsiveness to a  second 0~
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- 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 al., 1981; Gliner et al., 1983; McDonnell et al., 1983; Kulle et al., 1985).
Despite large  intersubject  variability,  individual responsiveness to a given
DO concentration is quite reproducible (Gliner et al., 1983; McDonnell et al.,
1985a).  Some  individuals,  therefore,  are consistently more responsive to 0™
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 CU 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  0.,.   Characterization  of individual responses to
03,  however,  is pertinent since it permits the  assessment of  a  segment of the
general population that  is  potentially at-risk to  0-  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 environ-
mental chambers to  03 (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, or ambient  air containing 03 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 03 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
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not characteristic of clinical exposures to 03, 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 CL,
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 control!ed-
exposure studies, however, have been designed  to examine the  effects of 03  on
exercise performance (Chapter 10).   In  one  study,  light intermittent exercise
(Vp = 20-25 L/min) at a high  03 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 result  of changes  in lung  mechanics or  both  is still
unclear and needs to be elucidated.
     Environmental conditions such as heat and  relative  humidity  may alter
subjective symptoms  and physiological  impairment associated with 0~ exposure.
Modification  of  the  effects  of 03  by these factors may be attributed  to  in-
creased 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
imtnunologic 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):
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     1.    Age.   Although changes  in  growth and development of the  lung with
age have been postulated as one of many factors capable of modifying responsive-
ness to 0~,  sufficient  numbers of studies have not been performed to provide
any sound conclusions for effects of different age groups on responsiveness to
°3'
     2.    Sex.   Sex  differences  in  responsiveness  to ozone  have not been
adequately studied.  Lung function of women, as assessed by changes in FEV-, QJ
might be affected  more  than that of men  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 0™ than nonsmokers.
     4,    Nutritional Status.   Antioxidant properties of vitamin E  in preventing
ozone-initiated peroxidation J_n vitro are well demonstrated and their protective
effects jji vivo are  clearly demonstrated  in  rats and  mice.  No evidence  indi-
cates, however, that man would benefit from increased vitamin E intake relative
to ambient ozone exposures.
     5.    Red Blood Cell EnzymeDeficiencies.  There have been too  few studies
performed to document  reliably that individuals with a hereditary  deficiency
of glucose-6-phosphate  dehydrogenase may  be  at-risk to significant  hematolog-
ical effects from  03 exposure.   Even if 0*3 or  a reactive product  of (k-tissue
interaction were to penetrate the red blood cell after j_n vivo exposure, 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, (<0.7 ppm
for  approximately  2  hr) induce a typical  temporal pattern of response (Chap-
ter 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  following 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  03 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
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responsiveness.   In  addition,  concentrations of 0, that  have no detectable
effect appear  not to invoke changes in  response  to  subsequent exposures at
higher 0, 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 pollution 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 standard-
setting  (<0.3  ppm On) 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 03 exposure to a similar degree as  normal, healthy  subjects.
Patients with  chronic obstructive lung disease  and/or asthma have  not shown
increased responsiveness to 03 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 0- can be adequately  determined.  None of these factors has been sufficiently
studied in relation  to 0-, exposures to give definitive  answers.
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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™ exposure.
Thus,  it  could be hypothesized that humans  exposed  to CU could experience
decrements in  their  host  defenses against infection.  At  the  present time,
however, these effects have not been studied in humans exposed to 03.
     Animal studies have also reported a number of extrapulmonary responses to
0,,  including  cardiovascular,  reproductive,  and teratological effects, along
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
0_.  While similar effects  have been described in circulating cells from  human
subjects exposed  to  high  concentrations  of 0,,,  the results were either incon-
sistent 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 pptn produce
remarkably similar types of responses in all species examined.  A characteristic
ozone  lesion  occurs  at  the junction of  the  conducting airways and the gas-
exchange regions of the lung after acute Q3 exposure.  Dosimetry model simula-
tions  predict that  the  maximal  tissue dose of  03 occurs  in this region of the
lung.  Continuation  of  the  inflammatory  process during longer  03 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 03 has yet been  pub-
lished, but centriacinar  inflammation has been shown to occur.
     Since substantial animal data exist for 03~induced changes in lung struc-
ture 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.
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1.11.4  Health  Effects of Other Photochemical Oxldants and PollutantMixtures
     Controlled human studies have not consistently demonstrated any modifica-
tion of respiratory effects for combined exposures of 03 with S02, NO-, CO, or
HgSO. and other particulate aerosols.   Ozone alone is considered to be respon-
sible 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  interac-
tions.  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 is  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  Identificationof Potentially At-Risk Groups
     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 pre-
existing  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.  Neverthe-
less, 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

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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
general population, may also impair or further curtail 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  potential  risk  from exposure to
ozone.  First unusual responsiveness to ozone has been observed in some individ-
uals  ("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 deter-
mining 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 influenc-
ing  responses  to ozone.   Data remain inconclusive at the present, however,
regarding  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

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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 parti-
     culate matter and sulfur oxides. Research  Triangle  Park, NC: U.S. Environ-
     mental 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 tech-
     niques. U.S.C. 42: §7408.


1.12.2  References for Properties, Chemistry, and Transport  of Ozoneand
        Other Photochemical Qxldants and Their  Precursors

Aikin, A.  C.;  Herman, J.   R.; Maier,  E.  J.  R.; McQuillan,  C.  J. (1983)  In-
     fluence 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 pollu-
     tion: a review.  Environ. Sci. Techno!. 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.: in press.

Atkinson,  R,;  Aschmann,  S. M. (1984)  Rate  constants for the reactions of 03
     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.;  Darna!!, 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

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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 N03  radicals  with  .
     series  of organics  in  air at 298 ± 1 K, J. Phys. Chem. 88: 1210-1215.
Atkinson,  R.;  Pitts,  J.  N., Jr.;
     actions of  dimethyl  sulfide
     1584-1587.
                              Aschmann,  S.  M.  (1984b)
                             with NOS and OH radicals.
Tropospheric re-
J. Phys. Chem. 88;
Atkinson, R.; Aschmann, S. M.; Winer, A. M.; Pitts, J. N. , Jr.  (1984c)
     Kinetics of  the gas-phase reactions  o,f  N03 radicals with a  series of
     dialkenes,  cycloalkenes,  and monoterpenes at 295 ± 1 K. Environ.  Sci.
     Techno!. 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 N03 radicals with  a  series
     of aromatics at 296 ± 2 K. Int. J. Chem. Kinet. 16: 887-898.
Atkinson, R.;  Plum,  C.  N. ; Carter, W.
     (1984e) Kinetics of the gas phase
     of alkanes at 296 ±2 K. J. Phys.
                                   P.  L.;  Winer, A. M.; Pitts, J.
                                   reactions of N03 radicals with
                                   Chem.  88: 2361-2364.
           N., Jr.
           a series
Atkinson, R.; Aschmann, S. M.; Winer, A. M.; Pitts, J. N., Jr.  (1985)  Kinetics
     and atmospheric  implications  of the gas-phase reactions  of  N03  radicals
     with a series of monoterpenes and  related organics  at 294 ±  2  K.  Environ.
     Sci. Techno!. 19: 159-163,
Bach
Bell
,  W.  D., Jr. (1975) Investigation of ozone and ozone precursor  concentra-
 tions  in nonurban locations in the eastern United States; phase II. meteo-
 rological  analyses.  Research Triangle Park,  NC:  U.S.  Environmental Protec-
 tion Agency,  Office of Air Quality Planning and Standards; EPA report no.
 EPA-450/3-74-034a.  Available  from  NTIS,  Springfield,  VA;  PB-246899.

