&EPA
               United States
               Environmental Protection
               Agency
              Environmental Criteria and
              Assessment Office
              Research Triangle Park NC 27711
EPA/600/8-84/020B
November 1 985
External Review Draft No. 2
               Research and Development
Air  Quality
Criteria for
Ozone and  Other
Photochemical
Oxidants
Review
Draft
(Do Not
Cite or Quote)
                Volume I  of V
                             NOTICE

                This document is a preliminary draft It has not been formally
                released by EPA and should not at this stage be construed to
                represent Agency policy. It is being circulated for comment on its
                technical accuracy and policy implications.

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                                            EPA/600/8-84/020B
Draft                                             November 1 985
Do Not Quote or Cite                     External Review Draft No. 2
                 Air Qualify  Criteria
                for  Ozone and  Other
             Photochemical  Oxidants

                     Volume I  of  V
                             NOTICE

This document is a preliminary draft. It has not been formally released by EPA and should not at this stage
be construed to represent Agency policy. It is being circulated for comment on its technical accuracy and
policy implications.
                  Environmental Criteria and Assessment Office
                  Office of Health and Environmental Assessment
                     Office of Research and Development
                     U.S. Environmental Protection Agency
                      Research Triangle Park, IM.C 2771 1

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                               PRELIMINARY DRAFT
                                    NOTICE
     Mention of trade names or commerical  products does not constitute endorse-
ment or recommendation for use.
                                     11
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                               PRELIMINARY DRAFT
                                   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 1985.
     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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                                PRELIMINARY  DRAFT
                                TABLE  OF  CONTENTS
 LIST OF  TABLES  	     vi i
 LIST OF  FIGURES 	     viii
 LIST OF  ABBREVIATIONS  	     ix
 CONTRIBUTING  AUTHORS  	     xi i i

 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  	     1-2
            1.2.1   Descriptions  and  Properties of Ozone and Other
                    Photochemical Oxidants  	     1-2
            1.2.2   Nature of Precursors  to Ozone and Other
                    Photochemical Oxidants  	     1-3
            1.2.3   Atmospheric Reactions of  Ozone and Other Oxidants
                    Including Their Role  in Aerosol  Formation 	     1-4
                    1.2.3.1   Formation and Transformation of Ozone
                              and Other Photochemical Oxidants  	     1-5
                    1.2.3.2   Atmospheric Chemical Processes
                              Involving Ozone 	     1-6
                    1.2.3.3   Atmospheric Reactions  of PAN, H202,
                              and HCOOH 	     1-7
            1.2.4   Meteorological  and  Climatological Processes  	     1-8
                    1.2.4.1   Atmospheric Mixing 	     1-8
                    1.2.4.2   Wind  Speed  and  Direction 	     1-10
                    1.2.4.3   Effects of  Sunlight and Temperature  ....     1-10
                    1.2.4.4   Transport of Ozone and Other
                              Oxidants  and Their Precursors 	     1-11
                    1.2.4.5   Stratospheric-Tropospheric Ozone
                              Exchange  	     1-12
                    1.2.4.6   Stratospheric Ozone at Ground Level  ....     1-13
            1.2.5   Sources,  Emissions, and Concentrations of
                    Precursors to Ozone and Other Photochemical
                    Oxidants  	     1-13
                    1.2.5.1   Sources and Emissions  of Precursors  ....     1-14
                    1.2.5.2   Representative  Concentrations in
                              Ambient Air 	     1-14
            1.2.6   Source-Receptor Models  	     1-16
                    1.2.6.1   Trajectory  Models	     1-16
                    1.2.6.2   Fixed-Grid  Models	     1-17
                    1.2.6.3   Box Models  	     1-17
                    1.2.6.4   Validation  and  Sensitivity Analyses
                              for Dynamic Models 	     1-17
      1.3   SAMPLING AND MEASUREMENT  OF OZONE AND OTHER
            PHOTOCHEMICAL  OXIDANTS  AND  THEIR  PRECURSORS  	     1-18
            1.3.1   Sampling  and  Measurement  of Ozone and  Other
                    Photochemical Oxidants  	     1-18
                    1.3.1.1   Quality Assurance and  Sampling 	     1-18
                    1.3.1.2   Measurement Methods for Total Oxidants
                              and Ozone 	     1-18
                    1.3.1.3   Calibration Methods	     1-21

                                       i v
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                               PRELIMINARY DRAFT
                               TABLE OF CONTENTS
                                  (continued)
                   1.3.1.4   Relationship of Total  Oxidants and
                             Ozone Measurements 	     1-23
                   1.3.1.5   Methods for Sampling and Analysis of
                             Peroxyacetyl Nitrate and Its
                             Homologues 	     1-24
                   1.3.1.6   Methods for Sampling and Analysis of
                             Hydrogen Peroxide 	     1-27
           1.3.2   Measurement of Precursors to Ozone and Other
                   Photochemical  Oxidants 	     1-29
                   1.3.2.1   Nonmethane Organic Compounds 	     1-29
                   1.3.2.2   Nitrogen Oxides	     1-31
     1.4   CONCENTRATIONS OF OZONE AND OTHER PHOTOCHEMICAL
           OXIDANTS IN AMBIENT AIR 	     1-32
           1.4.1   Ozone Concentrations in Urban Areas 	     1-33
           1.4.2   Trends in Urban and Nationwide Ozone
                   Concentrations 	     1-36
           1.4.3   Ozone Concentrations in Nonurban Areas 	     1-36
           1.4.4   Patterns in Ozone Concentrations 	     1-37
           1.4.5   Concentrations and Patterns of Other
                   Photochemical  Oxidants 	     1-40
                   1.4.5.1   Concentrations 	     1-40
                   1.4.5.2   Patterns	     1-42
           1.4.6   Relationship Between Ozone and Other
                   Photochemical  Oxidants 	     1-42
     1.5   EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS
           ON VEGETATION 	     1-44
           1.5.1   Limiting Values of Plant Response to Ozone 	     1-46
           1.5.2   Methods for Determining Ozone Yield Losses 	     1-49
           1.5.3   Estimates of Ozone-Induced Yield Loss 	     1-50
           1.5.4   Effects on Crop Quality 	     1-58
           1.5.5   Yield Loss from Ambient Exposures 	     1-58
           1.5.6   Statistics Used to Characterize Ozone Exposures ..     1-60
           1.5.7   Relationship Between Yield Loss and Foliar
                   Injury 	     1-62
           1.5.8   Physiological  Basis of Yield Reductions 	     1-63
           1.5.9   Factors Affecting Plant Response to Ozone 	     1-64
                   1.5.9.1   Environmental Conditions 	     1-64
                   1.5.9.2   Interaction with Plant Diseases 	     1-65
                   1.5.9.3   Interaction of Ozone with Other
                             Ai r Pol 1 utants 	     1-66
           1.5.10  Economic Assessment of Ozone Effects
                   on Agriculture 	     1-67
           1.5.11  Effects of Peroxyacetyl Nitrate on Vegetation ....     1-76
                   1.5.11.1  Factors Affecting Plant Response to
                             PAN 	     1-76
                   1.5.11.2  Limiting Values of Plant Response 	     1-77
                   1.5.11.3  Effects of PAN on Plant Yield 	     1-77
     1.6   EFFECTS OF OZONE ON NATURAL ECOSYSTEMS AND THEIR
           COMPONENTS 	     1-78
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                               PRELIMINARY DRAFT
                               TABLE OF CONTENTS
                                  (continued)
           1.6.1   Responses of Ecosystems to Ozone Stress 	    1-78
           1.6.2   Effects of Ozone on Producers 	    1-79
           1.6.3   Effects of Ozone on Other Ecosystem Components
                   and Ecosystem Interactions 	    1-80
           1.6.4   Effects of Ozone on Specific Ecosystems 	    1-81
           1.6.5   Economic Valuation of Ecosystems 	    1-83
     1.7   OTHER WELFARE EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL
           OXIDANTS  	    1-83
     1.8   TOXICOLOGIC EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL
           OXIDANTS  	    1-88
           1.8.1   Introduction 	    1-88
           1.8.2   Regional Dosimetry in the Respiratory Tract 	    1-90
           1.8.3   Effects of Ozone on the Respiratory Tract 	    1-92
                   1.8.3.1   Morphological Effects	    1-92
                   1.8.3.2   Pulmonary Function	    1-95
                   1.8.3.3   Biochemical Effects	    1-102
                   1.8.3.4   Host Defense Mechanisms	    1-107
                   1.8.3.5   Tolerance	    1-112
           1.8.4   Extrapulmonary Effects of Ozone 	    1-116
                   1.8.4.1   Central Nervous System and Behavioral
                             Effects 	    1-117
                   1.8.4.2   Cardiovascular Effects	    1-117
                   1.8.4.3   Hematological and Serum Chemistry
                             Effects 	    1-117
                   1.8.4.4   Cytogenetic and Teratogenetic Effects ..    1-119
                   1.8.4.5   Other Extrapulmonary Effects 	    1-120
           1.8.5   Interaction of Ozone with Other Pollutants	    1-121
           1.8.6   Effects of Other Photochemical Oxidants 	    1-124
     1.9   CONTROLLED HUMAN STUDIES OF THE EFFECTS OF OZONE AND
           OTHER PHOTOCHEMICAL OXIDANTS 	    1-128
     1.10  FIELD AND EPIDEMIOLOGICAL STUDIES OF THE EFFECTS OF
           OZONE AND OTHER PHOTOCHEMICAL OXIDANTS 	    1-136
     1.11  EVALUATION OF HEALTH EFFECTS DATA FOR OZONE AND OTHER
           PHOTOCHEMICAL OXIDANTS 	    1-141
           1.11.1  Health Effects in the General Human Population ...    1-141
           1.11.2  Health Effects in Individuals with
                   Pre-Existing Disease 	    1-146
           1.11.3  Extrapolation of Effects Observed in Animals
                   to Human Populations 	    1-146
           1.11.4  Health Effects of Other Photochemical Oxidants
                   and Pollutant Mixtures 	    1-147
           1.11.5  Identification of Potentially At-Risk
                   Groups 	    1-148
     1.12  REFERENCES 	    1-149
                                       VI

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                               PRELIMINARY DRAFT



                                LIST OF TABLES


Table                                                                   Page


1-1   Summary of ozone monitoring techniques	   1-19
1-2   Ozone calibration techniques 	   1-22
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 	   1-34
1-4   Ozone concentrations for short-term exposures that
      produce 5 or 20 percent injury to vegetation grown under
      sensitive conditions 	   1-47
1-5   Compilation of 03 concentrations predicted to cause 10% and
      30% yield losses as well as yield losses predicted to occur  .
      at 7-hr seasonal mean 03 concentrations of 0.04 and 0.06
      ppm 	   1-54
1-6   Ozone concentrations at which significant yield losses
      have been noted for a variety of plant species exposed
      under various experimental conditions 	   1-56
1-7   The effects of 03 on crop yield as determined by the use
      of chemical protectants 	   1-57
1-8   Effects of ambient oxidants on yield of selected crops 	   1-59
1-9   Summary of estimates of regional economic consequences of
      ozone pollution 	   1-69
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 	   1-97
1-12  Summary table:  Effects on pulmonary function of short-term
      exposures to ozone 	   1-101
1-13  Summary table:  Effects on pulmonary function of long-term
      exposures to ozone 	   1-104
1-14  Summary table:  Biochemical changes in experimental animals
      exposed to ozone 	   1-109
1-15  Summary table:  Effects of ozone on host defense mechanisms
      in experimental animals 	   1-114
1-16  Summary table:  Extrapulmonary effects of ozone in
      experimental animals 	   1-123
1-17  Summary table:  Interaction of ozone with other pollutants ....   1-126
1-18  Summary table:  Controlled human exposure to ozone 	   1-129
1-19  Summary table:  Acute effects of ozone and other photochemical
      oxidants in field studies with a mobile laboratory 	   1-138
                                      VI 1

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                               PRELIMINARY DRAFT



                                LIST OF FIGURES


Figure                                                                  Page


1-1   Relationship between 03 concentration, exposure duration,
      and a reduction  in plant growth or yield 	   1-48
1-2   Examples of effects of 03 on the yield of soybean and wheat
      cultivars.  The  03 concentrations are expressed as 7-hr
      seasonal mean concentrations.  The cultivars were selected as
      examples of 03 effects and to show year-to-year variations
      i n pi ant response to 03 	  1-52
1-3   Examples of the  effect of 03 on the yield of cotton, tomato,
      and turnip.  The 03 concentrations are expressed as 7-hr
      seasonal mean concentrations.  The species were selected as
      examples of 03 effects and to show year-to-year variations
      in plant response to 03 	   1-53
1-4   Summary of morphological effects in experimental animals
      exposed to ozone 	   1-96
1-5   Summary of effects of short-term ozone exposures on pulmonary
      function in experimental animals 	   1-100
1-6   Summary of effects of long-term ozone exposures on pulmonary
      function in experimental animals 	   1-103
1-7   Summary of biochemical changes in experimental animals
      exposed to ozone 	   1-108
1-8   Summary of effects of ozone on host defense mechanisms in
      experimental animals 	   1-113
1-9   Summary of extrapulmonary effects of ozone in experimental
      animals 	   1-122
1-10  Summary of effects in experimental animals exposed to
      ozone combined with other pollutants 	   1-125
                                      VI 1 1

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                               PRELIMINARY DRAFT
                             LIST OF ABBREVIATIONS
AChE                   acetylcholinesterase
avg                    average
BAKI                   boric acid buffered potassium iodide
Be                     beryllium
C                      carbon, concentration
°C                     degrees Celsius
CA                     chromotropic acid
CC                     closing capacity
CH3C(0)02              acetylperoxy radical
cm                     centimeter
CMS                    central nervous system
CO                     carbon monoxide
COp                    carbon dioxide
COLD                   chronic obstructive lung disease
cone.,  concn.           concentration
CV                     closing volume
dbh                    diameter at breast height
DNPH                   2,4-dinitrophenylhydrazine
ECD                    electron-capture detector
EDU                    ethylenediurea
EKMA                   Empirical Kinetic Modeling Approach
FEF                    forced expiratory flow
Fe2(S04)3              ferric sulfate
FEV                    forced expiratory volume
FEV,                   forced expiratory volume in 1 sec
FID                    flame ionization detector
fD                     respiratory frequency
 K
FTIR                   Fourier-transform infrared
FVC                    forced vital capacity
G-6-PD                  glucose-6-phosphate dehydrogenase
GC                     gas chromatography
GPT                    gas-phase titration
                                      IX
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                               PRELIMINARY DRAFT
                       LIST OF ABBREVIATIONS (continued)
GSH
HCOOH
HN03
HN04
H02
HONO
HPLC
HPPA
hr
hr/day
HRP
H2°2
H2S04
I
r
1C
I/O
IR
KI03
km
LAAPCD
LCV
LDH
L/min
M
m
MBTH
mi
NADPH
NAPBN
NBKI
NF
glutathione
formic acid
nitric acid
peroxynitric acid
hydroperoxy
nitrous acid
high-pressure liquid chromatograpy
3-(£-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
kilometer
Los Angeles Air Pollution Control District
leuco crystal violet
lactate deyhydrogenase
1iters per minute
molar
meter(s)
3-methyl-2-benzothiazolinone hydrazone
mile(s)
nicotinamide adenine dinucleotide phosphate
National Air Pollution Background Network
neutral buffered potassium iodide
ammonium sulfate
National Forest
OZSUM3/D
                                                11/22/85

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                               PRELIMINARY DRAFT
                       LIST OF ABBREVIATIONS (continued)
nm
NMHC
NMOC
NO
N02
N03
N0x
AN2
NPSH
NR
N20
OH
°2
°3
OZIPP
PAN
PA°2
PBzN
PEFR
pH
PPN
ppb
ppm
rad
RBC
RV
Sa02
SAROAD
SBR
sec
SGaw
SNAAQS
nanometer
nonmethane hydrocarbons
nonmethane organic compounds
nitric oxide
nitrogen dioxide
nitrogen trioxide
nitrogen oxides
nitrogen washout
non-protein sulfhydryls
natural rubber
nitrous oxide
hydroxyl radical
oxygen
ozone
ozone isopleth plotting package
peroxyacetyl nitrate
alveolar partial pressure of oxygen
peroxybenzoyl nitrate
peak expiratory flow rate
negative log of H ion concentration
peroxypropionyl nitrate
parts per billion
parts per million
radiation absorbed dose
red blood cell
residual volume
arterial oxygen saturation
Storage and Retrieval of Aerometric Data
styrene-butadiene rubber
second(s)
specific airway conductance
Secondary National Ambient Air Quality Standards
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                                                11/22/85

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                               PRELIMINARY DRAFT
                       LIST OF ABBREVIATIONS (continued)
S0«                    sulfur dioxide
S04                    sulfate
SO                     sulfur oxide
SR                     specific airway resistance
  aw
SRM                    Standard Reference Material
SURE                   Sulfate Regional Experiment Sites
T                      time, temperature
TF                     tropopause-folding events
tg/yr                  teragrams per year
TGS-ANSA               triethanolamine, guaiacol(o-methoxyphenol), sodium
                       metabisulfite, and 8-anilino-l-naphthalene sulfonic acid
TLC                    total lung capacity
TSH                    thyroid stimulating hormone
|jg/m                   microgram per cubic meter
utn/hr                  micrometer per hour
UV                     ultraviolet
Vj                     tidal volume
Vr                     minute ventilation; expired volume per minute
VOC                    volatile organic compounds
ZnSOd                  zinc sulfate
                                      XI 1
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                               PRELIMINARY DRAFT
                            CONTRIBUTING AUTHORS
Dr.  Richard M.  Adams
Department of Agricultural and Resource Economics
Oregon State University
Corvallis, OR  97331

Dr.  Robert Frank
Department of Environmental Health Sciences
Johns Hopkins School of Hygiene and Public Health
615 N. Wolfe Street
Baltimore, MD  21205

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-82
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
Professor, Department of Chemistry
407 Choppin Hall
Louisiana State University
Baton Rouge, LA  70803
(Present Address:
  U.S. Environmental Protection Agency
  Environmental Monitoring Systems Laboratory
  26 West St. Clair
  Cincinnati, OH  45268)

Mr.  Michael W.  Holdren
Battelle, Columbus Laboratories
505 King Avenue
Columbus, OH  43201
                                      XI 1 1
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                               PRELIMINARY DRAFT
                       CONTRIBUTING AUTHORS (continued)
Dr.  Donald H.  Horstman
Health Effects Research Laboratory
MD-58
U.S.  Environmental Protection Agency
Research Triangle Park, NC  27711

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

Dr.  Michael D. Lebowitz
Department of Internal Medicine
College of Medicine
University of Arizona
Tucson, AZ  85724

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

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)
Hilo, HI
                                      xiv
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                               PRELIMINARY DRAFT
                       CONTRIBUTING AUTHORS (continued)
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
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                               PRELIMINARY DRAFT
                          1.   SUMMARY AND CONCLUSIONS
1.1  INTRODUCTION
     This document consolidates  and  assesses knowledge regarding the origin
and distribution  of  ozone and other  photochemical oxidants and the effects of
these pollutants on humans,  experimental animals, vegetation, terrestrial eco-
systems, 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).
     While a  number  of photochemical oxidants  have been observed  in  or postu-
lated to occur in ambient air,  only data on ozone, peroxyacyl nitrates,  and
hydrogen peroxide are examined  in this document.   Coverage has been  limited to
these three oxidants  on  the basis of  available  information  on effects and
ambient air concentrations.  Of  these  oxidants,  only ozone  and peroxyacetyl
nitrate have been studied at concentrations  having relevance for potential ex-
posures 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  was  completed  in 1982  (U.S.   Environmental Protection Agency,
1982a).
     This document presents a  review and evaluation  of literature published
through early  1985.   The  document is not intended as a complete literature
review,  however;  but  is  intended, rather, to present  current data of probable
consequence for the  derivation  of national  ambient air quality standards for
protecting public health  and welfare.
     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 upon  their accurate measurement.  Similarly,  an overview  is  presented
of the chemical and  physical  processes in the  atmosphere by which precursors
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                               PRELIMINARY DRAFT
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.
     The   legislative  basis  for the development and issuance of  air quality
criteria  and related information is found in Sections 108 and 109 of the  Clean
Air Act (U.S.Code, 1982).
1.2  PROPERTIES, CHEMISTRY, AND TRANSPORT OF OZONE AND OTHER PHOTOCHEMICAL
     OXIOANTS AND THEIR PRECURSORS
1.2.1  Descriptions and Properties of Ozone and Other Photochemical  Oxidants
     Ozone (03)  and peroxyacetyl  nitrate  (PAN),  hydrogen peroxide (HpO^),
formic acid (HCOOH), and other photochemical oxidants occurring at low concen-
trations in  ambient  air 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 stan-
dard 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 stan-
dard potential  of  +2.07 volts  in aqueous  systems for the  redox pair, 03/H?0
(Weast,  1977).   Hydrogen peroxide, which is highly  soluble  in water and other
polar solvents, has a standard potential  of +1.776 in the redox pair,  H,,0?/H?0
(Weast,  1977).   No  standard potential  for peroxyacetyl  nitrate in neutral or
buffered aqueous  systems,  such as those that  occur in biological systems,
appears  in the  literature.   In acidic solution (pH  5  to 6),  PAN hydrolyzes

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fairly rapidly  (Lee et al., 1983; Holdren et al., 1984);  in  alkaline solution
it decomposes with the production of nitrite ion and molecular oxygen (Stephens,
1967; Nicksic et  al. , 1967).  An  important  property of PAN,  especially  in the
laboratory, is its thermal instability.   Its explosiveness dictates its synthesis
for 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  0,  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 HpO-) must  be generated jn situ for the calibration of measurement tech-
niques.   For  ozone and  H?0~,  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
                                                             A
hydroxyl  (OH) and  other  radicals,  oxygen,  and sunlight (see, e.g., Demerjian
etal.,  1974; National  Research  Council,  1977;  U.S.  Environmental Protection
Agency,  1978; Atkinson, 1985).  The oxidants are almost exclusively secondary
pollutants' formed  in the  atmosphere from their precursors by processes that
are a complex 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
present  in ambient air,  although at lower concentrations than the  hydrocarbons.
They are oxidized  through  the  same initial  step involved in  the oxidation of

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the hydrocarbons; that is, attack by hydroxyl radicals.   Alkenes, haloalkenes,
and aliphatic  aldehydes  are,  as  classes, among the  most  reactive organic
compounds found  in  ambient  air (e.g., Altshuller and Bufalini, 1971; Darnall
et al., 1976;  Pitts et al.,  1977; U.S. Environmental  Protection Agency, 1978,
and references  therein).   Alkenes and haloalkenes  are  unique among VOC in
ambient air  in  that they are susceptible both to attack by OH radicals (OH)
and by ozone  (Niki  et al.,  1983).  Methane,  halomethanes,  and certain naloe-
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?0)  is unimportant in  the production
of  oxidants  in  ambient  air  because it is virtually  inert in the  troposphere.

1.2.3  Atmospheric  Reactions  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
man-made  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
increasingly well-characterized.   The reactions of these  species  result  in
products and processes that may have significant environmental and health- and
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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  Formation and Transformation of Ozone and Other Photochemical Oxidants.
In the troposphere, ozone is formed through the dissociation of N0? 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 CL to
form NCL and an 0? molecule.  In the absence of competing reactions, a steady-
state or equilibrium  concentration of 0.,  is  soon established between  0,, NCL,
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/N02 and NMOC/NOx ratios (National  Research Council, 1977).
     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; Nik"!  et  al.,  1981).   Aldehydes,  which are constituents  of automobile
exhaust as  well as  decomposition  products of most  atmospheric photochemical
reactions  involving  hydrocarbons, and  nitrous  acid  (MONO),  are important
sources of  OH  radicals, as  is 0,  itself.  Other free  radicals, such as hydro-
and alkylperoxy radicals and the nitrate (N03) 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 N0?  from the reaction mixtures,  such that
the photochemical cycles  slowly come to an end unless fresh NO and N0? emis-
sions are  injected  into the atmosphere.  Compounds containing nitrogen,  such
as PAN, nitric  acid  (HN03), and peroxynitric acid (HNO.),  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 roaction  of OH  radicals with a  large number of organic compounds have
been measured  (e.g.,  Atkinson et al.,  1979;  Atkinson et al.,  1985).   The
mechanisms  of  the  reactions of paraffinic compounds  are fairly  well  under-
stood, as are those of olefinic compounds, at least for the  smaller compounds.

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Photooxidation reactions of the aromatic compounds, however, are poorly under-
stood.
     In the presence  of N0x,  natural hydrocarbons  (i.e.,  those organic com-
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  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  NO., 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.
                                                                           -21
Only for  organics whose ozone reaction rate  constants  are  greater than ~10
cm  molecule    sec    can consumption by ozone be considered to be atmospheri-
cally important (Atkinson and Carter, 1984).
     Ozone reacts rapidly  with  the  acyclic mono-,   di-, and  tri-alkenes  and
                                                                           _ -I Q
with cyclic alkenes.   The rate constants for these  reactions range from -10
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).
     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

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hydrocarbons (Atkinson and Carter, 1984), but their reactions with OH radicals
(Atkinson,  1985)  or NO,  radicals (Carter et al.,  1981a;  Atkinson  et a I...,
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
NOp, and  subsequently  with NO- 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 SO- to H?S04, 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, H.,0,,, and HCOOH.   Because PAN  is  in
equilibrium with acetyl peroxy radicals and NO,,, 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 .
     Although hydrogen peroxide formed in the gas  phase from the reactions of
hydroperoxyl radicals  plays  a role in HO  chemistry  in the  troposphere, and
especially  in the  stratosphere  (Crutzen  and Fishman,  1977;  Cox  and Burrows,
1979), its  major  importance  arises from its high  solubility in water.  The
latter ensures  that a large  fraction  of  gaseous H-Op will  be  taken  up  in
aqueous droplets.   Over  the  past  decade, evidence  has  accumulated that HjOp
dissolved in cloud,  fog,  and rainwater may play an important,  and,  in acidic
droplets (i.e., pH <5), even  a dominant role in  the oxidation of S0? to H?SO.
(e.g., Hoffman  and  Edwards,  1975; Martin and Damschen, 1981;  Chameides  and

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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 al., 1984).   Substantial uncertainties remain concerning
the quantitative role of H?0? 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 mechanisms by which ozone 1s brought
into the troposphere  from the stratosphere are  important in determining the
levels,  ground surface locations, and seasonality of incursions  of stratospheric
ozone into the troposphere.
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
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

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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  prob-
lems  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 afternoon  of  low-level  stable layers is a rare event,  occurring on <1 day
in 20  (Holzworth and Fisher, 1979).
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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  (<6  mi/hr)  occur  with  a
frequency ^50 percent  (Holzworth and Fisher, 1979).  These surface  inversions
break up by afternoon, however, permitting dispersion.
     The effects of wind  speed and direction  include the amount of dilution
occurring in the source areas, as well as along the trajectory 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., 1964).   Along the Pacific  Coast,  especially along the coast of California,
coastal winds  and a persistent low inversion layer  contribute to major pollutant
buildups in urban  source  areas and downwind along  the urban  plume trajectory
(Robinson,  1952;  Neiburger et al., 1961).
1.2.4.3  Effects of Sunlight and Temperature.   The effects  of  sunlight on
photochemical  oxidant  formation,  aside from the role of  solar  radiation  in
meteorological  processes, are  related  to  its intensity  and its  spectral  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 light intensity (Peterson, 1976;
Demerjian et al.,  1980)  and its  diurnal  variations  (Jeffries et  al.,  1975;
1976),  as well as  on  the  overall photooxidation process  (Jaffee et  al., 1974;
Winer et al.,  1979).
     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).

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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).
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,
including:   (1) the concentrations of respective precursors leaving the source
area; (2) induction time; (3) turbulent mixing;  (4) wind speed and wind direc-
tion;  (5) scavenging  during transport; (6) injection of  new  emissions from
source areas in  the  trajectory of the air  mass;  and  (7) local  and synoptic
weather conditions.
     Ozone and  other  photochemical  oxidants can  be transported  hundreds  of
miles  from  the place of  origin  of their precursors,  as  documented  by the
numerous studies on transport  phenomena that were described in the 1978 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;
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

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(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
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

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                               PRELIMINARY DRAFT
of which are consistent with theory, could cause substantial effects in terms
of high ozone concentrations at ground level.
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).   They also concluded from their review 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 intru-
sions.
     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)
concluded that "the experimental  technique  involving a  Be/03  ratio to esti-
mate the daily stratospheric component  of ground-level 0, is unverified and
considered to be  inadequate for air quality  applications" (p.  1009).
     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).

