PxEPA
United States
Environmental Protection
Agency
600884020A1
Environmental Criteria and
Assessment Office July 1984
Research Triangle Park NC 27711 External Review Draft
Research and Development
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(Do Not
Cite or Quote)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 bei ng circulated for comment on its
technical accuracy and policy implications.
-------
EPA-600/8-84-020A
Draft July 1984
Do Not Quote or Cite External Review Draft
Air Quality 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, N.C. 27711
U.S. Environmental Protection Agency
Region V, Library
230 South Dearborn Street
Chicago, Illinois 60604 X*'
-------
NOTICE
Mention of trade names or commercial products does not constitute
endorsement or recommendation for use.
S. Qfiflronment ~I n--t—tion Agency
-------
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 1983 and early 1984.
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. Separate chapters are 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 proper-
ties, chemistry, and measurement of ozone and other photochemical oxidants;
and the concentrations of ozone and other photochemical oxidants that are
typically found in ambient air.
The specific areas addressed by chapters on health and welfare effects
are the toxicological appraisal of effects of ozone and other oxidants; effects
observed in controlled human exposures; effects observed in field and epidemic-
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
0190LG/B May 1984
-------
CONTENTS
Page
VOLUME I
Chapter 1. Summary and Conclusions 1-1
VOLUME II
Chapter 2. Introduction 2-1
Chapter 3. Precursors to Ozone and Other Photochemical
Oxidants 3-1
Chapter 4. Chemical and Physical Processes in the Formation
and Occurrence of Ozone and Other Photochemical
Oxidants 4-1
Chapter 5. Properties, Chemistry, and Measurement of Ozone
and Other Photochemical Oxidants 5-1
Chapter 6. Concentrations of Ozone and Other Photochemical
Oxidants in Ambient Air 6-2
VOLUME III
Chapter 7. Effects of Ozone and Other Photochemical Oxidants
on Vegetati on 7-1
Chapter 8. Effects of Ozone and Other Photochemical Oxidants
on Natural and Agroecosystems 8-1
Chapter 9. Effects of Ozone and Other Photochemical Oxidants
on Nonbiological Materials 9-1
VOLUME IV
Chapter 10. Toxicological Effects of Ozone and Other
Photochemical Oxidants 10-1
VOLUME V
Chapter 11. Controlled Human Studies of the Effects of Ozone
and Other Photochemical Oxidants 11-1
Chapter 12. Field and Epidemiological Studies of the Effects
of Ozone and Other Photochemical Oxidants 12-1
Chapter 13. Evaluation of Integrated Health Effects Data for
Ozone and Other Photochemical Oxidants 13-1
0190LG/B
IV
May 1984
-------
TABLE OF CONTENTS
LIST OF TABLES ix
LIST OF FIGURES x
AUTHORS AND CONTRIBUTORS xi i
LIST OF ABBREVIATIONS AND SYMBOLS xv
1. SUMMARY AND CONCLUSIONS 1-1
1.1 INTRODUCTION 1-1
1.2 PRECURSORS TO OZONE AND OTHER PHOTOCHEMICAL OXIDANTS 1-2
1.2.1 Nature of Precursors 1-2
1.2.2 Measurement of Precursors 1-3
1.2.3 Sources and Emissions of Precursors 1-6
1.2.4 Ambient Air Concentrations of Precursors 1-8
1.3 CHEMICAL AND PHYSICAL PROCESSES IN THE FORMATION AND
OCCURRENCE OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS 1-12
1.3.1 Chemical Processes 1-12
1.3.2 Physical Processes 1-14
1.4 PROPERTIES, CHEMISTRY, AND MEASUREMENT OF OZONE AND
OTHER PHOTOCHEMICAL OXIDANTS 1-15
1.4.1 Properties 1-15
1.4.2 Reactions of Ozone and Other Oxidants in Ambient
Air 1-16
1.4.3 Reactions of Ozone and Peroxyacetyl Nitrate in
Aqueous (Biological) Systems 1-17
1.4.4 Sampling and Measurement of Ozone and Other
Photochemical Oxidants 1-18
1.4.4.1 Quality Assurance and Sampling 1-19
1.4.4.2 Measurement Methods for Total Oxidants
and Ozone 1-20
1.4.4.3 Calibration Methods 1-23
1.4.4.4 Relationship of Total Oxidants and
Ozone Measurements 1-25
1.4.4.5 Methods for Sampling and Analysis of
Peroxyacetyl Nitrate and Its
Homol ogues 1-27
1.4.4.6 Methods for Sampling and Analysis of
Hydrogen Peroxi de 1-32
1.5 CONCENTRATIONS OF OZONE AND OTHER PHOTOCHEMICAL
OXIDANTS IN AMBIENT AIR 1-36
1.5.1 Ozone Concentrations in Urban Areas 1-37
1.5.2 Trends in Urban and Nationwide Ozone
Concentrations 1-40
1.5.3 Ozone Concentrations in Nonurban Areas 1-42
1.5.4 Patterns in Ozone Concentrations 1-43
1.5.5 Concentrations and Patterns of Other
Photochemical Oxidants 1-45
1.5.5.1 Concentrations 1-45
1.5.5.2 Patterns 1-47
019GC1/B 6/29/84
-------
TABLE OF CONTENTS
(continued)
1.5.6 Relationship Between Ozone and Other
Photochemical Oxidants 1-48
1.6 EFFECTS OF OZONE AND PEROXYACETYL NITRATE ON VEGETATION .. 1-51
1.6.1 Effects of Ozone on Vegetation 1-51
1.6.1.1 Introduction 1-51
1.6.1.2 Limiting Values of Plant Response 1-52
1.6.1.3 Methods for Determining Ozone Yield
Losses 1-55
1.6.1.4 Estimates of Yield Loss 1-56
1.6.1.5 Effects on Crop Quality 1-64
1.6.1.6 Yield Loss from Ambient Exposures 1-64
1.6.1.7 Statistics Used to Characterize Ozone
Exposures 1-64
1.6.1.8 Relation Between Yield Loss and Foliar
Injury 1-66
1.6.1.9 Physiological Basis of Yield
Reductions 1-66
1.6.1.10 Factors Affecting Plant Response to
Ozone 1-67
1.6.1.11 Economic Assessment of Ozone Effects ... 1-69
1.6.2 Effects of Peroxyacetyl Nitrate on Vegetation 1-71
1.6.2.1 Introduction 1-71
1.6.2.2 Factors Affecting Plant Response to
PAN 1-71
1.6.2.3 Limiting Values of Plant Response 1-71
1.6.2.4 Effects of PAN on Plant Yield 1-72
1.7 EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS ON
NATURAL ECOSYSTEMS 1-72
1.7.1 Introduction 1-72
1.7.2 Oxidant-Induced Effects on a Western Coniferous
Forest Ecosystem 1-74
1.7.3 Effects of Ozone on Other Ecosystems 1-77
1.7.4 Effects on Interrelated Ecosystems 1-80
1.7.4.1 Aquatic Ecosystems 1-80
1.7.4.2 Agricultural Ecosystems 1-81
1.7.5 Ecosystem Responses to Stress 1-81
1.8 EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS ON
NONBIOLOGICAL MATERIALS 1-83
1.8.1 Introduction 1-83
1.8.2 Effects and Damage Functions 1-84
1.8.2.1 Elastomers 1-84
1.8.2.2 Textile Fibers and Dyes 1-85
1.8.2.3 Paints 1-87
1.8.3 Economic Assessment of Effects of Ozone on
Materi al s 1-87
1.9 INTRODUCTION TO HEALTH EFFECTS 1-89
1.9.1 Organization of Health Effects Information 1-89
1.9.2 Literature Coverage and Selection 1-92
vi
019GC1/B 6/29/84
-------
TOXICOL
OXIDANT
1.10.1
1.10.2
1.10.3
OGIC EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL
s
Introduction
Respiratory Transport and Absorption of Ozone ....