,  G.  B.  (1960)  Meteorological conditions during oxidant episodes in
 coastal  San Diego County  in October and November, 1959. Sacrament
 Department of Public Health.
                                                              i iouuea  in
                                                              Sacramento,  CA:
Bellinger, M.  J.;  Parrish, D. D. ; Hahn, C.; Albritton,  D.  L. ;
     C.  (1982)  NO   measurements in clean continental  air.  In:
     2nd  symposium  on composition of  the nonurban troposphere;
     burg, VA.
                                                           Fehsenfeld, F.
                                                           Proceedings of
                                                           May;  Williams-
Calvert, J.  G.;  Stockwell,  W.  R.  (1983) Acid generation in the troposphere by
     gas-phase chemistry. Environ. Sci.  Techno!.  17: 428A-443A.

Calvert, J. G.; Stockwell, W.  R.  (1984)  The  mechanism  and  rates  of the  gas-phase
     oxidation of  sulfur dioxide and  nitrogen  oxides  in the  atmosphere.   In:
     Calvert, J. G., ed., Acid precipitation: S02,  NO  and  N02 oxidation mechan-
     isms:  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. ;
     chamber  studies  of temperature effects  in
     Sci. Techno!. 13:  1094-1100.
                                             Pitts,  J.  N.,
                                            photochemical
   Jr.  (1979)  Smog
   smog.  Environ.
                                    1-167

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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.  Techno!. 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. Techno!.
     15: 831-834.

Chameides, W. L.; Davis, D. D,  (1982) The free radical chemistry of cloud  drop-
     lets 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 Basin.
     Environ. Sci.  Technol. 15: 933-939.

Clark, T. L.; Clarke, J. F. (1982) Boundary layer transport  of  NO  and 03  from
     Baltimore, Maryland—a  case  study.  Presented  at: 75th  annual 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 pollu-
     tion 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 environ-
     ment. 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. Health. A16: 1-8.

Cox, R. A.;  Burrows, J.  P. (1979) Kinetics  and mechanism of the disproportion-
     ation 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 composi-
     tion of the nonurban  troposphere;  May; Williamsburg,  VA.
                                    1-168

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References for Properties,Chemistry, Transport (cont'd.)

Crutzen, P. J.; Fishman, J. (1977) Average concentrations of OH in the tropos-
     phere, and the  budgets  of CH4, CO, H2, and CH3CC13. Geophys. Res. Lett.
     4: 321-324.

Daniel sen, E.  F.  (1968)  Stratospheric-tropospheric  exchange based on radioac-
     tivity, ozone and potential vorticity. J. Atmos. Sci.  25: 502-518.

Daniel sen, 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 trans-
     port, ID. SJ.^M measurements, and  meteorological  analyses of tropopause
     folding. JGR J.  Geophys. Res. 82: 5867-5877.

Darnall,  K.  R.;  Lloyd,  A. C. ; Winer,  A.  M.;  Pitts, J. N. , Jr. (1976) Reac-
     tivity scale for atmospheric hydrocarbons based on reaction  with  hydroxyl
     radical. Environ. Sci. Techno!. 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 photo-
     chemical  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) flux  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 forma-
     tion  in  the United  Kingdom.  Environ.  Sci. Techno!. 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:  191-506.

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 photo-
     chemical  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
     oxfdant- and N02-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-600/3-77-001b.

Diraitriades, B.  (19775)  Oxidant control strategies.  Part  I.  Urban oxidant-
     control strategy  derived  from existing smog chamber data. Environ. Sci.
     Techno!. 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 photo-
     chemical 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.; TommerdahlI, 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.  Avail-
     able from: NTIS, Springfield, VA; PB-300481.

F.R. (1979, November 14) 44: 65667-65670.

Ferman, M. Z, A.  (1981) Rural nonmethane hydrocarbon concentrations and  composi-
     tion. In:  Bufalini, J.  J.; Arnts, R. R., eds.  Atmospheric biogenic  hydro-
     carbons. 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 Asso-
     ciation; 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.; Seller, 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

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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.

Gertler, 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 particles,  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. Techno!. 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 mechanisms  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 monoter-
     pene  hydrocarbons  in  rural  atmospheres. JGR  J.  Geophys.  Res.   84:
     5083-5088.

Holdren,  M.  W.;  Spicer,  C.  W.;  Hales,  J.  M. (1984)  Peroxyacetyl nitrate solu-
     bility  and  decomposition  rate  in acidic water.   Atmos.  Environ. 18:
     1171-1173.

Holzworth, G. C. (1964) Estimates of mean maximum mixing depths in the contig-
     uous  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.

Hosier,  C.  R.  (1961)  Low-level 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

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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.  Techno!.  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  measure-
     ments 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. Techno!.  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 memo-
     randum  ERL  AR-55.  Available  from:  NTIS,  Springfield,  VA; PB-257368.

Lee, Y.-N.;  Senum,  G.  I.; Gaffney,  J. S.  (1983)  Peroxyacetyl nitrate (PAN)
     stability,  solubility,  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 role
     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; El Monte, CA.

Liu, M.-K.; Morris, R.  E.; Killus, 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
     potential ozone impacts from natural hydrocarbons.  I.  Development and
     testing of a chemical mechanism for the NO -air photooxidations of  isoprene
     and  crpinene under ambient conditions.  Atmos.  Environ. 17:  1931-1950.

Logan, J.  A.  (1983) Nitrogen oxides in  the  troposphere:  global  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 Pollu-
     tion; 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. Final  report to
     U.S.  Environmental  Protection   Agency,  SRI  Project  6780-8.  Research
     Triangle  Park,  NC:  U.S. Environmental 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

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References forProperties,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
     study 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+ CH3SCH3. 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. Environ-
     mental Protection  Agency, Environmental  Sciences Research  Laboratory;  EPA
     report  no.  EPA-600/4-76-025.  Available from: NTIS,  Springfield, VA;
     PB-24012S.

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:
     Diraitriades,  B.,  ed. International conference on  photochemical  oxidant
     pollution 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

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Referencesfor 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. Environ-
     mental 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. Bull. Am.  Meteorol. Soc. 33: 247-250.

Scheutzle, D.;  Rasmussen, R.  A.  (1978)  The  molecular 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., S02, NO and N02 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. Pre-
     sented at:  the 75th  annual  meeting of  the  Air Pollution  Control  Associa-
     tion; June; New Orleans,  LA.  Pittsburgh,  PA:  Air Pollution Control  Asso-
     ciation; 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
     regional  air pollution study, 1975-1976. Atmos.  Environ.  16:  1311-1321.