1.2.5  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
(NO ), emitted by manmade  and  by natural sources;  and on suitable conditions
   X
of sunlight, temperature,  and  other meteorological  factors.   Because of the
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intervening requirement for meteorological conditions conducive to the photo-
chemical  generation of  ozone,  emission inventories are not as direct predic-
tors of ambient concentrations of secondary pollutants such as ozone  and other
oxidants  as they are for primary pollutants.
1.2.5.1  Sources  and  Emissions  of  Precursors.   Emissions  of manmade  VOCs
(excluding  several  relatively  unreactive  compounds such as  methane)  in the
United States  have  been estimated  at 19.9 Tg/yr for 1983 (U.S.  Environmental
Protection  Agency,  1984).  An  examination of trends in manmade VOC emissions
for 1970 through  1983  shows  that the  annual emission  rate for manmade VOCs
decreased some 26 percent during this period.   The main sources nationwide are
industrial  processes,  which  emit  a  wide  variety of VOCs  such  as  chemical
solvents; and  transportation, which  includes the emission  of VOCs  in gasoline
vapor  as well  as  in  gasoline combustion products.   Estimates  of  biogenic
emissions of organic compounds in the United States are highly inferential but
data suggest that  the  yearly  rate  is  the same order of magnitude  as manmade
emissions.   Most of the biogenic emissions actually occur during the growing
season, however, and  the  kinds  of  compounds emitted are different from those
arising from manmade sources.
     Emissions of manmade NO  in the United States were estimated at  19.4 Tg/yr
for 1983.   Annual emissions of manmade NO   were some 12 percent higher in 1983
than in 1970, but the  rate leveled  off in  the late 1970s and exhibited a small
decline from about  1980 through 1982  (U.S.  Environmental  Protection Agency,
1984).   The  increase  over the period  1970 through  1983 had  two main causes:
(1) increased  fuel  combustion in stationary sources such as  power  plants;  and
(2) increased  fuel  combustion in highway motor vehicles, as  the result of  the
increase in  vehicle miles  driven.  Total vehicle miles driven  increased  by 42
percent over the 14 years in question.
     Estimated biogenic NO  emissions are based on uncertain extrapolations
from very  limited  studies,  but appear to  be about an order of magnitude less
than manmade NO  emissions.
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

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                               PRELIMINARY DRAFT
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,n 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
measured in urban areas (Ferman,  1981; Sexton and Westberg,  1984).   In samples
from sites  carefully  selected to guarantee their rural character,  total  NMHC
concentrations ranged  from  0.006  to 0.150 ppm C  (e.g.,  Cronn,  1982; Seila,
1981; Holdren  et al., 1979).  Concentrations of individual  species seldom
exceeded 0.010 ppm C.   The bulk of species present in rural  areas are alkanes;
ethane,   propane,  n-butane,  j_so-pentane,  and  n-pentane are  most abundant.
Ethylene and propene  are  sometimes present at <0.001  ppm  C,  and toluene is
usually  present  at  ~0.001  ppm C.    Monoterpene  concentrations are  usually
£0.020 ppm  C.   During  the summer months,  isoprene  concentrations as high  as
0.150 ppm C  have  been  measured (Ferman,  1981).   The maximum concentrations  of
isoprene usually  encountered, however, are in the  range  of  0.030 to 0.040
ppm C.
1.2.5.2.3  Nitrogen oxides in urban areas.  Concentrations of NO ,  like hydro-
               ~                      •                           A
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 N02,
initially by thermal  oxidation  and subsequently by ozone and peroxy radicals
produced in  atmospheric photochemical  reactions.  The  relative concentrations
of NO versus  N0? 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
ranged from  0.05  to 0.15  ppm in studies done in the last 5 to 7 years (e.g.,
Westberg and  Lamb,  1983;  Richter,  1983;  Eaton et  al.,  1979), although 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
ranged from 5 to 16.
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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
United States appear  to be higher than NO   concentrations  in  the  west by a
factor of  ten (Mueller  and  Hidy,  1983).   From the limited amount  of  data
available, NO   concentrations  in  unpopulated  nonurban areas  in  the  west
average <1 ppb;  but in  nonurban  northeastern areas  average  NO  can exceed
10 ppb.

1.2.6  Source-Receptor 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-empirical or computational-dynamic.   Empirical  models are
generally based on  a  statistical  analysis of historical air quality data or
upon  smog  chamber data,  and are not  explicity  concerned  with  atmospheric
chemistry or  meteorology.  An example  of empirical models is the linear roll-
back 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 conditons.
Trajectory models  provide  dynamic  descriptions of atmospheric source-receptor
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                               PRELIMINARY DRAFT
relationships that are simpler and less expensive to derive than those obtain-
ed from fixed-cell models.
     The simplest form  of  trajectory model is the empirical kinetic modeling
approach (EKMA), which does not account for vertical diffusion.   This approach
was developed from  earlier efforts (Hamming et al., 1973; 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 Hogo,  1978)  is
used to generate ozone isopleths at various levels of sophistication correspond-
ing to  "standard" EKMA,  "city-specific" EKMA, or the  simplified trajectory
model  (F.R. ,  1979).
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 pro-
cesses involved in photochemical air pollution formation.
1.2.6.3  Box Models.   Box  models (Hanna, 1973; Demerjian  and  Schere, 1979;
Derwent and  Hbv,  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
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 07-HC-NO  relationship.
                                        «J      A
     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

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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  Qxidants
     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 0, 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
quality control (U.S.  Environmental Protection Agency, 1977b). Design criteria
for 0,  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 0, in ambient air are summarized
in Table  1-1.   The earliest  methods  used for routinely monitoring  oxidants  in
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                                PRELIMINARY DRAFT
                                                TABLE  1-1.   SUMMARY OF OZONE MONITORING  TECHNIQUES
Principle
Continuous
colorimetric
Continuous
electrochemical
Cherai 1 umi nescence
Chemi 1 umi nescence
Ultraviolet
photometry
Reagent
10(20)% KI
buffered at
pH = 6.8
2% KI
buffered at
pH = 6.8
Ethylene,
gas-phase
Rhodamine-B
None
Response
Total
oxidants
Total
oxidants
03-specific
03-specific
Oj-specific
Minimum
detection limit
0.010 ppm
0.010 ppm
0.005 ppm
0.001 ppm
O.OOS ppm
Response
time, 90% FSa
3 to 5 minutes
1 minute
< 30 seconds
< 1 minute
30 seconds
Major
interferences
N02(+20%, 10%KI)
S02(-100%)
N02(+6t)
S02(- 10095)
Noneb
None
Species that
absorb at 254 nm
References
Littman and Benoliel (1953)
Tokiwa et al. (1972)
Brewer and MiJford (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)
FS = 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 nm (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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                               PRELIMINARY DRAFT
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  (N0?) and
sulfur dioxide (SCL)  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
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 absorption  by

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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 accu-
rately  known.   In the  gas-solid  chemiluminescence analyzer,  the reaction
between ozone and Rhodamine-B adsorbed on activated silica produces chemilumi-
nescence, the intensity  of which is directly proportional to  ozone concentra-
tion.
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 al.,  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 ozone-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
summarized in Table  1-2.  A number of  studies  conducted between 1974 and 1978
revealed several  deficiencies with KI  methods,  the most notable of which were
poor precision  or interlaboratory  comparability and a  positive bias of NBKI
measurements relative  to simultaneous absolute  UV absorption measurements.
The  positive bias observed  is  peculiar to the use of phosphate buffer in  the
NBKI techniques.   The  bias  was not observed  in the unbuffered  LAAPCD method
(which nevertheless suffered from poor precision),  nor  in the 1 percent EPA KI

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                                 PRELIMINARY DRAFT
                                                  TABLE  1-2.  OZONE CALIBRATION  TECHNIQUES
Method
1% NBKI
2% NBKIC
1% Unbuffered
KI
UV photometry
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 standard
Reagent grade
arsenious oxide
Reagent grade
potassium biiodate

03 absorptivity at
Hg 254 nm emission
line
Nitric oxide SRH
(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
Purpose
Primary reference
procedure
Primary reference
procedure
Primary reference
procedure
Primary reference
procedure
Alternative reference
procedure (1973-1979)
Transfer standard (1979-present)
Alternative reference
procedure
Bias,
[O3]i/[o3]uv
1.12 ± 0.05b
1.20 ± 0.05b
0.96d

1.030 ± 0.015f
1.00 ± 0.05
 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).
CUV 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 I   solution  absorptivity to be used instead of the preparation of standard iodine solutions.
                                             3

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                               PRELIMINARY DRAFT
method without phosphate buffer (Hodgeson et al., 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 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 0, 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., 1979).   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
03 photometers,  calibrated generators, and gas-phase titration (GPT) apparatus.
Guidelines on transfer  standards  have been published by EPA (McElroy, 1979).
1.3.1.4  Relationship of Total  Qxidants 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 (NOp) and negative (SCL)  interferences in  total oxidants measurements
of ambient air,  and  the change in the basis of  calibration.  In particular,
the presence  of NCL  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

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                               PRELIMINARY DRAM
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  N0» 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 0.^ + 0.005
                         (Correlation coefficient = 0.92)             (1-2)

The oxidant data were uncorrected for N0~ and S0? 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  N0«  and  SO™ 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 air 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
transform infrared (FTIR) spectrometry.   Atmospheric data on PAN concentrations
have been  obtained predominantly by GC-ECD because of its  relative  simplicity
and superior sensitivity.   These techniques have been described in this chapter
along with attendant  methods  of sampling, PAN generation, absolute analysis,
and calibration.
     By  far  the  most  widely used technique  for the quantitative determination
of  ppb  concentrations of PAN and  its  homologues is  GC-ECD  (Darley et al.,

019NCH/A                            1-24                                11/22/35

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                               PRELIMINARY DRAFT
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 1R
bands have been  assigned and the absorptivities reported  in  the literature
(Stephens,  1964; Bruckmann and Willner,  1983; Holdren and Spicer, 1984) permit
the quantitative analysis of PAN without calibration standards.   The absorptiv-
ity of the 990 cm   band of PBzN, a higher homologue of PAN,  has been reported
by  Stephens  (1969).  Tuazon  et  al.  (1978) describe  an FTIR system operable at
pathlengths up to 2 km for ambient measurements of PAN and other trace consti-
tuents.   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

019NCH/A                            1-25                                11/22/85

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                               PRELIMINARY DRAFT
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).
     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
019NCH/A                            1-26                                11/22/85

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                               PRELIMINARY DRAFT
analyze for nitrite (Nielsen et al., 1982) or acetate (Grosjean,  1983; Grosjean
et al., 1984)  ions.   Another calibration procedure has been proposed that is
based on the thermal decomposition of PAN in the presence of excess and measured
NO concentrations (Lonneman et al., 1982).  The acetylperoxy radical, CH3C(0)02,
and its decomposition products rapidly oxidize nitric oxide (NO)  to NO, with a
stoichiometry that has been experimentally determined.
1.3.1.6   Methods for Sampling and Analysis of Hydrogen Peroxide.    Hydrogen
peroxide (KLOp) is significant in photochemical smog as a chain terminator;  as
an index of the hydroperoxyl radical (HOp) concentration (Bufalini  and Brubaker,
1969; Demerjian et al., 1974); and as a reactant in the aqueous-phase oxidation
             -2
of SOp 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) report-
ing HpOp concentrations  of 0.01 to 0.18 ppm are now believed  to  be far too
high, and to be the result of artifact H?0? formation from reactions of absorbed
03 (Zika  and Saltzman, 1982; Heikes  et  al.,  1982;  Heikes, 1984).   Maximum
tropospheric 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 HpOp
have used aqueous  traps  for sampling.  Atmospheric  0,,  however, which is also
absorbed at  concentrations  much higher than H.Op,  reacts in the  bulk aqueous
phase and at surfaces to  produce H?0? 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
reduce this interference  (Zika and Saltzman, 1982;  Das  et al.,  1983).   Another
problem identified with aqueous sampling is that other atmospheric species (in
particular, SOp)  may  interfere  with the generation  of H_0p in aqueous  traps
and also react with collected H?0? 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 HpOp, 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.

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In addition, the use of a tunable diode infrared laser source should eliminate
the problem associated  with  nearby water bands, and this method is currently
under investigation for atmospheric measurements (unpublished work in progress,
Schiff, 1985).
     Hydrogen peroxide in the atmosphere may be detected at low concentrations
by the chemiluminescence obtained from copper(II)-catalyzed oxidaton of luminol
(5-amino-2,3-dihydro-l,4-phthalazinedione) by  H-O,,  (Armstrong  and Humphreys,
1965;  Kok et al., 1978a,b).   This technique as initially employed suffered the
interferences from 03  and  SO- discussed above for aqueous traps.   Das et al.
(1982) employed a static version of the method of Kok et al.  (1978a) to measure
HpO^ concentrations in  the  0.01 to 1 ppb  range.   In addition,  samples were
purged with argon  immediately after collection to eliminate, reportedly, the
0,  interference.   Recently,  a  modified  chemiluminescence method  has been
reported which  used hemin,  a blood component, as a catalyst for the luminol-
based Hp02 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 HpOp.   The production or decay of the fluorescence intensity of the substrate
or reaction product is  measured as it is oxidized by H_0?, 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 H905  concentration.   Detection limits have been reported to be
              li
quite low  (10     M).   The  chief disadvantage  of  this  approach  is that  the
concentration of H-O-  must  be within a narrow range to obtain an accurately
measureable decrease  in fluorescence.  Oxidation of  LCV  produces intensely
colored crystal  violet,  which has a molar absorption coefficient of  10  M
cm   at the analytical  wavelength,  596 nm.  The detection limit reported was
  _D
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 g-hydroxyphenyl acetic  acid  hontologue is being used
(Kunen et al.,  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 H?0p.

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                               PRELIMINARY DRAFT
     As with 0,, HpOp 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  hLCL is simply
the serial  dilution  of  commercial  grade 30 percent  HLO^  (Fisher Analytical
Reagent).   Techniques for the convenient generation of gas-phase standards are
not available.  A  technique  often  used for generating ppm concentrations of
HpO- in air involves the injection of microliter quantities of 30 percent H^O-
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  detector has been
utilized both  as  a stand-alone continuous  detection system (non-speciation
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 al., 1982).  The major problems
associated with the  non-speciation analyzers have been summarized  in  a recent
technical assistance document  published by the U.S.  Environmental Protection
Agency (1981).  The document also presents ways to reduce some of the existing
problems.
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                               PRELIMINARY DRAFT
     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 (McBride and  McClenny,  1980; Jayanty et al.,  1982;  Westberg
et al., 1980;  Ogle  et al.,  1982).   The preferred preconcentration method for
obtaining speciated data is  cryogenic collection.   Speciation methods involving
cryogenic preconcentration have also been compared with continuous nonspeciation
analyzers (e.g.,  Richter,  1983).  Results indicate  poor  correlation  between
methods at  ambient  concentrations  below 1 part-per-million carbon  (ppm C).
     Aldehydes, which  are both primary and secondary pollutants  in  ambient
air, are detected by  total  NMOC and NMHC speciation  methods  but can not be
quantitatively determined by those  methods.   Primary measurement techniques
for  aldehydes  include the  chromotropic  acid (CA)  method  for  formaldehyde
(Altshuller and McPherson,  1963;  Johnson et al.,  1981),  the 3-methyl-2-benz-
othiazolene (MBTH)  technique for total aldehydes (e.g., Sawicki et al.  ,  1961;
Hauser and  Cummins, 1964),   Fourier-transform infrared (FTIR) spectroscopy
(e.g., Hanst et al., 1982; Tuazon et al., 1978,  1980,  1981a),  and high-perfor-
mance liquid chromatography employing  2,4-dinitrophenyl-hydrazine derivatiza-
tion (HPLC-DNPH) for aldehyde speciation (e.g.,  Lipari  and Swarin, 1982; Kuntz
et al., 1980).  The CA and  MBTH methods utilize wet chemical procedures and
spectrophotometric  detection.   Interferences  from  other  compounds have  been
reported for both techniques.   The  FTIR method offers good specificity and
direct j_n situ analysis of ambient air.  These advantages are offset, however,
by the relatively high cost and lack  of portability of the instrumentation.
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 unsubsti-
tuted hydrocarbons  and  aldehydes.   With the  exception of  formic  acid,  other

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                               PRELIMINARY DRAFT
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, 0,, 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 (Osman et al.,  1979; Westberg et al., 1980).   Additional
research efforts should focus  on this area.
1.3.2.2  Nitrogen Oxides.  Aside from the essentially unreactive nitrous oxide
(N?0),  only two oxides of nitrogen occur in ambient air at appreciable concen-
trations:   nitric  oxide  (NO) and  nitrogen  dioxide (N0?).   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 N0?  is
the chemiluminescence method (F.R.,  1976).   The measurement principle is  the
gas-phase  chemiluminescent  reaction of  0-,  and NO (Fontijn et al., 1970).
                                          O
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 N0? converter.   The magnitude of these interferences
is  dependent upon  the type of converter  used (Winer et  al.,  1974;  Joshi and
Bufalini,   1978).   The detection limit of  commercial chemiluminescence instru-
                                     3
ments for N02 measurement is 2.5 ug/m  (0.002 ppm) (Katz, 1976).
     Development of an  instrument  based  on  the chemiluminescent  reaction of
N0? 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 Oo have been achieved.
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                               PRELIMINARY DRAFT
     Other acceptable methods for measuring ambient NCL 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-l-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
(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 03-   The  SRM  for
NO is a  cylinder  of compressed  NO in N~; the  mixture  is both accurate and
stable  (Hughes, 1975).  The  SRM  for N02  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  0,
to form N0? plus  0?.  The  U.S.  Environmental  Protection Agency (1975) recommends
the combined use of GPT plus SRM procedures, using one technique to check the
other.
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 concentrations of
oxidants other than ozone, singly, collectively, or in combination with ozone,
are cause for  concern;  and  (5)  evaluating the adequacy of ozone as a control
surrogate  for other photochemical oxidants.
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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 equals
or exceeds 0.12 ppm.  The data clearly show, as well,  that the highest 1-hour
ozone concentrations  in  the United States  occur  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.
     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
Cu; and populations of 0.5 to  1 million,  0.13 ppm 0,.   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 (> 75 percent of  possible
hourly values per year)  in 1979, 1980,  and 1981 (collectively, 906 station-years)
in the United States,  the median second-highest 1-hour ozone value was 0.12 ppm,
and 5 percent of the stations  reported second-highest 1-hour values > 0.28 ppm.
     A  pattern of  concern in  assessing human  physiological and vegetational
responses  to  ozone  is the occurrence of  repeated or prolonged periods, or
both, when  the  ozone  concentrations  in ambient air are in the range  of those
known to elicit responses.  In addition,  the number of days of respite between
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                               PRELIMINARY  DRAFT
   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
Northeast
New England
Middle Atlantic





South
South Atlantic





South
West South
Central



North Central
East North
Central






West North
Central


SMSA

Boston, MA
Buffalo, NY
Nassau-Suffolk, NY
Newark, NJ
New York, NY/NJ
Philadelphia, PA/NJ
Pittsburgh, PA

Atlanta, GA
Baltimore, MD
Ft. Lauderdale-Hollywood, FL
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

St. Louis, MO/IL
Minneapolis-St. Paul, MN/WI
Kansas City, MO/KS
SMSA
population,
mil 1 ions

>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


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

>2
>2
1 to <2
Second-highest
1983 03
concn. , ppm

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
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    TABLE 1-3 (continued).   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
West
Mountain
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 03
mil lions concn. , ppm
1 to <2
1 to <2
>2
>2
1 to <2
1 to <2
1 to <2
1 to <2
1 to <2
1 to <2
1 to <2
0.14
0.16
0.37
0.17
0.28
0.20
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).

such multiple-day periods of high ozone is of possible consequence.   Data show
that repeated, consecutive-day exposures to or respites from specified concen-
trations  are  location-specific.   At a  site  in  Dallas,  Texas,  for example,
daily maximum 1-hour  concentrations  were > 0.06 ppm for 2 to 7 days  in a row
37 times in a 3-year period (1979 through 1981).   A concentration of  >0.18 ppm
was recorded at that site on only 2 single days,  and no multiple-day  recurrences
of that  concentration  or greater were recorded over the 3-year period.   At a
site in  Pasadena,  California, however, 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  presented demonstrate the occurrence, at  least  in some urban
areas,  of  multiple-day  potential  exposures to relatively high concentrations
of ozone.
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1.4.2.   Trends in Urban and Nationwide Ozone Concentrations
     Trends in nationwide  ozone  concentrations,  gauged by annual  averages at
two subsets of stations,  show declines of  15 to 20 percent between 1978  and
1982.   Concentrations  monitored  at  California  stations declined  about 11
percent between  1978 and  1982.   Average concentrations  from  all  stations
together (i.e.,  including  California)  showed an increase of about 12 percent
from 1982 to 1983.   These trend data represent urban areas almost exclusively.
Interpretation of this  trend  is  complicated by four potentially significant
influences:  (1) a change  in  calibration procedure (1979); (2) improved data-
quality audits (1979);  (3) possible shifts in underlying meteorological  patterns;
and (4) changes in precursor emission rates.  The  exact portion of the decline
that is attributable to  the calibration change  can not be determined without
minute examination of  aerometric  data  records from each monitoring station,
since some monitoring  stations began using the UV calibration procedure  as
early as 1975, some changed to UV calibration in 1979 (but not  all  in the  same
month of 1979), and some used the interim BAKI calibration procedure permitted
by EPA for up to 18 months  after promulgation of the UV calibration procedure
(Hunt and Curran, 1982; also see  Chapter 4).

1.4.3.   Ozone Concentrations in Nonurban Areas
     Nonurban areas  are not  routinely  monitored  for ozone concentrations.
Consequently,  the aerometric data base for nonurban areas is considerably  less
substantial than  for urban areas.   Data are available from two  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 concentra-
tions at nonurban  sites  classified as rural (SURE study,  Martinez and Singh,
1979;  NAPBN studies,  Evans et al.,  1983) may exceed the concentrations observed
at sites classified  as  suburban  (SURE study, Martinez and Singh, 1979).  For
example,  maximum  1-hour  ozone concentrations measured in  1980 at  Kisatchie
National  Forest (NF), Louisiana;  Custer NF,  Montana;  and Green  Mt.  NF, Vermont,
were 0.105, 0.070, and 0.115 ppm, respectively.   Arithmetic mean  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

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study, maximum concentrations were 0.077, 0.099, 0.099, 0.080, and 0.118 ppm,
respectively.   The  mean 1-hour  concentrations  at those  sites were  0.023,
0.030, 0.025,  0.020, and 0.025 ppm,  respectively.
     Ranges of concentrations and the maximum 1-hour concentrations at some  of
the NAPBN and SURE sites show the probable influence of ozone transported from
urban areas.   In one documented case, for example,  a 1-hour peak  ozone 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  is  discernible  in the data  record  for  1979  through
1983 at the NAPBN sites.
     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.  Average concentra-
tions in nonurban areas are likely to be comparable to or  even higher than the
average concentrations  found in  urban  areas.  Reasons  for  these  phenomena
include the lack of NO in nonurban areas for titration  of ozone (scavenging);
induction and transport  times;  as well  as the possible additive  effects of
plumes from suburban  or  smaller areas  as air masses pass over them  downwind
from urban areas.

1.4.4.  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 morn'irg to a peak concentration  in early afternoon, and decreasing toward
minimal  levels again  in the  evening.  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

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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 an  upwind area where high ozone  levels have occurred earlier
in the  day.   Secondary  peak  concentrations may be higher than concentrations
resulting from  the photochemical   reactions  of locally  emitted  precursors
(Martinez and Singh,  1979).   At one nonurban site  in  Massachusetts, 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  occur  in
the summer and  fall  (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,  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  (cf.  data  for Tucson,  Arizona; and  for California sites).
Exceptions to seasonal  patterns are  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 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)  is higher  in  the
second quarter  of  the year (April, May,  June) at  seven  of the eight stations

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and is only negligibly lower than the third-quarter value at the eighth station.
The data also  show  that 99 percent of the 1-hour concentrations measured are
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, however; 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.
     In addition to temporal  patterns,  certain macroscale spatial  variations
in  ozone  concentrations occur that  are  generally  of little consequence in
exposure assessment.  For example, ozone concentrations increase with increasing
altitude (e.g., Seller and Fishman, 1981; Viezee et al., 1979).  The gradients
are of no  known  consequence for  inhabited elevations.   They could potentially
be  of  some  consequence  for high-altitude flights  unless compensated  for by
adequate  ventilation/filtration  systems.   Likewise, ozone  concentrations
exhibit hemispheric  asymmetry (Logan et al., 1981), with concentrations highest
in  the northern  hemisphere.  Aerometric  data sufficiently describe concentra-
tions  in the  latitudes  of the United States such  that  the  fact of asymmetry
has no practical  consequences for exposure assessment.
     Spatial variations  occur  on a smaller scale, however, that assume more
importance relative  to exposure assessment.   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 al., 1973; Thompson
et al., 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  al., 1984; Contant et
al., 1985).   Ratios of  indoor-to-outdoor  (I/O)  ozone concentrations are quite
variable,  however,  since the presence or  absence  of air conditioning, air
infiltration or exchange rates, interior air circulation rates, and the composi-
tion  of  interior surfaces all  affect indoor ozone  concentrations.   Ratios

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(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 office1 building (but with 100
percent outside air intake) to 10  to 25 percent in air-conditioned residences
(Berk et al.,  1981);  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 in this chapter show
relatively homogeneous ozone concentrations  in New Haven,  Connecticut (SAROAD,
1985),  which is a  moderately large city downwind of a reasonably well-mixed
urban plume (Cleveland et al.;  1976a,b).   In a large metropolis such as New
York City, however, appreciable  gradients  in  ozone concentrations can exist
from one side  of the city to the other (Smith, 1981).  Such gradients must be
taken into consideration  in  exposure  assessments.

1.4.5  Concentrations  and Patterns  of Other  Photochemical  Oxidants
1.4.5.1  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.   Peroxybenzoyl  nitrate
has not been clearly identified in ambient air in the United States.
     The highest concentrations of PAN reported in the older  literature, 1960
through the present, were those found in  the Los Angeles  area:  70  ppb (1960),
214 ppb (1965);  and 68 ppb  (1968) (Renzetti  and  Bryan,  1961; Mayrsohn and
Brooks, 1965;  Lonneman et al.,  1976;  respectively).
     The highest concentrations of PAN measured and reported in urban areas in
the past 5 years were  42 ppb at Riverside,  California,  in  1980  (Temple and
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

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concentrations measured  in the last decade  in the Los Angeles Basin have been
in the range of 11 to 37 ppb.   Average concentrations of PAN in the Los Angeles
Basin in the past 5 years have ranged from  4 to 13 ppb  (Tuazon et al., 1981a;
Grosjean, 1983; 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).
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 at Los Angeles in 1979 (Singh et al., 1981).
     Altshuller (1983) has  succinctly  summarized  the nonurban concentrations
of PAN and PPN by pointing out that they overlap the lower end of the range of
urban concentrations  at  sites  outside  California.   At  remote locations, PAN
and PPN  concentrations are  lower than even  the lowest of the urban concentra-
tions by a factor of 3 to 4.
     In urban areas,  hydrogen peroxide (H?0?) concentrations have been reported
to range from 
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                               PRELIMINARY DRAFT
however, since ozone is now thought to be an  interference in all methods used
to date except FTIR (Chapter 4).  Measurements by FT1R, 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-km-pathlength  FTIR  system is around
0.04 ppm.)
     Recent  data  indicate the  presence in  urban  atmospheres  of only trace
amounts of formic  acid:  < 15 ppb,  measured by FTIR  (Tuazon et al.,  1981b).
Estimates  in the  earlier  literature  (1950s) of 600  to 700 ppb of formic acid
in smoggy  atmospheres  were erroneous  because of faulty measurement methodology
(Hanst et  al.,  1982).
1.4.5.2  Patterns.  The patterns  of  formic acid (HCOOH), PAN, PPN, and H^
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  HJ^^ (PPN  was not  measured).
     Seasonally, winter concentrations (third  and fourth quarters) of PAN are
lower than summer  concentrations (second and  third quarters).   The percentage
of PAN  concentrations  (PAN/0,  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.
     Indoor-outdoor data  on PAN  are  limited to one  report (Thompson et al.,
1973),  which confirms  the pattern  to be expected from the known chemistry of
PAN; that  is,  it  persists longer indoors than ozone.   Data  are lacking on
indoor-outdoor ratios  for the other non-ozone oxidants.

1.4.6   Relationship Between Ozone and Other Photochemical  Oxidants
     The  relationship  between  ozone  concentrations  and the concentrations of
PAN, PPN,  H?0?,  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

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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.   Because 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.
     Chapters 7 through 9 document what  is known about the welfare  effects of
PAN.  No data  are  available  regarding the possible welfare effects  of HCOOH,
HpCL, or  PPN,  except  for slight evidence (Chapter  9) implicating  hLO^ in
damage to  latex paints.   Chapters  10 through  13 document  what is known about
the health effects  of  PAN, H^,  and HCOOH.   No health  effects data  are avail-
able for PPN.  The  health effects  data  reported in  Chapter 9 on H^O,, and on
HCOOH show that all  levels  tested  to date are orders of magnitude above even
the highest concentrations reported  for  ambient air; and, as  noted  above and
in Chapter 4, the  concentrations  reported for  H?0~ and  earlier,  high concentra-
tions reported for HCOOH  are now known to be  much too  high.   Thus,  the brief
discussion below focuses  on  the  relationship between ozone and PAN  concentra-
tions in ambient  air.
     The most straightforward evidence of the  lack of a quantitative,  monotonic
relationship between ozone and the other photochemical  oxidants is  the range
of  PAN-to-ozone ratios expressed as percentages, as  reported  in the review of
Altshuller (1983).   The correspondence of PAN and ozone concentrations  is not
exact but  is  similar  for most locations at which  both  pollutants have been
measured in the same study.  Disparities in PAN-to-ozone  ratios between  loca-
tions, however, point  up  the lack  of a consistent quantitative relationship.
Likewise, disparities  between  the  ratio  of the average concentrations of PAN
and ozone  and  the  ratio  of their concentrations when ozone is at its  maximum
level also point up  the  lack of a  monotonically  quantitative relationship.
     Certain other  information presented in this chapter bears out the lack of
a monotonic relationship  between PAN and ozone.  Not only are PAN-ozone  rela-
tionships  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 concentrations within the  same city.  Data obtained
in  Houston by  Jorgen  et  al.  (1978) show variations in  peak concentrations of
PAN and  in  relationships  to  ozone  concentrations of those peaks among  three
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separate monitoring  sites.   Temple and  Taylor (1983) have  shown  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) demon-
strated 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.  Not  all  that give rise to  both are equally
reactive toward both, however;  and therefore some precursors  preferentially
give 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,
H?0?, 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  Altshuller examined
the  issue  of 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.
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 0.,  injury.   The effects of 0.,  are  not limited to visible
injury, however;  impacts  can  range from  reduced  plant  growth  and decreased
yield, to changes in crop quality and alterations in susceptibility to abiotic
and biotic  stresses.   The plant foliage  is  the  primary site of 0, effects
019NCH/A                            1-44                                11/22/85

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                               PRELIMINARY DRAFT
although significant secondary  effects  including  reduced growth (both roots
and foliage) and yield can occur.
     Ozone exerts a phytotoxic  effect only if a sufficient amount reaches the
sensitive cellular sites  within the  leaf.   The 0, diffuses from the ambient
air into the  leaf  through the  stomata, which can  exert  some  control on (k
uptake, to  the  active  sites  within the leaf.   Ozone injury will  not occur if
(1) the rate of 03 uptake is  low enough so the plant can  detoxify or metabolize
0, or  its metabolites,  or (2)  the plant is able to repair or compensate for
the 03  impacts  (Tingey  and Taylor, 1982).   This is  analogous  to the plant
response to S0?  (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 and/or
reduced yield of fruits or seeds.
     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
organic compounds (assimilation) necessary  for  plant growth and development.
In addition to  photosynthesis,  the plant must extract the essential mineral
nutrients and water from the  soil  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 this  process becomes  the  step
limiting plant  growth  (Tingey,  1977).   Conversely, 03 will not  limit  plant
growth  if the process impacted  by  0~ is not or does not become rate  limiting.
This implies  that  not  all effects  of 0, on plants  are reflected in growth or
yield  reductions.  These  conditions suggest that there are combinations  of 0,
concentration and exposure duration  that the  plant can experience which  will
not result in visible  injury  or reduced plant  growth and  yield.  Indeed,  numer-
ous 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
019NCH/A                            1-45                                11/22/85

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                               PRELIMINARY DRAFT
reduced growth that does not impair yield or 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 as damage or
yield loss.  Although  foliar  injury is not  always classified as damage,  its
occurrence is an  indication that  phytotoxic  concentrations of CL are  present.
The occurrence of injury indicates that additional  studies should be conducted
in areas  displaying  foliar injury to assess the risk of CL to vegetation and
to determine if  the  intended use or  value  of  the  plants is being impaired.