Effects of Ozone on the Respiratory Tract
1.10.3.1 Morphological Effects
1.10.3.2 Pulmonary Function
1.10.3.3 Biochemical Effects of Ozone in the
Lung of Experimental Animal s
1.10.3.4 Effects of Ozone in Altering Host
Defense Against Microbes
1.10.3.5 Tolerance
TABLE OF CONTENTS
(continued)
1.10
1-93
1-93
1-94
1-96
1-96
1-99
1-105
1-110
1-115
1.10.4 Extrapulmonary Effects of Ozone 1-118
1.10.4.1 Central Nervous System and Behavioral
Effects 1-118
1.10.4.2 Cardiovascular Effects 1-119
1.10.4.3 Hematological and Serum Chemistry
Effects 1-119
1.10.4.4 Cytogenetic and Teratogenetic
Effects 1-121
1.10.4.5 Other Extrapulmonary Effects 1-122
1.10.5 Effects of Other Photochemical Oxidants 1-123
1.11 EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS IN
CONTROLLED EXPOSURES 1-127
1.11.1 Pulmonary Function Effects in Controlled Human
Studies: Mechanical Function of the Lung 1-127
1.11.1.1 General Population 1-127
1.11.1.2 Subjects with Preexisting Disease 1-136
1.11.1.3 Intersubject Variability 1-137
1.11.1.4 Attenuation with Repeated Exposures .... 1-137
1.11.2 Other Effects of Ozone in Controlled Human
Exposures 1-138
1.11.3 Effects of Peroxyacetyl Nitrate and Mixtures in
Control 1ed Human Exposures 1-139
1.12 FIELD AND EPIDEMIOLOGICAL STUDIES OF THE EFFECTS OF
OZONE AND OXIDANTS 1-139
1.12.1 Introduction 1-139
1.12.2 Field and Epidemiological Studies of Effects
of Effects of Acute Exposure 1-140
1.12.3 Epidemiological studies of Effects of Chronic
Exposure 1-143
1.13 SUMMARY OF THE EVALUATION OF INTEGRATED HEALTH EFFECTS
DATA ". 1-144
1.13.1 Health Effects in the General Human Population 1-144
1.13.2 Health Effects in Potentially Susceptible
Individuals 1-148
1.13.3 Extrapolation of Effects Observed in Animals
to Human Populations 1-149
vn
019GC1/B 6/29/84
-------
TABLE OF CONTENTS
(continued)
1.13.4 Health Effects of Other Photochemical Oxidants
and Pol 1utant Mixtures 1-150
1.13.5 Identification of Potentially At-Risk Populations
or Subpopulations 1-150
1.14 REFERENCES 1-153
viii
019GC1/B 6/29/84
-------
LIST OF TABLES
Table Page
1-1 Hydrocarbon (HC) composition typically measured in urban
areas (from sample collected in Milwaukee, 1981) 1-10
1-2 Summary of ozone monitoring techniques 1-22
1-3 Ozone calibration techniques 1-24
1-4 Summary of parameters used in determination of PAN by
GC-ECD 1-29
1-5 Infrared absorptivities of peroxyacetyl nitrate 1-30
1-6 Measurement methods for hydrogen peroxide 1-34
1-7 Second-highest 1-hr ozone concentrations in 1982 in
Standard Metropolitan Statistical Areas with populations
>1 million, given by census divisions and regions 1-38
1-8 Ozone concentrations for short-term exposures that
produce 5 or 20 percent injury to vegetation grown under
sensitive conditions 1-53
1-9 Seasonal 7-hour ozone concentrations (ppra) at which yield
losses of 10 percent or 30 percent are predicted from
exposure-response models 1-60
1-10 Ozone concentrations at which significant yield losses
have been noted for a variety of plant species exposed to
03 under various experimental conditions 1-62
1-11 Injury thresholds for 2-hour exposures to ozone 1-79
1-12 Morphological effects of ozone in experimental animals 1-101
1-13 Effects on pulmonary function of short-term exposures
to ozone 1-104
1-14 Effects on pulmonary function of long-term exposures
to ozone 1-107
1-15 Biochemical changes in experimental animals exposed to ozone .. 1-112
1-16 Effects of ozone on host defense mechanisms in experimental
animals 1-117
1-17 Extrapulmonary effects of ozone in experimental animals 1-125
1-18 Summary table: Results of controlled human exposures to
ozone 1-128
1-19 Estimated values of oxygen consumption and minute ventilation
associated with representative types of exercise 1-133
1-20 Summary table: Acute effects of ozone and other photochemical
oxidants in population studies 1-141
ix
019GC1/B 6/29/84
-------
LIST OF FIGURES
Page
1-1 National trend in estimated emissions of volatile organic
compounds, 1970 through 1982 1-7
1-2 National trend in estimated emissions of nitrogen
oxides, 1970 through 1982 1-9
1-3 Collective distributions of the three highest 1-hour
ozone concentrations for 3 years (1979, 1980, and 1981)
at valid sites (906 station-years) 1-41
1-4 Relationship between 03 concentration, exposure duration,
and a reduction in plant growth or yield (see Table 7-18;
also U.S. EPA, 1978) 1-54
1-5 Examples of effects of 03 exposure on yield of various
plants. 03 concentration (ppm) is expressed as 7-hr
seasonal mean. Soybean (A) data from Kress and Miller
(1983); peanut (B) data from Heagle et al. (1983) and
Heck et al. (1982); corn (C) and wheat (D) data from
Heagle and Heck (1980) and Heck et al. (1982) 1-57
1-6 Relative 03-induced yield reduction of selected crops
as predicted by the Weibull model (Heck et al., 1983) 1-58
1-7 Summation of abiotic and biotic agents involved in
diseases of trees, given by types of diseases and
functional parts of the tree. Decline diseases are
caused by a combination of biotic and abiotic agents 1-73
1-8 Conceptual sequence of levels showing continuum of
pi ant responses 1-82
1-9 Summary of morphological effects in experimental animals
exposed to ozone 1-100
1-10 Summary of effects of short-term ozone exposures on pulmonary
function i n experimental animals 1-103
1-11 Summary of effects of long-term ozone exposures on pulmonary
function in experimental animals 1-106
1-12 Summary of biochemical changes in experimental animals
exposed to ozone 1-111
1-13 Summary of effects of ozone on host defense mechanisms in
experimental animals 1-116
1-14 Summary of extrapulmonary effects of ozone in experimental
animal s 1-124
1-15 Group mean decrements in 1-sec forced expiratory volume
during 2-hr ozone exposures with different levels of
intermittent exercise: light (VE < 25 L/min); moderate
(VV = 26-43 L/min); heavy (Vp = 44r63 L/min); and very
he&vy (tf > 64 L/min) 1-135
019GC1/B 6/29/84
-------
Project Team: Air Quality Criteria for Ozone and Other Photochemical Oxidants
Ms. Beverly E. Til ton, Project Manager
and Coordinator for Chapters 1 through 6
Environmental Criteria and
Assessment Office
MD-52
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Dr. J. H. B. Garner
Coordinator for Chapters 8 and 9;
Co-coordinator for Chapter 7
Environmental Criteria and
Assessment Office
MD-52
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Mr. Thomas B. McMullen
Assistant Coordinator for Chapters 3 and 4
Environmental Criteria and
Assessment Office
MD-52
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Mr. James A. Raub
Coordinator for Chapters 10 through 13
Environmental Criteria and
Assessment Office
MD-52
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Dr. David T. Tingey
Coordinator for Chapter 7
Environmental Research Laboratory
U.S. Environmental Protection Agency
200 SW 35th Street
Corvallis, OR 97330
xi
019GC1/B 6/29/84
-------
AUTHORS AND CONTRIBUTORS
Chapter 1. Summary and Conclusions
Principal Authors
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. Jimmie A. Hodgeson
Professor, Department of Chemistry
407 Choppin Hall
Louisiana State University
Baton Rouge, LA 70803
*Dr. Thomas J. Kulle
Department of Medicine
School of Medicine
29 South Green Street, GSB-414
University of Maryland
Baltimore, MD 21201
Mr. James A. Raub
Environmental Criteria and Assessment Office
MD-52
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Ms. Beverly E. Til ton
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
xi i
019GC1/B 6/29/84
-------
Contributing Authors
*Dr. Robert Frank
Department of Environmental Health Sciences
Johns Hopkins School of Hygiene and Public Health
615 N. Wolfe Street
Baltimore, MD 21205
*Dr. Milan J. Hazucha
School of Medicine
Center for Environmental Health and Medical Sciences
University of North Carolina
Chapel Hill, NC 27514
Mr. Michael W. Holdren
BatteHe, Columbus Laboratories
505 King Avenue
Columbus, OH 43201
Dr. Donald H. Horstman
Health Effects Research Laboratory
MD-58
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Mr. James M. Kawecki
TRC Environmental Consultants
701 West Broad Street
Suite 401
Falls Church, VA 22046
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
xm
019GC1/B 6/29/84
-------
Contributing Authors (continued)
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
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
*These authors also reviewed portions of Chapter 1 at the request of the U.S.
Environmental Protection Agency. The evaluations and conclusions contained
herein, however, are not necessarily those of the reviewers.
xiv
019GC1/B 6/29/84
-------
LIST OF ABBREVIATIONS
ACh
APR
AM
ANOVA
AGO
APHA
aq
ASL
aim
ATPS
avg
b.p.