Singh,  H.  B.;  Ludwig, F.  L.;  Johnson,  W.  B. (1977)  Ozone in clean 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,  0..  H., ed.  (1968) Meteorology and atomic energy 1968. Washington, DC:
     U.S.  Atomic Energy  Commission.  Available  from:  NTIS, Springfield, VA;
     TID-24190.
                                   1-175

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References for Properties, Chemistry,, Transport (conf 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  concen-
     trations  in a  multiday smog episode in  the  California South  Coast Air
     Basin by long-path!ength Fourier-transform infrared spectroscopy.  Environ.
     Sci. Techno!.  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  re-
     quirements 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

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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.

Wellington, 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  Triangle 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 photo-
     chemistry 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

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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.
     Techno!. 14: 1257-1260.

Wolff, G. T.;  Lioy,  P. J.;  Meyers,  R.  E. ; Cederwall,  R.  T. ;  Wight, 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. Techno!. 11: 506-510.

Wolff, G. T.;  Lioy,  P.  J.;  Wight,  G.  D.;  Pasceri, R.  E. (1977b) Aerial inves-
     tigation 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 beryl-
     iium-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 andOther Photochemical
        Oxidarits and Their Precursors


Allen, A. 0.;  Hochanadel, C. J.; Ghormley,  J. A.;  Davis,  T. W.  (1952) Decom-
     position  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 analysis 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 H202. 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.  Environ-
     mental  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

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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.

Bruekmann, P. W.;  Winner,  H.  (1983) Infrared spectroscopic study of peroxy-
     acetyl nitrate (PAN) and its decomposition products. Environ. Sci. Techno!
     17: 352-357.

Bufalini, J, J.;  Brubaker,  K.  L. (1969)  Symposium on chemical reactions in
     urban atmospheres;  October.  Warren,  MI: General Motors Research Labora-
     tories.

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. Techno!. 6:  816-821.

Burton, C.  S.;  Bekowies, P. J.;  Pollack,  R. I.;  Connell,  P.  (1976) Oxidant/
     ozone  ambient measurement methods:  an  assessment and evaluation.  San
     Rafael, CA:  Systems Applications, Inc.; EF76-111R.

California 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:  July-
     August-September.   10(13):  2-3.  Available from:  Technical  Service  Div.,
     California Air Resources Board, Sacramento, CA.

Chameides,  W.L.;  Tan,  A. (1981).   The  two-demensional 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. Techno!. 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

-------
Referencesfor 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 a!., 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 photo-
     chemical  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  ozone determinations by
     ultraviolet photometry  and  gas-phase titration.  Environ. Sci.  Techno!.
     10: 897-899.

DeMore,  W. B.;  Romanovsky,  J. C.; Feldstein, M.; Hamming, W. J.;  Mueller, P.
     K.  (1976) Interagency comparison of iodometric methods for ozone determi-
     nation.  In:  Calibration in  air  monitoring:  a symposium; August  1975;
     Boulder, CO. Philadelphia, PA: American Society for Testing and Materials;
     pp. 131-143; ASTM special technical publication 598.

Dietz, W. A.  (1967)  Response factors  for gas chromatqgraphic  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 calibra-
     tion 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. Techno!. 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

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References for Sampling and Measurement (cont'd.)

Gay, B. W., Jr.; Bufalini, J. J. (1972a) Hydrogen'peroxide  in the  urban atmos-
     phere. In: Gould,  R.  F. ,  ed. ,  Photochemical  smog and ozone  reactions.
     Washington, DC:  American Chemical  Society; pp.  225-263.  (Advances  in
     chemistry series: 113.)
                                      o
Gay, B. W., Jr.; Bufalini, J. J. (1972b) Hydrogen peroxide  in the  urban atmos-
     phere. 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. Techno!. 10: 82-85.

Grosjean, D.  (1983)  Distribution of  atmospheric  nitrogenous  pollutants at a
     Los  Angeles area smog receptor  site. Environ.  Sci.  Techno!.  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.

Mauser, T.  R.;  Cummins, R.  L.  (1964) Increasing sensitivity of 3-methyl-2-
     benzothiazolone.hydrazone test for analysis  of  aliphatic aldehydes in air.
     Anal. Chem. 36: 679-681.

Heikes,  B.G.  (1984)  Aqueous H202  production  from  Q3 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  (R02N02).  Decomposition of peroxyacyl  nitrates.  Atmos. Environ.
     99:  3198-3199.

Hodgeson,  J.  A.;  Krost, K.  J.;  O'Keeffe, A.  E. ;  Stevens, R.  K.  (1970)  Chenri-
     luminescent 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-600/3-77-001a.  Available  from:  NTIS,  Springfield, VA;
     PB-264232.


                                    1-181

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References for Sampling and Measurement (cont'd.)

Holdren, M. W.;  Spicer,  C. W.  (1984)  Field compatible calibration procedure
     for peroxyacetyl nitrate.  Environ. Sci. Techno!.  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 methods 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  chemilumines-
     cent measurements of  NO  .  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  pollu-
     tion. 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. Technol.  12:  1072-1076.

Kravetz, T.  M.;  Martin,  S. W.;  Mendenhall,  G.  D.  (1980) Synthesis of peroxy-
     acetyl and  peroxyaroyl  nitrates:  complexion of peroxyadetyl  nitrate with
     benzene.  Environ. Sci. Technol. 14: 1262-1264.

Kunen,  S.  M.; Lazrus, A,  L.; Kok, G.  L.;  Heikes,  B.  G.  (1983) Aqueous oxida-
     tion  of  S02 by hydrogen peroxides. JGR J. Geophys. Res. 88: 3671-3674.

Kuntz,  R.;  Lonneman, W.;  Namie, G;;  Hull,  L. A. (1980) Rapid determination 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

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References for Sampling 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.; Darnschen, 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 instru-
     mentation 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:  technical  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 deter-
     mination  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  pre-
     paration  of  pure standards of peroxyacetyl  nitrate for atmospheric  analyses.
     Atmos.  Environ. 16:  2447-2450.
                                    1-183

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References for Sampling and Measurement (cont'd.)

Ogle, L. D.; Hall, R. C. ; Crow, W. L.; Jones, A. E.; Gise, J. P. (1982) Devel-
     opment of preconcentration and chromatographic procedures for the contin-
     uous and  unattended  monitoring  of hydrocarbons in ambient  air.  Presented
     at: 184th  national  meeting of the American Chemical Society; September;
     Kansas City, MO. Austin, TX: Radian Corporation.

O'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 S02, H202, Os, and HNOS. In:  Keith, L.  H.,  ed. Energy and environmental
     chemistry, v. 2: acid rain. Ann  Arbor, MI: Ann Arbor Science; pp. -245-262.

Paw,  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,  Office  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 chemilumine-
     scent 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.; Smith,  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

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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. Environ-
     mental 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.;  Mauser, 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 per-
     meation  devices and nitrite  ion  as standards  for the  colorimetric  deter-
     mination of nitrogen dioxide. Environ. Sci. Techno!.  4: 924-929.

Schiff, H.  (1985)  York University, Toronto, Canada.  Personal  communication:
     work in progress.

Sevcfk, J.  (1975) Detectors  in gas chromatography.  Prague, Czechoslovakia:
     Elsevier Scientific Publishing Company.

Sexton, F. W, ;  McElroy,  F.  F. ; Michie,  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 reac-
     tions  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 per-
     formance 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

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References for Sampling and Measurement (cont'd.)