1.5.1  Limiting Values of Plant Response to Ozone
     Several  approaches  have  been used to estimate the 03 concentrations and
exposure  durations  that induce foliar  injury.   Most of  these studies used
short-term exposures  (less than  I  day) and  measured visible injury  as  the
response  variable.  One  method to estimate the  0, concentrations and  exposure
durations that would induce specific amounts of visible injury involves exposing
plants to a range of 0, concentrations and exposure durations, and then evalu-
ating 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 to estimate the  03 concentrations and exposure
durations which  induce  foliar  injury is to  use the  limiting value approach
(Jacobson, 1977).  The  limiting  value method was developed  from a review of
the literature  and  represents  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  studies  of  tree
species.    The  analysis yielded  the following  range  of  concentrations and
exposure durations that were likely to induce foliar injury (U.S.  Environmental
Protection Agency, 1978):

     1.    Agricultural  crops --
               0.20 to 0.41 ppm for 0.5 hr
               0.10 to 0.25 ppm for 1.0 hr
               0.04 to 0.09 ppm for 4.0 hr
019NCH/A                            1-46                                11/22/85

-------
                               PRELIMINARY DRAFT
                 TABLE 1-4.   OZONE CONCENTRATIONS FOR SHORT-TERM
                                     OR 20
                                     SENSI1
                                     (ppm)
EXPOSURES THAT PRODUCE 5 OR 20 PERCENT INJURY TO VEGETATION
             GROWN UNDER SENSITIVE CONDITIONS3
Ozone
Exposure
time, hr
0.5

1.0

2.0

4.0

8.0



concentrations that may produce

Sensitive plants
0.
(0.
0.
(0.
0.
(0.
0.
(0.
0.
35 -
45 -
15 -
20 -
09 -
12 -
04 -
10 -
02 -
0.
0.
0.
0.
0.
0.
0.
0.
0.
50
60)
25 .
35)
15
25)
09
15)
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
go.

10.

gO.

£0.

go.
70 (0.

40 (0.

30 (0.

25 (0.

20 (0.
85)

55)

40)

35)

30)
 The concentrations in parenthesis are for the 20% injury level.
Source:   U.S.  Environmental Protection Agency (1978).
     2.    Trees and shrubs --
               0.20 to 0.51 ppm for 1.0 hr
               0.10 to 0.25 ppm for 2.0 hr
               0.06 to 0.17 ppm for 4.0 hr

     It should be  emphasized that while both described methods can estimate
concentrations and exposure  durations  that might induce visible injury, they
cannot predict impacts of 0., on crop yield or intended use.
     The concept of limiting values also was used to estimate the 0., concentra-
tions and  exposure durations which could potentially reduce plant growth and
yield (U.S.  Environmental  Protection  Agency,  1978).  The data were analyzed
and plotted  in  a  manner similar to Jacobson's  (1977) approach (Figure  1-1).
In Figure  1-1  the  line bounds mean 03  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 03  response  threshold  increased  to about 0.10 ppm  and  0.30 ppm
at 6 days.

019NCH/A                            1-47                                11/22/85

-------
 1.0
Q.
Q.

z'
O
z
HI
O
Z
o
o
ui

O
N
O
 0.1
0.01
                  I
                                I      1    1   1   1   1 1 1  1
\    440  19C918 045

 \

  XO24

    \       1514    30
                                      21D  11D
                                    » 46        • 48 52
                                               ,10
                                  59
      i     »      (
      v  12 13    41     ,
       \      26        (
         \  10«  CTJ29

          \      39

           \

                      6
7 an 20


 • 42 430D9

    5«    33
       54 •• 55, 56 •• 58
             3«
                                                 2*
                                                       57
                                             53
          EXPOSURE, hr/day

            A < 1.99

            D   2 TO 3.99

            O   4 TO 5.99
       1   1  1  II  1
                               1      1    1   1   1  1  1  1  1
          6   8  10
                               20
                             40
        60  80 100
200
400
                             EXPOSURE PERIOD, days


    Figure 1-1. Relationship between 03 concentration, exposure duration, and a
    reduction in plant growth or yield (see Table 7-18).  Numbers on the figure re-
    fer to reference numbers in Table 11-4, U.S. Environmental Protection Agency
    (1978).


    Source: Derived from National Research Council (1977); cited in U.S. Envi-
    ronmental Protection Agency (1978).
                                   1-43

-------
                               PRELIMINARY DRAFT
1.5.2  Methods for Determining Ozone Yield Losses
     Diverse experimental procedures have been used to study the effects of 03
on plants,  ranging  from  studies in highly controlled conditions to exposures
in open-top chambers  and field exposures without  chambers.   In general, the
more controlled  conditions are most appropriate  for  investigating specific
responses and providing the scientific basis for interpreting and extrapolating
results.   These  systems  are  powerful  tools to  increase our  understanding  of
the biological effects of air pollutants.  However, to assess the impact of 03
on plant yield and  to provide data for economic assessments, it is desirable
to minimize deviations  from  the typical  environment  in  which the plant is
grown.   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 magni-
tude of crop  losses caused by 0., (Heck et al.,  1982).  The primary objectives
of NCLAN were:

     1.   To define the relationships between yields of major agricultural
          crops and 0.,  exposure as required to support the needs of the
          economic assessments  and  the  development of National Ambient
          Air Quality Standards;
     2.   To  assess  national economic consequences  resulting from the
          exposure of major agricultural  crops to 03;
     3.   To advance the understandng of the cause and effect relationships
          that determine crop responses to pollutant exposures.

     The NCLAN experimental  sites were selected on the basis  of (1) differing
climatic conditions,  (2)  distribution  of crop species, and (3) the existence
of established  research groups  studying air  pollution  effects  on plants.
Cultural  conditions  approximate typical  agronomic practices, and open-top
field exposure chambers are used to minimize perturbations to the plant environ-
ment during the  exposure.   The studies  have  attempted  to use realistic (L
concentrations and sufficient replication to permit the development of exposure-
response models.  The data have been analyzed  using  regression approaches.
The exposures are typically  characterized by a 7-hr  (0900 to 1600) seasonal
mean 0, concentration.  This  is the time period when 0- is added to the exposure
chambers.
019NCH/A                            1-49                                11/22/85

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                               PRELIMINARY DRAFT
1.5.3  Estimates of Ozone-Induced Yield Loss
     Yield loss is defined as an impairment or decrease in the intended use of
the plant.  Included in the concept of yield  loss are reductions in aesthetic
values,  the occurrence of  foliar injury (changes in plant  appearance),  and
losses in terms of weight,  number, or size of the plant part that is  harvested.
Yield loss may  also include changes in physical appearance, chemical  composi-
tion, or  ability  to withstand storage; collectively,  these traits  are  termed
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  the  same  impact  on  a plant  of the  same species  growing as a part of
natural  plant community would have.   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  constitute  a  yield  loss.   Attainment of  the  limiting  values for 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 rela-
tionship  between  yield  loss  and ozone concentration have focused on yields,
measured  as effects on  weight of the marketable plant  organ,  and will  be the
primary focus of this  section.
     Studies, frequently  using open-top field exposure chambers,  have been
conducted 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 0., exposure to  plant response,  and (2)
studies that compared discrete  treatment  levels to a  control.  The advantage
of  the regression  approach  is that exposure-response models  can  be  used to
interpolate results between treatment levels.
     When the  regression  approach was used  to  estimate yield loss,  0, 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 0, impact on plant yield

019NCH/A                            1-50                                11/22/85

-------
                               PRELIMINARY DRAFT
over the range  of  concentrations,  not just at the treatment means as  is the
case with analysis of variance methods.
     Examples of the relationship between 0, concentration and plant yield are
shown in Figures  1-2  and 1-3.  These cultivars/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  CL
concentration.   Both approaches  have  been used to summarize the data on  crop
responses to 0,  using  the Weibull  (Rawlings and Cure, 1985) function.   As an
example of response, the CL 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
(10%) were predicted when  the 7-hr seasonal mean 03  concentration  exceeded
0.04 to  0.05 ppm.   Concentrations of 0.028  to  0.033  ppm were predicted to
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 0 in sorghum, barley, and a corn cultivar to a high of 28.8 percent
in Vona wheat.   A  review of the data  in  Table 1-5  indicates that the grain
crops were  apparently  generally  less  sensitive  to 03 than were  the other
crops.   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 1~2  and  1-3 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
that the  fitted equations  do not show systematic deviation  from  the data
                                                                2
points and that  there  is a high coefficient of determination (R ).   Although
linear  regression  equations  have  been  used to estimate  yield loss, there
appears to be systematic deviations from the data for some species and cultivars
even though  the  equations  had moderate-to-high coefficients of determination
  2
(R ).   The use  of  plateau-linear or polynomial equations appeared to fit the
019NCH/A                            1-51                                11/22/85

-------
   6000
   5000
oi 4000
jc
Q
ui
>
Q
   3000
   2000
   1000
         (A)
                    SOYBEAN (DAVIS)
                    RALEIGH. 1981 AND 1982
           1981 (Ol
        0 0.02 0.04 0.06 0.08 0.1 0.12 0.14

            O3 CONCENTRATION, ppm
   6000
   5000
•*  4000
Q
_j
UJ
>


M  3000
   2000
   1000
           19B2IQI
           V = S23S'IO,/0.153I2272
           1983 (A|
                  V° 'OS)1
            I
                 I    I    I    I
                                  I
        0  0.020.040.060.080.10120.14

            03 CONCENTRATION, ppm
                                                 6000
                                                  5000
                                               O
                                               ui
                                                  3000
                                                 2000
                                                  1000
(B)\ SOYBEAN (WILLIAMS)
  A N.BELTSVILLE. MO. 1981 AND 1982
                                                           1981 IOI
                                                           1982 I A)
                                                           , = 5884-(0./0.1621
                                                                        1.577
                                                                   I
                                                                           j
                                                      0  0.020.040.060.08010.12014

                                                            03 CONCENTRATION, ppm


                                                    6000
                                                    5000
                                                    4000
                                                   ! 3000
                                                    2000
                                                    1000
                                                                      WHEAT (ARTHUR 71)
                                                                      ARGONNE. 1982 AND 1963
                                                          -  1983 (A)
                                                              I    I     I    I
                                                                               I     I
                                                         0  0.02 0.04 0.06 0.08 0.1  0.12 0.14

                                                              O3 CONCENTRATION,  ppm
         Figure 1-2.  Examples of the effects of 03 on the yield of soybean and wheat
         cultivars. The 03 concentrations are expressed as 7-hr seasonal mean concen-
         trations. The cultivars were selected as examples of 03 effects and to show
         year-to-year variations in plant response to 63.

         Source:  Soybean data from Heck et al.,  1984; wheat data from Kress et al.,
         1985.
                                          1-52

-------
6000




5500




5000




4500




4000




3500




3000




2500




2000




1500
(A)      COTTON (SJ-2)

        SHAFTER. CA. 1981 AND 1982
                         ,1.228
                          I   I    I   I
o

\
o>
                                     X
                                     w
                                     m
                                     cc
34



33



32



31



30



29



28



27



26



25



24



23
           (S|
! TOMATO IMUHIETTAI

 TRACY. CA. 1981 AND 1982
       0.02 0 04 0.06 0.08 0.1 0.12 0.14 0.16 0.18 0.2



           0, CONCENTRATION, ppm
                                           0  0.02  0.04 006  0.08  0.1  012 0.14 016



                                                   03 CONCENTRATION, ppm
                     (/>
                     u
                     tt
                     O
                     O
                     oc
                16


                15


                14


                13


                12


                11


                10


                 9


                 8


                 7


                 6


                 5


                 4


                 3


                 2


                 1
                                           TURNIP (TOKYO CROSSI

                                           RALEIGH. 1979 AND 1980
                                             Y=15.25-l°i/0-094l
                                                           394
                                             1979 IOI

                                              = «.8S-<°,/0.086|3
                                                 I     I
                                                          I
                            0  0.02 004  0.06  0.08 0.1  0.12  014 0.16



                                  O, CONCENTRATION, ppm
    Figure 1-3. Examples of the effects of 63 on the yield of cotton, tomato, and turnip.
    The 03 concentrations are expressed as 7-hr seasonal mean concentrations. The species
    were selected as examples of 63 effects and to show year-to-year variations in plant

    response to 03.


    Source:  Cotton and tomato data from Heck et al., 1984; turnip data from Heagle et

    al., 1985.

                                       1-53

-------
                                   PRELIMINARY DRAFT
          TABLE 1-5.   COMPILATION OF 03 CONCENTRATIONS PREDICTED TO CAUSE
      10* AND 30% YIELD LOSSES AS WELL AS YIELD LOSSES PREDICTED TO OCCUR AT
             7-HR SEASONAL MEAN 03 CONCENTRATIONS OF 0.04 AND 0.06 PPMa
    Species
03 concentrations, ppm,
predicted to causes
yield losses of:
Percent yield losses predicted
to occur at 7-hr seasonal
mean Oa concentration of:

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, Vona
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, Stonevllle
Horticultural crops
Tomato, Murrleta (81)
Tomato, Murrleta (82)
Lettuce, Empire
Spinach, America
Spinach, Hybrid
Spinach, Vlroflay
Spinach, Winter Bloom
Turnip, Just Right
Tur;,1p, Pur Top W. G.
T .'••<-. :p, Shogoln
Turnip, Tokyo Cross
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
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
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
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
aThe yield losses are derived from Welbull  equations and are based on the control
 yields 1n charcoal-filtered air.

 AK.-ce:  :«:• ived from Heck et al.  (1984).

                                    1-5-1

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                               PRELIMINARY DRAFT
data better.  More  recently  a Weibull model  has been  used  to  estimate  percent
yield loss (Heck et al., 1983).   The Weibull model yields a curvilinear response
line which  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 (L.
     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
03 concentration  that  significantly  reduced yield  was determined from the
authors'  analyses (Table  1-6).   The lowest  concentration  reported to  reduce
yield was  frequently the  lowest concentration  used  in the  study;  hence  it was
not always possible to estimate a no-effect exposure concentration.   In general,
the data  indicate that 0., 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 03 concentration was required to
cause an  effect than was estimated from the regression studies, it should be
noted that  the  concentrations  derived from the regression studies were based
on a 10 percent yield loss,  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.
     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 is  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 and
result  in an underestimation of yield loss.   However,  with an understanding  of
these limitations,  researchers have concluded that chemical protectants are  an
objective  method of  assessing  the effects  of  0..  on  crop yield.   Results ol:
several  studies with chemical  protectants  showed that ambient oxidants did
decrease  crop yield  (Table  1-7).   Crop yields were reduced  18  to M  percent

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                                        PRELIMINARY DRAFT
                               TABLE 1-6.  OZONE CONCENTRATIONS AT WHICH SIGNIFICANT YIELD LOSSES HAVE BEEN NOTED  FOR

                                      A VARIETY OF PLANT SPECIES EXPOSED UNDER VARIOUS EXPERIMENTAL CONDITIONS
01
cr*
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
Wi How 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 weight
24, height growth
19, height growth
12, height growth
03 concentration,
ppm
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 Maas, 1973
Pell et al. , 1980

Bennett et al. , 1979
Oshima 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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                                  PRELIMINARY DRAFT
                     TABLE 1-7.   THE EFFECTS OF 03 ON CROP YIELD
                   AS DETERMINED BY THE USE OF CHEMICAL PROTECTANTSC
   Species
Yield reduction
 % of control
   03 exposure,
       ppm
     Reference
Beans (green)



Onion


Tomato


Bean (dry)



Tobacco


Potato



Potato
      41



      38


      30


      24



      18


      36



      25
>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
Manning et al.,  1974
Wukasch and Hofstra, 1977
Legassicke and Ormod, 1981
Temple and Bisessar, 1979
Bisessar and Palmer, 1984
Bisessar, 1982
                        Clarke et al.,  1983
 All 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.

cThis study was run over 2 years when the 03 doses were 65 and 110 ppnrhr,
 respectively, but the yield loss was similar both years.
   019NCH/A
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                                        11/22/85

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                               PRELIMINARY DRAFT
when the ambient oxidant concentration exceeded 0.08 ppm for 5 to 18 days over
the crop's growing season.

1.5.4  Effects on Crop Quality
     Based on results  of  the few studies that  have  been conducted, 0,  can
reduce crop quality,  in  addition to reducing the  total  yield of the crop.
Quality is a  general  term that  includes many  features  of the crop such as
nutritional composition, appearance,  taste,  and ability to withstand storage
and shipment.   Examples of 0.,-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. , 1976;
Neely et  al.,  1977);  and increased reducing sugars that  are  associated  with
the undesirable darkening when potatoes are used to make potato chips (Pell et
al., 1980).

1.5.5  Yield Loss From Ambient Exposures
     Of studies  to  determine  the impact  of  ambient oxidants (primarily 03) 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%
increase  to  a 22%  decrease  in response to 03  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_ has reduced
the radial growth of sensitive individuals 30 to 50% annually over  the last 15
to 20 years  (Mann et al., 1980;  Benoit  et  al.,  1982).   Field studies in the
San Bernardino National Forest showed that during the last 30 years ambient 0^
reduced height  growth of  ponderosa pine  by  25%,  radial  growth by  37%, and  the
total wood volume produced by 84% (Miller et al., 1982).  A number  of research
studies have  demonstrated that  ambient CL  concentrations  in a number  of
locations  in  the United States  are sufficently  high  to impair plant yield.
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                                 PRELIMINARY  DRAFT
                                 TABLE  1-8.   EFFECTS OF  AMBIENT  OXIDANTS  ON  YIELD  OF  SELECTED CROPS
Plant species
Tomato
(Fireball 861 VR)
Bean
(Tendergreen)
Snap bean (3 cultivars:
Astro, BBL 274, BBL
03
concentration,
ppm
0.035
(0.017-0.072)
0.041
(0.017-0.090)
0.042
Exposure duration
99 day average (0600-2100)
43 day average (0600-2100)
3 mo average (0900-2000)
Percent yield
reduction
from control
33, fruit fresh
weight
26, pod fresh wt
1, pod weight
Location
of study
New York

Maryland
Reference
MacLean and
Schneider, 1976

Heggestad and
Bennett, 1981
  290)

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


 0.051


 0.035



>0.08
313 of hr between
(0800-2200) from late
June to mid-September
over three summers, 5%
of the time the concen-
tration was above 0.08 ppm

1979, 8 hr/day average
 (1000-1800), April-
 September
1980, 8 hr/day average
 (1000-1800), April-
 September
1981, 8 hr/day average
 (1000-1800), April-
 September

58% of hr (0600-2100)
between 1 July and
6 September
                                                 20, seed wt
                      Maryland
32, total  above
 ground biomas

20, total  above
 ground biomass

21, total  above
 ground biomass
9, ear fresh wt
Vi rginia


Vi rginia
California
                Howell  et al. ,
                1979;  Howell  and
                Rose,  1980
Duchelle et al. ,
1983
Thompson et al.,
1976a
  (Monarch Advance)
>0.08
                               28, ear fresh wt

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                               PRELIMINARY DRAFT
1.5.6  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 03 concentra-
tions,  although  various  averaging  times  have been used.   Some  studies have
also used  cumulative CL dose.  The difficulty  of selecting an appropriate
statistic to characterize  plant  exposure has been summarized  by  Heagle and
Heck (1980).  Ambient  and  experimental  0^ exposures  have  been  presented  as
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 has  adequately characterized the
relationships among  CL concentration, exposure  duration,   interval  between
                      «J
exposures, and plant  response.   The  use  of a mean  concentration  (with long
averaging times) (1)  implies that all  concentrations of 0,  are equally effective
in causing  plant  responses  and  (2) minimizes the contributions of  the peak
concentrations to the response.   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  03
concentrations.   For example, Oshima  et  al. (1977a,b) and  Lefohh and Benedict
(1982)  have summed only the ppm-hours of exposure greater than some  preselected
value.    Larsen  and  Heck (1983)  have  introduced  the  concept of "impact"  to
describe the effects of 0, and SO- on soybeans.   The "impact (I)"  is calculated
similarly to total dose,  except the  concentration  is  raised  to an  exponent
                        W
greater  than 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"  as an approach to  describe the
greater  importance of  higher  concentrations.  The "effective mean" is  defined
as the average hourly impact raised to an exponent and divided by  the duration.
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                               PRELIMINARY DRAFT
     Several lines of  evidence  suggest that higher concentrations should be
given a  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  the  plant 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  compen-
sate for the impact.
     Studies with  beans  and  tobacco  (Heck et al., 1966)  showed that a  dose
(concentration  X 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  CL flux exceeded 115 umoles/m  in one hour (Bennett,
1979).   However, a  single 3-hr exposure at approximately half the  concentration
(0.27 compared  with 0.49  ppm)  required a 64% greater internal  flux  of  0^ to
produce   the  same amount of  foliar injury as did the 1-hr  exposure.  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  03 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  0,   for  a  few days became more  sensitive to subsequent 0^
exposures.   In  studies  with  tobacco, Mukammal  (1965) showed  that  a  high 0.,
concentration on one day caused substantial  injury, whereas an equal  or  higher
concentration on the   second  day  caused only slight injury.   Using  stress
ethylene as  an  indicator of 0., 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 0., for  several

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                               PRELIMINARY DRAFT
weeks.   They  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 CL.  The newer leaves also displayed a slower
rate of  senescence.   The observations by Elkiey and Ormrod (1981) that the CL
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 also the dynamic nature
of the 03 exposure, i.e., is the exposure at a constant or variable concentra-
tion?  Musselman et al.  (1983) recently showed that constant concentrations of
03 caused  the same types of plant  responses  as  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  CL  in  open-top exposure chambers showed that significant
yield reductions  occurred when  the  maximum 0~ concentration exceeded 0.06 ppm
at least 10%  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  which  had 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 the daily peak exposure.   This study also illustrates the
problem with  the  7-hr seasonal  mean  concentration;  i.e., it fails to consider
properly the  peak concentrations.   The  plants showing  the  greater growth
reduction (in the  episodic  exposure) were exposed to  a  significantly  lower
7-hr seasonal mean  concentration.   Studies with S0?  also showed that plants
exposed  to  variable concentrations exhibited a greater  plant  response than
those exposed to  a constant concentration (Mclaughlin et al., 1979; Male et
al., 1983).

1.5.7  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

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                               PRELIMINARY DRAFT
with yield  loss  (Heagle  et a!., 1974; Oshima  et  al.,  1975).   The  relative
sensitivities of  two potato cultivars were  reversed  when judged by  foliar
injury or yield  reductions  (Pell et al., 1980).   In field corn,  foliar  injury
occurred at  a  lower 0, concentration than yield  reductions;  but as  the 0.,
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).

1.5.8  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  translocation.   An impairment in these processes may
lead to reduced plant yield if the process is limiting.
     For plant growth to occur, plants must assimilate CCL and convert it into
organic substances;  an  inhibition  in carbon assimilation may be reflected in
plant growth or yield.  In several  species 0., (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 which  catalyzes the  assimilation  of  CO,, (Pell and
Pearson, 1983).
     Ozone,  in addition  to  decreasing  the  total amount of C0? 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 translocated
to the roots and to the reproductive organs (e.g., Tingey et al., 1971;  Jacobson,
1982; Oshima et  al.,  1978, 1979;  Bennett  et  al.,  1979).   This reduces root
size and marketable yield  as well  as  rendering  the plant more sensitive to
injury  from environmental   stresses.   Another consequence of  reduced root
growth and  altered  carbon  allocation is an  impairment of symbiotic nitrogen
fixation (U.S.  Environmental Protection Agency,  1978; Ensing and  Hofstra,
1982).
     The reproductive  capacity  (flowering  and seed set)  is reduced by 0.,  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

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                               PRELIMINARY DRAFT
concentrations of 0, (0.05 to 0.10 ppm) for a few hours (Feder, 1968; Mumford,
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
0,-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.

1.5.9  Factors Affecting Plant Response to Ozone
     Numerous factors  influence  the  type and magnitude of  plant  response to
0,.   Most  studies  of the factors  influencing plant response have  been limited
to effects on  foliar  injury;  however,  some  studies  have  measured yield and
some have  researched the physiological  basis for those  influences.   The para-
meters studied include  environmental  factors,  biological  factors, and inter-
actions with other air pollutants.
1.5.9.1  Environmental  Conditions.  Environmental  conditions before and during
plant exposure are  more  influential  in  determining the  magnitude  of  the plant
response than are  post-exposure  conditions.   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  03  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 as they are under more moderate conditions.
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     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
          (1980) demonstrated that plants absorb significantly more 0, at high
          humidity than at low humidity.   It is generally accepted that plants
          in the eastern United States are injured by lower concentrations of
          0., 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 (L sensitivity is apparently related
          to stomatal  closure,  which reduces CL  uptake  (U.S.  Environmental
          Protection Agency,  1978;  Olszyk  and  Tibbitts,  1981; Tingey et al.,
          1982).  Water  stress  does not  confer a permanent tolerance  to CL;
          once the water  stress  has been alleviated,  the plants regain their
          sensitivity to 03 (Tingey et al.,  1982).

1.5.9.2  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 or more hours)  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 0,  were more
readily injured  by Botrytis  than  plants  not exposed  to  0., (Manning et al.,
1970a,b; Wukasch and Hofstra, 1977a,b; Bisessar, 1982).   Both field and labora-
tory studies have confirmed that the roots and  cut stumps of 0-,-injured ponderosa
                                                              «J
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 al.,  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).
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                               PRELIMINARY DRAFT
1.5.9.3  Interaction of Ozone with Other Air Pollutants.   The report of Menser
and Heggestad  (1966) provided the initial impetus to study the interaction of
03 with SOp.   They showed that Bel W-3 tobacco plants exposed to  03 (0.03 ppm)
or SO,, (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 0~
                                                                           «J
and SO- 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 individ-
ual reports  (e.g.,  Reinert et al.,  1975; Ormrod, 1982; Jacobson and Colavito,
1976;  Heagle and Johnston, 1979; Olszyk and  Tibbitts, 1981;  Flagler and Younger,
1982;  Foster et al., 1982; Heggestad and Bennett,  1981; Heagle et al.,  1983a).
     There have been fewer studies of the effects  of 0, and  SO- on plant yield
than on visible  injury.   The addition of low concentrations  of S0? to 0^ has
caused greater effects  on plant growth than  0, alone.  At this time, however,
there are insufficient data to indicate whether the  effects  tend  to be greater
or less than  additive.   Although the effects were not  always synergistic, the
effects of the  pollutant combination were usually greater than the effect of
03 alone.   Field studies  have  investigated  the influence of  S0»  on  plant
response to 03 at ambient and higher concentrations  on several plant species:
soybean (Heagle  et  al.,  1983; Reich and Amundson, 1984), beans (Oshima,  1978;
Heggestad and  Bennett,  1981),  and potatoes   (Foster  et al., 1983).  In these
studies,  0.,  altered  plant yield but S0? had  no significant effect and  did not
interact with  0., to  reduce plant yield unless the S0?  exposure concentrations
and frequency of occurrence were much greater  than  the concentrations  and
frequencies of occurrence  typically found in the ambient air  in the  United
States.
     The applicability of the yield results  from pollutant combination studies
to ambient conditions  is not known.  An analysis of ambient air monitoring
data indicated that  at sites where the two  pollutants were  co-monitored, ten
or fewer  periods  of co-occurrence occurred  during the growing season  (Lefohn

019NCH/A                            1-66                                11/22/85

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                               PRELIMINARY DRAFT
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 (On and S0?) on plant yield have used a longer exposure duration
and a higher  frequency  of  pollutant co-occurrence than occur in the ambient
air.
     Only a few studies have investigated the effects of 0., when combined with
other pollutants, and no clear trend is available.  Preliminary studies using
three pollutant mixtures (0.,,  SOp, N02) showed  that the additions of SOp and
N02 (at low concentrations)  caused a greater growth reduction than 0.,  alone.

1.5.10  Economic Assessment of  Ozone Effects on  Agriculture
     Evidence  from the  plant science literature clearly demonstrates that 0,
at ambient  levels will  reduce  yields of some crops (see Section 7.4.3.2.2).
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 03  control  to  agriculture.   Many of these assessments have been
performed since publication of the 1978 0~  criteria document.  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 sepcific criteria, as discussed in Section 7.5.
     While a  complete  discussion  of the criteria  for  evaluating  economic
assessments is  not appropriate  here, it is  instructive to highlight certain
key issues.    First,  the evidence  on crop response  to  0~  should reflect how
crop yields  will  respond  under  actual  field conditions.  Second,  the air
quality data  used to frame current or  hypothetical effects  of  0., on  crops
should represent the actual exposures experienced by crops in each production
area.   Finally, the  assessment  methodology  into which such data are entered
should 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.
     The assessments  of 0, damages  to  agriculture  found  in the literature
display a range of procedures  for calculating  economic  losses,  from simple
019NCH/A                            1-67                                11/22/85

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                              PRELIMINARY DRAFT
monetary calculation procedures to more complex economic assessment methodol-
ogies.   The simple  procedures  calculate  monetary effects by multiplying pre-
dicted yield or production changes resulting from exposure to CL by an assumed
                                                               •J
constant crop price, thus  failing to recognize possible crop  price  changes
arising from yield  changes as well as not accounting for the processes under-
lying  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 0., 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 on 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,
aerometric,  or  economic information and  models  currently  available.   The
estimates can then be ranked relative to  the strength  of these data and assump-
tions.   Of  the  eight  regional  studies  reviewed,  most have  adequate economic
models, but only four are judged adequate across all  input categories.   Further,
most regional  studies  abstract  from  the  interdependencies  that exist between
regions, which  limits their utility in evaluating 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

OZNORM/A                            1-68                                11/22/85

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    PRELIMINARY DRAFT
TABLE 1-9.   SUMMARY OF ESTIMATES OF REGIONAL ECONOMIC CONSEQUENCES OF OZONE POLLUTION
Annual benefits

Study Region
Adams et al.
(1982)
Southern
California







Lueng et al.
(1982)
Southern
Cal ifornia







Hewitt et al.
(1984)
Cal ifornia











Crops
14 annual crops:
beans, broccoli,
cantaloupes,
carrots, cauli-
flower, celery,
lettuce, onions,
potatoes, tomatoes
cotton, and sugar
beets.