BTPS
bz
C
°C
CA
CAMP
CARB
cc
CC
°dyn
CE
CHEM
CH4
CHESS
CL
CLst
cm
acetylcholine
air:fuel ratio
alveolar macrophage
analysis of variance
airway obstructive disease
American Public Health Association
approximately
aqueous
above sea level
atmosphere
ATPS condition (ambient temperature and pressure, saturated
with water vapor)
average
boiling point
BTPS conditions (body temperature, barometric pressure,
and saturated with water vapor)
benzene
carbon
degrees Celsius
chromotropic acid
Continuous Air Monitoring Program
California Air Resources Board
cubic centimeter
closing capacity
dynamic lung compliance
continuous exercise
gas phase chemiluminescence
methane
Community Health Environmental Surveillance System
lung compliance
static lung compliance
centimeter
019DH/G
xv
6/30/84
-------
LIST OF ABBREVIATIONS (continued)
CNS
CO
co2
COHb
COLD
concn
COPD
CV
DBH
DL
DLCO
DNPH
DOT
E
ECD
ECG, EKG
EEC
EKMA
E0
EPA
ERV
FEF
max
FEF
FEF
200-1200
FEF
25-75%
FEF
75%
central nervous system
carbon monoxide
carbon dioxide
carboxyhemogl obi n
chronic obstructive lung disease
concentration
chronic obstructive pulmonary disease
closing volume
tree diameter at breast height
diffusing capacity of the lungs
carbon monoxide diffusion capacity of the lungs
2,4-di nitrophenylhydrazi ne
Department of Transportation
elastance
electron-capture detector
electrocardi ogram
electroencephalogram
Empirical Kinetic Modeling Approach
normal electrode potential
U.S. Environmental Protection Agency
expiratory reserve volume
maximal forced expiratory flow achieved
during an FVC
forced expiratory flow
mean forced expiratory flow between 200 ml and 1200 ml of
the FVC [formerly called the maximum expiratory flow rate
(MEFR)]
mean forced expiratory flow during the middle half of the
FVC [formerly called the maximum mid-expiratory flow rate
(MMFR)]
instantaneous forced expiratory flow after 75% of the FVC
has been exhaled
019DH/G
xvi
6/30/84
-------
LIST OF ABBREVIATIONS (continued)
FEV
FEV1
FEVt/FVC
FID
FIVC
fR
FRC
FRM
ft
FTIR
FVC
G
g
G-6-PD
Gaw
GC
g/mi
GPT
GS-CHEM
GSH
Hb
HC
HCN
HCOOH
Hct
HFET
Hg
HO-
H02
MONO
HONO,,
forced expiratory volume
forced expiratory volume in 1 sec
a ratio of timed forced expiratory volume (FEV.) to
forced vital capacity (FVC)
flame ionization detector
forced inspiratory vital capacity
respiratory frequency
functional residual capacity
Federal Reference Method
foot
Fourier-transform infrared
forced vital capacity
conductance
grams(s)
glucose-6-phosphate dehydrogenase
airway conductance
gas chromatography
grams per mile
gas-phase titration
gas-solid chemiluminescence
glutathione
hemoglobin
hydrocarbons
hydrogen cyanide
formic acid
hematocrit
Highway Fuel Economy Driving Schedule
mercury
hydroxy radical
hydroperoxy
nitrous acid
nitric acid
019DH/G
xvn
6/30/84
-------
LIST OF ABBREVIATIONS (continued)
HPLC
HPPA
hr
hr/day
HRP
H2°2
hv
1C
IE
in
IR
IRV
IVC
k
kg
kgm/min
KI
km
LDH
LD50
LM
L/min
In
L/s
1ST
M
m
MAST
•
max Vp
max V0«
high-pressure liquid chromatograpy; also,
3-(p_-hydroxyphenyl)propionic acid
hour(s)
hours per day
Horseradish peroxidase
water
hydrogen peroxide
sulfuric acid
photon
inspiratory capacity
intermittent exercise
inch(es)
i nfrared
inspiratory reserve volume
inspiratory vital capacity
constant
kilogram
ki1ogram-meter/mi n
potassium iodide
kilometer
lactate deyhydrogenase
lethal dose (50 percent)
light microscopy
liters/min
natural logarithm (base e)
liters/sec
local standard time
molar
meter(s)
Kl-coulometric (Mast meter)
maximum ventilation
maximal aerobic capacity
019DH/G
xvm
6/30/84
-------
LIST OF ABBREVIATIONS (continued)
mb
MBC
MBTH
MEFR
MEFV
MetHb
mg
mg/m
MGE
min
ml
mm
mM
MMAD
MMC
MMFR or MMEF
m.p.
mph
MS
MSL
MT
MTBE
MVV
NA
NAAQS
NADB
NAMS
NAPBN
NAS
NBS
NBKI
NECRMP
millibar(s)
maximum breathing capacity
3-methyl-2-benzothiazolinone hydrazone
maximum expiratory flow rate
maximum expiratory flow-volume curve
methemoglobin
mil 1igram(s)
milligrams per cubic meter
modified graphite electrode
minute(s)
mil 1iliter(s)
mil 1imeter(s)
mi 11imolar
mass median aerodynamic diameter
mean meridional circulation
maximum mid-expiratory flow rate
melting point
miles per hour
mass spectrometry
mean sea level
metric tons
methyl tertiary butyl ether
maximum voluntary ventilation
not available
National Ambient Air Quality Standard
National Aerometric Data Bank
National Aerometric Monitoring Stations
National Air Pollution Background Network
National Academy of Sciences
National Bureau of Standards
neutral buffered potassium iodide
Northeast Corridor Regional Modeling Project
019DH/G
xix
6/30/84
-------
LIST OF ABBREVIATIONS (continued)
NEDS
NEROS
NH
NF
nm
NMHC
NMOC
NO
N02
N03
N0x
AN2, dN
NR
NYCC
°2
V
°3
P(A-a)0
PABA
PAco2
PaCO£
PAN
PA°2
Pa02
PBZN
PEF
PEFV
PG
PH
National Emissions Data System
Northeast Regional Oxidant Study
ammonia
ammonium sulfate
ammonium nitrate
National Forest
nanometer
nonmethane hydrocarbons
nonmethane organic compounds
nitric oxide
nitrogen dioxide
nitrogen trioxide
nitrogen oxides
nitrogen washout
natural rubber
New York City Driving Schedule
oxygen
oxygen radical
ozone
alveolar-arterial oxygen pressure difference
para-aminobenzoic acid
alveolar partial pressure of carbon dioxide
arterial partial pressure of carbon dioxide
peroxyacetyl nitrate
alveolar partial pressure of oxygen
arterial partial pressure of oxygen
peroxybenzoyl nitrate
peak expiratory flow
partial expiratory flow-volume curve
prostaglandin
reciprocal of H ion concentration
arterial pH
019DH/G
xx
6/30/84
-------
LIST OF ABBREVIATIONS (continued)
L
PMN
PNA
PPN
ppb
ppm
PPt
PSD
psig
Pst
PST
PUFA
R
RAPS
Raw
RBC
Rcoll
rh
RL
RQ, R
Rt
Rti
RTI
RV
S.D.
SAROAD
SBNT
SBR
SCAB
SCE
Se
transputmonary pressure
polymorphonuclear leukocyte
peroxynitric acid
peroxypropionyl nitrate
parts per billion
parts per million
parts per trillion
prevention of Significant Deterioration
pounds per square inch gauge
static transputmonary pressure
Pacific Standard Time
polyunsaturated fatty acid
resistance to flow
Regional Air Pollution Study
airway resistance
red blood cell
collateral resistance
relative humidity
total pulmonary resistance
respiratory quotient
total respiratory resistance
tissue resistance
Research Triangle Institute
residual volume
standard deviation
arterial oxygen saturation
Storage and Retrieval of Aerometric Data
single-breath nitrogen test
styrene-butadiene rubber
South Coast Air Basin
sister chromatid exchange
selenium
019DH/G
xxi
6/30/84
-------
LIST OF ABBREVIATIONS (continued)
sec
SEM
SGaw
SH
SLAMS
SMSA
SOD
so2
so4
SPF
SRaw
SRM
SSET
STA
STP
STPD
SURE
TEL
TEM
Tenax GC
TF
tg/yr
TGV
THC
TLC
TML
TNMHC
TV
TWC
UV
second(s)
scanning electron microscopy
specific airway conductance
sulfhydryls
State and Local Air Monitoring Stations
Standard Metropolitan Statistical Area
superoxide dismutase
sulfur dioxide
sulfate
specific pathogen-free
specific airway resistance
standard Reference Material
small-scale eddy transport
seasonal tropopause adjustment
standard temperature and pressure
STPD conditions (standard temperature and
pressure, dry)
Sulfate Regional Experiment Sites
tetraethyl lead
transmission electron microscopy
adsorbent used in NMOC analysis
tropopause-folding events
teragrams per year
thoracic gas volume
total hydrocarbons
total lung capacity
tetramethyl lead
total nonmethane hydrocarbons
tidal volume
three-way catalyst
ultraviolet photometry
microgram per cubic meter
019DH/G
xxn
6/30/84
-------
LIST OF ABBREVIATIONS (continued)
MM
U
UHAC
U.S.