Stevens, R.  K. ;  Hodgeson,  J.  A.; Ballard, -L. 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 Angeles, 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 atmos-
     pheres.  Atmos. Environ. 12: 865-875.

Tuazon, E. C.; Winer, A.  M.; Graham,  R.  A.; Pitts,  J.  N.,  Jr.  (1980)  Atmos-
     pheric  measurements  of trace  pollutants  by kilometer-pathlength FTIR
     spectroscopy. Adv.  Environ. Sci.  Techno!.  10: 259-300.

Tuazon, E. C.; Winer, A.  M.; Graham,  R. A.; Pitts,  J. N.,  Jr. (1981a) Atmos-
     pheric  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 concen-
     trations in  a multiday smog episode  in the  California South  Coast Air
     Basin by long path  length  Fourier  transform   infrared  spectroscopy.
     Environ. Sci. Techno!. 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

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References for Sampling andMeasurement (cont'd.)

U.S.  Environmental  Protection  Agency.  (1978) Air quality  criteria for ozone
     and other photochemical oxidants. Research Triangle Park, NC: U.S. Environ-
     mental 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.; Cantrell, C. A.  (1983) Luminol-based nitrogen
     dioxide detector.  Anal. Chem. 55: 937-940.

Westberg, H. H.; Holdren, M. W.;. H111, 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.  CAPA-
     11-71.                             '             .-...-

Winer,   A.  M.;  Peters, J. - M. ; .Smith,. J. P.;  Pitts, J. N. ,. Jr.  (1974) Response
     of commercial  chemiluminescent N0-N02  analyzers  to other  nitrogen-containing
     compounds. Environ. Sci. Techno!. 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 pero-
     xidase: 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 analysis of H202 -in  air. Geophys. Res. Lett.
     9: 231-234.      •          '  -.. v..'  ,       :       .   i '•  •


1.12.4  References  for  Concentrations of Ozone  and  Other  Photochemical Oxidants
        in  Ambient  Air  -  .    .   .  ,    ,•--'.,  -,-••-   '        •.•"-,..

Altshuller, A.  P.  (1983) Measurements of  the  products of atmospheric photo-
     chemical  reactions in  laboratory studies  and  in ambient air—relation-
     ships  between  ozone and other products.  Atmos.  Environ.  17: 2383-2427.
                                    1-187

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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 Assoc-
     ciation; June;  Philadelphia,  PA.  Pittsburgh, PA:  Air  Pollution Control
     Association; paper no. 81-22.1

Cleveland, W. S.; Graedel, T. E.; Kleiner, B. (1976a) Photochemical  air pollu-
     tion: transport  from  the New York City area  into  Connecticut and Massa-
     chusetts. 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.; Stasiuk,  W. N.; Mohnen, V.  (1977) Ozone in  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.

Parley, 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.
                                   1-188

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References for Ambient Air Concentrations (cont'd.')

Grosjean, D.  (1981)  Critica-1  evaluation  and comparison of measurement methods
     for nitrogenous  compounds  in  the  atmosphere.  Final  report,  A 706-05,  for
     Coordinating  Research  Council.  Environmental  Research and Technology.
     Westlake Village, 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 south-
     eastern 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 measure-
     ment 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

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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.;
     O'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.

Sabersky, 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

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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  Retrieval  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.

Seller, 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. ; Sh-igeishi, 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). Albany, 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. ;  Holguin, 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 peroxy-
     acetyl 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

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References for Ambient Air Concentrations (cont'd.)

Tuazon, E. C. ;  Winer,  A.  M. ; Graham, R. A.; Pitts, J. N. , Jr. (1981a) Atmos-
     pheric 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 concen-
     trations  in a  multiday smog episode in  the  California South Coast Air
     Basin by long path length Fourier transform infrared  spectrometry. Environ.
     Sci.  Techno!.  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. Environ-
     mental 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

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Westberg, H.; Allwine,  K.;  Robinson,  E,  (1978)  Measurement of light hydrocar-
     bons and oxidant  transport:  Houston area  1976.  Research Triangle Park,
     NC: U.S. Environmental Protection Agency, Office of Research and  Develop-
     ment; 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  Control  Association,
     Boston, MA:  June.   Pittsburgh,  PA:  Air Pollution  Control  Association.
     Paper no.  75-58.6.

Wolff, G. T.; Lioy, P. J.; Taylor,  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 Oxidantson
         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 information.  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-6QO/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)  Ozone  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

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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.; Qshima, 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 assess-
     ment 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.;  Unswprth,  M.  H.  (1982)  Effects of low concentra-
     tion 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 03 expo-
     sures  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

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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  air  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.;  Campbell, F. J.  (1968) Influence of  low  levels 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.  Qua!.  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:  phytotoxi-
     city 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.,  eds.  Crop loss
     assessment: proceedings of E. C. Stakman  commemorative  symposium. Univer-
     sity  of Minnesota,  Agricultural Experimental  Station;  miscellaneous
     publication no. 7; pp. 296-305.

                                   1-195

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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.  Phyto-
     pathology 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. Phytopathol-
     ogy 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. I., 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.  Techno!.
     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, Con/all is,  OR.
                                    1-196

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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  cultivars after  acute ozone exposure  in  the seedling stage.  J.
     Am. Soc. Hortic. Sci. 104: 754-759.

Hoffman, G.  J.;  Maas, E.  V.; Rawlins, S.  L. (1975)  Salinity-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, Loll urn perenne and Phalaris  aquatica to  chronic ozone
     exposure. Aust. J.   Plant Physio!. 7: 511-517.

Howell, R.  K.;  Rose,  L.  P.,  Jr.  (1980) Residual air pollution effects on soy-
     bean 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).


                                   1-197

-------
References for Vegetation Effects (cont'd.)

Jacobson, J.  S.  (1982) Ozone and the growth and productivity of agricultural
     crops.  In:  Unsworth,  M.  H.; Qrmrod, 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.;  Miller, 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.
     Qua!. 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.,  Miller,  J.  E.; Smith,  H.  J.  (1985) Impact of ozone on winter
     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 air  quality data analysis  system for
     interrelating effects,  standards,  and needed source reductions:  Part 8.
     An  effective mean 03 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.
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References for Vegetation Effects(confd.)

Lefohn, A. S.; Tingey, D. T. (1984) The co-occurrence of potentially 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 yield  effects  from
     ambient air pollutants  in the Ohio River Valley.  J. Air Pollut. Control
     Assoc.  32:  146-150.

Maclean, D.  C.;  Schneider, P. E. (1976) Photochemical oxidants  in Yonkers, New
     York: effects on yield of bean and  tomato.  J.  Environ.  Qua!.  5:  75-78.

Male, L.; Preston, E.; Neely, G. (1983) Yield response  curves of crops exposed
     to S02 time 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.
                                      1  • i    '   i
Manning,  W.  J.; Feder,  W.  A.;  Perkins, I.  (1970a)  Ozone and  infection  of
     geranium flowers by Botrytis clnerea. Phytopathology 60: 1302.

Manning,  W.  J.; Feder,  W.  A.; Perkins,  I.  (1970b)  Ozone injury increases
     infection of geranium leaves by Botrytis 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.