9 crops: lemons,
granges, (Valencia
and Navel), straw-
berry, tomato,
alfalfa, avocado.
lettuce, and celery.





13 crops: alfalfa.
barley, beans.
celery, corn.
cotton, grain sor-
ghum, lettuce,
onions, potatoes,
rice, tomatoes,
and wheat.





of control ,
$ million
$45 (in 1976
dollars)









$103 (in 1975
dollars)









From $35 (bene-
fit of control
to 0.04 ppm) to
$157 (loss for
increase to
0.08 ppm) in
1978 dollars.






Evaluation of critical data and assumptions
Plant response data
Inadequate; uses Larsen-
Heck foliar injury models
converted to yield losses.








Inadequate; 0, -yield
response functions
estimated from second-
ary data on crop yields.







Adequate for some crops;
most response functions
derived from NCLAN data
through 1982. Surrogate
responses used for celery,
onions, rice and potatoes
are questionable.






Aerometric data
Adequate; Exposure
measured as cumu-
lative seasonal
exposure in
excess of Cali-
fornia standard
(0.08 ppm), from
hourly data col-
lected for sites
closest to produc-
tion regions.
Adequate for some
regions; exposure
measured in aver-
age monthly con-
centration in ppm
for 12 hr period
(0700 to 1900 hr).
Data from 61
Calfornia Air
Resources Board
monitoring sites.
Adequate; Califor-
nia Air Resources
Board data for
monitoring sites
closest to rural
production areas.
Exposure measured
as the seasonal
7-hr average in
each production
area for compara-
bility with NCLAN
exposure.
Economic model data
Adequate; a price endo-
genous mathematical
(quadratic) programming
model reflecting
agronomi c , envi ronmental ,
and economic conditions
in 1976.




Adequate on demand side;
economic model is compo-
sed of linear supply
and demand curves for
each crop estimated
with data from 1958-
1977, but ignores
producer-level adjust-
ments.


Adequate; economic model
similar to Adams et al.
(1982) but includes some
perennial crops and re-
flects 1978 economic and
technical environment.







Additional comments
Economic effect measured as a
change in economic surplus (sum
of consumers and producers'
surpluses) between base case
base case (actual 0, levels 1n
1976) and economic surplus
that would be realized if all
regions were in compliance with
1971 photochemical oxidant
standard of 0.08 ppm.

Economic effect is measured as
a change in economic surplus
between base case (1975) and a
clean air environment reflecting
zero 0,.
J





Economic effects measured as
changes in economic surplus
across three 0, changes from
1978 actual levels. These
include changes in ambient 0,
to 0.04, 0.05, and 0.08 ppm
across all regions.







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                                       PRELIMINARY DRAFT
                             TABLE 1-9 (continued).   SUMMARY OF ESTIMATES OF  REGIONAL ECONOMIC  CONSEQUENCES  OF  OZONE  POLLUTION
Study Region
     Crops
                                 Annual  benefits
                                   of control,
                                   $ mi 11 ion
                   	Evaluation of critical  data and assumptions
                  Plant response dataAerometric data"
                                                                                                   Economic  model  data
                                                                                                                                Additional  comments
Rowe et al.
(1984)
San Joaquin
Valley in
California
13 annual & peren-
nial crops:  alfal-
fa, barley,  beans,
carrots, corn,
cotton, grain,
sorghum, grass hay,
grapes, pasture,
potatoes, saf-
flower, tomatoes,
and wheat.
$43 to $117
depending on
degree of con-
trol ,  measured
in 1978 dollars.
Adequate for some crops;
response functions based
on both experimental  data
and secondary data.   Most
crops from NCLAN data.
Responses for the remain-
ing crops were based  on
surrogate responses of
similar crops in the  data
set.
Adequate; 4 expo-
sure levels were
tested.   The aver-
age hourly concen-
tration was used
in most functions
to predict changes.
Al 1 data were from
California Air
Resources Board
monitoring sites in
predominantly rural
areas.
Adequate; same as in
Howitt, et al. (1984).
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 number of hrs. >_ 0.10 ppm; (2)
meeting the current standard of
0.10 ppm; and (3) meeting an 0,
standard of 0.08 ppm.
Adams and      3 crops:  corn,       $668 (in 1980
McCarl (1985)  soybeans, and       dollars)
Corn Belt      wheat.
                                     Adequate; 0,-yield
                                     response information
                                     from NCLAN for 3 years
                                     (1980-1982).   Yield
                                     adjustments estimated
                                     from Weibull  response
                                     models.
                                            Adequate except
                                            for attempt to link
                                            7-hr seasonal  mean
                                            to hourly stand-
                                            ards.   Data are
                                            interpolated from
                                            SAROAD monitoring
                                            sites by Kriging
                                            procedure, mea-
                                            sured as 1980
                                            seasonal 7-hr
                                            average.  Regu-
                                            latory analysis
                                            assumes that 0,
                                            is log-normally
                                            distributed.
                                               Adequate;  economic esti-
                                               mates are  generated by a
                                               mathematical  programming
                                               model of U.S.  agriculture
                                               reflecting 1980 condi-
                                               tions.   Farm level
                                               response is portrayed
                                               by 12 individual
                                               "representative"  farm
                                               models to generate
                                               supply adjustments
                                               used in the national
                                               level mode 1.
                                              Economic estimates represent
                                              changes in economic surplus (sum
                                              of consumers' and producers'
                                              surpluses) between current
                                              (1980) 0, levels and increases
                                              and decreases in ambient 0,
                                              levels.  Reduction to a uniform
                                              ambient level of 0.04 ppm across
                                              all regions results in benefits of
                                              $668 mi 11 ion.
Mjedle et al.
(1984)
II1inois
3 crops: corn,
soybeans, and
wheat.
Ranges from $55  Adequate when cross-
to $220 annually checked against NCLAN
                                   for period
                                   1976 to 1980.
                                     data; responses are
                                     estimated from secon-
                                     dary (non-experimental)
                                     data on actual farmer
                                     yield, input, and 0,
                                     concentrations.  Results
                                     are translated into yield
                                     effects and compared to
                                     NCLAN data from II Mnois.
                           Adequate; Same
                           Kriged data set as
                           used in Adams and
                           McCarl (1985),
                           except that are
                           only for Illinois
                           and cover 5 years
                           (1976-1980).
                           Exposure is mea-
                           sured as seasonal
                           7-hr, average to
                           facilitate compa-
                           rison with NCLAN
                           response estimates.
                    Adequate at producers
                    level: economic model
                    consists of a series
                    annual relationships
                    on farmers' profits
                    (profit functions).
                    These  functions are
                    adjusted to represent
                    changes in 0, (+ 25%)
                    for each year.  Model
                    does not include consumer
                    (demand) effects.
                          The estimates  represent  increases
                          in farmers' profits  that could
                          arise  for a 25%  reduction  in 0,
                          for each year  (1976-1980).  Years
                          with higher ambient  levels  have
                          highest potential  increase  in
                          profits for changes.

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                                      PRELIMINARY DRAFT
                            TABLE  1-9 (continued).   SUMMARY OF ESTIMATES  OF  REGIONAL  ECONOMIC  CONSEQUENCES  OF  OZONE  POLLUTION
Study Region
                   Crops
Annual benefits
  of control ,
  $ million
                                                              Evaluation  of  critical  data  and  assumptions
                    Plant response data
                                              Aerometric data
                                                                  Economic  model  data
                                                                                                                               Additional  comments
Page et al.
(1982)
Ohio River
Basin
              3 crops:  corn,
              soybeans  and wheat,
  $7.022 measured  Inadequate; crop losses
  as present value provided by Loucks and
                                  of  producer
                                  losses  for
                                  period  1976 to
                                  2000.   Annual-
                                  ized  losses are
                                  approx.  $270 in
                                  1976  dollars.
                   Armentano (1982),
                   responses derived  by
                   synthesis of existing
                   experimental data.
                                                                               Inadequate;  dose
                                                                               measured  as  cumula-
                                                                               live  seasonal  expo-
                                                                               sure  for  a 7-hr
                                                                               period  (0930-1630
                                                                               hr)  for 1977.
                                                                               Monitoring sites
                                                                               at only 4 loca-
                                                                               tions were used to
                                                                               characterize the
                                                                               regional  exposure,
                                                                                                   Inadequate;  the economic
                                                                                                   model  consists of  region-
                                                                                                   al  supply  curves for each
                                                                                                   of  the 3 crops.  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.
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.
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-0, data
               limited to one per                   from other researchers.
               crop.                                 Crop loss modeling
                                                    includes  both chronic
                                                    and espisodic response
                                                    and crop  development
                                                    stage as  factors in
                                                    yield response, by
                                                    regressing yield on 0.,
                                                    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 sum 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 mere
                                                                                                                            prices.
                                                                                                           increases in crop
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.

-------
                              PRELIMINARY DRAFT
last criteria documents  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 secondary national  ambient air quality standards (SNAAQS).   Two of
the studies,  however,  are judged to be adequate  in terms of the three critical
data  inputs.   Together,  they provide defensible  estimates  of the economic
consequences of changes in ambient air 0, levels  on agriculture.
     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  places  emphasis on developing producer-level  responses  to
0.,-induced yield changes  (from  NCLAN data)  in 200 production  regions.   The
 J
results of the  Kopp  et al.  (1984) study indicate 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,
an  increase  in  03  to  an assumed ambient concentration of 0.08 ppm (seasonal
7-hr average) across  all  regions  produces a net  loss  of approximately $3.0
billion.
     The second study,  by  Adams et al.  (1984),  is  a  component of the NCLAN
program.   The results  are 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 03 adjustments are  sub-
stantial,   but  make up a relatively  small  percentage  of total agricultural
output (about 4 percent).   Specifically, a 25 percent reduction in ozone from
1980 ambient levels results in benefits of $1.7  billion.   A 25 percent increase

OZNORM/A                            1-72                               11/22/85

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                                                 PRELIMINARY DRAFT
                                           TABLE  1-10.  SUMMARY OF ESTIMATES OF NATIONAL ECONOMIC CONSEQUENCES OF OZONE POLLUTION
•—i
U)
Study Region
Ryan et a).
1981
Shriner et al.
(1982)
Adams and
Crocker (1984)
Annual benefits
of control ,
Crops $ bill ion
16 crops: alfalfa, $1.747 in 1980
beets, broccoli, dollars.
cabbage, corn
(sweet and field),
hay, lima beans,
oats, potatoes,
sorghum, soybeans,
spinach, tobacco,
tomatoes, and
wheat.
4 crops: corn, $3.0 in 1978
soybeans, wheat, dollars.
and peanuts.
Multiple cultivars
of al 1 crops but
peanuts.
3 crops: corn, $2.2 in 1980
soybeans, and dollars.
Evaluation of critical data and assumptions
Plant response data
Inadequate; yield-response
information derived from
a synthesis of 5 yield
studies in the literature
prior to 1980. Synthe-
sized response functions
estimated for both chronic
and acute type of expo-
sures for six crops. For
the remaining 10 crops
surrogates are used.
Yield changes are based
on reduction in 0, to
meet 1980 Federal stan-
dard of 0.12 ppm in non-
compliance counties.
Adequate; analysis uses
NCLAN response data for
1980. Functions esti-
mated in linear form.
Yield changes reflect
difference between 1978
ambient 0, levels of
each county and assumed
background of 0.025 ppm
ppm concentration.
Adequate; analysis uses
NCLAN 0,-yield data for
Aeronetric data
Inadequate; dose
measured in sev-
eral ways to
correspond to
underlying
response function.
0, data derived
ffom National
Aerometric
Databank and
from Lawrence
Berkeley
Laboratory, for
period 1974-1976.
Economic model 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.
Unknown; exposure Inadequate; same as Ryan
may be measured as et al. (1981) except
highest 7-hr. uses 1978 crop prices.
average, rather
than 7-hr NCLAN
average. Rural
ambient concen-
trations for 1978
estimated by Kriging
procedure applied
to SAROAD data.
Adequate; 1980
ambient 0, levels
Adequate on demand side
inadequate on modeling
Additional comments
Dollar estimate is for the 531
counties exceeding the
Federal standard of 0. 12 ppra.
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.
Economic estimate measured in
terms of changes in consumer
                          cotton.   Two  corn
                          cultivars,  three
                          soybean,  two
                          cotton.
1980 and 1981.  Functions
estimated in  linear form.
Yield changes measured
between 1980  ambient
levels and an assumed 0,
concentration of 0.04 ppm
across all  production
regions.
estimated by
Kriging of SAROAD
monitoring sites,
translated into a
seasonal 7-hr aver-
age.
producer behavior; eco-
nomic model consists of
crop demand and supply
curves.  Corresponding
price and quantity adjust-
ments result in changes in
economic surplus.   No pro-
ducer level responses
modeled, only measures
aggregate effects.
and producer surpluses associated
with the change in 0^.

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                                      PRELIMINARY DRAFT
                             TABLE  1-1C (continued).  SUMMARY OF ESTIMATES OF NATIONAL ECONOMIC CONSEQUENCES OF OZONE POLLUTION
Study Region
Adams et a).
(1984a)
Annual benefits
of control ,
Crops $ bil lion
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 0, -yield data for as Adams and
1980 through 1982. Yield Crocker (1984).
changes measured between
1980 ambient levels and
25 percent reduction in
0, 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 due
to sample size and func-
tional 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 qua
dratic response function.
Kopp et al.
(1984)
5 crops:  corn,
soybeans, wheat,
cotton, and
peanuts.   Multiple
cultivars of each
crop except peanuts.
$1.2 in 1978     Adequate; analysis uses
dollars.          NCLAN 0,-yield response
                 data for 1980 through
                 1982.   Yield losses (for
                 estimates reported here)
                 measured as the differ-
                 ence between ambient 1978
                 0, and a level assumed to
                 represent compliance with
                 an 0.08 ppm standard.
Adequate; same as
Adams and Crocker
and Adams, et al.
(1984) 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 0, levels, the
analysis also includes a examina-
tion of the sensitivity of the
estimates to the nature of the
demand relationships used in the
model.
Adams et al
(1984b)
6 crops: barley, $1.7 in 1980
corn, soybeans, dollars.
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.
Adequate; analysis uses
NCLAN 0,-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
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 0,
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
  biologi-, aerometric,  or economic information and  models  currently available.

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                              PRELIMINARY DRAFT
in ozone results 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. (1984)
are derived from conceptually sound economic models and from the most defensi-
ble 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 0.,-moisture  stress  interactions,  in many of  the  response experiments.
Also, the CL  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  0.,  levels at  selected  validation points,  validation  requires more
monitoring sites  in  rural  areas.   The economic models,  with the large number
of variables, parameters, and the underlying data used to derive these values,
are also potential sources of uncertainty.
     It is unlikely,  however,  that the  inclusion  of these possible  improve-
ments  in  future assessments will  greatly alter the  range  of agricultural
benefits provided  in  the Kopp  et al. (1984) and Adams et al.  (1984) studies,
for several  reasons.   First, the current  studies cover  about  75 to 80 percent
of U.S. agricultural  crops  (by value).  For  inclusion of the  other 20 percent
to change  the  estimates significantly would require that their sensitivities
to 0., be much  greater than  for  the  crops included to date.  Second, model
sensitivity analyses  from  existing studies  indicate  that changes in  key plant
science parameters  must be  substantial  to  translate into  major changes in
economic estimates.   From  experience to date it seems  unlikely  that use of
different  dose measures  or  interaction  effects would result in changes of the
magnitude  already  addressed  in some  of  the sensitivity  analyses.  Third, even
if there are  such changes, there are likely  to  be countervailing responses;
e.g., longer exposure periods  may predict greater yield losses but  0.,-water
stress tends to  dampen or reduce the yield estimates.   Finally, it should be
noted that potential  improvements  in economic estimates are  policy-relevant
only to the extent that they alter the relationship between total  benefits and
total costs  of  that  policy.   Uncertainties in other  effects  categories  are
probably greater.
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     In conclusion,  the  recent  economic estimates of benefits to agriculture
of 0... control, particularly those estimates by Kopp et al. (1984) and Adams et
al.  (1984b),  meet  the general criteria  discussed  in  Section 7.5 and  hence
provide defensible  evidence  of  the general magnitude of such effects.  Rela-
tive to estimates given in the 1978 criteria document and economic information
on most other  CL effects categories, these two  studies,  in  combination with
the  underlying NCLAN  data on yield effects, are the most defensible economic
information to date by which to judge the economic efficiency of alternative
vegetation-related  SNAAQS.   As  noted above, there  are  still gaps in  plant
science and aerometric  data  and a strong need for meteorological modeling of
0-, formation and transport processes for use in formulating rural 0., scenarios.
Further, none of the studies has accounted for the compliance costs of meeting
any 0.,  changes.   For a cost-benefit analysis  to be complete, the annualized
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.

1.5.11  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.,  and both
compounds 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) have subsequently been 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.
1.5.11.1   Factors Affecting  Plant  Response to  PAN.   Herbaceous  plants are
sensitive to PAN and cultivar differences in sensitivity have been observed in
field and  controlled  studies.   Trees and other woody  species,  however,  are
apparently resistant  to  visible  foliar injury from PAN (Taylor, 1969; Davis,
1975, 1977).
     There is  an absolute requirement  for  light  before,  during, and  after
exposure or visible injury from PAN will  not  develop  (Taylor et al.,  1961).
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                              PRELIMINARY DRAFT
Field observations have shown that crops growing under moisture stress devel-
oped 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  (L  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).
1.5.11.2   Limiting Values  of Plant Response.   The  limiting-value  method has
been  used  to  estimate  the lowest PAN concentration  and  exposure duration
reported to cause visible  injury on  various plant species (Jacobson, 1977).
The analysis yielded the following range of concentrations and exposure 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.
     More recent 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 for 7 hours  (Fukuda and Terakado,  1974).   Under field conditions,
injury symptoms may develop on sensitive species when PAN concentrations reach
approximately 15 ppb  for 4 hours (Taylor,  1969).
1.5.11.3   Effects of  PAN on  Plant  Yield.   Only  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 hours per day, twice per
week, from germination to crop maturity (Taylor et al.,  1983).   No significant
effects on  yield were  detected.   This is supportive  of field observations,  in
which  foliar  injury occurred  on these species  from ambient PAN exposures 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 hours  per
day,  twice a week, from germination to crop maturity showed yield   losses up to
13  percent (lettuce)   and  23  percent (Swiss  chard)  without  visible  foliar
injury  symptoms  (Taylor et  al.,  1983).   The  results indicate  that  PAN at
concentrations below  the  injury  threshold  can  cause significant yield losses
in sensitive cultivars of leafy  vegetable crops.  In addition to  reduced yield
without visible injury, photochemical  oxidant events have caused  foliar injury
on leafy vegetables (Middleton et al., 1950).   After severe  PAN damage, entire

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                              PRELIMINARY DRAFT
crops may  be unmarketable or  else  extensive  hand work may be  required  to
remove the injured leaves before the crop may  be marketed.
     A comparison of PAN concentrations  likely to cause either visible injury
or reduced yield with measured ambient concentrations (see  Chapter 5)  indicates
that it is unlikely that ambient PAN will impair the intended  use of plants in
the United States except  in  some areas  of California  and  in  possibly 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 7).   The responses elicited by
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).
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                              PRELIMINARY DRAFT
1.6.2  Effects of Ozone on Producers
     In forest ecosystems, tree populations  are the producers  and the control-
ler organisms.   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 7).   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 O.J; sweetgum, 29 percent (0.10 ppm 0,); green ash,  24 per-
cent (0.10 ppm);  willow oak, 19 percent (0.15 ppm  0.,);  and sugar  maple,  25 per-
cent (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 radial growth, and in root growth in  slash  pine seedlings
exposed for up to 112  days to 7-hour  seasonal mean concentrations of 0.104 ppm
0.,  (with a  1-hour daily maximum of 0.126 ppm  0.,)  and  0.076 ppm  0.,  (with  a
1-hour daily maximum of 0.094 ppm  0.,).
     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-hour)  (Mann et al.,  1980), with  1-hour 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 reduc-
tions in radial  growth  in the  last 4 years  (1976 to  1979) of  the 1962 to  1979
period for which  growth was examined than those 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-hour  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.
     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

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                              PRELIMINARY DRAFT
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 Gingham,
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 7).
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 7).

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  have  provided  some  evidence of
successional shifts and of predisposition to infestation  by pests and pathogens
as  the  result  of oxidant-induced changes in ponderosa and  Jeffrey pines (see
Section 8.9.4 belcw).  Of  particular  note  here,  however,  are the  effects  of
ozone  on mycorrhizae,  which are  considered  essential  for the  survival  of most
producer species  because of the  functions they perform (see,  e.g., Hacskaylo,
1972).  McCool et al.  (1979),  McCool  and Menge (1983),  and Parmeter et al.
(1962)  have reported  decreases  in  mycorrhizal infections  and  rootlets in
ozone-stressed citrange (a citrus hybrid),  Virginia  pine,  and ponderosa pine,
respectively.  Mahoney (1982), on the other hand,  found no  evidence of impair-
ment in the development of mycorrhizal associations  in loblolly pine seedlings
exposed to  ozone plus sulfur dioxide.
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                              PRELIMINARY DRAFT
     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 pollant-insect
interactions in determining the  growth impact of a pollutant.   Manion (1985)
has emphasized the necessity of taking non-pollutant stresses,  both biotic and
abiotic, into account when attempting to attribute changes in forest ecosystems
to air pollutants.

1.6.4  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
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-hour-average ozone concentrations ranged from
about 0.03-0.04 ppm to  about  0.10-0.12 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-hour-
average  ozone  concentrations  were  0.05  to 0.06 ppm (Miller et al.,  1982).
Injury,   decline, and  death  of these species were  associated  wit.h the major
ecosystem changes observed (Miller et al., 1982).
     Calculated 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  calcu-
late an  oxidant.-induced decrease in diameter ot 40 percent.  On the basis of

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                              PRELIMINARY DRAFT
the 3-year growth  of  samplings in filtered and  nonfiltered  air in portable
greenhouses,   they  calculated  oxidant-induced  reductions of  26 percent  in
height growth (McBride et al., 1975).
     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.   Heavy  litter accumulation hindered  pine seed  establishment
but encouraged  the growth  of oxidant-tolerant  understory  species  (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 (Stark and
Cobb,  1969).    Fewer western  pine  beetles were required to kill weakened trees
(Miller et al., 1982); and  stressed pines became more  susceptible to root rot
and showed a  decrease in  mycorrhizal rootlets and their  replacement by sapro-
phytic fungi  (Parmeter et al., 1962).
     Death of  ponderosa  and Jeffrey pine in the  forest  overstory resulting
from 0,  injury,  root  rot, and pine beetle attack,  and in some cases,  removal
by fire, changed the basic structure of the forest ecosystem (Phase IV,  Table I,
Bormann, 1985)  by causing replacement of  the  dominant conifers with self-
perpetuating,  fire  adapted, 0.,-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-hour ozone concentra-
tions ranged  from  0.08  to 0.10 ppm in the  3-year  study  period, with 1-hour
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.
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     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  have not been controller species and have
not had a role equal  in importance to the  role of ponderosa and Jeffrey pines
in that 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 ecosystem deterioration, (2) on the point at which ecosystems
lose the capacity  for self-repair,  and (3) on the points at which they begin
to lose their  ability to  provide,  respectively,  priced and unpriced  benefits
to society.   To  estimate  the  economic losses  that might  be  associated with
ozone-induced ecosystem changes  requires even  more 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  OTHER WELFARE EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS
     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.   Theore-
tically, 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.
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     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 consid-
erably, although  the  extent  of  reduction differs widely  according to  the
material  and the type  and amount of protective measures used.
     The formation of cracks  and  the depth of cracking in elastomers are 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.   Cracking occurred at a  rate  of  0.02
to 0.03 ppm/hr over the entire range of concentrations.
     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  um/hr for
cold SBR and 4.01 (jm/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 (jm/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
0.05 ppm, it would take 2.5 years for a crack  to penetrate cord depth.

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     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 antioxrdants 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 NO,, with or without high relative
humidity.
     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 N0».   Subsequent work by Schmitt (1960, 1962)  confirmed
the fading  action of ozone and  the importance of  relative humidity in the ab-
sorption 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  1n  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

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importance of surface area in relation to the degree of fading.   In explaining
this relationship, Kamath  et  al.  (1982) found that ozone penetrated into the
fiber itself and  caused  most  of the  fading  through  subsequent  diffusion to
the surface.
     Field studies by Nipe (1981) and laboratory work by Kamath et al. (1982)
showed a  positive  association  between ozone levels and  dye  fading of nylon
materials at an ozone concentration of 0.2 ppm and various  relative humidities.
In summary, dye fading is a complex function of ozone concentration, relative
humidity, and  the presence of  other gaseous pollutants.  At present,  the
available research is insufficient to quantify the amount of damaged material
attributable to ozone alone.  Anthraquinone  dyes incorporated into cotton and
nylon fibers appear to be the most sensitive to ozone damage.
     The degradation of  fibers from exposure to ozone is poorly  characterized.
In general,  most synthetic fibers like modacrylic  and polyester  are relatively
resistant, whereas cotton, nylon, and acrylic fibers have greater but varying
sensitivities to the gas.   Ozone reduces the breaking strength  of these fibers,
and the  degree of  reduction depends on  the amount of moisture present.  Under
laboratory conditions, Bogaty et al.  (1952) found  a 20 percent  loss in breaking
strength in cotton textiles under high-moisture conditions  after exposure to a
0.06 ppm concentration of ozone for 50 days;  they  equated these  conditions to a
500-to 600-day exposure  under natural  conditions.   Kerr et  al.  (1969) found a net
loss of 9 percent in breaking strength of moist cotton fibers exposed to ozone
at a concentration of 1.0 ppm for 60  days.   The limited  research 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,

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little was  (and is)  known  about the  physical  damage functions, and cost
estimates were  simplified to  the point of not  properly  recognizing many of
the scientific  complexities of  the  impact of ozone.   Assumptions about expo-
sure  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 mere-
ly 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
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

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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:

     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 CL 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 0,, 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 0., through appropriate
animal models.  This  summary highlights the significant results  of selected

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studies that will provide useful data for better predicting and assessing,  in
a scientifically sound manner, the possible human responses to (L.
     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 (L
     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 CL  have not
     been included.

2.   Cited studies report the effects of 0., 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 10.

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

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usually broad  and very  general.   For example,  the  category  "decreases in
macrophage function"  includes  such diverse endpoints as measurements  of  lyso-
somal and phagocytic  activity,  macrophage mobility,  or chemotactic response.
These responses may or may not  be related to one another.  Thus,  care must  be
taken in  how these data  are  used and  interpreted. The  only appropriate  use  is
to gain an overview of the broad array of the effects of ozone and the 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 0~ in  the upper airways
and  in  a  reduction  of the amount of 0, reaching sensitive tissues.  The site
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
     o
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  0., uptake in  the  respiratory
tract.  Experiments on the  nasopharyngeal  removal  of  0,  in  animals suggest
that the  fraction of  CL  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.

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     To further our  understanding  of C>3 absorption, mathematical models have
been developed to simulate the processes  involved and to predict (L 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
CL 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;  Miller et al., 1978b,  1985).  These models are very
similar in their treatment of 0, 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
reactions, as well  as in the  fact that the newer model  includes chemical  reac-
tions of OT 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 the animals simulated (guinea pig and rabbit)  but it
is  also  a 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 CL and its role in toxicity, but also to

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support and to  lend  confidence to the modeling  efforts.   With experimental
confirmation,  models which further our understanding of the role of 0, 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 CL.  In the
past, extrapolations have usually  been qualitative in nature.   With additional
research in areas which are  basic to the  formulation  of dosimetry models,
quantitative dosimetric  differences  among  species can be  determined.  If  in
addition,  more information is obtained on species sensitivity to  a given dose,
significant advances can be made  in quantitative extrapolations and in making
inferences about the likelihood of effects  of 03 in man.   Since animal  studies
are the only available  approach for investigating the full array of potential
disease states  induced  by  exposure  to 0~,  quantitative use of animal  data  is
in the  interest  of  better  establishing 03 levels to which man can safely be
exposed.