UV
V
YQ
vc
vco
v
V
D
>D
D anat
max
vo
, Q0
v/v
VHAC
VOC
vol %
w/w
WCOT
XAD-2
XO
micromolar
uranium
uranium hydroxamic acid chelates
United States
ultraviolet
vanadium
alveolar ventilation
ventilation/perfusion ratio
vital capacity
carbon dioxide production
physiological dead space
dead-space ventilation
anatomical dead space
minute ventilation; expired volume per minute
inspired volume per minute
lung volume
maximum expiratory flow
oxygen uptake
oxygen consumption
volume - volume
vanadium hydroxamic acid chelates
volatile organic compounds
volume percent
weight - weight
wall-coated open tubular (column)
absorbent used in NMOC analysis
xylenol orange
year(s)
wavelength
019DH/G
xxm
6/30/84
-------
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 can not at present be quantified, these atmospheric effects
and phenomena are not addressed in this document. They have been fully ad-
dressed, however, in other, recent air quality criteria documents (U.S. Envi-
ronmental 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. A separate
criteria document is issued for oxides of nitrogen, as specified by the Clean
Air Act. The second criteria document prepared by the U.S. Environmental
Protection Agency (EPA) on the oxides of nitrogen was published in 1982 (U.S.
Environmental Protection Agency, 1982a).
This document presents a review and evaluation of literature published
through 1983, and in some cases, through early 1984. 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
019GC1/A 1-1 6/29/84
-------
of the chemical and physical processes in the atmosphere by which precursors
give rise to the production of ozone and other photochemical oxidants. In
subsequent chapters, the properties and generic reactions responsible for the
effects ascribed to ozone and other photochemical oxidants are presented as
background for understanding the detailed information presented in the chapters
on health and welfare effects. Likewise, techniques for the measurement of ozone,
total oxidants, and individual oxidant species other than ozone are evaluated,
since the significance of aerometric and exposure data on these pollutants is
dependent upon the accuracy and specificity of the analytical techniques used.
Typical concentrations of the respective oxidants are presented to permit assess-
ment 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 as amended in 1977 (U.S. Congress, 1977).
1.2 PRECURSORS TO OZONE AND OTHER PHOTOCHEMICAL OXIDANTS
1.2.1 Nature of Precursors
Photochemical oxidants are products of atmospheric reactions involving
volatile organic compounds (VOC), oxides of nitrogen (NO ), hydroxyl radicals,
P\
oxygen, and sunlight. They 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.
Although vapor-phase hydrocarbons (compounds of carbon and hydrogen only)
are the predominant organic compounds in the ambient air that serve as precur-
sors to photochemical oxidants, other volatile organic compounds are also
photochemically reactive in those atmospheric processes that give rise to the
oxidants. In particular, halogenated organics (e.g., haloalkenes) that parti-
cipate in photochemical reactions are present in ambient air, although at lower
concentrations than the hydrocarbons. They are apparently oxidized through the
same initial step involved in the oxidation of the hydrocarbons; that is, attack
019GC1/A 1-2 6/29/84
-------
by hydroxyl radicals (HO-)- Alkenes, haloalkenes, and aliphatic aldehydes
are, as classes, among the most reactive organic compounds found in ambient
air. Alkenic hydrocarbons and halocarbons are unique among VOC in ambient air
in that they are susceptible both to attack by HO- and to ozonolysis (oxida-
tion by ozone) (Niki et al., 1983). Methane, halomethanes, and certain
haloethenes are of negligible reactivity in ambient air and have been classed
as unreactive by the U.S. Environmental Protection Agency (1980).
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, 1982a). Nitrogen dioxide is an important precursor to ozone and other
photochemical oxidants (1) because its photolysis in ambient air leads to the
formation of oxygen atoms that combine with molecular oxygen to form ozone;
and (2) because it reacts with acetylperoxy radicals to form peroxyacetyl
nitrate (PAN), a relatively potent phytotoxicant (Taylor, 1969; Qshima et al.,
1974) and lachrymator (Heuss and Glasson, 1968). Although ubiquitous, nitrous
oxide (NpO) is unimportant in the production of oxidants in ambient air because
it is virtually inert in the troposphere. (In the stratosphere, where the
wavelength distribution is different, N^O is photolyzed.)
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).
1.2.2 Measurement of Precursors
Numerous analytical methods have been employed to determine nonmethane
organic compounds (NMOC) in ambient air. To present an overview of the most
pertinent information, measurement methods for the organic species may be
arranged in 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
019GC1/A 1-3 6/29/84
-------
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). This detector has been utilized
both as a stand-alone continuous detection system (non-speciation) and also
with gas chromatographic techniques that provide for speciation of the many
organics present in ambient air. A number of studies of non-speciation analy-
zers have indicated an overall poor performance of the commercial instruments
when calibration or ambient mixtures containing NMOC concentrations less than
1 ppm C were analyzed (e.g., Reckner, 1974; McElroy and Thompson, 1975; Sexton
et al. , 1981). The major problems associated with the non-speciation analyzers
have been summarized in a recent technical assistance document published by
the U.S. Environmental Protection Agency (1981). The document also presents
ways to reduce some of the existing problems.
Because of the above deficiencies, other approaches to the measurement of
nonmethane hydrocarbons are currently under development. The use of gas
chromatography coupled to an FID system circumvents many of the problems
associated with continuous non-speciation analyzers. This method, however,
requires sample preconcentration because the organic components are present at
part-per-billion (ppb) levels or lower in ambient air. The two main preconcen-
tration techniques in present use are cryogenic collection and the use of
solid adsorbents (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 involv-
ing cryogenic preconcentration have also been compared with continuous non-
speciation 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-
othiazolone (MBTH) technique for total aldehydes (e.g., Sawicki et al., 1961),
Fourier-transform infrared (FTIR) spectroscopy (e.g., Hanst et al. , 1982;
Tuazon et al., 1978, 1980, 1981b), and high-performance liquid chromatography
employing 2,4-dinitrophenyl-hydrazine derivatization (HPLC-DNPH) for aldehyde
019GC1/A 1-4 6/29/84
-------
that release light energy that is proportional to the NO concentration. Al-
though 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, 1976). Other NO and NO- measuring methods have also
been summarized in Chapter 3. None of the other techniques is widely used to
monitor air quality.
1.2.3 Sources and Emissions of Precursors
The photochemical production of ozone, the principal component of "smog,"
depends both on the presence of precursors, volatile organic compounds (VOCs)
and nitrogen oxides (NO ), that are emitted by manmade and by natural sources,
J\
and on suitable conditions of sunlight, temperature, and other meteorological
factors. Because of the intervening requirement for meteorological conditions
conducive to the photochemical generation of ozone, emission inventories are
not as direct predictors of ambient concentrations in the case of secondary
pollutants such as ozone and other oxidants as they are for primary pollutants.
Emissions of manmade VOCs (excluding several relatively unreactive com-
pounds such as methane) in the United States have been estimated at 18.2 tg/yr
for 1982. Trends in manmade VOC emissions for 1970 through 1982 are shown in
Figure 1-1 (U.S. Environmental Protection Agency, 1983). The annual emission
rate for manmade VOCs has decreased some 28 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 magni-
tude as manmade emissions. Biogenic emissions are temperature-dependent and
those of isoprene are light-dependent, as well. In addition, isoprene emissions
are produced mainly by deciduous trees and therefore should be lower in winter
than when the trees have leaves. These factors result in diurnal and seasonal
variations in emission rates.
Emissions of manmade NO in the United States were estimated at 20.2 tg/yr
/\
for 1982. Annual emissions of manmade NO were some 12 percent higher in 1982
/\
than in 1970, but the rate leveled off in the late 1970s and exhibited a small
decline from about 1980 through 1982. The increase over the period 1970
019GC1/A 1-6 6/29/84
-------
30
20
(/)
z
o
o
o
10
i—r
TRANSPORTATION
IND. PROC., STAT. SOURCE
SOUD WASTE
NON-IND~SOLVENTS~
MISC.
I I
i—r
1970 1971 1972 1973 1974 1975 1976 1977 1978 1979 1980 1981
YEAR
Figure 1-1. National trend in estimated emissions of volatile organic com-
pounds, 1970 through 1982.
Source: U.S. Environmental Protection Agency (1983).
1-7
-------
through 1982 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 13 years in question.
Trends in manmade NO emissions over 1970 through 1982 are shown in Figure 1-2
(U.S. Environmental Protection Agency, 1983). 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 emissions.
1.2.4 Ambient Air Concentrations of Precursors
1.2.4.1 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 disper-
sion is limited that early in the morning, NMHC concentrations measured then
generally reflect maximum diurnal levels. Representative data for urban areas
show mean NMHC concentrations between 0.4 and 0.9 ppm.
The hydrocarbon composition of urban atmospheres is dominated by species
in the C? to CIQ 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).
Table 1-1 shows a typical example of the hydrocarbon composition in
ambient air in urban areas (Westberg and Lamb, 1982).
1.2.4.2 Hydrocarbons in Rural Areas. Rural nonmethane hydrocarbon concentra-
tions 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 concentra-
tions 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, ijo-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 about <0.020 ppm C.
019GC1/A 1-8 6/29/84
-------
20
05 1C
«•• 15
Z
g
w
CO
UJ
X
10
TRANSPORTATION
FUEL COMBUSTION
IND. PROC., SOLID WASTE, MISC. V
I j I I I
1970 1971 1972 1973 1974 1975 1976 1977 1978 1979 1980 1981
YEAR
Figure 1-2. National trend in estimated emissions of nitrogen oxides, 1970
through 1982.