Mclaughlin,  S.  B.;  Shriner, D. S.; McConathy,  R.  K.; Mann,  L.  K.  (1979) The
     effects  of  S02  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.)

Middle-ton, J. T.; Kendrick, J. B., Jr.; Schwalm, H. W. (1950)  Injury to herba-
     ceous 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: Con/all is
     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. Techno!. 6: 427-430.

Musselman, R. C.; Oshima, R.  J.;  Gallavan, R.  E. (1983) Significance of pollut-
     ant  concentration distribution  in the response of 'red  kidney' beans to
     ozone. J. Am. Soc, Hortic.  Sci. 108: 347-351.

Neely, G.  E.; Tingey,  D. J.;  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 photochemi-
     cal  oxidant  pollution and its control:  proceedings,  volume II;  September
     1976; Raleigh, NC. Research Triangle Park,  NC: U.S.  Environmental Protec-
     tion  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) Foliar  injury response of petunia
     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. Qua!. 2: 518-520.

Olszyk, D.  M.;  Tibbitts, T.  W.  (1981)  Stomatal  response and  leaf injury  of
     Pi sum sativum  L.  with S02  and  03  exposures.  Plant Physio!.  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

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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
     specific gravity of Populus 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-l,5-biphosphate  carboxylase  in alfalfa  foliage.  Plant  Physio!.
     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.
     Techno!. 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  03  and/or S02  exposure causes
     a linear decline in soybean yield. Environ.  Pollut. (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

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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, CO:
     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  meeting the secondary national ambient  air
     quality  standards:  final  report. Menlo Park,  CA:  SRI  International; pro-
     ject 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  t°  ':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. Qua!.  5: 410-412.
                                    1-202

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References for Vegetation Effects (cont'd.)

Thompson, C. R.; Kats, G.; Pippen, E. L ; Isom, W. H. (1976b) Effect of photo-
     chemical 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-600/3-77-001b.

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.  Available from:  NTIS, Spring-
     field,  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 control:  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 onion-
     leaf  dieback: open-top  chamber studies.  Phytopathology 67: 1080-1084.
                                    1-203

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References for VegetationEffects (cont'd.)

Wukasch, R, T.;  Hofstra, G. (1977b)  Ozone  and Botrytis spp.  interaction  in
     onion-leaf dieback: field studies. <3. 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. Techno!. 17: 371-373.


1.12.6  References for Effects of Ozone on Natural  Ecosystems  and  Their Components


Adams, H.  S.;  Stephenson, S,  L.;  Biasing, T.  J.;  Duvick,  D. N. (1985) Growth-
     trend declines  of ^spruce 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 sensi-
     tivity 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.
                                                                      m
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.

Hacskaylo,  E.  (1972)  Mycorrhizae:   the  ultimate in  reciprocal  parasitism?
     BioScience 22: 577-583.

Hacskaylo, E. (1973) The Torrey  symposium on current aspects of fungal develop-
     ment;  IV.  Dependence  of  mycorrhizal fungi  on  hosts.  Bull.  Torrey Bot.
     Club 100: 217-223.

Hogsett, W. E.; Plocher, M.; Wildman, V.; Tingey, 0. 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, R."L.; Cobb, F. W., Jr.;  Wilcox, W. W.; Rowney,  D. L. (1980)  Effects of
     photochemical  oxidant injury  of ponderosa and  Jeffrey  pines on  suscepti-
     bility 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'. Techno!. 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 03,  N02,
     and/or  S02 on  Platanus occidental is. 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  dis-
     cussion  papers. J. Air Pollut.  Control  Assoc.  35:  919-922.
                                    1-205

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References forEcosystem 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 G1omus fasciculatus and growth of
     'Troyer1 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 pollu-
     tant  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.

Miller,  P.  R.;  Parmeter,  J. R.,  Jr.; Flick,  B.  H.; Martinez,  C.  W. (1969)
     Ozone dosage response of  ponderosa pine seedlings.  J.  Air  Pollut. Control
     Assoc. 19: 435-438.

Miller,  P.  R.;  Taylor, 0. C.;  Wilhour,  R.  G.  (1982) Oxidant air  pollution
     effects  on a western  coniferous  forest ecosystem. Con/all is, 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, 1st 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

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References for Ecosystem Effects (cont'd.)

Parmeter, J,  R.,  Jr.;  Bega, R. V.;  Neff,  T.  (1962) A chlorotic  decline of
     ponderosa  pine  in southern  California.  Plant  Dis.  Rep.  46: 269-273.

Pattern, R.  L.  (1981)  Effects of ozone  and sulfur dioxide on height  and stem
     specific gravity of Populus 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  photo-
     synthesis 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 commun-
     ities. 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.  Environ-
     mental 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. Techno!. 17:  371-373.
                                                                i

1-12.7. References for Effectsof 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

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References for Nonbiologlcal 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. Techno!. 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.  Environ-
     mental 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) Microspectrophotometnc
     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 laun-
     dering 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.

Sehmitt,  C.  H.  A.  (1960)  Lightfastness  of dyestuffs on textiles.  Am.   Dyest.
     Rep. 49: 974-980.
                                    1-208

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References for NonbiologicalMaterials (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:  evaluation  of the scientific Basis  for Ozone/Oxidants Stan-
     dards, Houston, TX,  November 28-30,  1984.  Pittsburgh, PA: Air Pollution
     Control Association.


1-12.8  References  for ToxicologicalEffects  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 trachea!
     mucous velocity in detecting airway  responses to Og.  J.  Appl.  Physio!.:
     Respir. Environ. Exercise Physio!.  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 03-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 toxi-
     city.  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.  Physio!.  31:  247-252.
                                    1-209

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References for Toxicologi calEffects  (cont'd.)

Amdur, M. 0.; Ugro, V.; Underbill, 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.;  Renters,  J.  D.; Graham,
     J, A.;  Miller,  F.  J. (1983)  Effects of subchronic exposure to a mixture
     of 63,  S02,  and  (NH4)2S04 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,  ultra-
     structural,  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. Physio!.  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 ef-
     fects of ozone and related photochemical oxidants; March 1982; Pinehurst,
     NC.  Princeton,  NJ:  Princeton Scientific Publishers, Inc.;  pp. 459-467.
     (Advances in modern environmental  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

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References for TgxicologicalEffects (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  environ-
     mental  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  spon-
     taneous activity of mice. Science  (Washington, DC) 131:  1733-1734.

Boorman,  G.  A.;  Schwartz, L. W. ; McQuillan, •• 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 mutagem'city,  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.;  McQuillan,  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.

Calabrese,  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,  NJ:  Princeton Scientific Publishers, Inc.; pp. 103-117.  (Ad-
     vances  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 atmos-
     pheric  contaminant peroxyacetyl  nitrate. Arch.  Environ.  Health  15: 739-744.
                                    1-211

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References for Toxlcological Effects (cont'd.)

Castleman, W. L.; Dungworth, D. L.; Tyler, W. S. (1973a) Cytochemically detec-
     ted  alterations  of lung  acid phosphatase  reactivity following ozone
     exposure. Lab. Invest. 29: 310-319.