1.8.3  Effects of Ozone on the Respiratory Tract
1.8.3.1  Morphological  Effects.  The morphological  changes which  follow exposure
to less than 1960 (jg/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 0, 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 0, exposure of experi-
mental  animals,  damaged ciliated  cells have been  reported  in all  of these
conducting airways (Schwartz et al., 1976; Castleman et al., 1977).  In rats,
damage to ciliated cells appears most severe at the junction of the conducting
airways with the  gas exchange area  (Stephens et al., 1974a;  Schwartz et al.,
1976).  Damage  to type  1 alveolar epithelial cells is  limited to those cells
located near this junction, i.e.,  the centriacinar or proximal alveolar region
of the  pulmonary acinus  (Stephens  et al.,  1974b;  Schwartz  et al., 1976;
Castleman et  al.,  1980; Barry et al.,  1983; Crapo et al., 1984).   Type  1
alveolar cells  form most  of  the blood-air barrier where  gas exchange occurs.
Severely damaged ciliated and type 1 alveolar epithelial  cells are shed (sloughed)

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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 al., 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
epithelium in rats has been well documented as early as 2 hours after exposure
to 0, 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
epithelial  cells  after  2 hours exposure to  392 ug/m   (0.2 ppm)  0,, but this
portion of  their  report is  not documented by published micrographs (Stephens
et  al.,  1974a).    Loss  of cilia  from  cells  in  the  rat terminal  bronchiole
occurs following  exposure to 980  ug/m  (0.5 ppm)  0, for 2 hours  (Stephens et
al., 1974a).  Damage  to ciliated  cells has  been  seen  following  exposure of
both rats and monkeys to 392 ug/m  (0.2 ppm) 0-, 8 hr/day for 7 days (Schwartz
                                              
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                              PRELIMINARY DRAFT
490 |jg/m3  (0.25 ppm) 0,,  12  hrs/day  for 42 days  (Barry et al., 1983; Crapo et
                                                                        T
al., 1984).  Changes in type 1  cells were not detectable after 392 ug/m   (0.2
ppm) 0,, 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
changes persist during 180-day exposures of rats to 980 ug/m  (0.5 ppm) 0.,,  24
hr/day  (Moore  and  Schwartz,  1981)  and one-year  exposures of monkeys to 1254
|jg/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 0,. .  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
extracellular matrix   (Last  et al., 1984a;  Fujinaka  et  al.,  1985).   Three
studies provide morphological evidence of mild fibrosis (i.e., local increase
of  collagen) in centriacinar interalveolar septa  following prolonged exposure
to  < 1960  |jg/m3  (< 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 al.,  1980; Moore and Schwartz,  1981).
     While  morphometry of  small  pulmonary arteries is not commonly studied in
(L-exposed  animals, pulmonary artery walls  thickened by muscular hyperplasia
                                                      3
and edema were reported in rabbits exposed to 784 ug/m  (0.4 ppm) 0,, 6 hr/day,
5 days/week for 10  months  (P'an  et al. , 1972).   Thickened intima and media in
pulmonary arterioles were reported in monkeys exposed to 1254 ug/m  (0.64 ppm)
03,  8 hr/day for 1 year (Fujinaka et al.,  1985).
     Several of the effects of 0~ inhalation persisted after the 0., inhalation
ended and  the  animals breathed  only  filtered air  several days or weeks. Lungs
from rats  exposed  to  1568 ug/m   (0.8 ppm) 0., 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 ug/m  (0.8 ppm) 0, (Castleman
OZNORM/A                            1-94                               11/22/85

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                              PRELIMINARY DRAFT


et al., 1980)  and  in mice 10 days after a 20-day exposure to 1568 (jg/m  (0.8
ppm) OT,  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 ug/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 03  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.
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  1-4 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

OZNORM/A                            1-95                               11/22/85

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 {
i 1

» |

I


)



> 1
1


1 {




1 1
1
1
i 	 1

\





•


\



\ •




|
|
Figure 1-4. Summary of morphological effects in experimental animals exposed to
ozone. See Table 1-11 for reference citations of studies summarized here.

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                              PRELIMINARY DRAFT
         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
                           26
                           5
                           5
                           5
                           5,
                           5,
       0.50, 1.0
      0.8
      0.8
       0.88
                         0.54
                         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,
                         0.54
                         0.54
                         0.64
                         0.8
                         1.0
      0.8
      0.8
      0.8
     ,  0.88
     ,  0.88
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)
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                     11/22/85

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                              PRELIMINARY DRAFT
    TABLE 1-11 (continued).   SUMMARY TABLE:   MORPHOLOGICAL EFFECTS OF OZONE
                           IN EXPERIMENTAL ANIMALS
Effect/response
Distal airway
remodel ing




Thickened pulmonary
arteriolar wal Is
03 concentration, ppm
[0.2], 0.5, 0.8
0.2, 0.5, 0.8
0.5
0.64, 0.96
0.64
1.0
0.4
0.64
References
Boorman et al . (1980)
Schwartz et al. (1976)
Moore and Schwartz (1981)
Last et al. (1984a)
Fujinaka et al. (1985)
Freeman et al. (1973)
P'an et al. (1972)
Fujinaka et al. (1985)
the effects  of  ozone  on  the respiratory tract, particularly  after  longer
exposure periods.   A  number  of  newer studies reported  here  reflects  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
exposure for 2 hr to  concentrations of 431 to  980  ug/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 al.,  1973; Amdur
et al.,  1978).   The  onset of these effects is rapid and the abnormal  breathing
pattern usually disappears within  30 min after  cessation 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).
     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  |jg/m3 (0.56  to 0.85  ppm) of  0-3  (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

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                              PRELIMINARY DRAFT
to 5 days  (Osebold  et  al.,  1980).   In addition,  increased airway sensitivity
to histamine or cholinomimetic drugs administered by aerosol or  injection has
been noted in several species after exposure to 980 to 5880 (jg/m  (0.5 to 3.0
ppm) of 03 (Easton  and  Murphy,  1967;  Lee et al.,  1977;  Abraham et al.,  1980,
1984a,b; Gordon and Amdur,  1980;  Gordon et 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.,  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
hypersectetion,  thereby limiting the airway penetration  of inhaled bronchocon-
strictors (Abraham et al.,  1984a).
     The time course of  airway  hyperreactivity after exposure to 980 to  5880
ug/m (0.5  to 3.0 ppm) of 0^ suggests a possible association with inflammatory
cells and  pulmonary  inflammation  (Holtzman et al. , 1983a,b;  Sielczak et  al.,
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 0- 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  1-5  and
Table 1-12 (see Section  1.8.1  for  criteria used  in developing this  summary).
     Exposures of 4  to  6 weeks to  ozone  concentrations  of  392 to 490 jjg/m
(0.2 to 0.25 ppm) increased lung distensibi1ity at high  lung volumes in young
rats (Bartlett  et al.,  1974;  Raub  et  al.,  1983).   Similar increases in  lung

OZNORM/A                            1-99                               11/22/85

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o
C3

00
.  	 1
of
o^

)








i










I


                                   Figure 1-5. 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.

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                              PRELIMINARY DRAFT
          TABLE 1-12.   SUMMARY TABLE:   EFFECTS ON PULMONARY FUNCTION
                       OF SHORT-TERM EXPOSURES TO OZONE
  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)
distensibility were found  in  older rats exposed to 784 to 1568 (jg/m  (0.4 to

0.8 ppm) for  up  to  180 days (Moore and  Schwartz,  1981;  Costa et al.,  1983;

Martin et al., 1983).   Exposure to 0, concentrations of 980 to 1568 \ig/m  (0>5
to 0.8 ppm)  increased  pulmonary  resistance  and caused Impaired  stability of
the small peripheral airways  1n  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 fibrosls which has  also  been suggested morphologically and

biochemically.

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                              PRELIMINARY DRAFT
     The effects of  long-term  exposures  to ozone on  pulmonary  function  and
airway  reactivity  in  experimental  animals are summarized  in  Figure  1-6  and
Table 1-13 (see Section  1.8.1  for  criteria used  in developing this summary).
1.8.3.3  Biochemical Effects.  The  lung  is metabolically active,  and several
key steps in metabolism have been studied after 0, 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
oxygen  in air, from  oxidants produced during metabolic  processes,  and  from
oxidizing air pollutants  such  as ozone.   Obviously,  this  protection is only
partial  for 03 since exposure  to ozone causes numerous effects on  lung struc-
ture,  function,  and  biochemistry.   Acute exposure  to  high ozone levels
(2920 \jg/m , 2 ppm) typically decreases antioxidant metabolism,  whereas repeated
                                                     o
exposures to  lower  levels  (between 272 and 1568 ug/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/m  (0.2 ppm) 0., (Mustafa,  1975;  Mustafa and Lee,  1976;
Plopper et al.,  1979).   Similar responses are seen in monkeys  and  mice,  but at
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
high  ozone  levels  (^  3920 ug/m  ;  > 2  ppm)  decreases  metabolism (and thus,
oxygen consumption);  repeated exposure to lower levels (> 1568 ug/m ,  0.8 ppm)
increases oxygen  consumption (Mustafa et al., 1973;  Schwartz  et  al. ,  1976;
Mustafa  and  Lee,  1976).   Effects in rats  on  normal diets  have been observed
after a short-term  exposure to ozone  levels  as  low  as 392 ug/m   (0.2 ppm)
(Schwartz et al.,  1976; Mustafa et  al., 1973;  Mustafa and Lee,  1976).   Monkeys
are affected at a higher level  of ozone (980 ug/m ,  0.5 ppm).
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                                                                                               o*
o
00

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                              PRELIMINARY DRAFT
          TABLE 1-13.   SUMMARY TABLE:   EFFECTS ON PULMONARY FUNCTION
                        OF LONG-TERM EXPOSURES TO OZONE
  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
  (FEF)
   [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)
Kotllkoff et al., 1984

Eustis et al.  (1981)
Wegner (1982)

Raub et al. (1983)
Costa et al.  (1983)
Wegner (1982)
     Similar patterns of  response  for both antioxidant metabolism and oxygen

consumption are observed  after  exposure  to ozone.   A 7-day exposure to ozone

produces linear concentration-related  increases  in  activities of glutathione

peroxidase,  glutathione  reductase,  glucose-6-phosphate  dehydrogenase, and

succinate oxidase (Mustafa and  Lee,  1976; Chow et al., 1974; Schwartz  et al.,

1976; Mustafa et al., 1973).   Rats on a vitamin E-deficient diet experience an

increase in  enzyme  activities at  196 ug/m   (0.1 ppm)  ozone  as compared to

392 ug/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).
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            1-104
                   11/22/85

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                              PRELIMINARY DRAFT
     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
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
substrate and  the enzyme.   Acute exposure to 1470 to 1960 |jg/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-
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.

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                              PRELIMINARY DRAFT
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
                                                      3
been shown in the lungs  of rats exposed to > 1372 (jg/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 i_n 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
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
                       3
observed,  with 980 ug/m   (0.5 ppm) Cu 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
392 and 1568 ug/m  (0.2  and 0.8 ppm)  03 after an intermittent exposure for  62
days.
     The effects  of  0,   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 j_n vitro  is well  established,  few jn vivo studies of lung  lipids have

OZNORM/A                            1-106                              11/22/85

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                              PRELIMINARY DRAFT
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
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
of the  lung,  which  regulates  fluxes of various substances  with  potential
physiological  activities  across the alveolar walls.
     The biochemical effects  observed  in experimental animals exposed to 0,
are summarized  in  Figure 1-7  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  ug/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.
OZNORM/A                            1-107                              11/22/85

-------
                              rf-" ,<•<
                                                          *+•'
AH




o
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                     Figure 1-7.  Summary of biochemical changes in experimental animals exposed to ozone.
                     See Table 1-14 for reference citations of studies summarized here.

-------
                              PRELIMINARY DRAFT
               TABLE 1-14.   SUMMARY TABLE:   BIOCHEMICAL CHANGES
                   IN EXPERIMENTAL ANIMALS  EXPOSED  TO  OZONE
Effect/response
Increased 02
consumption
03 concentration, ppm
[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 '
References
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)
Increased lysosomal
  enzyme activities
Increased lung
  hydroxyproline
  and prolyl
  hydroxylase
  activity
Altered mucus
  glycoprotein
  secretions
[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
Increased alveolar
protein and
permeabi 1 ity
changes
Increased LDH
activity
[0.1],- 0.26, 0.51,
[0.25], 0.5, 1.0
0.6, 1.0
1.0
[0.1]
[0.5], 0.8
0.8
1.0

Increased NADPH
  cytochrome c
  reductase
  activity

Increased GSH
 metabolism
0.2, 0.35, 0.8
0.2, 0.5, 0.8
0.2, 0.5, 0.8
[0.1]
     0.2
     0.35
                      0.2,
                      0.32
                      0.45
                      0.5
 0.5,
0.8
0.8
0.8
1.0
                                      0.8
                   Chow et al.  (1974)
                   Dillard 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)
                   Reasor 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)
OZNORM/A
              1-109
                                       11/22/85

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                              PRELIMINARY DRAFT
         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
                      0.8
                           Fukase et al.  (1978)
                           Chow and Tappel  (1972,  1973)
                           Elsayed et al.  (1982a,b;
                             1983)

Increased NPSH
Decreased
unsaturated
fatty acids
0.8
0.9
0.9
0.1, 0.2
0.2, 0.5, 0.8
0.45
0.8
0.5
Chow et al. (1976b)
Tyson et al. (1982)
Lunan et al. (1977)
Plopper et al. (1979)
DeLucia et al. (1975b)
Mustafa et al. (1982)
Chow et al. (1976b)
Roehm et al. , 1972
     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).
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             1-110
                 11/22/85

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                              PRELIMINARY DRAFT
     Ciliated cells are  damaged  by CL inhalation, as  demonstrated  by major
morphological changes in  these  cells  including necrosis and sloughing or by
the shortening  of  the cilia in cells attached  to the bronchi.  Sufficient
ciliated cell damage  should  result in decreased transport of viable and non-
viable particles from the lung.   Rats exposed  to  784,  1568,  1960,  or 2352
ug/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  tracheal
explants from exposed rats, was inhibited  by short-term continuous  exposure  to
1568 (jg/m3 (0.8 ppm)  of  03 for 3  to  5  days (Last and Cross,  1978;  Last and
Kaizu, 1980;  Last et al., 1977).   Glycoprotein synthesis and secretion recovered
to control values after  5 to 10 days  of  exposure and increased to greater than
control  values after 10  days of exposure.   With this increase in  production  of
mucus, investigators have  found  that  the  velocity of the tracheal mucus was
                                                            3
significantly reduced following a 2 hr exposure to 1960 ug/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  03  effect  in  humans
might be  the  increased  prevalence of  infectious  respiratory  illness  in  the
community.  Such a  comparison may be  proper since both mortality  from  respira-
tory  infections (animals)  and  morbidity  from respiratory infections (humans)
can result from a  loss  in pulmonary defenses (Gardner,  1984).   Whether the

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                              PRELIMINARY DRAFT
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  host defenses should be performed in man,
using epidemiological  or volunteer methods  of study.   Unfortunately,  such
studies have  not  been reported yet.   Attention must therefore be paid to the
results of host-defense experiments conducted with animals.
     In the  area  of host  defense  of the  lung against infection, present  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
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 0, on host defense mechanisms in experimental animals are
summarized in Figure  1-8  and  Table  1-15  (see Section 1.8.1 for criteria used
in developing this summary).
1.8.3.5  Tolerance.  Examination of responses  to  short-term,  repeated exposures
to 0, clearly  indicates  that with some of the parameters  measured, animals
have an increased capacity to resist the effects  of subsequent exposure.  This
tolerance persists for  varying  times, depending  on the degree of development
of the  tolerance.  Previous exposure  to  low concentrations of 0, will protect
against the effects of subsequent exposure  to lethal  doses and the development
of lung edema  (Stokinger  et  al.,  1956; Fairchild, 1967; Coffin and  Gardner,
1972a;  Chow, 1984).  The prolongation of mucociliary clearance reported for CL

OZNORM/A                            1-112                              11/22/85

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                                                  \v*
                                                          ~o°


0. 1 -
0.2-
£
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Figure 1-8. Summary of effects of ozone on host defense mechanisms in experimental
animals.  See Table 1-15 for reference citations of studies summarized here.

-------
                              PRELIMINARY DRAFT
        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 no.
  cells
of defense
              [0.1]
              0.4, 0.8,  1.0
              [0.5]
              1.0
              0.8

              0.5
              0.99
              0.62
                          0.4
                          0.4
                   1.0
0.1,
0.5
0.5
0.5, 1.0

0.25,  0.5
                               0.67
                               0.67
                          0.8
                          1.0
                          1.0
0.2
              0.2,  0.35
              0.2,  0.35
              0.2,  0.5, 0.8
              0.25
              0.5
              0.5,  0.88
              0.5
              0.54, 0.88
              0.8
              1.0
              1.0
              0.5,  0.88
              0.5,  0.8
              0.2
              0.2
           0.5, 0.8
Grose et al.  (1980)
Kenoyer et al.  (1981)
FHberg et al.  (1972)
Abraham et al.  (1980)
Phalen et al.  (1980)

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

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)
Freeman et al.  (1974)
Castleman et al.  (1980)
Freeman et al.  (1973)
Cavender et al. (1977)
Brummer et al.  (1977)
Eustis et al.  (1981)
Dungworth (1976)
Stephens et al. (1976)
OZNORM/A
                        1-114
                                             11/22/85

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







Increased suscepti-
bility (cont'd)

Altered immune
activity



03 concentration, ppm
0.08
0.08, 0.1
0.1
0.1
0.1, 0.3
0.4, 0.7
[0.2]
0.5
[0.64]
0.3
0.7, 0.9
1.0
0.1
0.5, 0.8
0.5, 0.8
0.59

References
Coffin et al. (1968)
Miller et al. (1978a)
Ehrlich et al. (1977)
Aranyi et al. (1983)
Illing et al. (1980)
Bergers et al. (1983)
Bergers et al. (1983)
Wolcott et al. (1982)
[Sherwood et al. (1984)]
Abraham et al. (1982)
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)
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 0.,.   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 03 exposures.
These  investigators suggest that  during continuous exposure to 03  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  03  as
the pre-exposed counterpart  (Plopper  et al., 1978).  This information is an
important observation because  it  implies  that the decrease in susceptibility
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11/22/85

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                              PRELIMINARY DRAFT
to CL persists only as  long as the exposure to 0., continues.  The biochemical
studies of Chow et al.  (1976)  support this conclusion.
     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 CL  exposure, the increase in
antioxidant metabolism  reaches a plateau and  recovery occurs a  few days after
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 CL  and respiratory system fluids or
tissue can produce effects in  lymphocytes, erythrocytes, and serum, as well as
in the parathyroid  gland,  the  heart, the liver,  and the CNS.  Ozone exposure
also  produces  effects  on  animal  behavior that may be  caused  by pulmonary
consequences of 0^,  or  by nonpulmonary (CNS) mechanisms.   The  mechanism by
which 0,  causes extrapulmonary changes is unknown.  Mathematical models of 03
dosimetry predict that  very little 03  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.
OZNORM/A                            1-116                              11/22/85

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                              PRELIMINARY DRAFT
1.8.4.1  Central Nervous System and Behavioral Effects.   Ozone significantly
affects the  behavior of rats  during  exposure to concentrations  as  low as
235 ug/m  (0.12 ppm) for 6 hr.  With increasing concentrations of 03, 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 ug/m ,  0.25 ppm),  an increase in activity is observed after exposure
ends.  Higher 0,  concentrations  (980  ug/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 0, impairs  the inclination to respond.
Two  studies  indicate that mice will  respond to remove  themselves  from an
atmosphere containing greater than 980 ug/m   (0.5 ppm)  (Peterson and Andrews,
1963, Tepper et al.,  1983).   These  studies suggest that the aversive effects
of 03 may be  due  to lung irritation.   It  is  unknown whether lung irritation,
odor, or a direct effect on the CNS causes change in rodent behavior at lower
0., concentrations.
1.8.4.2  Cardiovascular Effects.   Studies  on  the effects  of 0, 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 0,  alone or in combination with
                  3
cadmium (1176 ug/m , 0.6 ppm 0.,)  resulted  in  measurable  increases in systolic
pressure and heart  rate  (Revis  et al., 1981).  No additive  or antagonistic
response was observed with the  combined exposure.   Pulmonary capillary blood
flow and PaO? decreased  30 min following  exposure of dogs to  588 ug/m  (0.3
ppm) of On (Friedman et al.,  1983).   The decrease in pulmonary capillary blood
flow persisted for as long  as 24 hr following exposure.
1.8.4.3  Hematological and Serum  Chemistry Effects.   The data base  for the
effects of 03 on  the hematological  system is extensive and indicates that 0.,
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.
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                              PRELIMINARY DRAFT
     Effects of 0.,  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
RBCs isolated from monkeys exposed to 1470 |jg/m  (0.75 ppm) of 0, 4 hr/day for
                                                                 3
4 days (Clark et al.,  1978).   A single 4-hr exposure to  392 ug/m  (0.2 ppm)
also caused increased fragility as well as sphering of RBCs of rabbits (Brinkman
et al.,  1964).   An increase in the number of RBCs  with Heinz bodies was detected
following a  4-hr  exposure to 1666 ug/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
                                                           o
biochemical  effects.  RBCs of  monkeys exposed to  1470 ug/m  (0.75 ppm) of 0.,
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).
     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
a decrease  in RBC GSH after exposure  to 1568 ug/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,
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
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
showed an increase in G-6-PD activity after an exposure of 627 ug/m  (0.32 ppm)
of 03 for 6 hr.   Decreases observed in AChE activity occurred in both groups
(Moore et al., 1980).
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                              PRELIMINARY DRAFT
     Other blood changes  are  attributed to Ov  Rabbits exposed for 1 hr to
        3
392 |jg/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 |jg/m  (0.4 ppm)
of 03 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 0.,  concentration in both studies was  1568 (jg/m  (0.8 ppm) of 0.,.
     Short-term exposure  to low concentrations  of  0,  induced an immediate
change in the serum creatine phosphokinase level in mice.  In this  study, the
OT 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 i_n vitro exposure  of RBCs  from humans (Freeman
and Mudd, 1981; Menzel  et al.,  1975b;  Verweij and Van Steveninck,  1981).  A
common effect observed  by a number of  investigators is that 0,  inhibits the
membrane ATPase activity of RBCs (Koontz and Heath,  1979;  Kesner et al.,  1979;
Kindya and  Chan,  1976;  Freeman  et al., 1979; Verweij  and  Van Steveninck,
1980).  It has been postulated that this inhibition of ATPase could be related
to the spherocytosis  and  increased fragility  of  RBCs seen in animal and  human
cells.
     Although these j_n 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 Teratogenic Effects.  Uncertainty still  exists regard-
ing possible  reproductive,  teratogenic,  and  mutational effects of exposure to
ozone.  Based on  various ijn 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
etal., 1979; Dubeau  and Chung,  1979,  1982).  The  interpretation,  relevance,

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                              PRELIMINARY DRAFT


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 i_n 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 in vivo.
     Important questions  still exist  regarding i_n vivo cytogenetic effects of
ozone in  rodents and  humans.  Zelac et al.  (1971a,b) reported chromosomal
abnormalities in  peripheral  leukocytes  of hamsters exposed to 0,  (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
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  0, 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 |.ig/m3 (1.0 ppm), effects were observed after 1,  2,  and 3
days of  exposure.   As  the concentration of 0->  was reduced,  increasing  numbers
of daily 3-hr exposures were  required to produce a significant effect.   At the
lowest  concentration  studied (196 ug/m  ,  0.1 ppm),  the increase was observed
at days 15 and 16 of exposure.  It appears that this effect is not specific to

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                              PRELIMINARY DRAFT
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 03  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 ug/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 0.,.   The  authors hypothesyzed  that  0, alters serum
binding of these hormones.
     The extrapulmonary effects of ozone in experimental animals are summarized
in  Figure 1-9  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  03 exposure in
combination  with  NO,  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

OZNORM/A                            1-121                              11/22/85

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                                                     .a
    0.
    0.1-
 E   0-2H
 a
 a
 ,  0.3H
 c
 0
~   0.4-1
 0

-2   e.sH
 0
 u
 c   0.6H
 u
 «   0.7-
 c

I   0  8H
    0.9-


     1  0
  Figure 1-9. Summary of extrapulmonary effects of ozone in experimental animals.
  See Table 1-16 for reference citations of studies summarized here.

-------
                              PRELIMINARY DRAFT
         TABLE 1-16.   SUMMARY TABLE:   EXTRAPULMONARY  EFFECTS  OF  OZONE
                            IN EXPERIMENTAL ANIMALS
Effect/response
CNS effects









Hematological effects
















Chromosomal, reproduc-
tive, teratological
effects



Liver effects



Endocrine system
effects




03 concentration, ppm
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
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
0.44
1.0
0.24, 0.3
0.43
0.1, 0.25, 0.5, 1.0

0.82
1.0
0.75
0.75
0.75
0.75
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)
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. Q972)
Larkin et al. (1983)
Clark et al. (1978)
Chow and Kaneko (1979)
Chow et al. (1974)
Menzel et al. (1975a)
Schlipkbter and Bruch (1973)
Dorsey et al. (1983)
Mizoguchi et al. (1973)
Christiansen and Giese (1954)
Brinkman et al. (1964)
Veninga (1967)
Kavlock et al. (1979)
Kavlock et al. (1980)
Zelac et al. (1971a)
Tice et al. (1978)
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 Pemsingh (1981, 1984)
Pemsingh and Atwal (1983)
demons and Garcia (1980a,b)
demons and Wei (1984)
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                              PRELIMINARY DRAFT
(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
Oj and (NH.)^ 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 03>  Fep(SO.)3,
HpSO., and (NH.KSO. produced the same  effect on clearance rate as exposure to
Cu alone.  However, when  measuring changes in host defenses,  the combination
of 03 with N02 and ZnSO.  or 0., with SOp and (NH^SO^ produced  enhanced effects
that can not be attributed to 0, 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 03 with other pollutants  are  summarized in
Figure 1-10 and Table 1-17.

1.8.6  Effects of Other Photochemical Oxidants
     There have  been  far  too few controlled  toxicological  studies with the
other oxidants to permit any sound scientific evaluation of their contribution
to the toxic  action of photochemical oxidant  mixtures.  When the effects seen
after exposure to 0, and PAN are examined and compared,  it is obvious that the
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 (0.037 ppm).
     Similarly, most of the investigations reporting HpO- toxicity have involved
concentrations much higher than those  found in the ambient air (0.1 ppm),  or
the  investigations were  conducted  by using various j_n  vitro techniques for
exposure.  Very  limited information is  available on the health  significance of
inhalation exposure to gaseous  HpOp.   Because HpO,, 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 pos-
sible effects in this region of the respiratory tract.
OZNORM/A                            1-124                              11/22/85

-------
PO
Ul







0.2-
e
a
Q.
0.3-
c
•: 0 4~
0
i 05-
c
Q)
£ 0.6-
0
u
« 0 7-
c
0
£ 0 8-
Q 9-

1 C)
»' r»'
\° »" \-
,-S ,-H ^or r
0 or o^^ \-x
A V" 1 ?° A °C 09° a
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                                Figure 1-10. Summary of effects in experimental animals exposed to ozone combined
                                with other pollutants.  See Table 1-17 for reference citations of studies summarized here.