Source: U.S. Environmental Protection Agency (1983).
1-9
-------
TABLE 1-1. HYDROCARBON (HC) COMPOSITION TYPICALLY MEASURED IN URBAN AREAS
(FROM SAMPLE COLLECTED IN MILWAUKEE, 1981)
HC concn. ,
ppb C
Hydrocarbon
HC concn.,
ppb C
Hydrocarbon
,5
5
14.0
25.5
16.0
18.5
9.
28.
65.0
2.0
3.5
3.5
49.0
24.0
2.0
0.5
2.0
4.5
13.0
10.0
11.0
6.5
4.5
9.5
2.0
Ethane 4.5
Ethylene 5.5
Acetylene 8.0
Propane 5.0
Propene 8.0
j/-Butane 3.0
n-Butane 1.5
1-butene 1.5
i^-Butene 33.5
t-2-Butene
c-2-Butene 2.5
^-Pentane 2.5
ri-Pentane 2.5
1-Pentene
t-2-Pentene 6.5
c-2-Pentene 18.5
Cyclopentene
Cyclopentane 6.5
2,3-Dimethylbutane 4.0
2-Methylpentane
c-4-Methyl-2-pentene 3.0
3-Methylpentane 5.0
1-Hexene 3.0
n-Hexane 22.0
t-2-Hexene 3.0
c-2-Hexene 17.0
Methylcyclopentane 7.0
2,4-Dimethylpentane
Benzene
Cyclohexane
2-Methylhexane
2,3-Di methylpentane
3-Methylhexane
2,2,3-Tri methylpentane
ri-Heptane
Methyl eyelohexane
2,4-Dimethylhexane
2,3,4-Trimethylpentane
Toluene
2,3-Dimethylhexane
2-Methylheptane
3-Ethylhexane
n-Octane
Ethylcyclohexane
Ethyl benzene
g, m-Xylene
Styrene
o-Xylene
n-Nonane
v-Propylbenzene
rt-Propyl benzene
p_-Ethyl toluene
m-Ethyltoluene
o-Ethyl toluene
1,3,5-Tri methyl benzene
1,2,4-Trimethyl benzene
1,2,3-Trimethyl benzene
Methylstyrene
1,3-Di ethyl benzene
1,4-Di ethyl benzene
Total identified
hydrocarbons
I Olefin
HC concn.,
PPb c
46
Total unidentified
hydrocarbons
HC concn.,
ppb C
87
Z Aromatic
2 Paraffin
Acetylene
134
301
16
497
27
60
3
Total NMHC
summing i
species
by
ndividual
584
Source: Westberg, H.; Lamb, B. (1982)
019GC1/A
1-10
6/29/84
-------
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.
1.2.4.3 Aldehydes in Urban Areas. Aldehydes observed in urban atmospheres
include formaldehydes, acetaldehyde, chloral, propanal, n-butanal, and benz-
aldehyde. Formaldehyde concentrations are the best characterized of these
aldehydes because the chromotropic acid methodology for formaldehyde was
established in the early 1960s. With the exception of early data from Los
Angeles (1961), reported concentrations of formaldehyde in urban areas fall in
the 0.01 to 0.03 ppm range, with maximum concentrations ranging up to 0.09
ppm.
Comparing these concentrations with concentrations of NMHC in urban
areas, it is apparent that formaldehyde probably constitutes less than 3
percent of the total NMOC in most urban areas. Acetaldehyde concentrations
are generally lower than formaldehyde in a given urban area. Concentrations
of total aldehydes in urban atmospheres can vary from a few ppb up to about
0.2 ppm (200 ppb). In polluted atmospheres, acrolein, propanal, butanal, and
benzaldehyde have each been measured at concentrations <0.015 ppm.
1.2.4.4 Aldehydes jn Rural Areas. Very few total aldehyde measurements have
been made in rural areas. Breeding et al. (1973) reported values for total
aldehydes of 0.001 to 0.002 ppm in rural Illinois and Missouri. Formaldehyde
levels in remote atmospheres apparently range from 0.1 to 10 ppb, with global
background formaldehyde concentrations varying from 0.3 to 0.5 ppb (Duce et
al., 1983).
1.2.4.5 Nitrogen Oxides in Urban Areas. Concentrations of NO , like hydrocar-
~~~ J\
bon concentrations, tend to peak in urban areas during the early morning, when
atmospheric dispersion is limited and automobile traffic is dense. Most NO
is emitted as nitric oxide (NO), but the NO is rapidly converted to N0? by
ozone and peroxy radicals produced in atmospheric photochemical reactions.
The relative concentrations of NO versus NO- 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
J\
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). Concurrent NMHC
measurements for these 10 cities showed that NMHC/NO ratios ranged from 5 to
16.
019GC1/A 1-11 6/29/84
-------
1.2.4.6 Nitrogen Oxides in Rural 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
X
et al., 1982). Concentrations of NO at nonurban sites in the north-central
f\
northeastern United States appear to be higher than NO concentrations in the
xv
west by a factor of 10 (Mueller and Hidy, 1983). From the limited amount of
data available, NO concentrations in unpopulated rural areas in the west
s\
average £ 1 ppb; but in nonurban northeastern areas average NO can exceed 10
ppb.
1.3 CHEMICAL AND PHYSICAL PROCESSES IN THE FORMATION AND OCCURRENCE OF OZONE
AND OTHER PHOTOCHEMICAL OXIDANTS
The photochemistry of the polluted atmosphere is exceedingly complex, but
an understanding of the basic phenomena is not difficult to acquire. Three
processes occur: the emission into the atmosphere of precursors to ozone,
from predominantly manmade sources; photochemical reactions that take place
during the dispersion and transport of these precursors; and chemical and
physical scavenging that reduces the concentrations of ozone (03) and other
oxidants, and their precursors, along the trajectory. Because transport and
dispersion of the precursors together determine the ambient concentrations
ozone may finally reach, an understanding of certain meteorological phenomena,
in addition to photochemical reactions, is also necessary.
1.3.1 Chemical Processes
In the troposphere, 0_ is formed indirectly through the action of sunlight
on nitrogen dioxide (N0?). In the absence of competing reactions, a steady-
state or equilibrium concentration of 0_ is soon established between the 0_,
NO,,, and NO (nitric oxide). The injection of organic compounds (primarily
hydrocarbons) into the atmosphere upsets the equilibrium and allows the ozone
to accumulate at much higher than steady-state concentrations. Recent work on
the photochemistry of smog has demonstrated fairly conclusively that the
hydroxyl radical, HO-, is the key species in causing organic compounds to play
a major role in smog reactions.
The length of the induction period before the accumulation of 03 begins
depends heavily on the initial concentration of HO radicals. There is evidence
that nitrous acid (HONO), which is a good source of HO radicals, occurs in the
019GC1/A 1-12 6/29/84
-------
atmosphere, but at very low concentrations. The most important source of HO*,
appears, rather, to be aldehydes, which are constituents of automobile exhaust,
as well as decomposition products of most atmospheric photochemical reactions
involving hydrocarbons.
The occurrence of organic compounds and sunlight does not mean that the
photochemical reactions will continue indefinitely. Terminating reactions
gradually remove N0? from the reaction mixtures, such that the photochemical
cycles would slowly come to an end unless fresh NO and N0? emissions were
injected into the atmosphere. Besides ozone, other oxidants that contain
nitrogen, such as peroxyacetyl nitrate (PAN), nitric acid (HNO,), and peroxy-
nitric acid (HNO.), as well as organic nitrates and inorganic nitrates, are
some of the terminating compounds.
The maximum concentration that 0~ can reach in polluted atmospheres
appears to depend on the hydrocarbon-nitrogen oxides ratio. At a low ratio
(1:1 to 2:1), insufficient HO- radicals are available from the hydrocarbon
species to effect the conversion of NO to N0?, a necessary first step. At
high ratios (greater than 12:1 to 15:1), conversion of NO to N0? occurs rapidly,
but the terminating reactions remove N0? from the reaction cycles and CL
cannot build up to high concentrations. Only at intermediate ratios (4:1 to
10:1) are conditions favorable to the formation of appreciable concentrations
of 03.
Recent studies on the fundamental photochemistry of organic compounds have
been reasonably successful. The reactions of paraffinic compounds (alkanes) are
fairly well understood, as are those of olefinic compounds (alkenes). Photo-
chemical reactions of the aromatic compounds, however, are poorly understood.
Natural hydrocarbons (i.e., those organic compounds emitted from vegeta-
tion), as well as hydrocarbons from manmade sources, can react photochemically
with nitrogen oxides to yield 0,, although natural hydrocarbons are reported
to be mainly scavengers of 0, rather than producers of 0,.