Castleman, W.  L.;  Dungworth,  D.   L.; Tyler,  W.  S.  (1973b) Histochemically
     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
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Cavender,  F.  L.; Singh,  B.;  Cockrell,  B.  Y.  (1978)  Effects in rats  and guinea
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Chow,  C.  K.;  Kaneko,  J. J.  (1979) Influence of dietary vitamin E on the red
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Chow,  C.  K.;  Tappel,  A. L. (1973) Activities of pentose shunt and  glycolytic
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Chow,  C.  K.; Dillard,  C.  J.;  Tappel,  A.  L.  (1974) Glutathione  peroxidase
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Chow,  C.  K.; Mustafa, M. G.;  Cross, C.  E.; Tarkington, B.  K.  (1975) Effects  of
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Chow, C.  K. ;  Hussain,  M.  Z. ; Cross, C.  E.;  Dungworth,  D.  L. ;  Mustafa,  M.  G.
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Chow, C. K.; Cross, C.  E.; Kaneko, J. J. (1977) Lactate dehydrogenase activity
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Chow, C. K. ; Plopper, C. G.; Chiu, M.; Dungworth, 0. L. (1981)" Dietary  vitamin E
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Coffin, D.  L.; Gardner,  D.  E.;  Holzman,  R.  S.;  Wolock,  F.  J.  (1968) Influence
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DeLucia,  A.  J.;  Mustafa, M. G.;  Hussain,  M.  Z.;  Cross, C. E.  (1975b) Ozone
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Dowell,  A.  R.; Lohrbauer, L.  A.; Hurst,  D.; Lee, S. D.  (1970) Rabbit alveolar
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Dubeau,  H.;  Chung, Y. S.  (1979)  Ozone response in wild type and  radiation-
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Dungworth, D. L.; Clarke, G. L.; Plata, R. L. (1969) Pulmonary  lesions  produced
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Ehrlich,  R. (1980) Interaction between environmental pollutants and respiratory
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Ehrlich,   R.  (1983)  Changes  in susceptibility to  respiratory  infection  caused
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     effects of azone and related photochemical  oxidants; March 1982; Pinehurst,
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Ehrlich,   R.;  Findlay,  J. C.;  Fenters, J.  D.;  Gardner, D. E.  (1977)  Health
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Ehrlich,  R.; Findlay, J.  C.; Gardner,  D.  E,  (1979) Effects of repeated  exposures
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Elsayed,   N.  M.; Mustafa, M.  G.;  Postlethwait, E. M.  (1982a) Age-dependent
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Elsayed,   N.  M. ; Hacker,  A.;  Mustafa,  M.; Kuehn, K.;  Schrauzer,  G.  (1982b)
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Elsayed,   N.  M.;  Hacker,  A.  D.;  Kuehn, K.; Mustafa, M.  G.;  Schrauzer,  G.  N.
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Erdman, H.  E. ; Hernandez, t.  (1982) Adult toxicity and dominant lethals induced
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Eustis, S.  L. ;  Schwartz, L. W.;  Kosch, P. C.; Dungworth, D.   L. (1981) Chronic
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Evans, M. J.; Mayr, W.;  Bils,  R.  F.;  Loosli,  C.  G.  (1971) Effects of ozone on
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Evans, M. J. ; Johnson,  L.  V.;  Stephens,  R. J.;  Freeman, G.  (1976a) Renewal of
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Evans, M. J.; Johnson, L. V.; Stephens, R. J.;  Freeman,  G.  (1976b)  Cell  renewal
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     24:  70-83.

Evans, M.  J.;   Stephens,  R.  J.;  Freeman, G.  (1976c).  Renewal of  pulmonary
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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 hyperresponsive-
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Fafrchild, E. J., II. (1967) Tolerance mechanisms:  determinants  of lung responses
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Fetner, R. H. (1962)  Ozone-induced chromosome breakage  in human  cell cultures.
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Fletcher, B. L.; Tappel, A. L. (1973)  Protective effects of dietary crToco-
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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
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Friberg,  L,;  Holma, B.;  Rylander,  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.
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Fujimaki, H.; Ozawa, M.; Imai, T. ; Shimizu,  F.  (1984) Effect of  short-term
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Fujinaka, L.  E.; Hyde,  D. M.;  Plopper,  C. G.;  Tyler, W.  S. ;  Dungworth, D. L.;
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Fukase, 0.; Isomura, K. ; Watanabe,  H.  (1975)  Effect of ozone on glutathione
     i_n vivo.  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
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Gardner,  D.  E. ; Graham, J. A.  (1977) Increased pulmonary  disease mediated
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Gardner, D. E.; Pfitzer, E. A.; Christian; R. T.; Coffin, D.  L.  (1971) Loss  of
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Gardner,  D.  E. ; Lewis,  T,  R.;  Alpert,  S.  M.;  Hurst,  D.  J.; Coffin,  D.  L.
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Gardner,  D.  E. ; Illing, J.  W.;  Miller,  F. J.;  Coffin, D.  L.  (1974) The effect
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     Pathol.  Pharmacol.  9:  689-700.

Gardner,  D.  E. ;  Miller, F. J. ;  Illing,  J.  W.'; Kirtz, J.  M.  (1977) Increased
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Gershwin, L. J.; Osebold, J. W.; Zee, Y. C. (1981) Immunoglobulin  E-containlng
     cells  in  mouse lung following allergen  inhalation and ozone exposure.
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Gertner, A.;  Bromberger-Barnea, B.; Dannenberg,  A.  M., Jr.; Traystman, R.;
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Gertner, A.;  Bromberger-Barnea,  B.;  Traystman,  R.;  Berzon, D. ; Menkes,  H.
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Gertner, A.;  Bromberger-Barnea, B.; Traystman,  R.; Menkes, H.  (1983c) Effects
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Gertner, A.; Bromberger-Barnea, B,; Kelly, L.; Traystman,  R.; Menkes, H. (1984)
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Gillespie,  J.  R.  (1980)  Review of the  cardiovascular and pulmonary function
     studies on  beagles  exposed for 68 months  to auto exhaust and other air
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Goldstein,  E.; Tyler,  W.  S.; Hoeprich,  P.  D. ;  Eagle, C. (1971a) Ozone and the
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Goldstein,  E.; Tyler, W.  S.; Hoeprich, P.  D.; Eagle,  C. (1971b) Adverse influ-
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Goldstein,  E.; Eagle, M.  C.; Hoeprich, P.  D.  (1972)  Influence of ozone on pulmo-
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Goldstein,  B.  D.; Hamburger, S. J.;  Falk,  G.  W.;  Amoruso, M.  A.  (1977) Effect
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Gooch,  P.  C.;  Creasia, D. A.;  Brewen, J.  G.  (1976)  The cytogenetic effect  of
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Gordon, T.; Taylor,  B,  F.; Amdur,  M.  0.  (1981) Ozone  inhibition of tissue
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Gordon, T.; Venugopalan,  C. S.; Amdur, M. 0.; Drazen, J. M.  (1984)  Ozone-induced
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Graham, J.  A.;  Menzel,  D.  B.; Miller,  F.  J.;  111 ing,  J.  W. ;  Gardner,  D.  E.
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Graham, J.  A.;  Menzel,  D.  B. ; Miller,  F.  J. ;  II ling,  J.  W. ;  Gardner,  D.  E.
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     with  mixed-function oxidase  inducers  and  inhibitors.  Toxicol.  Appl.
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Graham, J.  A.;  Miller,  F. J.; Gardner,,D.  E.; Ward, R.; Menzel, D. B. (1982b)
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Graham, J. A.; Menzel, D. B.; Miller, F. J.;  111 ing, J.  W.;  Ward, R.; Gardner,
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Graham,  J.  A.; Menzel, D.  B.;  Mole, M.  L. ;  Miller, 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.; Miller, F.  J.  (1980) Response of ciliated epi-
     thelium  to ozone and sulfuric  acid.  Environ.  Res.  22:  377-385.