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

Increased anti-
oxidant metabolism
and 02 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 03
     + 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 |jg/m3 (NH4)2S04
   0.05 ppm 03
     + 100-400 jjg/m3 N02
     +1.5 mg/m3 ZnS04
   0.1 ppm 03
     +0.9 mg/m3 H2S04
     (sequential exposure)
   0.1 ppm 03
     +4.8 mg/m3 H2S04
   0.1 ppm 03
     + 940 pg/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 et al. (1983)
                                                     Gardner et al. (1977)


                                                     Grose et al.   (1982)

                                                     Ehrlich (1980)

                                                     Aranyi et al. (1983)
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              1-126
                  11/22/85

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                              PRELIMINARY DRAFT
         TABLE 1-17 (continued).   SUMMARY TABLE:
                           WITH OTHER POLLUTANTS
                            INTERACTION OF OZONE
Effect/response
Pollutant concentrations
  References
Altered upper
respiratory
clearance
mechanisms
   [0.1 ppm 03
     +1.1 mg/m3 H2S04]
     (sequential exposure)
   0.4 ppm 03
     +7.0 ppm N02
   0. 5- ppm 03
     + 3 mg/m3 H2S04
   [0.8 ppm 03
     +3.5 mg/m3
       {Fe2(S04)3
        + H2S04
        + (NH4)2S04}]
Grose et al.  (1980)

Goldstein et al. (1974)
Last and Cross (1978)
Phalen et al. (1980)
     A few HI vitro studies have reported cytotoxic, genotoxic, and biochemical
effects of HpOp  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.
     Field and epidemiological  studies  have  shown that  human  health  effects
from exposure  to ambient  mixtures of oxidants and  other airborne pollutants
can produce  human health  effects (Chapter 12).   Few  such studies  have been
conducted with laboratory animals,  because  testing  and measuring  of such
mixtures is not only complicated, but extremely costly.    In these studies, the
investigators  attempted to simulate the photochemical reaction products 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  etal.,  1972;  Hueter etal.,  1966).   Certain
other  biological  responses were observed in both  treatment  groups, including a
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                              PRELIMINARY DRAFT
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
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  0,),  the observed decrements  in  FEV,  0 primarily
reflect FVC  decrements  of similar magnitude,  with  little  or no  contribution
from changes in resistance.
     Results from studies of at-rest  exposures to  0, have  demonstrated  decre-
                                                                            3
ments  in  forced expiratory  volumes  and flows  occurring  at  and above 980 (jg/ra
(0.5 ppm) of 03 (Folinsbee et al., 1978;  Horvath et al., 1979).   Airway resis-
tance  is  not clearly affected at these 0,  concentrations.   At or below 588
    3
|jg/m   (0.3  ppm)  of  0.,,  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 (Konig et al., 1980).
     With moderate intermittent exercise at a Vp of 30  to 50 L/min, decrements
in forced  expiratory  volumes and flows have  been  observed at  and above 588
ug/m   (0.30 ppm)  of  0   (Folinsbee  et al.,  1978).   With heavy  intermittent
exercise  (VV  = 65 L/min), pulmonary  symptoms are  present  and  decrements   in
forced  expiratory volumes  and  flows  are  suggested to  occur following  2-hr
exposures  to  235  (jg/m  (0.12 ppm)  of  03  (McDonnell  et  al., 1983).  Symptoms
019END/A                            1-128                         11/22/85

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                                                 PRELIMINARY DRAFT
                                                     TABLE 1-18   SUMMARY  TABLE:   CONTROLLED  HJMAN  EXPOSURE TO OZONE
I
ro
Ozone b
concentration Measurement ' Exposure
ug/m3
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 (VE) 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

13 male 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
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
IE (65) Decrement in forced expiratory volume and
@ 15-min 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 J 0.24 ppm.
CE (57) Small decrements in forced expiratory
volume at 0.16 ppm with larger decrements
at >0.24 ppm; lower-respiratory symptoms
increased at >0. 16 ppm.
IE (65) Individual responses to 03 were highly
615-min intervals reproducible for periods as long as 10
months; large Intersubject variability
1n response due to intrinsic responsiveness
to 03.
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

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                                               PRELIMINARY DRAFT
                                                   TABLE 1-18 (continued).  SUMMARY TABLE:  CONTROLLED HUMAN EXPOSURE TO OZONE
OJ
o
Ozone
concentration
ug/nr1
392
666




392
823
980



392
490


412


588
980







725
980
1470
784



784



ppm
0.20
0.35




0.2
0.42
0.50



0.20
0.25


0.21


0.3
0.5







0.37
0.50
0.75
0.4



0.4




Measurement >c Exposure Activity
method duration level (V_)
UV, UV 1 hr IE (77.5) @ vari-
(mouth- able competitive
piece) intervals
CE (77.5)


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)


CHEM, NBKI 2 hr R (10), IE (31,
50, 67)
@ 15-min intervals






MAST, NBKI 2 hr R (11) & IE (29)
@ 15-min intervals

UV, NBKI 2 hr IE (2xR)
@ 15-min intervals


CHEM, NBKI 4 3 hr IE (4-5xR)
MAST, NBKI




Observed effects(s)
Decrement in forced expiratory volume and
flow with IE and CE; subjective symptoms
increased with 03 concentration and may
limit performance; respiratory frequency
increased and tidal volume decreased with
CE.
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.
Decrement in forced expiratory volume and
flow; the magnitude of the change was
related to 03 concentration and V
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 ppm.
Good correlation between dose (concen-
tration x V_) and decrement in forced
expiratory volume and flow.
Specific airway resistance increased with
histamine 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 Reference
10 male Adams and Schelegle,
(distance runners) 1983




8 male Gliner et al. , 1983
13 female




20 male Kulle et al. , 1985



6 male Folinsbee et al.,
1 female 1984
(distance cyclists)
40 male Folinsbee et al.,
(divided into four 1978
exposure groups)






20 male Silverman et al. .
8 female (divided into 1976
six exposure groups)
12 male Dimeo et al., 1981
7 female
(divided into three
exposure groups)
10 male Farrell et al. , 1979
4 female



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                                      PRELIMINARY DRAFT
                                          TABLE 1-18 (continued).   SUMMARY TABLE:   CONTROLLED HUMAN EXPOSURE TO OZONE
Ozone .
concentration Measurement ' Exposure
ug/m3 ppm method duration
784 0.4 CHEM, UV 3 hr
Ac t i v i ty
level (VE)
IE (4-5xR)
for 15 min
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 bronchoreactivHy with
methachol ine on the first 3 days;
attenuation of response occurred by
the 4th and 5th day and persisted
for > 7 days.
No. and sex
of subjects Reference
13 male Kulle et al. , 1982
11 female
(divided into two
exposure groups)
823    0.42
                 UV, UV
                                 2 hr
IE (30)
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 intersubject variability.
                                                                                                                     24 male
                                                                                                                                              Horvath et al.,  1981
921 0.47 UV, NBKI
980 0.5 MAST, NBKI
1176 0.6 UV, NBKI
1470 0.75 MAST, NBKI
2 hr IE (3xR)
6 hr IE (44) for two
15-min periods
2 hr IE (2xR)
(noseclip) ? 15-min Intervals
2 hr IE (2xR)
@ 15-min intervals
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 1n 7
nonatopic subjects with histamine and
methachol ine and In 9 atoplc subjects
with histamine.
Decrements in spirometric variables
(20%-55%); residual volume and closing
capacity increased.
8 male
3 female
19 male
1 female
11 male
5 female (divided
by history of atopy)
12 male
Ltnn et al
Kerr et al
. , 1982b
. , 1975
Hoi tzman et al . ,
1979
Hazucha et
1973
al. ,
EXERCISING HEALTHY CHILORFN
235 0.12 CHEM, UV
2.5 hr IE (39)
015-min intervals
Small decrements in forced expiratory
volume, persisting for 24 hr. No subjec-
tive symptoms.
23 male
(8-11 yrs)
McDonnel 1
1985b.c
et al. ,

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                                       PRELIMINARY DRAFT
                                           TABLE  1-18.  (continued)   SUMMARY  TABLE:   CONTROLLED  HUMAN  EXPOSURE  TO  OZONE
Ozone .
concentration Measurement ' Exposure
Mg/nr* ppm method duration
Activity
level (V£)
Observed effects(s)
No. and sex
of subjects Reference
ADULT ASTHMATICS
392 0.2 CHEM, NBKI 2 hr
490 0.25 CHEM, NBKI 2 hr
IE (2xR)
@ 15-min intervals
R
No significant changes in pulmonary func-
tion. Small changes in blood biochemistry.
Increase in symptom frequency reported.
No significant changes in pulmonary func~
tion.
20 male Linn et al. , 1978
2 female
5 males Silverman, 1979
12 female
ADOLESCENT ASTHMATICS
235 0.12 UV 1 hr
(mouthpiece)
R
No significant changes in pulmonary function
or symptoms.
4 male Koenig et al. , 1985
6 female
(11-18 yrs)
SUBJECTS WITH CHRONIC OBSTRUCTIVE LUNG DISEASE
235 0.12 UV, NBKI 1 hr
i
'
-------
                              PRELIMINARY DRAFT
are present and  decrements  in forced expiratory volumes and flows definitely
occur at 314 to 470 pg/"1  (0.16 to 0.24 ppm) of 0., following 1 hr of continuous
heavy exercise at  a V_  of 57  L/min  (Avol et al.,  1984)  or very heavy exercise
at a VE  of  80  to 90 L/min (Adams  and  Schelegle, 1983; Folinsbee et  al., 1984)
and following 2 hr of intermittent heavy exercise at a VF of 65 L/min (McDonnell
et al.,  1983).   Airway resistance  is  only  modestly affected with  moderate
exercise (Kerr et al., 1975; Farrell et al., 1979) or even with heavy exercise
while exposed  at levels as  high as  980 (jg/rn  (0.50  ppm) 0,  (Folinsbee et al.,
1978; McDonnell et al., 1983).  Increased fD and decreased VT) while maintain-
                                           K                I
ing the  same  VV,  occur with prolonged heavy exercise when  exposed  at 392  to
        •3      b
470 ug/m  (0.20 to 0.24 ppm) of 0, (McDonnell  et al., 1983;  Adams and Schelegle,
                                 •J
1983).   While  an  increase  in RV has been reported to result from exposure to
1470 ug/m   (0.75  ppm) of  0.,  (Hazucha  et al.,  1973), changes in RV have not
                                             3
been observed  following exposures to  980 ug/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 980 ug/m   (0.50 ppm) of 0, or less,
with moderate and heavy exercise (Folinsbee et al.,  1978).
     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  0.,  concentration, V.-, and exposure duration  (Silverman  et
al. , 1976).   The relative contribution of these variables to  pulmonary  decre-
ments is greater for  0, concentration than for Vp.   A greater degree of predic-
tive accuracy  is obtained if  the  contribution  of  these  variables  is appropri-
ately 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 03 concen-
tration  have been  shown to be  quite reproducible  (Gliner et al., 1983; McDonnell
et al.,  1985a), indicating that some  individuals  are consistently more respon-
sive  to  0,  than  are others.   No information is  available  to account for these
differences.   Considering the great variability  in  individual  pulmonary  re-
sponses  to  0^  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 03  concentrations
 019END/A                             1-133                          11/22/85

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                              PRELIMINARY DRAFT
>588 \jg/m  (0.3 ppm) (Holtzman et al.,  1979;  Kb'nig et al.,  1980;  Dimeo el al.,
1981).   Exposure to 392 (jg/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 CL exposure
reflect reduced maximal inspiratory position (inspiratory capacity) (Folinsbee
et al.  ,  1978).  These  changes, as well as altered  ventilatory  control and the
occurrence of  respiratory  symptoms,  most likely result from sensitization or
stimulation of  airway  irritant receptors  (Folinsbee et al.,  1978; Holtzman et
al., 1979; McDonnell et al., 1983).   The increased airways  resistance observed
following 0, 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
                                                      3W
et al.  ,  1983).   The increased  responsiveness  of  airways  to histamine  and
methacholine  following 0,  exposure most  likely results from  an  0.,-induced
increase in airways permeability or from an alteration of smooth muscle charac-
teristics.
     Decrements in  pulmonary  function  were not observed for adult asthmatics
exposed  for  2  hours  at rest (Silverman, 1979)  or with  intermittent light
exercise  (Linn  et  al.,  1978)  to  0, 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 pg/m  (0.12
ppm) of 03 (Koenig  et al.,  1985).  Although these  results indicate that asthma-
tics are not more sensitive to 0.. than are normal  subjects, experimental-design
considerations  in reported  studies suggest that  this issue is  still unresolved.
For  patients  with  COLD performing  light  to moderate intermittent  exercise,  no
decrements  in  pulmonary function are observed  for  1-  and 2-hr  exposures  to  0.,
concentrations  of  588  ug/m3 (0.30 ppm) and  less (Linn  et  al., 1982a, 1983;
Solic  et al.,  1982; Kehrl et al., 1983,  1985) and only small decreases  in
forced expiratory volume are observed  for 3-hr exposures of chronic bronchitics
to  804 ug/m3  (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 0., exposure of smokers and nonsmokers is
                                       •J
sparse  and  somewhat  inconsistent,  perhaps partly because  of undocumented
variability in  smoking  histories.  Although some degree of attenuation appears
 019END/A                            1-134                         11/22/85

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                              PRELIMINARY DRAFT
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  (L 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 07 exposure,
                                                                    •J
but the results  so far  indicate that the effects are no more than  additive.
In addition,  there may  be considerable  interaction between these  variables
that may  result  in modification of interpretations made based  on  available
information.
     During  repeated daily  exposures  to  0,, decrements in pulmonary function
are greatest on the second exposure day  (Farrell  et al., 1979;  Horvath et al.,
1981;  Kulle  et al., 1982;  Linn et al.,  1982b); thereafter, pulmonary respon-
siveness to  0., is attenuated with smaller  decrements on each successive day
than on  the day  before until  the  fourth or fifth exposure  day  when small
decrements or no changes are observed.   Following a sequence of repeated daily
exposures, this  attenuated pulmonary responsiveness  persists  for  3  (Kulle
et al., 1982;  Linn et al.,  1982b)  to 7 (Horvath  et al., 1981) days.   Repeated
daily  exposures to a given low effective dose of 0~ does not affect the magni-
tude of decrements in  pulmonary function resulting from exposure at a higher
effective dose of 0, (Gliner et al., 1983).
     There is  some evidence suggesting that exercise  performance may be limited
by exposure  to 0,.   Decrements in forced expiratory  flow  occurring with 0.,
exposure  during  prolonged heavy exercise (Vp =  65  to 81 L/min) along with
increased f0 and decreased VT might be expected to produce ventilatory limita-
           ry                I
tions  at  near  maximal  exercise.   Results from exposure to  ozone during high
019END/A                            1-135                         11/22/85

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                              PRELIMINARY DRAFT
exercise levels (68 to 75 percent of max VO-) 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 CL 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 0, levels.   Limited data have indicated that 0,
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 0- with SO,,, N0?, 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
higher  than  the  daily maximum concentrations of  PAN  reported for  relatively
high  oxidant  areas (0.037 ppm).  One  study  (Dreschler-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
019END/A                            1-136                         11/22/85

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                              PRELIMINARY DRAFT
such as temperature and relative humidity;  proper exposure assessments,  including
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 hygiene practices, smoking habits,  and socioeconomic  status.
     The most quantitatively useful  information  of the effects  of acute  exposure
to  photochemical  oxidants  presented  in  this chapter comes  from  the  field
studies of symptoms and pulmonary function.   These studies offer the advantage
of studying the effects of  naturally-occurring,  ambient  air on  a local  subject
population using  the methods  and  better experimental  control  typical  of
controlled-exposure  studies.   In addition,  the  measured responses in  ambient
air can be compared  to clean,  filtered  air without pollutants  or to filtered
air containing artificially-generated concentrations of  0., 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)  have demonstrated
that  respiratory  effects  in Los  Angeles area residents  are related  to CL
concentration and level of exercise.  Such effects include:  pulmonary function
                                                  3
decrements seen at  0~ 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 |jg/m  (0.153 ppm) in heavily exer-
                                                     3
cising athletes and  at 0,  concentrations of 341 ug/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) showing no differences in response between chamber
exposures  to  oxidant-polluted ambient air with  a mean  0, concentration of
        3
294 |.ig/m  (0.15 ppm)  and purified air containing a controlled concentration of
generated  0^  at 314 ug/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

019END/A                            1-137                          11/22/85

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                                                PRELIMINARY  DRAFT
                         TABLE 1-19.   SUMMARY  TABLE:   ACUTE  EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS IN FIELD STUDIES WITH A MOBILE LABORATORY
CO
Mean ozone ^
concentration Measurement '
ug/ro3 ppro method
2152 0.144 UV,
UV
i'"300 0.153 UV,
UV
306 0.156 UV,
NBKI
323 0.165 UV,
NBKI
341 0.174 UV,
NBKI
Exposure Activity
duration level (V£)
1 hr CE(32)
1 hr CE(53)
1 hr CE(38)
1 hr CE(42)
2 hr IE(2 x R)
9 15-min
interval s
Observed effect(s)
Small significant decreases in FVC (-2.1*), FEV0 75
(-4.0%), FEV, o (-3.7%), and PEFR (-4.4%) relative
to control with no recovery during a 1-hr post-
exposure rest; no significant increases in
symptoms.
Mild increases in lower respiratory symptom scores
and significant decreases in FEV, (-5.3%) and
FVC; mean changes in ambient air were not statisti-
cally different from those in purified air contain-
ing 0. 16 ppm 03.
No significant changes for total symptom score or
forced expiratory performance in normals or
asthmatics; however, FEV, remained low or
decreased further (-3%) 3 hr after ambient air
exposure in asthmatics.
Small significant decreases in FEV, (-3.3%) and
FVC with no recovery during a 1-hr postexposure
rest; TLC decreased and AN2 increased slightly.
Increased symptom scores and small significant
decreases in FEV, (-2.4%), FVC, PEFR, and TLC
in both asthmatic and healthy subjects however,
25/34 healthy subjects were allergic and "atypi-
cally" reactive to 03.
No.
of subjects Reference
59 healthy Avol et al., 1985a,b
adolescents
(12-15 yr)
50 healthy Avol et al . , 1984
adults (compe-
titive bicy-
clists)
48 healthy Linn et al., 1983;
adults Avol et al. , 1983
50 asthmatic
adults
60 "healthy" Linn et al., 1983;
adults Avol et al. , 1983
(7 were
asthmatic)
34 "healthy" Linn et al., 1980, 1983
adults
30 asthmatic
adults
          Ranked by lowest  observed effect  level  for  03  in  ambient air.
          Measurement method:   UV = ultraviolet photometry.
         ""Calibration method:   UV = ultraviolet photometry  standard;  NBKI  = neutral  buffered potassium iodide.
          Minute ventilation  reported  in  L/min or as  a multiple of resting ventilation.   CE = continuous  exercise,  IE = intermittent exercise.

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                              PRELIMINARY DRAFT
the results  from  field  studies  relative to those factors are consistent with
results from controlled human exposure studies (Chapter 11).
     Studies of the  effects  of  both acute  and  chronic exposures have been
reported in the epidemiological  literature on photochemical  oxidants.   Investi-
gative approaches  comparing communities with high CL concentrations  and communi-
ties 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 incorpor-
ation 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.
     Studies of effects  associated with acute exposure  that are considered to
be qualitatively useful for standard-setting purposes include those on irritative
symptoms, pulmonary function, and aggravation of existing respiratory disease.
Reported effects on the incidence of acute respiratory illness and on physician,
emergency  room, and hospital  visits are not clearly related  with  acute exposure
to ambient  0.,  or  oxidants  and,  therefore, are not useful for deriving health
effects criteria.   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  al., 1974;  Makino and Mizoguchi,
1975; Okawada  et  al.,  1979).  Discomfort  caused  by  irritative symptoms may be
responsible  for the  impairment of athletic performance reported in high school
students during cross-country track meets  in  Los  Angeles (Wayne  et al.,  1967;

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Herman, 1972) and is consistent with the evidence from controlled human exposure
studies indicating  that exercise performance may be  limited by exposure to CL
                                                                            O
(Chapter 11).  Although  several  additional  studies  have shown  respiratory
irritation apparently related to exposure to ambient CL or oxidants in community
populations, none of these epidemiological studies provide satisfactory quanti-
tative data on acute respiratory illnesses.
     Epidemiological studies in children and young adults suggest an association
of decreased peak  flow and  increased airway  resistance with acute  ambient air
exposures to daily maximum 1-hr 0.,  concentrations ranging from 20 to 294 |.ig/m
(0.01  to  0.15  ppm)  over  the entire study  period  (Kagawa and Toyama,  1975;
Kagawa et al.,  1976; Lippmann  et  al., 1983;  Lebowitz et al.,  1982,  1983;
Lebowitz, 1984;  Bock et al., 1985;  Lioy et al., 1985).   None  of  these  studies
by themselves  can  provide  satisfactory quantitative data on acute effects of
0,, because  of  methodological problems  along  with the  confounding  influence of
other pollutants and environmental  conditions in the ambient air.  The aggrega-
tion  of  individual  studies, however,  provides reasonably good  qualitative
evidence for an  association between ambient 0, exposure and  acute  pulmonary
function effects.  This qualitative association is strengthened by the consis-
tency  between  the  findings  from the epidemiological  studies  and the  results
from the field studies in exercising adolescents (Avol et al., 1985a,b) which
have shown  small  decreases  in  forced expiratory volume and flow at 282 |jg/m
(0.144 ppm) of 0, in the ambient air;  and with the results from the controlled
                »}
human exposure studies in exercising children which have  shown small decrements
in forced expiratory volume  at 235  ug/m   (0.12 ppm)  of 0,  (Section  11.2.9.2).
     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 occurred,
and the possible concurrence of symptomatic attacks resulting from the presence
of other environmental  conditions in ambient air.   For example, Whittemoro 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) 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  temperature.   All  of  these
studies have questionable effects from other pollutants,  particularly  inhalable

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                              PRELIMINARY DRAFT
particles.   There have  been  no consistent findings of symptom aggravation or
changes in  lung  function  in  patients with chronic  lung  diseases  other than
asthma.
     Only a few prospective studies have been reported on morbidity,  mortality,
and chromosomal  effects  from  chronic exposure to 0..  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
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 CL 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 CL or
oxidants affect the peripheral lymphocytes of the exposed population.
1.11  EVALUATION OF HEALTH EFFECTS DATA FOR OZONE AND OTHER PHOTOCHEMICAL
      OXIDANTS
1.11.1  Health Effects in the General Human Population
     Controlled human  studies  of  at-rest exposures to 0^  lasting  2 to 4 hr
have demonstrated decrements in forced expiratory volume and flow occurring at
and above 0.5 ppm of 0.. (Chapter 11).  Airway resistance was not significantly
changed at  these  03 concentrations.   Breathing 0., at rest  at concentrations
< 0.5 ppm did  not  significantly impair pulmonary  function although  the occur-
rence of  some  0--related  pulmonary symptoms has been suggested  in a number  of
studies.
     One  of  the  principal modifiers  of the magnitude of  response  to 0.,  is
minute  ventilation (V_),  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 Vp not only  increase the overall  volume of inhaled pollutant, but
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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
V.- from nasal to oronasal.
     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.   Despite large interindividual  variability,
the magnitude of  group mean lung function  changes  is  positively associated
with the level of exercise and ozone concentration.  Based on reported studies
of 1 to  3  hr duration  (Chapter  11 and  references  therein), significant pulmo-
nary function  impairment  (decrement)  occurs when  exercise  is  combined  with
exposure to ozone:

     1.   Light exercise (V£ < 23 L/min) -  Effects at > 0.37 ppm 0"3;
     2.   Moderate exercise  (V£ = 24 to 43  L/min)  -  Effects  at > 0.30 ppm 03;
     3.   Heavy exercise (V£ = 44 to 63 L/min) - Effects at > 0.24 ppm 0.,; and
     4.   Very heavy exercise (V_ >  64 L/min) - Effects at > 0.18 ppm 0,, with
          suggestions of decrements  at 0.12 ppm 0,.

For the  majority of  the  controlled studies,  15-min intermittent exercise
alternated with  15-min rest was employed for  the  duration  of the exposure.
The maximum  response to 0, exposure  can be observed within 5 to 10 min follow-
ing the  end  of  each exercise period.    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 within  24 hr.   In some individuals, despite apparent func-
tional  recovery, other regulatory systems may still exhibit abnormal responses
when stimulated; e.g., airway hyperreactivity might persist for days.
     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 but the  differences between intermittent and  continuous exercise are
not clearly  established.  More experimental data are needed to make  any quanti-
tative evaluation of  the differences in  effects induced  by these two modes  of
exercise.

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     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  CL  (Chapter 11)  or to ambient  air  containing 0., as the
predominant pollutant  (Chapter 12).   This  association holds  for  both the
time-course and magnitude  of effects.   Studies on  children  and  adolescents
exposed to 03 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., 1985a,b).   Epidemiological
studies of  exposure to  ambient photochemical pollution are of  limited  use  for
quantifying exposure-response  relationships  for  0, 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
not characteristic of clinical  exposures to 0,, even at concentrations  several
times  higher  than any  likely  to  be encountered in ambient  air.   There is
limited qualitative  evidence to  suggest  that  at  low  concentrations of 0.,,
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 12).
     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 12).   Only a few controlled-
exposure studies, however, have been designed  to  examine the effects of CL  on
exercise performance (Chapter  11).  In one study,  light intermittent exercise
(Vr =  20-25 L/min)  at a high 0, 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 On 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

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also be an independent effect of elevated body temperature on pulmonary function
(VC).
     Numerous additional factors have the potential for altering responsiveness
to ozone.  For example, children and older  individuals may be more  responsive
than young adults.   Other  factors  such as  gender  differences  (at any age),
personal habits  such  as smoking,  nutritional deficiencies,  or differences in
immunologic status may  predispose  individuals to susceptibility to  ozone.   In
addition, social, cultural, or economic factors  may be involved.   Those actually
known to alter  sensitivity,  however,  are few,  largely because they have  not
been examined adequately to determine definitively their effects on sensitivity
to 0_.  The following briefly summarizes what is actually known from the data
regarding the  importance of  these  factors  (see Section  13.3.3 for  details):

     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 u\ in different age groups.
     2.    Sex.    Sex  differences in  responsiveness to ozone  have not been
adequately studied.  Lung function of women, as  assessed by changes in FEV, 0,
might be affected  more  than  that of men  under  similar exercise and exposure
conditions, but  the  possible  differences  have not  been tested systematically.
Further research is needed to determine whether there are systematic differences
in response that are related to sex.
     3.    Smoking Status.   Differences  between  smokers  and  nonsmokers have
been studied often,  but the  smoking histories are  not documented  well.  There
is some evidence, however,  to suggest that  smokers may be less sensitive to 03
than nonsmokers.
     4.    Nutritional Status.  Antioxidant properties of vitamin E  in preventing
ozone-initiated peroxidation i_n vitro are well demonstrated and their protective
effects _i_n 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 Enzyme Deficiencies.  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  0., exposure.  Even if 0.,  or a reactive product  of 0.,-tissue

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interaction were to penetrate the red blood cell  after rn 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 07 (<0.7 ppm
                                                                    O
for approximately  2  hr)  induce  a typical temporal  pattern of response (Chap-
ter 11, Section 11.3).  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 to develop full  attenuation, with more sensitive subjects requiring
more time.  The magnitude  of a  peak  response  to 0- appears to  be directly
related to  0., concentration.  It  is  not known  how variations in  the  length or
            •3
frequency  of exposure will modify the time course of  this altered responsive-
ness.   In addition, concentrations of 0- that have  no detectable effect appear
not to invoke changes in response to subsequent exposures at higher CL concen-
trations.   Full attenuation,  even in ozone-sensitive subjects,  does not persist
for more than 3 to 7 days 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.
     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 CL) are due to inhibition of maximal inspiration rather than
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.
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1.11.2  Health Effects in Individuals with Pre-Existing Disease
     Currently available evidence  indicates that  individuals with preexisting
disease respond to CL exposure to a similar degree as normal subjects.   Patients
with chronic  obstructive  lung disease and/or asthma have not shown increased
sensitivity to 0,  in controlled human exposure  studies,  but there is some
indication from epidemiological studies that asthmatics may be symptomatically
and possibly  functionally  more sensitive 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 sensitivity to 0, can be
adequately determined.  None of these factors has been sufficiently studied in
relation to CL exposures to give definitive answers.

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 03  could  experience
decrements in  their  host  defenses against infection.  At  the  present time,
however,  these effects  have  not been  described  in  humans  exposed to 0^, so
that concentrations  at  which effects might occur  in man or the severity of
such effects are unknown and difficult to predict.
     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 morpho-
logy 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
 0
subjects  exposed  to  high  concentrations  of 0.,, the  results  were either incon-
sistent or of questionable physiological significance  (Section 13.3.8).   It is
not known, therefore, if extrapulmonary  responses would  be likely  to occur in
humans  when  exposure schedules are used that are representative of exposures
that the  population  at  large might actually experience.
     Despite  wide  variations  in  study techniques and experimental  designs,
acute  and subchronic exposures of  animals  to levels  of ozone < 0.5 ppm produce

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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 0.,  exposure.   Dosimetry model simulations
predict that the  maximal tissue dose of CL occurs in this region of the lung.
Continuation of the  inflammatory  process  during longer 0. exposures is espe-
cially 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 CL has yet been pub-
lished, but centriacinar inflammation has  been shown to occur.
     Since substantial animal  data exist for  0,-induced changes in  lung struc-
ture and  function, biochemistry,  and host  defenses,  it is conceivable  that man
may experience  more types of  effects  than have been  established  in  human
clinical  studies.   It is important to note, however, that this is a qualitative
probability; it does  not  permit  assessment of  the  ozone  concen-trations  at
which man might experience similar effects.

1.11.4  Health  Effects  of Other Photochemical Oxidants  and  Pollutant Mixtures
     Controlled human studies  have not consistently  demonstrated any modifica-
tion of respiratory effects for combined exposures  of 0., with S0?,  N0?, CO, or
H?S(L 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 13.6.3).   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
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exposure regimens that  are  more closely representative of ambient air ratios
of peak concentrations,  frequency,  duration,  and time intervals between events.

1.11.5  Identification of Potentially At-Risk Groups
     Despite uncertainties  that may  exist  in the data,  it  is  possible  to
identify the groups  that may be at particular  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  particular  risk  from  exposure  to
ozone  is  that  subgroup  of  the general population  characterized  as  having
preexisting  respiratory  disease.   Available  data on actual  differences in
sensitivity between these and healthy members of the general  population indicate
that  under  the exposure  regime used  to  date, individuals with preexisting
disease may not be more  sensitive to ozone than healthy individuals.   Neverthe-
less,  two  considerations place these individuals among  groups  at potential
risk from exposure to ozone.  First, it must be noted that concern with trigger-
ing untoward reactions  has  necessitated the  use of  low  concentrations and  low
exercise levels  in  most studies on subjects  with mild  preexisting disease.
Therefore,   few or  no  data on  responses at  higher concentrations  and higher
exercise levels are available for comparison with responses in healthy subjects.
Thus, definitive data on responses in individuals with preexisting disease  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.   Such  declines  may  be  expected  to  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 apparent special  risk from exposure to ozone consists
of individuals  ("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

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                              PRELIMINARY DRAFT
of determining  in  advance  those members of  the  general  population who are
"responders" has been devised.
     Data presented  in  this  chapter underscore the importance of exercise in
the potentiation  of effects  from  exposure to ozone.  Thus,  a  third group
potentially at  risk  from  exposure  to ozone  is composed of those individuals
(healthy and otherwise) whose  activities  out of doors, whether vocational or
avocational, result in increases in minute ventilation.  Although many individ-
uals with preexisting respiratory disease would not be expected to exercise at
the same  levels one  would  expect  in healthy  individuals, any  increase  in
activity level  would bring about a  commensurate increase in minute ventilation.
To the  extent   that  the aged,  the  young,  males, or  females  participate  in
activities  out  of  doors  that raise their  minute ventilations,  all of these
groups  may  be   considered to be potentially at  risk,  depending upon other
determinants of total  ozone dose,  CL concentration,  and  exposure duration.
     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.
1.12  REFERENCES
1.12.1  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.
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1.12.2  References for Properties, Chemistry and Transport  of Ozone  and
        Other Photochemical Oxidants and Their  Precursors


Aikin, A.  C. ;  Herman,  J.  R. ; Maier,  E.  J.  R. ; McQuillan,  C.  J.  (1983)  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.; 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 0.,
     and OH radicals with a series of alkynes.  Int.  J.  Chem. Kinet.  16:  259-'?68.

Atkinson,  R. ; Carter, W.  P. L. (1984) Kinetics  and mechanisms of  the reactions
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019END/A                            1-150                          11/22/85

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019END/A                            1-151                          11/22/85

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019END/A                             1-153                          11/22/85

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     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. ;  Viezee,  W. ; Johnson,  W.   B.;  Ludwig, F. L. (1980) The  impact of
     stratospheric ozone  on tropospheric air quality.   J.  Air  Pol Kit. Control
     Assoc. 30:   1009-1017.

Slade,   D.  H. ,  ed.  (1968) Meteorology and atomic energy  1968. Washington, DC:
     U.S.  Atomic Energy Commission.  Available  from:  NTIS, Springfield, VA;
     TID-24190.

Stephens,  E. R.  (1967) The formation of  molecular oxygen by alkaline hydrolysis
     of peroxyacetyl nitrate.  Atmos.  Environ. 1: 19-20.
019END/A                            1-157                         11/22/85

-------
                              PRELIMINARY DRAFT
References for Properties, Chemistry, Transport (conl'd.)

Tiao, G.  C. ;  Box,  G.  E.   P.;  Hamming,  W.  J.  (1975) Analysis  of  Los  Angeles
     photochemical smog daLa:  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-pathlength Fourier-transform infrared spectroscopy.  Environ.
     Sci.  Technol. 15:  1232-1237.

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.

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.

Viezee, W. ;  Singh,  H.  B.  ; Shigeishi,  H.  (1982)  The impact of stratospheric
     ozone  on tropospheric  air  quality-implications from  an  analysis of
     existing field  data: final report.  Atlanta,  GA:  Coordinating  Research
     Council. Available from: NTIS,  Springfield, VA; PB82-256231.

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.
019END/A                            1-158                         11/22/85

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

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. ;  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.