Besides direct adverse effects on human health and on vegetation, CL con-
tributes to visibility degradation and to acidic deposition. Through its
photolysis by sunlight, with subsequent generation of HO radicals, ozone par-
ticipates only indirectly, but not insignificantly, in the formation of both
sulfate and nitrate aerosols, which cause reduced visibility. These sulfate
and nitrate species, on further reaction, result in acidic deposition.
019GC1/A 1-13 6/29/84
-------
1.3,2 Physical Processes
Meteorological processes are quite important in determining the extent to
which 03 precursors can accumulate, and thereby the concentration of 03 that
can result. Atmospheric mixing depends principally on the amount of turbulent
mixing, wind speed and direction, or all three. Geography can have a significant
impact, also, particularly at land-sea interfaces.
The degree of turbulent mixing can be characterized by atmospheric stabi-
lity. Pollutants do not spread rapidly in stable layers, nor do they mix
upwards rapidly through stable layers to higher altitudes. Rather, stable
layers are usually characterized by temperature inversions, in which the tem-
perature increases with increasing altitude. Since pollutants emitted below or
into an inversion layer will not readily mix across the inversion layer, they
may persist for a considerable time and distance until the inversion is broken,
usually by surface heating resulting from sunlight.
The extent to which surface heating can cause mixing heights to increase
(and to cause dilution of 0- and its precursors) is highly dependent on geo-
graphy. Along both the Pacific Coast and the Northeast Coast, as well as near
the Great Lakes, low-level inversions (i.e., the mixing height is not great)
frequently persist through the afternoon, making these areas prone to local
and regional air pollution episodes.
Wind speed and direction determine the extent to which pollutants can be
increased by passing over successive sources, or can be diluted by being
rapidly removed from the source area. The plumes of precursors and resulting
0- from large metropolitan areas have been shown to persist for hundreds of
miles. Three kinds of transport of ozone and other pollutants have been
described, in terms of transport distance. In urban-scale transport, maximum
concentrations of 0, are produced about 20 miles or so (and about 2 to 3
hours) downwind from the major pollutant source areas. In mesoscale transport,
0« has been observed up to 200 miles downwind from the sources of its precur-
sors. Synoptic-scale transport is associated with large-scale, high-pressure
air masses that may extend over and persist for many hundreds of miles.
The significance of sunlight in photochemistry is related to its intensity
and its spectral distribution, both of which have direct effects on the speci-
fic chemical reaction steps that initiate and sustain oxidant formation. Days
on which significant ozone-oxidant concentrations occur are usually days with
warm, above-normal temperatures. These are also characteristic of high pressure
019GC1/A 1-14 6/29/84
-------
systems with inversions and low winds. The photolysis of aldehydes is affected
by the spectral distribution of light, since it is strongly dependent on wave-
length in the near ultraviolet region.
Ozone formed in the stratosphere can be brought downwards to the earth's
surface by events called "tropopause folds." These events are most commonly
observed in the mid-latitudes during spring and early summer. Relatively high
concentrations of 0- can occur for short periods of time, minutes to a few
hours, over local areas.
1.4 PROPERTIES, CHEMISTRY, AND MEASUREMENT OF OZONE AND OTHER PHOTOCHEMICAL
OXIDANTS
1.4.1 Properties
Ozone, peroxyacetyl nitrate, and hydrogen peroxide, along with other photo-
chemical oxidants occurring at very low concentrations 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 standard potential) and is expressed in
volts. Ozone has a standard potential of +2.07 volts in aqueous systems (for
the redox pair, 0-/H?0). Hydrogen peroxide has a standard potential of +1.776
in the redox pair, H^Op/H^O. No standard potential for peroxyacetyl nitrate in
neutral or buffered aqueous systems, such as those that occur in biological sys-
tems, appears in the literature. In acidic solution (pH 5 to 6), PAN hydrolyzes
fairly rapidly; in alkaline solution it decomposes with the production of nitrite
ion and molecular oxygen.
The toxic effects of oxidants are attributable to their oxidizing ability.
Their oxidizing properties also form the basis of the measurement techniques
for all three of these pollutants. The calibration of ozone and PAN measurements,
however, is achieved via their spectra in the ultraviolet and infrared, respec-
tively. The calibration of measurement methods for H?02 is achieved with iodo-
metric techniques that depend on the oxidizing properties of H^Op-
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. All three pollutants must be generated ijn situ
019GC1/A 1-15 6/29/84
-------
for the calibration of measurement techniques. For ozone and H?0?, generation
of calibration gases is reasonably straightforward.
1.4.2 Reactions of Ozone and Other Oxidants in Ambient Air
The atmospheric reactions of ozone and of other photochemical oxidants such
as peroxyacetyl nitrate (PAN) and hydrogen peroxide (H?02) are complex and diverse,
but are becoming increasingly well-characterized. The reactions of these species
result in products and processes that may have significant environmental and
health- and welfare-related implications, including effects on biological systems,
nonbiological materials, and such phenomena as visibility degradation and acidi-
fication of cloud and rain water. Ozone may play a role in the oxidation of SO,,
to H2$04, both indirectly in the gas phase (via formation of OH radicals and
Criegee biradicals) and directly in aqueous droplets. Evidence is also accumu-
lating that hydrogen peroxide, like ozone, is involved in both gas-phase photo-
chemistry and aqueous-phase oxidations. For example, studies of the rates of
oxidation of S02 by H202 in solution suggest that this reaction is sufficiently
fast that it could be the major aqueous-phase route for the oxidation of S02
under certain atmospheric conditions. In addition, the importance of oxidants
such as PAN in various aspects of atmospheric chemistry, such as long-range
transport of NO and multi-day air pollution episodes, is now being recognized.
/\
Ozone can react with organic compounds in the troposphere. It is important
to recognize, however, that organics undergo competing reactions with OH radicals
in the daytime (Atkinson et al., 1979; Atkinson and Lloyd, 1984) and, in certain
cases, with NO- radicals during the night (Japar and Niki, 1975; Carter et al.,
1981; Atkinson et al. , 1984a,b,c,d), as well as photolysis. Only for organics
whose ozone reaction rate constants are greater than ~10 cm molecule sec
can consumption by ozone be considered to be atmospherically important (Atkinson
and Carter, 1984).
Ozone reacts rapidly with the acyclic mono-, di-, and tri-alkenes and with
_"| Q
cyclic alkenes. The rate constants for these reactions range from ~10 to
~10~14 cm3 molecule"1 sec'1 (Atkinson and Carter, 1984), corresponding to
atmospheric lifetimes ranging from a few minutes for the more reactive cyclic
alkenes, such as the monoterpenes, to several days. In polluted atmospheres,
a significant portion of the consumption of the more reactive alkenes will
occur via reaction with ozone, rather than with OH radicals, especially in the
afternoons during photochemical oxidant episodes. Reactions between ozone and
019GC1/A 1-16 6/29/84
-------
alkenes can result in aerosol formation (National Academy of Sciences, 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.
The aromatics react with ozone, but quite slowly (Pate et al. , 1976;
Atkinson et al. , 1982), such that their reactions with ozone are expected to
be unimportant in the atmosphere. Cresols are more reactive toward ozone than
the aromatic hydrocarbons (Atkinson et al., 1982), but their reactions with OH
radicals (Atkinson et al., 1978, 1982) or N03 radicals (Carter et al., 1981;
Atkinson et al., 1984a) 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 et al., 1981).
The kinetics of the reactions of ozone with a variety of nitrites, ni-
triles, nitramines, nitrosamines, and hydrazines have been studied (Atkinson
and Carter, 1984), but only for the hydrazines are these reactions sufficiently
rapid to be of atmospheric importance. Chamber studies have shown that N-
nitrosodimethylamine can result from the reaction of ozone with simple hydra-
zines (Tuazon et al. , 1981). Whether this product would ever be formed by
reaction with ozone in the atmosphere obviously depends upon the presence, and
level, of the precursor hydrazines in ambient air.
Certain reactions of ozone other than its reactions with organic compounds
are important in the atmosphere. Ozone reacts rapidly with NO to form N0?,
and subsequently with N0? 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.
1.4.3 Reactions of Ozone and Peroxyacetyl Nitrate in Aqueous (Biological)
Systems
Both ozone and PAN can react directly and rapidly with many organic mole-
cules, including many types occurring in biological systems. Additionally,
active species such as singlet oxygen, hydroxyl radicals, and superoxide are
019GC1/A 1-17 6/29/84
-------
produced either as products of primary reactions or from the decomposition of
ozone or PAN in water; these species also have the potential for causing bio-
logical damage.
The reactions of ozone with biologically important functional groups have
been described in the literature, although such information remains relatively
sparse and is based on j_n vitro work that is not always pertinent to reactions
that occur under the conditions of iji vivo exposure. Among the functional
groups with which ozone reacts relatively rapidly are the carbon-carbon double
bonds (alkenic group) found in biologically important compounds such as some
of the essential fatty acids and polyunsaturated fatty acids (PUFA) of the kind
found in the lipids of cell membranes. Amines are, in general, close to alkenes
in their reactivity toward ozone, although amino groups existing as the amide
or salt are less susceptible to ozone than unprotected amino groups. Sulfur-
containing compounds, such as methionine, can also undergo electrophilic attack
by ozone, resulting in the formation of both sulfoxides and sulfones. Under
some conditions (e.g., pH > 9), ozone is rapidly converted to hydroxyl radicals,
which are less selective than ozone in reactions with organic molecules. The
conversion of ozone to superoxide (O-O and hydroperoxy radicals (HQ^*) has
also been reported.