Grose,  E.  C. ; Richards,  J. H. ;  tiling,  J. W. ; Miller,  F.  J. ; Davies, D. W.;
     Graham,  J.  A.;  Gardner,  D.  E.  (1982) Pulmonary host defense responses to
     inhalation  of sulfuric acid and ozone.  J. Toxieol.. 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 i_n vitro based on
     sister chromatid exchange analysis.  Environ.  Res.  18:  336-346.
                                    1-219

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Hartley, J. G.;  Gardner,  D. E.;  Coffin  D.  L.;  Menzel,  D.  B.  (1977)  Enhanced
     binding of autologous cells to the macrophage plasma  membrane as  a  sensi-
     tive 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;   Rich!and,  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  poiI, rec, and  DNA  gene products
     in the repair of  lesions  produced in  Escherichia coli DNA by ozone.  Stud.
     Biophys. 68: 229-335.

Hamelin, 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.

Hamelin, C.;  Sarhan, F.;  Chung,  Y.  S.  (1977b)  DNA degradation caused by ozone
     in mucoid  mutants  of Escherichia coll 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  methyl-
     prednisolone.  Am. Rev. Respir. Dis. 123:  47-52.

Holtzman, M. J.; Fabbri,  L. M.;  Skoogh, B.-E.; O'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
     Physio!. 55: 1232-1236.

Holtzman, M.  J.; Fabbri,  L.  M.; O'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.
                                                        i>
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

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Hurst, D. J.;  Coffin,  D.  L. (1971)  Ozone  effect on lysosomal hydrolases  of
     alveolar macrophages jjn 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) Hydroxy-
     proline  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 chronically  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. ;  Miller, F.  J.; Gardner,  D.  E.  (1980)  Decreased resistance to
     infection  in exercised mice exposed to N02 and 03.  J. Toxicol.  Environ.
     Health 6: 843-851.

Inoue,  H. ;  Sato,  S.; Hirose, T.;  Kikuchi,  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
     level  of ozone:  functional  aspects.   Nikkyo  Shikkai-Shi  17:  288-296.

Jegier,  Z.  (1973)  L1ozone  en tant que polluant atmospherique [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 developmental
     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  on  short and
     long term  clearance.  Exp. Lung  Respir. 2: 111-120.

Kesner,  L.. ; ]£indya,  R. J. ;  Chan,  P.  C.  (1979)  Inhibition  of erythrocyte1  membrane
     (Na +  K  )-activated ATPase  by ozone-treated phospholipids.  J.  Biol.  Chem.
     254: 2705-2709.
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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.;  (Jealjh, 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)  Oscillatory mechanics
     of the  respiratory system  in ozone-exposed  rats.  J. Appl.  Physio!.:
     Respir.  Environ. Exercise Physio!. 56: 182-186.

Kyei-Aboagye, K,; Hazueha,  M.; Wyszogrodski,  I.;  Rubinstein,  D.; Avery, M. E.
     (1973) The  effect  of ozone  exposure  i_n  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 pol-
     lutants: 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  trachea!  explants:
     effects of pollutants. EHP  Environ.  Health Perspect.  35:  131-138.

Last, J. A.; Jennings,  M. D.;  Schwartz, L. W.; Cross, C. E. (1977) Glycoprotein
     secretion  by trachea!  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 altera-
     tions 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.


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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.  Physio!.:  Respir.
     Environ. Exercise Physio!.  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. Physio!.: Respir. Environ. Exercise Physio!.  46:  1108-1114.

Lee, L.-Y.;  Djokic, T. D.;  Dumont, C.; Graf, P.  D.; Nadel, J. A.  (1980)  Mechanism
     of ozone-induced tachypneie response to hypoxia  and  hypercapnia in  conscious
     dogs.  J. Appl. Physio!.: 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 beagle. Arch. Environ. Health 29: 102-106.

Lum, H.; Schwartz,  L. W.;  Dungworth, D.  L.;  Tyler, W. S.  (1978) A comparative
     study of eel! 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 N02 and 03.  In:  Sanders,
     C.  L.;  Schneider,   R.  P.;  Dagle, G. E.;  Ragan,  H.  A.,  eds.  Pulmonary
     tnacrophage  and epithelial   cells:  proceedings of  the  sixteenth annual
     Hanford  biology  symposium;  September  1976;  Richland, 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 alveo-
     lar 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
     iji vivo ozone exposure on  i_n y 1 tro pulmonary  alveolar macrophage mobility.
     J. Toxicol. Environ. Health 7:  373-381.

McJilton, C..; Thielke, J.;  Frank, R.  (1972) Ozone  uptake  model  for the  respira-
     tory  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

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Mellick, P.  W.;  Mustafa,  M.  G.;  Tyler,  W.  S.;  Dungworth, D.  L.  (1975) Morpho-
     logic 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) Preven-
     tion  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
     levels  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.

Miller,  F.  J.; Overton,  J.  H.,  Jr.; Jaskot,  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.  App'l.  Pharmacol. 79: 11-27.

Mizoguchi, I.; Osawa, M.  j 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.  Contain.  Toxicol.
     26; 273-280.


                                    1-224

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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  PolTut.  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  sensiti-
     vity 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)  Biochemical  effects of  environmental oxidants  pollutants in  animal
     lungs.  In:  Lee, S.  D., ed.  Biochemical effects of environmental pollu-
     tants.  Ann  Arbor,  MI: Ann  Arbor Science  Publishers,  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 Dohlen, F.  M.; Hassett,  C.  M.;  Postlethwait,
     E. M.;  Quinn,  C.  L.; Graham, J. A.; Gardner, D. E.  (1984)  A  comparison of
     biochemical  effects of nitrogen dioxide,  ozone, and their combination in
     mouse lung.  I.  Intermittent  exposures. Toxicol. AppT.  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 photochemical, oxidants and automo-
     bile  exhaust.   Osaka-furitsu  Koshu  Eisei  Kenkyusho  Kenkyu Hokoku  Rodo
     Eisei Hen 10:  35-42.

Nambu,  I.; Yokoyama, E.  (1983) Antitoxidant  system and .ozone tolerance.  Environ.
     Res.  32: 111-117.
                                    1-225

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References for Toxicologleal Effects  (cont'd.)

O'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.