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. Technol. 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-
     lium-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.
019END/A                             1-159                          11/22/85

-------
                              PRELIMINARY DRAFT
1.12.3  References for Sampling and Measurement of Ozone and Other Photochemical
        Oxiclants and Their Precursors
Allen, A. p.;  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,  5.  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.

Brewer, A. W. ; Milford, J.  R.   (1960) The Oxford-Kew ozone sonde. Proc. R.  Soc.
     London Ser. A 256: 470-495.

Bruckmann, P.  W. ;  Willner, H.  (1983) Infrared spectroscopic study  of  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. Technol. 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:  15t.h
     conference  [on] methods   in  air pollution  studies; January;  Long Beach,
     CA.  Berkeley,  CA:  California Air Resources  Board, Air  and  Industrial
     Hygiene  Laboratory.
 019END/A                            1-160                          11/22/85

-------
                              PRELIMINARY DRAFT
References for Sampling and Measurement (cont'd.)

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.

Oarley,  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.M.;  Rao, K.N. (1982).   Chemiluminescent method  for the
     determination of  low concentrations of  hydrogen peroxide.   J.  Indian
     Chen. 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.

Dasgupta, P.   K.   (1980a) Discussion on "The importance of atmospheric ozone and
     hydrogen peroxide  in oxidizing sulphur dioxide in cloud and rainwater [on
     Penkett  et al.,  1979]." Atmos. Environ.  14: 272-275.

Dasgupta,  P.  K.   (1980b)  The importance of atmospheric ozone and hydrogen
     peroxide  in oxidizing sulfur  dioxide  in cloud and  rainwater—further
     discussion  [on Penkett et al., 1979].  Atmos. Environ. 14: 620-621.

Dasgupta,  P.  K. ;  Hwang,  H. (1985).  Application of a  nested  loop  system for
     the  flow injection  analysis  of trace aqueous peroxide.   Anal.  Chem.  In
     press.

Demerjian, K.   L. ;  Kerr,  J. A.; Calvert,  J.  G. (1974) The mechanism of 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.  Technol.
     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.


019END/A                           1-161                         11/22/85

-------
                              PRELIMINARY DRAFT
References for Sampling and Measurement (cont'd.)

Dietz, W.  A.  (1967) Response factors for gas chromatographic analyses.  J. Gas
     Chromatogr.  5: 68-71.

F.  R.  (1971,  April 30) 36: 8186-8201.   National  primary and  secondary  air
     quality standards.

F.R.   (1975, February  18)  40: 7042-7070.  Ambient  air  monitoring  reference and
     equivalent methods.

F.R.  (1976, December 1) 41: 52686-52692. National primary and  secondary ambient
     air quality standards: nitrogen dioxide measurement principle and 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 dio-
     xide  in  the gas-phase titration of  nitric  oxide  with ozone.   Anal.  Chem.
     54: 278-282.

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.)

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.

Hauser, T. R.; Cummins, R. L.  (1964) Increasing sensitivity of 3-methyl-2~benzo-
     thiazolone hydrazone test  for analysis of  aliphatic  aldehydes  in air.
     Anal. Chem. 36: 679-681.
019END/A                            1-162                         11/22/85

-------
                              PRELIMINARY DRAFT
References for Sampling and Measurement (cont'd.)

Heikes, B.C.  (1984) Aqueous  H202  production  from  03 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) Chemi-
     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.

Holdren,   M.  W. ;  Spicer,  C.  W. (1984) Field compatible calibration procedure
     for peroxyacetyl nitrate. Environ.  Sci. Technol. 18: 113-116.

Hughes, E.  E.  (1975)  Development  of standard reference  materials for air
     quality measurement.  ISA Trans.  14: 281-291.

Jayanty,   R.  K.  M. ;  Blackard, A.;  McElroy, F.   F.; McClenny,  W.  A.   (1982)
     Laboratory  evaluation of nonmethane  organic  carbon  determination  in
     ambient air by cryogenic preconcentration and flame ionization detection.
     Research Triangle Park,  NC:   U.S.  Environmental Protection Agency;  EPA
     report  no.  EPA-600/4-82-019.  Available   from:   NTIS,  Springfield, VA;
     PB82-224965.

Johnson,   D.  F.; Kok, G. L.; Sonner,  R. J.   (1981) Improved chromatographic acid
     technique for the determination of formaldehyde.  In:  Grosjean,  D.; Kok,
     G. L. , eds.   Interlaboratory  comparison  study  of 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.


019END/A                             1-163                          11/22/85

-------
                              PRELIMINARY DRAFT
References for Sampling and Measurement (cont'd.)

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 peroxyacetyl  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.

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.
                                     i
Martin, L.  R. ;  Damschen,  D.  E.  (1981) Aqueous oxidation of sulfur dioxide  by
     hydrogen peroxide at  low pH. Atmos. Environ. 15:  1615-1621.

Mast,  G.  M. ;  Saunders,  H. E.  (1962) Research  and development of the instru-
     mentation of ozone sensing.  ISA Trans.  1: 325-328.

McBride, J.  M. ;  McClenny, W.  A.  (1980) Analysis of NMOC by cryogenic precon-
     centration and  flame ionization detection:  draft  report.   U.  S.  Environ-
     mental  Protection Agency, Research Triangle Park, NC.

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.
019END/A                            1-164                         11/22/85

-------
                              PRELIMINARY DRAFT
References for Sampling and Measurement (cont'd.)

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  submicrogram 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.

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, 03, and  HN03.  In: Keith,  L.   H., ed. Energy and  environmental
     chemistry, v. 2:  acid  rain.  Ann Arbor,  MI: Ann Arbor Science; pp. 245-262.

Paur,  R.  J.  ; McElroy,  F.   F.  (1979) Technical  assistance  document for the
     calibration  of ambient ozone monitors.  Research Triangle Park, NC: U.S.
     Environmental Protection Agency,  Environmental  Monitoring and Support
     Laboratory;  EPA  final report no.  EPA-600/4-79-057.  Available  from:  NTIS,
     Springfield, VA; PB80-149552.

Penkett,  S.  A.;  Jones,  B.  M.  R.; Brice, K.  A.; Eggleton, A. E. J. (1979)  The
     importance of atmospheric ozone and hydrogen peroxide in oxidising sulphur
     dioxide in cloud and  rainwater. Atmos.  Environ. 13: 123-137.

Perschke, H.; Broda, E. (1961) Determination of very small amounts of  hydrogen
     peroxide. Nature (London) 190: 257-258.


019END/A                            1-165                          11/22/85

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                              PRELIMINARY DRAFT
References for Sampling and Measurement (cont'd.) .

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.

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. ; Hauser, T. R.; Stanley, T.  W.; Elbert,  W.  (1961).  The 3-methyl-2-
     benzothiazolone hydrazone test: sensitive new  methods  for the  detection,
     rapid estimation, and  determination of aliphatic  aldehydes.  Anal.  Chem.
     33: 93-96.

Scaringelli, F. P.; Rosenberg,  P. E. ;  Rehme,  K.  A.  (1970) Comparison of per-
     meation devices  and  nitrite  ion as standards for  the  colorimetric  deter-
     mination of nitrogen dioxide.  Environ.  Sci. Technol. 4: 924-929.

Schiff, H. (1985).   York University, Toronto,  Canada.   Personal communication:
     work in progress.
Sevcfk, J.  (1975) Detectors in gas chromatography.
     Elsevier Scientific Publishing Company.
                 Prague, Czechoslovakia:
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.
019END/A
1-166
11/22/85

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                              PRELIMINARY DRAFT
References for Sampling and Measurement (cont'd.)

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.

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-pathlengtn FTIR
     spectroscopy. Adv.  Environ. Sci. Technol. 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.
019END/A                            1-167                         11/22/85

-------
                              PRELIMINARY DRAFT
References for Sampling and Measurement (cont'd.)

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. Technol. 15: 1232-1237.

U.S.  Environmental Protection Agency.  (1975) Technical assistance document for
     the chemiluminescence measurement of nitrogen dioxide.  Research Triangle
     Park, NC: U.S.  Environmental  Protection Agency; EPA report no.  EPA-600Y
     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.

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.   Research  Triangle  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. ; Hill, H.  H. (1980) Analytical methodology for
     the  identification  and quantification of vapor  phase  organic  pollutants.
     New  York, NY:  Coordinating  Research  Council;  CRC-APRAC project  no.  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.  Technol. 8: 1118-1121.

Yoshizumi,  K. ; Aoki ,  K. ;  Nouchi , I.; Okita, T. ; Kobayashi, T.; Kamakura. S.;
     Tajima, M.  (1984).   Measurement  of the  concentration  in rainwater  and  of
     the Henry's Law  constant of hydrogen peroxide.   Atmos. Environ.  18:395-401.

019END/A                            1-168                         11/22/85

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                              PRELIMINARY DRAFT
References for Sampling and Measurement (cont'd.)

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.
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  aii—relation-
     ships between  ozone  and other products. Atmos.  Environ.  17:  2383-2427.

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

Bufalini, J.  J. ;  Gay,  B.  W. , Jr.;  Brubaker,  K.  L.  (1972) Hydrogen peroxide
     formation  from formaldehyde photooxidation  and  its presence  in  urban
     atmospheres. Environ. Sci.  Technol. 6:  816-821.

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.

Contant,  C.  F. ; Gehan,  B. M. ;  Stock,  T.  H. ; Holguin,  A. H. ; Buffler, P. A.
     (1985)  Estimation  of individual  ozone  exposures using microenvironment
     measurements.   In: APCA Specialty Conference:  Scientific  Basis  for the
     Ozone Standard,  Houston, TX, November  28-December  1,  1984.  Pittsburgh;
     APCA. In Press.

Darley,  E.  F. ;  Kettner,  K.  A.;  Stephens, E.  R.  (1963) Analysis of peroxyacyl
     nitrates  by gas chromatography  with electron capture  detection.  Anal.
     Chem. 35:  589-591.

Davies,  T.  D. ;  Ramer, B.  ;  Kaspyzok,  G. ;  Delany,  A. C.  (1984)  Indoor/outdoor
     ozone concentrations  at  a contemporary  art gallery. J. Air Pollut. Control
     Assoc.  31:  135-137.
019END/A                             1-169                          11/22/85

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

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.

Farmer, J. C. ;  Dawson,  G.  A.  (1982)  Condensation sampling of soluble  atmos-
     pheric trace gases. JGR J.  Geophys.  Res. 87: 8931-8942.

Grosjean, D.   (1982) Critical 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, 0.   (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.  0.  (1982) Evidence of aqueous phase hydrogen peroxide
     synthesis in the troposphere. JGR J. Geophys. Res.  87: 3045-3051.

Hunt, W.  F.,  Jr.; Curran, T. C.   (1982) National and regional  trends in ambient
     ozone measurements, 1975-1981.  Research Triangle Park,  NC:  U.S.  Environ-
     mental  Protection  Agency,  Office of Air Quality Planning and Standards.

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, T. J. ; Stedman,  D. H.; Kok, G.  L. (1979)  Measurements  of  H202  and HN03
     in rural air. Geophys.  Res. Lett. 6: 375-378.

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.
019END/A                            1-170                          11/22/85

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

Lonneman, W.  A.; Bufalini, J. J.;  Seila, R.  L. (1976) PAN and oxidant measure-
     ment in ambient atmospheres.  Environ.  Sci.  Techno!. 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.

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.

Peterson, G.   A.;  Sabersky,  R.  H.  (1975) Measurements of pollutants inside an
     automobile. J. Air Pollut. Control Assoc. 25: 1028-1032.

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.

SAROAO,  Storage  and Retrieval  of Aerometric  Data [data base].   (1985)  Data
     file for  1976. Research Triangle  Park, NC: U.S. Environmental Protection
     Agency,  Office of Air Quality Planning and Standards.  Disc; ASCII.

Seiler,  W. ;  Fishman,  J.  (1981) The distribution  of carbon monoxide and ozone
     in  the free troposphere. JGR J. Geophys.  Res. 86:   7255-7265.

Singh, H. B.  ; Salas, L. J.;  Smith, A.  J.; Shigeishi, 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.
019END/A                            1-171                          11/22/85

-------
                              PRELIMINARY DRAFT
References for Ambient Air Concentrations (cont'd.)

Stock, T.  H. ;  Holguin,  A. H. ;  Selwyn,  B.  J. ;  Hsi , B.  P.;  Content,  C.  f.  ;
     Buffler, P.  A. ;  Kotchmar, 0. 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.

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.  Technol.  15:  1232-1237.

U.S.  Department of Commerce, Bureau of the Census. (1982) Statistical Abstract
     of the United States, 1982-1983. 103rd Ed. Washington, DC.

U.S.  Environmental Protection Agency.  (1978)  Air  quality criteria for ozone
     and other photochemical oxidants.  Research Triangle Park, NC: U.S.  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. (1984) National air quality and emission
     trends  report,  1985.  Research  Triangle  Park,  NC:  U.S. Environmental
     Protection Aency.  Office  of Air  Quality  Planning  and Standards.  EPA
     report no. EPA-450/4-84-029.

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.

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.
019VEE/A                           1-172                               11/22/85

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                              PRELIMINARY DRAFT
1.12.5   References for Effects of Ozone and Other Photochemical Oxidants on
        Vegetation


Adams,  R.  M. ;  McCarl,  B.  A.  (1985) Assessing  the  benefits of alternative
     oxidant standards  on  agriculture:  the role of  response  information.  J.
     Environ.  Eton. Manage.: in press.

Adams,  R. M. ;  Crocker,  R.  M. ;  Katz, R.  W.  (1984a)  The adequacy  of natural
     science information  in economic  assessments  of pollution control.:  a
     Bayesian  methodology.  Rev.  Econ. Stat. 66: 568-575.

Adams,  R. M. ;  Hamilton, S.  A.; McCarl, B.  A.  (1984b) The economic  effects of
     ozone on  agriculture.  Corvallis, OR: U.S. Environmental Protection Agency;
     EPA report  no.  EPA-600/3-84-090.  Available from: NTIS, Springfield, VA;
     PB85-168441/XAB.

Adams, R. M.;  Crocker, T.  D.;  Thanavibulchai,  N. (1982) An economic assessment
     of air pollution damages to selected annual crops in southern  California.
     J. Environ.  Econ. Manage.  9:  42-58.

Adedipe, N. 0.;  Ormrod, 0.  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  fulx  density.  Atmos.  Environ.  18:  1207-1215.

Ashmore, M. R.  (1984) Effects  of ozone on  vegetation in the  United Kingdom.
     Proceedings of the OECD workshop on ozone; Gothenburg, Sweden.

Benedict, H. M.;  Miller,  C.  J. ; Olson,  R.  E.  (1971) Economic  impact  of air
     pollutants  on  plants  in  the  United States. Research  Triangle  Park,  NC:
     U.S. Environmental  Protection  Agency; report  no.  APTD-0953.  Available
     from:  NTIS, Springfield,  VA;  PB-209265.

Bennett, J.  H.  (1979) Foliar exchange of gases. In:  Heck, W. W.; Krupa, S. V.;
     Linzon, S.  N. ,  eds.  Methodology   for  the  assessment  of air pollution
     effects on  vegetation:  a  handbook from  a specialty conference;  April
     1978;  Minneapolis, MN. Pittsburgh, PA: Air Pollution Control Association;
     ch. 10.

Bennett, J.  H.; Hill, A. C. (1974) Acute inhibition of apparent photosynthesis.
     In: Dugger,  J. ,  ed.  Air pollution  effects  on  plant growth.  Washington,
     DC: American Chemical  Society.  (ACS symposium series 3.)

Bennett, J.  P.;  Oshima, R. J. ;  Lippert, L. F.  (1979)  Effects of  ozone on
     injury and  dry  matter partitioning in pepper plants.   Environ.  Exp. Bot.
     19: 33-39.
019VEE/A                           1-173                               11/22/85

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                              PRELIMINARY DRAFT
References for Vegetation Effects (cont'd.)

Benoit, L. F. ;  Skelly,  J.  M. ;  Moore,  L.  D. ;  Dochinger, L. S.  (1982) Radial
     growth reductions in FMnus strobus L. correlated with foliar ozone sensi-
     tivity as  an  indicator  of ozone-induced losses in eastern forests. Can.
     J. For.  Res.  12:  673-678.

Benson, E. J. ;  Krupa,  S.;  Teng, P.  S. ; Welsch, P. E. (1982)  Economic assess-
     ment of  air  pollution  damages  to agricultural  and si 1vicultural  crops.
     In:  Minnesota final report to Minnesota Pollution  Control  Agency. St.  Paul,
     MN:  University of Minnesota.

Bisessar,  S.   (1982) Effect of  ozone,  antioxidant  protection,  and  early  blight
     on potato in the field.  J. Am.  Soc.  Hortic. Sci. 107:  597-599.

Bisessar,  S. ;  Palmer,  K.  T.  (1984) Ozone,  antioxidant  spray  and  Meloidogyne
     hapla effects on tobacco.  Atmos.  Environ.  18: 1025-1027.

Black,  V.  J.;  Ormrod, D. P.; Unsworth, M.  H. (1982)  Effects of low 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.

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.
019VEE/A                           1-174                               11/22/85

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                              PRELIMINARY DRAFT
References for Vegetation Effects (cont'd.)

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.

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.
019VEE/A                           1-175                               11/22/85

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                              PRELIMINARY DRAFT
References for Vegetation Effects (cont'd.)

Heagle, A. S. ;  Letchworth,  M.  B.;  Mitchell,  C.  A.  (1983a)  Effects of growth
     medium and  fertilizer  rate  on the yield response of soybeans exposed  to
     chronic doses of ozone. Phytopathology 73: 134-139.

Heagle, A. S. ;  Heck,  W.  W.  ; Rawlings, J. 0.; Philbeck, R.  B. (1983b)  Effects
     of chronic  doses of ozone  and  sulfur dioxide  on  injury and yield of
     soybeans in open-top field chambers. Crop Sci.  23: 1184-1191.

Heagle, A. S. ;  Cure,  W.  W.  ; Rawlings, J.  0.  (1985) Response of  turnips to
     chronic  doses  of ozone  in open-top  field chambers.  Environ.   Poll.
     (Series A) 38:  305-320.

Heck, W.  W. ;  Tingey,  D.  T.  (1971) Ozone time-concentration model  to predict
     acute foliar injury.  In:  Englund, H.  M. ; Beery, W. T., eds.  Proceedings
     of the second international  clean air congress; December 1970;  Washington,
     DC. New York, NY: Academic Press; pp.  249-255.

Heck, W.  W. ;  Dunning, J.  A.;  Hindawi, I. J.   (1966)  Ozone:  nonlinear relation
     of dose  and injury to plants.  Science   (Washington, DC)  151:  511-515.

Heck, W.  W. ;  Taylor,  0.  C.  ; Adams, R.; Bingham, G.; Miller, J.; Preston, E.;
     Weinstein,  L. (1982) Assessment of crop loss  from ozone.  J.  Air  Pollut.
     Control  Assoc.  32: 353-361.

Heck, W.  W. ;  Adams,   R. M. ; Cure,  W.  W. ; Heagle,  A.  S. ;  Heggestad,  H.  E. ;
     Kohut, R.  J. ;  Kress,   L.  W. ;  Rawlings,  I.  0.;  Taylor,  0.  C.  (1983) A
     reassessment  of  crop  loss  from  ozone.  Environ.   Sci.   Technol.
     17: 573A-581A.

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.
019VEE/A                           1-176                               11/22/85

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                              PRELIMINARY DRAFT
References for Vegetation Effects (cont'd.)

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,  0.  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, 0.  C. ; Nicholls,  A.  0.; Calder, D.  M.  (1980) Growth  responses  of
     Dactyl is glomerata,  Lolium  perenne and Phalaris  aquatica to chronic ozone
     exposure. Aust.  J.  Plant Physiol. 7: 511-517.

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

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).

Jacobson, J.  S. (1982)  Ozone  and the growth and productivity of agricultural
     crops.   In: Unsworth,  M.  H. ; Ormrod, D.   P. , eds.  Effects  of gaseous air
     pollution  in  agriculture  and  horticulture.  London, United  Kingdom:
     Butterworth Scientific; pp. 293-304.

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.
     Qual. 12: 276-281.

Kress,  L. W. ;  Skelly,  J. M.  (1982)  Response of  several  eastern forest  tree
     species  to chronic  doses  of ozone  and nitrogen dioxide.  Plant  Dis.
     66: 1149-1152.

Kress,  L. W. ,  Miller,  J. E. ;  Smith,  H.  J.  (1985) Impact of ozone on winter
     wheat yeild.  Environ.  Exp.   Bot. (in press).


019VEE/A                           1-177                                11/22/85

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                              PRELIMINARY DRAFT
References for Vegetation Effects (cont'd.)

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.

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.

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.  Qual.  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.

Manning,   W.  J. ;  Feder,  W.  A.;  Perkins, I.  (1970a)  Ozone  and  infection of
     geranium flowers by Botrytis cinerea. 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.  (1980)  Relative  humidity:  important modifier
     of pollutant  uptake by  plants.  Science  (Washington, DC)  22:  167-169.
019VEE/A                           1-178                               11/22/85

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                              PRELIMINARY DRAFT
References for Vegetation Effects (cont'd.)

Mclaughlin, S. B. ;  Shriner,  D.  S. ; McConathy,  R.  K. ;  Mann,  L.  K.  (1979)  The
     effects of  S02  dosage  kinetics and exposure freguency on photosynthesis
     and transpiration  of kidney  beans  (Pnaseolus  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.

Middleton, 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: Corvallis
     Environmental  Research  Laboratory;  EPA report  no.  EPA-600/D-82-276.
     Available from: NTIS, Springfield, VA; PB83-189308.

Mjelde, J. W. ; Adams,  R.  M. ; Dixon, B.  L. ;  Garcia,  P.  (1984) Using farmers'
     actions to measure crop loss due to air pollution. J. Air Pollut. Control
     Assoc. 31: 360-364.

Mukammal,   E.  I.   (1965)  Ozone  as  a cause of tobacco  injury. Agricultural
     Meteorology 2: 145-165.

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. T.;  Wilhour, R. G. (1977) Effects of ozone and sulfur
     dioxide  singly  and in  combination on yield,  quality and N-fixation of
     alfalfa.  In: Dimitriades,  B., ed.  International  conference on  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. Qual. 2: 518-520.

Olszyk, D. M. ;  Tibbitts,  T.  W.  (1981)  Stomatal  response  and leaf  injury of
     Pisum sativum  L. with  S02  and 03 exposures. Plant Physiol. 67: 539-544.

Ormrod, D. P.  (1982) Air pollutant  interactions  in  mixtures.  In:   Unsworth,
     M. H.; Ormrod, D.   P., eds.  Effects of gaseous air pollution in agriculture
     and  horticulture.   London,  United  Kingdom:   Butterworth  Scientific;
     pp. 307-331.

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                              PRELIMINARY DRAFT
References for Vegetation Effects (cont'd.)

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.

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.  Qtial. 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 Physiol.
     73: 185-187.

Pell,  E.  J. ;  Weissberger,  W.  C.  ; Speroni,  J.  J.   (1980)  Impact of  ozone  on
     quantity and  quality of greenhouse-grown  potato  plants.  Environ. Sci.
     Technol. 14: 568-571.

Rawlings, J.  0.;  Cure,  W.  W.  (1985) The  Weibull  function as  a  dose-response
     model to describe ozone  effects on crop yields. Crop Science (in  press).

Reich,  P.  B. ;  Amundson,  R.  G. (1984) Low level 0,  and/or  SO,, exposure causes
     a  linear decline in soybean yield. Environ.  Pollut.   (Series  A) 34: 345-355.
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                              PRELIMINARY DRAFT
References for Vegetation Effects (cont'd.)

Reinert, R. A. ; Nelson,  P. V.  (1979) Sensitivity  and  growth  of  twelve  elatior
     begonia cultivars to ozone.  HortScience 14: 747-748.

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  to  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.

Thompson,  C.  R. ;  Kats,  G.; Cameron,  J. W.  (1976)  Effects of  photochemical  air
     pollutants on  growth, yield,  and ear characteristics  of  two sweet  corn
     hybrids.  J.  Environ. Qual.  5:  410-412.
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                              PRELIMINARY DRAFT
References for Vegetation Effects (cont'd.)

Tingey, D. T. (1977). (To be supplied).

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. ;  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.

Wukasch, R.  T. ;  Hofstra,  G.  (1977b) Ozone and  Botrytis spp.  interaction  in
     onion-leaf dieback:  field studies. J. Am.  Soc.   Hortic. Sci.  102:  543-546.

Yang,  Y.-S.; Skelly,  J.  M.; Chevone,  B.  I.;  Birch, J.  B.   (1983) Effects  of
     long-term ozone exposure  on photosynthesis and  dark respiration  of eastern
     white pine. Environ. Sci. Technol. 17: 371-373.
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                              PRELIMINARY DRAFT
1.12.6  References for Effects of Ozone on Natural Ecosystems and Their Components


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. Can.
     J. For.  Res.  12:  673-678.

Bormann, F. H.  (1985)  Air pollution and  forests:  an  ecosystem perspective.
     BioScience 35: 434-441.

Botkin, D. B. ;  Smith,  W.  H.  ; Carlson,  R.  W. ;  Smith,  T.  L.  (1972)  Effects  of
     ozone on white pine saplings:  variation in inhibition  and recovery of  net
     photosynthesis. Environ. Pollut. 3: 273-289.

Carlson, R. W.  (1979)  Reduction in the photosynthetic  rate of Acer, Quercus,
     and Fraxinus species caused by sulfur dioxide and  ozone. Environ. Pollut.
     18: 159-170.

Cowling, E. B.  (1985)  Effects of air  pollution on forests: Critical review
     discussion papers.  J.  Air Pollut.  Control  Assoc.  35: 916-919.

Coyne,  P.   E. ;  Bingham,  G.  E. (1981) Comparative  ozone  dose response of gas
     exchange  in a  ponderosa pine  stand exposed  to long-term fumigations.   J.
     Air Pollut. Control Assoc.  31:  38-41.

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.

Ehrlich, P.  R. ;  Mooney,  H.  A. (1983) Extinction,  substitution, and ecosystem
     services. BioScience 33: 248-254.

Farnworth, E.  G. ;  Tidrick,  T. H. ;  Jordan, C. F. ;  Smathers, W.  M.,  Jr. (1981)
     The value  of  natural  ecosystems:  an  economic and  ecological  framework.
     Environ. Conserv.  8: 275-282.

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

Hogsett, W. E. ; Plocher, M.;  Wildman, V.; Tingey,  D.  T.; Bennett, I. P. (1985)
     Growth response of two varieties of slash pine seedlings to chronic ozone
     exposures. Can. J.  Bot.   (In press).
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                              PRELIMINARY DRAFT
References for Ecosystem Effects (cont'd.)

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's.  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.

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.  (1983)  Influence of ozone on carbon  partitioning
     in tomato: potential role of carbon flow in regulation of the  mycorrhizal
     symbiosis under conditions of stress.  New Phytol. 94: 241-247.

McCool, P. M.; Menge, J. A.; Taylor,  0.  C.  (1979) Effects of ozone  and HC1  gas on
     the development of the mycorrhizal  fungus Glomus  faciculatus and growth of
     'Troyer'  citrange.  J. Amer. Soc. Hort. Sci. 104:   151-154.

McLaughlin, S. B.  (1985) Effects of air pollution on forests: A critical review.
     J. Air Pollut.  Control Assoc. 35:  512-534.

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.)
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                              PRELIMINARY DRAFT
References for Ecosystem Effects (cont'd.)

Miller, P. R. ;  Elder-man,  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. Corvallis, OR: Corvallis
     Environmental  Research  Laboratory;  EPA  report  no.  EPA-600/D-82-276.
     Available from: NTIS, Springfield, VA; PB83-189308.

Mooi,  J.  (1980)  Influence  of ozone  on  the growth of  two poplar cultivars.
     Plant Dis.  64: 772-773.

National Park Service.   (1985)  Testimony of the National  Park Service before  the
     Subcommittee on Parks and  Recreation.  Washington,  D.C.:  U.S.  House of
     Representatives, Committee on Interior and Insular Affairs; 99th Congress,
     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.

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.

Patton, 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.

Risser,  P. G.  (1985) Toward a  holistic management  perspective.  BioScience.
     35: 414-418.

Stark,  R. W. ;  Cobb,  F.  W. , Jr. (1969)  Smog injury,  root diseases and bark
     beetle damage in ponderosa pine. Calif. Agric.  23: 13-15.
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                              PRELIMINARY DRAFT
References for Ecosystem Effects (cont'd.)

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;
     EPA  report  no.  EPA-600/8-78-004.  Available from: NTIS, Springfield, VA;
     PB83-163337.

Woodwell,  G.  M.  (1970)  Effects of pollution on the structure and physiology of
     ecosystems.  Science (Washington, DC)  168: 429-433.

Yang, Y.-S.; Skelly,  J. M. ; Chevone, B.  I.;  Birch,  J.  B. (1983) Effects of
     long-term ozone exposure on photosynthesis and dark respiration of eastern
     white pine.   Environ.  Sci.  Technol. 17: 371-373.


1.12.7  References for Other Welfare Effects of Ozone and Other Photochemical
        Oxidants
Beloin, N. J.  (1972)  Fading of dyed fabrics by air pollution: a field study.
     Text. Chem.  Color. 4: 77-78.

Bogaty, H. ;  Campbell,  K. S.; Appel, W.  D. (1952) The oxidation of cellulose by
     ozone in small concentrations.  Text. Res. J. 22: 81-83.

Bradley,  C.   E. ;  Haagen-Smit,  A.  J.  (1951)  The  application of rubber in the
     quantitative determination of  ozone.  Rubber Chem. Technol. 24: 750-775.

Edwards,  D.  C. ;  Storey,  E.  B.  (1959)  A quantitative  ozone test for small
     specimens. Chem.  Can. 11: 34-38.

Haylock, J.  C.; Rush,  J. L. (1976) Studies on the ozone fading of anthraquinone
     dyes on nylon fibers. Text.  Res.  J. 46: 1-8.

Haylock, J.  C.; Rush,  J. L. (1978) Studies on the ozone fading of anthraquinone
     dyes on  nylon fibers; part II: in-service  performance.  Text.  Res. J.  48:
     143-149.