Aromatic compounds are much less reactive toward ozone than alkenic com-
pounds in aqueous systems. In compounds containing both aromatic and alkenic
groups, such as the indole ring of tryptophan, the initial ozone attack occurs
exclusively at the alkenic part of the molecule. Aldehydes react with ozone
with and without the involvement of oxygen. Either way, acyl hydrotrioxides
are formed that subsequently decompose to peroxides and carboxylic acids. Sim-
ple ketones react slowly or not at all with ozone.
Reactions between ozone and specific molecules of importance in biological
systems have been described in Chapter 10.
Knowledge of the solution chemistry of PAN is limited. It is known, how-
ever, that PAN can react with alkenes, with sulfur-containing compounds, and
with aldehydes. The half-life of PAN in water (pH 7.2) is only about 4.4 min-
utes. Thus, some of the toxicological effects ascribed to PAN should possibly
be attributed to its decomposition products instead.
1.4.4 Sampling and Measurement of Ozone and Other Photochemical Oxidants
The analysis of ozone and other, related atmospheric oxidants includes
requirements for representative sampling, specific and sensitive measurement
methodologies, methods for the generation of standard samples, absolute methods
019GC1/A 1-18 6/29/84
-------
for the calibration of these standards, and procedures by which to provide
quality assurance for the whole measurement process. In the summary presented
below, recommended procedures are given for all of these analytical steps. Sam-
pling and quality assurance are discussed in general terms for all of the oxidants.
Methods of analysis, sampling, and generation and calibration are discussed speci-
fically for ozone, peroxyacetyl nitrate (PAN) and its homologues, and hydrogen
peroxide. Because of the large existing data base that employed measurements
for "total oxidants," non-specific iodometric techniques are discussed and
compared to current specific CL measurements.
1.4.4.1 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 cohorts, multiple-point calibration procedures, prevention and remedial
maintenance requirements; procedures for air pollution episode monitoring;
methods for recording and validating data; and information on documentary
quality control (U.S. Environmental Protection Agency, 1977a).
A crucial link in the measurement cycle involves sampling strategies and
techniques. Sampling strategies, which involve the design and operation of a
sampling network, must be consistent with the specific purpose of the measure-
ments. Ambient air monitoring data are collected for a variety of purposes,
each of which may have different requirements that affect sampling strategy.
For example, a sampling strategy for health effects research studies may
require a number of monitoring stations carefully situated to assess human
exposure for a given urban population over a finite period of time. In addi-
tion, since ozone, PAN, and HLCL are all secondary pollutants formed after an
initial induction period, stations for monitoring peak concentrations should
be located downwind of the urban center of precursor emissions.
The reactivity and instability of CL and other photochemical oxidants
dictate special sampling techniques. Samples of air containing 0, cannot be
collected and stored and must be analyzed dynamically. Analysis for PAN must
likewise be performed as soon as possible after collection. Hydrogen peroxide
019GC1/A 1-19 6/29/84
-------
collected in aqueous media is fairly stable, but samples are subject to inter-
fering reactions from ozone trapped in solution. Sampling probes should be
constructed of Teflon or some similarly inert material, and inlet residence
times should be as short as possible. Other design criteria for 03 monitoring
stations have been given (Standing Air Monitoring Work Group, 1977; National
Academy of Sciences, 1977). The most important of these are that inlets of
the sampling probe should be positioned 3 to 15 m (10 to 49 ft) above ground
and at least 4 m (13 ft) from large trees and 120 m (349 ft) from heavy auto-
mobile traffic.
1.4.4.2 Measurement Methods for Total Oxidants and Ozone. Techniques for the
continuous monitoring of total oxidants and 0- in ambient air are summarized
in Table 5-13. The earliest methods used for routinely monitoring oxidants in
the atmosphere were based on iodometry. When atmospheric oxidants are absorbed
in potassium iodide (KI) reagent, the iodine produced,
03 + 3I~ + H20 = I3~ + 02 + 20H~ (1-1)
is measured by ultraviolet absorption in colorimetric instruments and by
amperometric means in electrochemical instruments. The term "total oxidants"
is of historical significance only and should not be construed to mean that
such measurements yield a sum of the concentrations of the oxidants in the
atmosphere. The various oxidants in the atmosphere react to yield iodine at
different rates and with different stoichiometries. Only ozone reacts imme-
diately to give a quantitative yield of iodine. Hydrogen peroxide, for example,
produces iodine at a slow rate and because of its low concentration compared
to ozone would be expected to have little effect upon a total oxidants measure-
ment. As discussed below, the total oxidants measurement correlates fairly
well with the specific measurement of ozone, except during periods when signi-
ficant N02 and SO™ 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 concen-
trations were measured by "total oxidants" methods.
The reference method promulgated by EPA for compliance monitoring is the
chemiluminescence technique based on the gas-phase ozone-ethylene reaction
(U.S. Environmental Protection Agency, 1971b). The technique is specific for
019GC1/A 1-20 6/29/84
-------
ozone, the response (luminescence intensity) is a linear function of concentra-
tion, detection limits of 0.001 to 0.005 ppm are readily obtained, and response
times of 30 seconds or less are readily obtained. 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 (U.S. Environmental Protection Agency,
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.
Commercial analyzers that have been designated as reference methods were
listed in Chapter 5 (Table 5-7). An acceptable equivalent method must meet
the prescribed performance specifications and also show a consistent relation
with the reference method. Commercial analyzers that have been designated as
equivalent methods were also listed in Chapter 5 (Table 5-7).
The designated equivalent methods are based on either the gas-solid
chemiluminescence procedure or the ultraviolet absorption procedures (Table
1-2). The first designated equivalent method was based on ultraviolet absorp-
tion of the mercury 254 nm emission line. The absorption coefficient of ozone
is accurately known at this wavelength with an accepted value of 134 M cm .
Detection limits of 0.005 ppm are readily obtained by modern digital capabili-
ties for making precise measurements of weak absorbancies at moderate path-
lengths. Compensation for potential interferences that also absorb at 254 nm
is made by comparing an averaged transmission signal of ozone in air to the
transmission signal through an otherwise identical air sample from which the
ozone has been preferentially scrubbed. Advantages of this UV absorption
technique are that a reagent gas is not required and control of sample air
flow is not critical. In addition, the measurement is in principle an absolute
one, in that the ozone concentration can be computed from the measured trans-
mission signal since the absorption coefficient and pathlength are accurately
known.
In the gas-solid chemiluminescence analyzer, the reaction between ozone
and Rhodamine-B adsorbed on activated silica produces chemiluminescence, the
intensity of which is directly proportional to ozone concentration. The
sensitivity is greater than the gas-phase chemiluminescence method and a
controlled reagent gas flow is not required. The sensitivity of the reaction
surface decays gradually with time, but the analyzer contains internal means
to compensate for the decay.
019GC1/A 1-21 6/29/84
-------
I
ro
ro
Principle
Continuous
col or 1 metric
Continuous
electrochemical
Chemi luminescence
Chemi luminescence
Ultraviolet
photometry
Reagent
10(20)X KI
buffered at
pH = 6.8
2% KI
buffered at
pH = 6.8
Ethyl ene ,
gas-phase
Rhodamine-B
None
TABLE 1-2.
Response
Total
oxldants
Total
oxidants
03-spec1f1c
Os-spec1f1c
03-spec1fic
SUMMARY OF OZONE MONITORING TECHNIQUES
Minimum
detection limit
0.010 ppm
0.010 ppm
0.005 ppm
0.001 ppm
0.005 ppm
Response
time, 90% FSa
3 to 5 minutes
1 minute
< 30 seconds
< 1 minute
30 seconds
Major
1 nterf erences
N02(+20%, 10XRI)
S02(-100%)
N02(+6%)
S02(-100X)
Noneb
None
Species that
absorb at 254 nm
References
Llttman and Benollel (1953)
Toklwa et al. (1972)
Brewer and Mllford (1960)
Mast and Saunders (1962)
Toklwa et al. (1972)
Nederbragt et al. (1965)
Stevens and Hodgeson (1973)
Regener (1960, 1964)
Hodgeson et al. (1970)
Bowman and Horak (1972)
aFS = full response.
A signal enhancement of 3 to 12% has been reported for measurement of 03 1n humid versus dry air (California Air Resources Board, 1976).
No significant interferences have been reported 1n 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.
-------
1.4.4.3 Calibration Methods. All the analyzers discussed above must be
periodically calibrated with ozonized air streams, in which the ozone concen-
tration has been determined by some absolute technique. This includes the UV
absorption analyzer, which, when used for continuous ambient monitoring, may
experience ozone losses in the inlet system because of contamination.