O'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,  I.  (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.;  Atwals  0. S.  (1983) Occurrence of  APUD-type cells in the
     ciliated cyst of the parathyroid gland of ozone-exposed dogs. Acta Anat.
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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 morpho-
     logical and biochemical study. Arch.  Environ.  Health 34:  390-395.
                                    1-226

-------
References for Toxicological Effects (cont'd.)
Raub, J. A. ;  Miller,  F.  J. ;
     exposure on  pulmonary
     S.  D. ; Mustafa, M.  G. ;
     the blomedical effects
     1982;
     Inc.;
                             A. (1983) Effects of  low-level  ozone
                              adult and neonatal  rats.  In:  Lee,
                              A., eds. International  symposium  on
                              related photochemical oxidants; March
Pinehurst,  NC Princeton,  NJ:  Princeton  Scientific  Publishers,
 Graham, J.
function  in
 Mehlman,  M.
of ozone and
pp. 363-367.  (Advances  in modern environmental toxicology: v. 5).
Reasor, M. J.; Adams, G. K. , III; Brooks, J. K.;
     of albumin  and  IgG in the airway secretions
     Environ. Sci. Health C13: 335-346.
                                      Rubin, R. J. (1979) Enrichment
                                       of dogs breathing ozone. J.
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; Raleigh, NC. Research Triangle Park, NC: U.S. Environmental
     Protection Agency, Health Effects  Research Laboratory;  EPA-600/9-81-Q01;
     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
     reactivity  by different  testing  methods.  J.  Appl.
     Environ. Exercise  Physio!. 57: 1783-1789.
                                              muscarinic bronchial
                                               Physio!.: Respir.
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:  influ-
     ence 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 permea-
     bility of Escherichia coli. J. Bacteriol.  85:  567-576.
Sherwood,  R.  L.;  Kimura,  A.; Donovan, R.;  Goldstein, E.
     ppm ozone on  rats with  chronic  pulmonary  bacterial
     Environ. Health 13:  893-904.
                                              (1984) Effect of 0.64
                                              infection. J. Toxicol.
                                    1-227

-------
References for lexicological 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 03 or N02  exposure. Am.  J.
     Pathol. 93: 183-200.

Stewart, R. M.;  Weir,  E. K.; Montgomery, M.  R.;  Niewoehner, D,  E.  (1981)  Hydro-
     gen peroxide contracts airway smooth muscle: a possible  endogenous mecha-
     nism. Respir. Physio!. 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. Inter-
     national symposium on the biomedical  effects of ozone and related photo-
     chemical oxidants;  March 1982; Pinehurst,  NC.  Princeton, NJ: Princeton
     Scientific  Publishers, Inc.; pp. 515-526. (Advances in modern  environmen-
     tal 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. (19815) Effects of
     exposure to  ozone on  susceptibility to experimental tuberculosis. Toxicol.
     Lett. 9: 11-17.

                                    1-228

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References for lexicological Effects (cont'd.)

Tice,  R.  R.;  Bender, M.  A.;  Ivett,  J. L. ;  Drew,  R.  T.  (1978) Cytogenetic
     effects of,inhaled ozone. Mutat.  Res. 58; 293-304.

Trams, E. G.;  Lauter, C. J.; Brown, E. A.  B,; Young, 0. (1972) Cerebral corti-
     cal 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 N02~  or  03-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 mea-
     suring  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 altera-
     tions  in phenol red absorption  from the  rat lung.  Toxicol. Lett. 6:
     213-219.


                                   1-229

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References for Toxlcological 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.;  Spbecki,  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 S02, N02  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  chromo-
     some  aberrations  observed in irradiated Chinese  hamsters.  Environ.  Res.
     4: 325-342.

Zitnik,  L.  A.;  Schwartz,  L. W.; McQuillen, N.  K.;  Zee, Y.  C.; Osebold,  J.  W.
     (1978)  Pulmonary changes  induced  by  low-level  ozone: morphological  obser-
     vations. 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. Physio!.: Respir.
     Environ. Exercise Physio!.  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. Physio!.  59: 1879-1885.

Bedi, J.  F.;  Drechsler-Parks, D. M.;  Horvath,  S.  M.  (1985) Duration  of  in-
     creased  pulmonary function  sensitivity  to an initial ozone  exposure.
     Am. Ind. Hyg.  Assoc. J. 46:  731-734.

Dimeo,  M.  J.;  Glenn, M.  G.;  Holtzman,  M.  J.; Sheller, 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.; Drinkwater, B.  L.; Gliner, J.  A.;  Bedi,  J.  F.,  eds.  Environmental
     stress:  Individual  human  adaptations.  New 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.
     Physio!.:  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.; Mcllhany,  M. L.;  Swidersky, P. (1975) Effects of
     ozone on  pulmonary function in  normal subjects;  Am.  Rev.  Respir.  Dis.
     Ill: 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 adoles-
     cents. Am. Rev.  Respir. Dis. 132: 648-651.

Konig,  G.;  Rb'mmelt,  H.;  Kienele,  H.;  Dirnagl,  K.;  Polke, H.; Fruhmann, G.
     (1980) Changes in  the bronchial  reactivity of humans  caused by the influ-
     ence of ozone. Arbeitsmed. Sozialmed.  Praeventivmed.  151: 261-263.

Kulle,  J.  J.; Sauder,  L.  R.;  Kerr,  H.  D.; Parrel!, 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.

Kulle,  T.  J.; Milman,  J.  H.;  Sauder, L. R.;  Kerr,  H.  D.; Parrel!,  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.

Linn,  W.  S.;  Fischer, D. A.; Medway, D.  A.;  Anzar,  U. T. ;  Spier, C.  E. ;
     Valencia, L.  M.;  Venct, T. G.;  Hackney, J.  D. (1982a) Short-term respira-
     tory  effects of 0.12 ppm ozone  exposure  in  volunteers with chronic ob-
     structive lung disease. Am.  Rev.  Respir.  Dis. 125:  658-663.


                                    1-232

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References forControlled 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.

Linn,  W.  S.;  Shamoo, D. A.;  Venet,  T.  G.; Spier, C.  E.; Valencia,  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. Physio!.:  Respir.
     Environ. Exercise Physio!.  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. Physio!. 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 forField andEpidemiologicalStudies 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.
                                          5

                                   1-233

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References for Field and Epidemiological 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.; Linn,  W.  S.;  Shamoo, D.  A.;  Valencia, 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  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  perfor-
     mance  [master's  thesis].  Chapel  Hill, NC: University 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.;  O'Rourke, M.  K.; Dodge,  R.;  Holberg,  C.  J.  ; Corman, G.;
     Hoshaw, R.  W.; Pinnas, J. L.; Barbee, R.  A.;  Sneller,  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

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References for Field and Epidemiological 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)  Persistence  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. Interna-
     tional  symposium on the  biomedical effects  of ozone  and related photo-
     chemical 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  Evaluation 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.;  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.
                                    1-235

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References for Evaluation of Health Effects Data  (cont'd.)

Avol,  E.  L.;  Linn,  W.  S.;  Shamoo, D.  A.;  Valencia, 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.  Physio!.:
     Respir.   Environ. Exercise Physio!. 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.;  Hebe!, 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.  Physio!.:  Respir.
     Environ. Exercise  Physio!.  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.;  Strops,  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.
                                    1-236

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References for EvaluationofHealthEffects 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  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).
                                    1-237

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