Haynie, F. H.; Spence, J.  W.; Upham, J. B.  (1976) Effects of gaseous pollutants
     on materials—a  chamber  study. Research  Triangle  Park,  NC:  U.S.  Environ-
     mental  Protection Agency, Environmental Sciences Research Laboratory; EPA
     report  no.  EPA-600/3-76-015.  Available  from:   NTIS,  Springfield,  VA;
     PB-251580.
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                              PRELIMINARY DRAFT
References for Other Welfare Effects (cont'd.)

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)  Microspectrophotontetric
     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.

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

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.
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                              PRELIMINARY DRAFT
1.12.8  References for Toxicological Effects of Ozone and Other  Photochemical
        Oxidants
Abraham, W.  M. ;  Januszkiewicz, A. J.;  Mingle,  M.;  Welker, M.;  Wanner,  A.;
     Sackner, M.  A.  (1980)  Sensitivity of bronchoprovocation  and tracheal
     mucous  velocity  in  detecting airway responses to 03. J. Appl.  Physiol.:
     Respir. Environ. Exercise Physiol. 48: 789-793.

Abraham, W. M.;  Lauredo, I.; Sielczak, M.; Yerger,  L.; King,  M.  M.;  Ratzan,  K.
     (1982) Enhancement of bacterial pneumonia  in sheep by ozone exposure.  Am.
     Rev. Respir.  Dis.  Suppl. 125(4 pt. 2): 148.

Abraham, W.; Chapman, G. A.; Marchette, B. (1984a)  Differences  between  inhaled
     and intravenous carbacnol in detecting 03-1nduced airway effects.  Environ.
     Res. 35: 430-438.

Abraham, W.  M. ;  Delehunt,  J. C. ; Yerger,  L. ;  Marchette,  B. ;  Oliver, W. ,  Jr.
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Cavender, F.  L. ; Singh, B. ; Cockrell,  B.  Y.  (1978)  Effects  in  rats  and guinea
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                              PRELIMINARY DRAFT
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Elsayed, N.  M. ;  Hacker, A.; Mustafa,  M. ;  Kuehn,  K. ; Schrauzer,  G.  (1982b)
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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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Freeman,  G. ;   Juhos,  L.  T. ; Furiosi, N.  J. ;  Mussenden,  R. ; Stephens, R.  J. ;
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Friberg,   L. ;  Holma,  B. ;  Rylander,  R.  (1972)  Animal lung  reactions after
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Friedman,  M. ; Gallo, J. M.; Nichols,  H.  P.;  Bromberg,  P.  A.  (1983)  Changes in
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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
     j_n vivo. Taiki Osen Kenkyu 10: 58-62.

Fukase, 0.;  Watanabe, H.;  Isomura,  K.  (1978)  Effects  of exercise on mice
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Gardner,  D.  E.  (1984) Oxidant-induced  enhanced sensitivity to  infection  in
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Gardner,  0.  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.  VI.;  Miller,  F.  J.;  Coffin,  D.  L.  (1974) The effect
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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-containing
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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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     Environ.  Exercise Physiol. 57:  1079-1088.

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Goldstein, E. ;  Tyler, W.  S.; Hoeprich,  P.  0.;  Eagle, C.  (1971a)  Ozone  and  the
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     127: 1099-1102.

Goldstein, E.;  Tyler, W.  S.; Hoeprich, P.  D.; Eagle, C. (1971b) Adverse  influ-
     ence of ozone  on pulmonary bactericidal  activity  of  murine  lungs.  Nature
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Goldstein, E.;  Eagle, M.  C. ; Hoeprich, P.  D.  (1972)  Influence of ozone on pulmo-
     nary defense mechanisms of silicotic mice. Arch. Environ. Health 24: 444-448.

Goldstein, B.  D. ;  Lai,  L.  Y. ;  Cuzzi-Spada, R. (1974) Potentiation  of comple-
     ment-dependent  membrane   damage  by  ozone.  Arch.  Environ.  Health  28:
     40-42.

Goldstein, B.  D. ;  Hamburger, S. J.;  Falk,  G.  W.;  Amoruso, M.  A.  (1977)  Effect
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     phages by concanavalin A.   Life Sci. 21:  1637-1644.

Gooch,  P.  C. ;  Creasia,  D.  A.;  Brewen, J.  G.  (1976)  The cytogenetic  effect of
     ozone: inhalation  and HI vitro  exposures.  Environ.  Res. 12:  188-195.

Gordon,  T. ; Amdur,  M.  0.  (1980)  Effect of  ozone  on respiratory response of
     guinea pigs to histamine.   J.  Toxicol. Environ.  Health 6: 185-195.

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.  (1979) Alteration of hepatic xenobiotic metabolism by  ozone [dis-
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     Microfilms, Ann Arbor, MI: publication no. 80-09646.

Graham,  J.  A.;  Menzel,  D.  B. ;  Miller,  F.  J. ; Illing,   J. W. ; Gardner, D. E.
     (1981) Influence of ozone  on pentobarbital-induced sleeping time in mice,
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                              PRELIMINARY DRAFT
References for Toxicological Effects (cont'd.)

Graham, J. A.;  Menzel,  D.  B. ;  Miller,  F.  J. ;  Illing, J. W. ; Gardner, D. E.
     (1982a) Effect  of  ozone on  drug-induced  sleeping time  in mice pretreated
     with  mixed-function oxidase  inducers  and  inhibitors.  Toxicol.  Appl.
     Pharmacol.  62: 489-497.

Graham, J. A.;  Miller,  F. J. ;  Gardner,  D.  E.;  Ward,  R.;  Menzel,  D.  B.  (1982b)
     Influence  of  ozone and  nitrogen dioxide  on  hepatic  microsomal  enzymes  in
     mice. J. Toxicol.   Environ. Health 9: 849-856.

Graham, J. A.; Menzel,   D. B.; Miller, F. J.; Illing,  J. W.; Ward,  R. ; Gardner,
     D. E.  (1983) Influence of  ozone  on  xenobiotic metabolism.  In:  Lee,
     S. D. ; Mustafa, M.  G. ;  Mehlman,  M. A.,  eds.  International  symposium on
     the biomedical effects  of ozone and related photochemical oxidants;  March
     1982; Pinehurst,  NC.  Princeton,  NO:  Princeton  Scientific  Publishers,
     Inc.; pp.  95-117.  (Advances in modern environmental toxicology:  v.  5).

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.  ;  Illing,  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.  Toxicol.  Environ.  Health 10:
     351-362.

Guerrero,   R. R. ;  Rounds, D.  E.;  Olson,  R.  S. ;  Hackney,  J. D.  (1979) Mutagenic
     effects of  ozone  on human cells exposed  i_n vivo and j_n vitro based on
     sister chromatid exchange analysis. Environ. Res. 18: 336-346.

Hadley, J. G. ;  Gardner, D.   E.  ; Coffin  0.  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;  Richland,  WA. Washington,  DC:   Energy  Research and
     Development  Administration;  pp.  1-21.  (ERDA  symposium  series: v.   43).
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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  col i  K-12   isolated after  exposure  to ozone. J.   Bacteriol.
     122:   19-24.
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Hamelin, C. ;  Chung,  Y.  S.  (1978) Role of the pol, rec, and DNA gene products
     in the repair of lesions produced in Escherichia coli DNA by ozone. Stud.
     Biophys.  68:  229-335.

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 coli K12.  FEMS  Microbiol.  Lett. 2:
     149-151.

Hesterberg, T. W. ;  Last,  J.  A.  (1981) Ozone-induced acute pulmonary fibrosis
     in rats:  prevention of increased rates of collagen  synthesis by 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.

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
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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.

Hurst,   D.   J. ; Coffin,  D.   L.  (1971) Ozone  effect on lysosomal hydrolases  of
     alveolar macrophages  ui 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.
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Hussain, M. Z. ;  Cross, C.   E. ; Mustafa, M. G.; Bhatnagar,  R. S. (1976b)  Hydroxy-
     prol ine  contents  and   prolyl  hydroxylase  activities  in lungs of  rats
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                              PRELIMINARY DRAFT
References for Toxicological Effects (cont'd.)

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) L'ozone 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_. ;  j£indya,  R.  J. ; Chan, P. C. (1979)  Inhibition of erythrocyte membrane
     (Na + K )-activated  ATPase by ozone-treated phospholipids.  J.  Biol.  Chem.
     254:  2705-2709.

Kindya, R. J. ; Chan,  P.  C.  (1976)  Effect of ozone  on  erythrocyte membrane
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Konigsberg,  A. S. ;  Bachman,  C.  H. (1970) Ozonized atmosphere and  gross motor
     activity of rats.   Int.  J.  Biometeorol.  14: 261-266.

Koontz, A. E. ; yeatlj,  R.  L. (1979)  Ozone alteration of transport of cations
     and  the  Na  3    ATPase in  human  erythrocytes.  Arch.   Biochem.  Biophys.
     198:  493-500.

Kotlikoff, M.  I.; Jackson,  A.  C. ; Watson, J. W. (1984) Oscillatory mechanics
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     Respir.  Environ. Exercise Physiol. 56:  182-186.
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                              PRELIMINARY DRAFT
References for Toxicologlcal Effects (cont'd.)

Kyei-Aboagye, K.;  Hazucha,  M. ; Wyszogrodski,  I.;  Rubinstein,  D.;  Avery,  M.  E.
     (1973) The effect  of ozone  exposure  ui  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 tracheal 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  tracheal  explants  cultured from rats  exposed to ozone. Am.
     Rev.  Respir.  Dis.  116:  695-703.

Last, J.  A.;  Greenberg,  D.  B.  ; Castleman,  W. L.  (1979)  Ozone-induced  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.

Last, J.  A.;  Reiser,  K.  M.; Tyler, W.  S.; Rucker, R.  B.  (1984b) Long-term
     consequences  of exposure  to  ozone. I.  Lung collagen content.  Toxicol.
     Appl. Pharmacol.  72:  111-118.

Lee, L.-Y.; Bleecker, E.  R.; Nadel, J.  A.  (1977)  Effect  of ozone  on bronchomotor
     response to inhaled  histamine aerosol  in dogs. J. Appl.  Physiol.: Respir.
     Environ. Exercise Physiol. 43: 626-631.

Lee, L.-Y.; Dumont,  C. ;  Djokic,  T. D. ;  Menzel ,  T.  E. ;  Nadel,  J.  A.  (1979)
     Mechanism of  rapid,  shallow  breathing after ozone  exposure  in conscious
     dogs. J. Appl. Physiol.:  Respir.  Environ. Exercise  Physiol.  46: 1108-1114.
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                              PRELIMINARY DRAFT
References for Toxicological Effects (cont'd.)

Lee, L.-Y.; Djokic, T. D. ;  Dumont, C. ; Graf, P. D. ; Nadel, J. A.  (1980) Mechanism
     of ozone-induced tachypneic response to hypoxia and hypercapnia  in conscious
     dogs. J. Appl.  Physiol.:  Respir.  Environ.  Exercise Physio!.  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
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Lum, H. ;  Schwartz,  L. W.;  Dungworth, D.  L.;  Tyler, W.  S.  (1978)  A comparative
     study of cell  renewal after  exposure  to  ozone or oxygen:  response  of
     terminal bronchiolar  epithelium in the rat.  Am.  Rev.  Respir.  Dis.  118:
     335-345.

Lunan,  K.   D. ; Short,  P.; Negi,  D.;  Stephens,  R.  J.  (1977)  Glucose-6-phosphate
     dehydrogenase  response  of  postnatal  lungs to  N02  and 03.  In: Sanders,
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     macrophage  and epithelial cells:  proceedings of  the sixteenth  annual
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MacRae, W. D. ; Stich, H. F.  (1979)  Induction of  sister chromatid exchanges in
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Martin, C. J.; Boatman,  E.  S.; Ward, G. (1983) Mechanical properties  of alveo-
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Mellick,  P. W. ;  Dungworth,  D.  L.  ; Schwartz, L. W. ; Tyler, W. S.  (1977) Short
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                              PRELIMINARY DRAFT
References for lexicological Effects (cont'd.)

Menzel, D. B. ; Slaughter,  R. J.;  Bryant,  A.  M.;  Jauregui,  H.  0.  (1975a)  Heinz
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Menzel, D. B.; Slaughter, R. J.; Bryant, A.M.; Jauregui, H. 0. (1975b) Preven-
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Miller, F. J. ;  Illing,  J.  W. ;   Gardner,  D.  E.  (1978a) Effect of urban ozone
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Miller, F. J.; Menzel, D. B.;  Coffin, D. L.  (1978b) Similarity between man and
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Miller, F.  J. ;  Overton, J. H.,  Jr.; Jaskot, R. H.;  Menzel,  D.  B.;  (1985)
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Mizoguchi, I.; Osawa,  M. ;  Sato, Y.  ; Makino,  K. ; Yagyu,  H.  (1973)  Studies  on
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Moore, P.  F.;  Schwartz, L.  W.  (1981) Morphological effects of prolonged exposure
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Moore, G.  S. ; Calabrese, E. J.;  Grinberg-Funes,  R.  A.  (1980)  The C57L/J  mouse
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                              PRELIMINARY DRAFT
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Murphy, S. D. ;  Ulrich,  C.  E. ; Frankowitz, S. H.; Xintaras, C.  (1964)  Altered
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Mustafa, M.  G. (1975) Influence of  dietary vitamin E on  lung  cellular  sensiti-
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Mustafa, M.   G.; Lee,  S.  D.  (1976) Pulmonary  biochemical  alterations resulting
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Mustafa, M.  G.; Tierney, 0. F.  (1978) Biochemical and metabolic changes  in  the
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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
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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
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     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. Appl.  Pharmacol.  72:  82-90.

Nakajima,  T. ;  Kusumoto,  S.;  Tsubota,  Y.;  Yonekawa,  E.;  Yoshida,  R.; Motomiya,
     K.; Ito,  K. ;  Ide,  G. ; Otsu, H. (1972).  Histopathological studies on  the
     respiratory  organs  of mice  exposed to photochemical  oxidants and  automo-
     bile exhaust.  Osaka-furitsu Koshu Eisei Kenkyusho Kenkyu  Hokoku Rodo
     Eisei Hen 10: 35-42.

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

O'Byrne, P.   M.; Walters, E.  H.;  Gold,  B.  0.; Aizawa, H. A.;  Fabbri,  L. M. ;
     Alpert, S. E.; Nadel,  J. A.; Holtzman,  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
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                              PRELIMINARY DRAFT
References for lexicological Effects (cont'd.)

Osebold, J.  W.;  Owens, S. L. ;  Zee, Y. C.; Dotson, W. M.; LaBarre, D. D.  (1979)
     Immunological alterations  in the  lungs  of mice following ozone exposure:
     changes  in  immunoglobulin levels  and  antibody-containing cells.  Arch.
     Environ. Health 34:  258-265.

Osebold, J.  W. ; Gershwin,  L. J.;  Zee,  Y.  C.  (1980)  Studies  on the enhancement
     of allergic  lung  sensitization by inhalation  of ozone and sulfuric  acid
     aerosol. J.  Environ. Pathol.  Toxicol. 3:  221-234.

P'an, A. Y.  S. ; Jegier,  Z.  (1971) The  serum  trypsin inhibitor capacity during
     ozone exposure.  Arch.  Environ. Health 23:  215-219.

P'an, A. Y.  S. ;  Jegier,  Z. (1972)  Trypsin  protein esterase  in  relation to
     ozone-induced vascular damage. Arch. Environ.  Health 24:  233-236.

P'an, A. Y.  S.;  Jegier, Z.  (1976) Serum protein changes during exposure  to  ozone.
     Am. Ind. Hyg. Assoc. J. 37:  329-334.

P'an, A. Y.  S.; Beland,  J. ; Jegier,  Z.  (1972) Ozone-induced arterial lesions.
     Arch.  Environ. Health  24:  229-232.

Pemsingh, R.  S. ;  Atwal,  0. S.   (1983)  Occurrence  of APUD-type cells  in  the
     ciliated cyst of  the parathyroid  gland  of ozone-exposed  dogs.  Acta  Anat.
     116: 97-105.

Peterson, D. C.; Andrews, H. L. (1963) The role of  ozone in radiation  avoidance
     in the mouse. Radiat.  Res. 19: 331-336.

Phalen, R.  F. ;  Kenoyer,  J. L.  ; Crocker, T.  T.; McClure, T. R. (1980)  Effects
     of sulfate aerosols  in combination with  ozone on elimination of  tracer
     particles inhaled by rats. J. Toxicol.  Environ. Health 6: 797-810.

Plopper, C.  G. ;  Chow,  C. K. ;   Dungworth,  D.  L. ; Brummer, M. ;  Nemeth,  T.  J.
     (1978)  Effect of low  level  of ozone on rat lungs.  II.  Morphological
     responses during recovery and re-exposure. Exp. Mol. Pathol. 29:  400-411.

Plopper, C.  G. ;  Chow,  C. K. ;  Dungworth, D.  L.; Tyler, W. S.  (1979)  Pulmonary
     alterations in rats exposed  to 0.2 and 0.1 ppm ozone:  a  correlated  morpho-
     logical and biochemical study. Arch. Environ.  Health 34:  390-395.

Raub, J. A.;  Miller,  F.  J. ; Graham, J.  A.  (1983) Effects  of low-level ozone
     exposure on  pulmonary function  in adult and  neonatal rats.  In:  Lee,
     S. D.;  Mustafa,  M.  G. ; Mehlman, M.  A.,  eds.  International  symposium on
     the biomedical effects of ozone and  related  photochemical oxidants;  March
     1982;  Pinehurst,  NC   Princeton,  NJ: Princeton  Scientific  Publishers,
     Inc.;  pp.  363-367.  (Advances in modern  environmental  toxicology: v.  5).

Reasor, M.  J.; Adams, G.   K., III; Brooks, J.  K.;  Rubin, R.  J.  (1979) Enrichment
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                              PRELIMINARY DRAFT
References for lexicological Effects (cont'd.)

Revis,  N. W. ; Major, T.; Dalbey, W.  E.  (1981)  Cardiovascular effects  of  ozone
     and  cadmium  inhalation in  the rat. In:  Northrop  Services,  Inc., ed.
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     Protection Agency, Health  Effects  Research  Laboratory;  EPA-600/9-81-001;
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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:
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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
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Roum, J.  H. ; Murlas,  C.  (1984) Ozone-induced changes in muscaranic bronchial
     reactivity by  different  testing  methods.  J.  Appl.  Physiol.:  Respir.
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Schlipkb'ter, 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,
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Sherwood, R. L. ;  Kimura, A.; Donovan,  R. ; Goldstein, E.  (1984)  Effect of  0.64
     ppm ozone on rats with chronic pulmonary bacterial infection.  J. Toxicol.
     Environ. Health 13:  893-904.

Shingu,  H. ;  Sugiyama,  M. ;  Watanabe, M.; Nakajima, T. (1980) Effects of ozone
     and  photochemical oxidants on interferon production  by  rabbit alveolar
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Sielczak, M. W. ;  Denas,  S.  M. ;  Abraham,  W.  M.  (1983)  Airway cell  changes  in
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                              PRELIMINARY DRAFT
References for Toxicologlcal Effects (cont'd.)

Stephens, R.  J. ;  Sloan, M.  F. ;  Evans, M. J. ; Freeman, G. (1974a) Early  response
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     1 cell response  to  exposure to 0.5  ppm  03  for  short  periods.  Exp.  Mol.
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Stephens, R. J. ;  Sloan,  M.  F. ;  Groth, D. G.  (1976) Effects of long-term, low
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Stephens, R. J. ;  Sloan,  M.  F.; Groth,  D.  G.;  Negi, D.  S.;  Lunan,  K.  D.  (1978)
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Tepper, J.  L. ; Weiss,  B.; Cox, C.  (1982) Microanalysis  of  ozone  depression  of
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     national  symposium  on  the biomedical  effects  of  ozone and related  photo-
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Thomas, G. ; Renters,  J.  D. ; Ehrlich, R. (1979) Effect  of  exposure to PAN and
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                              PRELIMINARY DRAFT
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Trams, E.  G.;  Lauter, C.  J.; Brown, E.  A. B.;  Young, 0. (1972) Cerebral corti-
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Tyson, C.  A.; Lunan,  K.  D.;  Stephens,  R.  J. (1982)  Age-related  differences  in
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Veninga, T. S. ; Wagenaar, J.;  Lemstra, W.  (1981)  Distinct enzymatic  responses
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     Perspect. 39:  153-157.

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     processes  in human  red blood  cell membranes.  Biochim. Biophys.  Acta  602:
     591-599.

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     p-aminobenzoic acid against ozone toxicity.  Biochem. Pharmacol.  30: 1033-
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     of cats.  I. Functional. Am. Rev.  Respir.  Dis. 108: 1141-1151.

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     monkeys  (Macaca radiata):  including the  effects  of long-term  exposure  to
     low-level  ozone [dissertation].   Davis,  CA:  University of  California.
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     rat  operant  behavior  by  ozone  exposure.   Toxicol.  Appl.   Pharmacol.
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                              PRELIMINARY DRAFT
References for lexicological Effects (cont'd.)

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     influenza disease severity and alters  distribution of influenza viral
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     exposed to ozone. Nipon Kyobu Shikkan Gakkai  Zasshi  12: 556-561.

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     Environ.  Health 25: 132-138.

Yokoyama, E.; Ichikawa,  I.; Nambu, Z.; Kawai, K.;  Kyono,  Y. J.  (1984) Respiratory
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     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.  Physiol.: Respir.
     Environ. Exercise Physiol.  55: 805-812.
019VEE/A                            1-209                                11/22/85

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                              PRELIMINARY DRAF1
References for Controlled Human Studies (cont'd.)

Avol,  E.  L. ;  Linn,  W.  S. ; Venet, T. G.; Shamoo, D. A.; Hackney, J.  D.  (1984)
     Comparative  respiratory  effects  of ozone and  ambient  oxidant pollution
     exposure during heavy exercise. J. Air Pollut. Control Assoc.  34:  804-809.

Beckett, W.  S. ;  McDonnell,  W. F. ;  Horstman,  D.  H. ;  House,  D.  E.  (1985) Role
     of the parasympathetic nervous system in the acute lung response  to  ozone.
     J.  Appl. Physiol.:  in press.

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. P.;  Horvath,  S.  M.  (1984) Interaction  of
     peroxyacetyl  nitrate and ozone on pulmonary functions. Am. Rev.  Respir.
     Dis.  130: 1033-1037.

Parrel 1, 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.
     Physiol.: Respir.  Environ.  Exercise Physiol. 57:  984-988.

Gliner, J.  A.;  Horvath,  S.  M. ;  Folinsbee,  L.  J.  (1983) Pre-exposure  to  low
     ozone concentrations does not  diminish the pulmonary function response on
     exposure  to higher  ozone  concentration.  Am. Rev.  Respir. Dis.  127: 51-55.

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.

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.
019VEE/A                            1-210                                11/22/85

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                              PRELIMINARY DRAFT
References for Controlled Human Studies (cont'd.)

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. ;  Rommelt,  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, T. J. ;  Sauder,  L.  R.; Kerr, H.  D.; Parrel 1, 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.;  Farrell, 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.

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.
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                              PRELIMINARY DRAFT
References for Controlled Human Studies (cont'd.)

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. Physiol.: Respir.
     Environ. Exercise Physiol.  54: 1345-1352.

McDonnell, W. F., III; Hortsman, D. H.  ; Abdul-Salaam,  S.;  House, D. E.  (1985a)
     Reproducibility  of individual  responses  to  ozone exposure.  Am.   Rev.
     Respir.  Dis. 131: 36-40.

McDonnell, W.  F. ,  III;  Chapman, R. S.  ; Leigh, M.  W.;  Strope, G. L.; Collier,
     A.  M. (1985b)  Respiratory  responses of  vigorously exercising  children to
     0.12 ppm ozone exposure.  Am.  Rev.  Respir. Dis.: in press.

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:  Proceedings of  an  international  specialty  conference
     in the  evaluation  of  the scientific basis for an  ozone/oxidant standard;
     November 1984; Houston, TX. Pittsburgh, PA:  Air Pollution  Control  Associ-
     ation; in press.   (APCA transaction v.  4).

Silverman, F.  (1979)  Asthma  and respiratory  irritants (ozone).  EHP Environ.
     Health Perspect.  29: 131-136.

Silverman, F.; Folinsbee, L.  J.; Barnard, J.;  Shephard, R. J. (1976) Pulmonary
     function changes in ozone  - interaction of concentration and ventilation.
     J.  Appl. Physiol. 41: 859-864.

Solic, J.  J. ;  Hazucha,  M.  J.; Bromberg,  P.  A.  (1982) The  acute  effects of 0.2
     ppm  ozone  in patients with chronic obstructive pulmonary disease.  Am.
     Rev.  Respir. Dis. .125: 664-669.


1.12.10   References  for Field  and Epidemiological  Studies of the Effects of
        Ozone and Other Photochemical Oxidants


Avol, E.   L. ;  Linn,  W. S. ; Shamoo, D. A.; Venet,  T.  G.; Hackney, J. D.  (1983)
     Acute respiratory  effects  of Los Angeles smog  incontinuously  exercising
     adults.  J. Air Pollut. Control Assoc.  33: 1055-1060.

Avol, E.   L.;  Linn,  W. S. ; Venet,  T. G.; Shamoo,  D.  A.; Hackney, J. D.  (1984)
     Comparative  respiratory  effects  of  ozone and ambient oxidant  pollution
     exposure during  heavy exercise.  J. Air Pollut.  Control Assoc.  34:  804-809.

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.
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                              PRELIMINARY DRAFT
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. (1985b) Short-term health effects of ambient air pollution
     in adolescents.  In: Proceedings of an international specialty conference
     on the evaluation  of  the  scientific  basis  for  an  ozone/oxidant  standard;
     November 1984; Houston, TX.  Pittsburgh,  PA: Air Pollution  Control  Assoc-
     iation; in press.  (APCA transactions: v.  4).

Bock,  N. ;  Lippmann, M.;  Lioy, P.; Munoz, A.; Speizer, F. (1985) The effects of
     ozone on the pulmonary function of children.   In:  Proceedings of an inter-
     national  specialty  conference on the evaluation of the scientific basis
     for an ozone/oxidant standard; November 1984;  Houston, TX. Pittsburgh, PA:
     Air Pollution  Control  Association;  in  press.   (APCA transactions:  v.  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. J.; 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:
     Proceedings of an international specialty  conference on the evaluation of
     the  scientific basis  for  an ozone/oxidant  standard;  November  1984;
     Houston,  TX. Pittsburgh, PA: Air Pollution Control  Association; in press.
     (APCA transactions: v. 4).

Kagawa, J. ;  Toyama, T.   (1975)  Photochemical  air pollution:  its  effects  on
     respiratory function of elementary school  children. Arch.   Environ. Health
     30: 117-122.

Kagawa, J. ; Toyama, T.;  Nakaza,  M.  (1976) Pulmonary function test in  children
     exposed to  air pollution.  In: Finkel,  A.  J. ;  Duel, W. C. , eds. Clinical
     implications  of  air pollution  research:   proceedings of  the 1974 air
     pollution medical  research  conference; December 1974; San  Francisco,  CA.
     Acton, MA:  Publishing Sciences Group,  Inc.; pp. 305-320.

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. ;  Gorman, 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.
019VEE/A                           1-213                                11/22/85

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                              PRELIMINARY DRAFT
References for Field and Epidemiological Studies (cont'd.)

Linn, W.  S. ;  Jones, M.  P.; Bachmayer, E. A.; Spier, C. E. ; Mazur, S. F. ; Avol,
     E.  L. ;  Hackney, J.  D.  (1980) Short-term respiratory effects of polluted
     ambient air:  a laboratory study of volunteers in a  high-oxidant community.
     Am.  Rev.  Respir.  Dis. 121: 243-252.

Linn, W.   S.  ;  Avol,  E.  L. ; Hackney,  J.  D.  (1983) Effects of ambient oxidant
     pollutants on  humans: a  movable environmental chamber  study.  In:  Lee,  S.
     D. ;  Mustafa, M. G. ; Mehlman, M. A., eds. International symposium  on the
     biomedical effects  of ozone and  related  photochemical  oxidants;  March
     1982; Pinehurst,  NC. Princeton,  NJ:  Princeton  Scientific  Publishers,
     Inc.; pp. 125-137.   (Advances in modern toxicology:  v. 5).

Lioy, P.   J.  ;  Vollmuth,  T. A.; Lippman,  M.  (1985)  Persistance of peak  flow
     decrement in children  following ozone exposures exceeding  the National
     Ambient Air Quality Standard. J. Air Pollut. Control Assoc.: 35: 1068-1071.

Lippmann,  M.;  Lioy, P.  J. ; Leikauf, G.; Green, K. B.; Baxter, D.; Morandi, M.;
     Pasternack, B. S.  (1983) Effects of ozone  on the  pulmonary function  of
     children. In:  Lee,  S.  D. ; Mustafa, M. G.; Mehlman, M.  A.,  eds. 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.

Okawada,  N. ;  Mizoguchi,  I.;  Ishiguro, T. (1979) Effects of photochemical air
     pollution on the human  eye—concerning eye irritation, tear lysome and
     tear pH.  Nagoya J.  Med.  Sci. 41: 9-20.

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.;  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.:  in press.

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
     on the evaluation  ofthe scientific basis  for an ozone/oxidant standard;
     November 1984; Houston,  TX.  Pittsburgh, PA: Air Pollution Control Asso-
     ciation;  in press.  (APCA transactions:  v.  4).
019VEE/A                           1-214                               11/22/85

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                              PRELIMINARY DRAFT
References for Evaluation of Health Effects Data  (cont'd.)
McDonnell, W.  F. ,  III;  Chapan,
     A. M.  (1985a) Respiratory
     to 0.12 ppm ozone exposure.
            R.  S. ;  Leigh, M. W. ;  Strope,  G.  L. ;  Collier,
            responses of  vigorously exercising children
             Am.  Rev.  Respir.  Dis.:  in press.
McDonnell, W. F.; Champan, R. S. ; Horstman,  D.  H.;  Leigh,  M.  W. ;  Abdul-Salaam,
     S. (19855)  A  comparison of the responses of children and adults to acute
     in the  evaluation  of the scientific basis for an ozone/oxidant standard;
     November  1984;  Houston,  IX.  Pittsburgh,  PA:  Air Pol'lution  Control
     Association;  in press.  (APCA transaction v.  4).
019VEE./A
US GOVEI1NUENI F'HINIIWC OFKCt.   6 46-0 J 4/200 ?5


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