An ozone calibration system for a primary laboratory calibration system
consists of a clean air source, an ozone generator, and a sampling manifold.
The ozone generator most often used is a photolytic source employing a mercury
pen-ray lamp that irradiates a quartz tube through which clean air flows at a
controlled rate (Hodgeson et al., 1972). The ozone concentration may be
varied by means of a mechanical sleeve over the lamp envelope or by changing
the lamp voltage or current. Once the output of the generator has been cali-
brated 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 this country
are summarized in Table 1-3.
The original reference calibration procedure promulgated by EPA was the
1 percent neutral buffered potassium iodide (NBKI) method (U.S. Environmental
Protection Agency, 1971). This technique was employed in most of the United
States, with the exception of California, which routinely used a 2 percent
NBKI procedure that was quite similar to the EPA method except for the use of
humidified air through the ozone source (California Air Resources Board, 1976).
The Los Angeles Air Pollution Control District (LAAPCD) used a 1 percent un-
buffered KI procedure and measured the iodine produced by a titration technique
rather than the photometric technique used in the California and EPA methods.
A number of studies conducted between 1974 and 1978 revealed several deficien-
cies with KI methods, the most notable of which were poor precision or inter-
laboratory comparability and a positive bias of NBKI measurements relative to
simultaneous absolute UV absorption measurements. The positive bias was also
observed with respect to gas-phase titration (GPT) of ozone with standard
nitric oxide (NO) samples. The positive bias observed is peculiar to the use
of phosphate buffer in the NBKI techniques. The bias was not observed in the
unbuffered LAAPCD method (which nevertheless suffered from poor precision), nor
in the 1 percent EPA KI method without phosphate buffer (Hodgeson et al., 1977),
nor in a KI procedure that used boric acid as buffer (Flamm, 1977). A summary
019GC1/A 1-23 6/29/84
-------
TABLE 1-3. OZONE CALIBRATION TECHNIQUES
I
ro
Method
IX NBKI
2X NBKI
IX Unbuffered
KI
UV photometry
Gas-phase
titration (GPT)
IX BAKI
Reagent
IX KI,
phosphate buffer
pH = 6.8
2X KI
phosphate buffer
pH = 6.8
IX KI
pH = 7
None
No standard
reference gas
IX KI,
boric acid buffer
pH » 5
Primary standard8
Reagent grade
arsenious oxide
03 absorptivity at
Hg 254 nm emission
line
No SRM (50 ppm in N2)
from NBS
Standard KI03f
solutions
Method used,
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,
[oa]t/[o3]uv
1.12 ± 0.05b
1.20 ± 0.05b
0.96C
1.030 ± 0.015*
1.00 i 0.05
aln 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.
C0nly one study available (Demore et al., 1976).
dUV photometry used as reference method by CARB since 1975. This technique used as an interim, alternative reference procedure by
EPA from 1976 to 1979.
eTMs is the value reported in the latest definitive study (Fried and Hodgeson, 1982). Previous studies reported biases ranging from
0 to 10 percent (Burton et al., 1976; Paur and McElroy, 1979).
This procedure also recommended a standard I3~ solution absorptivity to be used instead of the preparation of standard iodine solutions.
-------
of results of these prior studies was presented in the previous criteria docu-
ment (U.S. Environmental Protection Agency, 1978a) and in a review by Burton
et al. (1976). Correction factors for converting NBKI calibration data to a
UV photometry basis were given in Chapter 5.
Subsequently, EPA evaluated four alternative reference calibration proce-
dures based on UV photometry, GPT with excess NO, GPT with excess ozone and the
boric acid buffered KI technique (BAKI). The results of these studies (Rehme
et al., 1981) showed that UV photometry was superior in accuracy, precision,
and simplicity of use; and in 1979 regulations were amended to specify UV
photometry as the reference calibration procedure (U.S. Environmental Protection
Agency, 1979a,b,c,d). Laboratory photometers used as reference systems for ab-
solute 0» measurements have been described by Demore and Patapoff (1976), Bass et
al. (1977), and Paur and Bass (1983).
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 and low ozone concentrations. A primary standard UV
photometer, such as those above, is one that meets the requirements and specifi-
cations given in the revised ozone calibration procedures (U.S. Environmental
Protection Agency, 1979d). 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 stand-
ards that have been used are commercial 0, photometers, calibrated generators,
and GPT apparatus. Guidelines on transfer standards have been published by EPA
(McElroy, 1979).
1.4.4.4 Relationship of Total Oxidants and Ozone Measurements. The temporal
and quantitative relationship between simultaneous total oxidants and ozone
measurements has been examined in this chapter because of the existence of a
data base obtained by "total oxidants" measurements. Such a comparison is com-
plicated by the relative scarcity of data, the presence of both positive (N0?)
and negative (S0?) interferences in total oxidants measurements, and the change
in the basis of calibration. In particular, the presence of N0? and S0? inter-
ferences prevents the establishment of a definite quantitative relationship be-
tween ozone and oxidants data. Nevertheless, some interesting conclusions can
be drawn and are summarized below.
019GC1/A 1-25 6/29/84
-------
An expected relationship between total oxidants and specific 0., measurements
can be predicted based upon the known response of oxidant instrumentation to
oxidizing and reducing species in the atmosphere. The predicted relation in
this document assumes that N0? is the only significant positive interference
and that SCL is the predominant negative interference. Because of the potential
presence of oxidizing (NO^) and reducing (S0~) interferences, it is difficult
or impractical to intercompare measurements during evening and early morning
hours when ozone concentrations are at a minimum. The relationship is best
compared at the midday to early afternoon diurnal maximum of ozone when NCL
concentrations are approaching a minimum; the S0» concentration at this time
will depend on local emissions. A comparison of maximum hourly averages is
appropriate since the primary and secondary ambient air quality standards are
based on this value. If legitimate corrections or compensations have been made
for SO £ and NOp interferences, the corrected total oxidants concentrations should
always be higher than simultaneous CL concentrations by an amount dependent on
type and concentrations of other oxidants present. The major other oxidants
known to exist in the atmosphere are PAN and hLCL. Maximum concentrations of
these oxidants occur near the ozone diurnal maximum (Chapter 6) with values
that are only a fraction of the CL maximum (section 6.6 and 6.7). In addition,
both of these are classified as slow oxidants in that they release iodine at a
slow rate in aqueous solution. Therefore, if a contribution from these species
is discernible at all in the total corrected oxidants reading, it should be only
a small fraction of the ozone contribution. For most of the aerometric data
base, particularly outside the state of California, no attempts were made to
correct total oxidants concentrations for NCL and S02 because such corrections
were impractical or impossible. For uncorrected total oxidants data, the
counterbalancing effects of S02 and N02 interferences make it even more diffi-
cult to discern contributions from oxidants other than ozone. The uncorrected
total oxidants data should then be either higher than or lower than correspond-
ing ozone data, depending on the relative concentrations of SO,, and NO^.
The simultaneous comparisons that have been made in large part confirm the
predictions above. Studies concluded in the early to mid-1970s were reviewed
in the previous criteria document (U.S. Environmental Protection Agency, 1978a).
Averaged data showed fairly good qualitative and quantitative agreement between
diurnal variations of total oxidants and ozone. Uncorrected data showed distinct
019GC1/A 1-26 6/29/84
-------
morning and evening peaks resulting from N0? interference. Data taken from indi-
vidual days of respective studies showed considerably more variation, with total
oxidants measurements both higher and lower than ozone measurements.
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 corre-
lated (Chock et al., 1982) and yielded the following regression equation for 1978,
in which a large number (927) of data pairs were available:
Oxidant (ppm) = 0.870 03 + 0.005
(Correlation coefficient = 0.92) (1-2)
The oxidant data were uncorrected for N02 and S0~ interferences, and, again, on
individual 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 S0? interferences, and in such corrected total oxi-
dants measurements ozone is the dominant contributor to total oxidants. Indeed,
it is difficult to discern the presence of other oxidants in most total oxidant
data. There can, however, be major temporal discrepancies between ozone and
oxidants data, which are primarily a result of oxidizing and reducing inter-
ferences with KI measurements. As a result of these interferences, on any
given day the total oxidant values may be higher than or lower than simultaneous
ozone data. The measurement of ozone is a more reliable indicator than total
oxidant measurements of oxidant air quality.
1.4.4.5 Methods for the Sampling and Analysis of Peroxyacetyl Nitrate and Its
Homologues. Only two analytical techniques have been used to obtain
significant data on ambient peroxyacetyl nitrate (PAN) concentrations. These
are gas chromatography with electron capture detection (GC-ECD) and long-path
Fourier transform infrared (FTIR) spectrometry. Atmospheric data on PAN con-
centrations 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. Since PAN is thermo-
dynamically unstable, standards must be generated and analyzed by some absolute
technique for the purpose of calibrating the GC-ECD. Thus, PAN generation
techniques and absolute methods for analyzing these samples have also been
summarized.
019GC1/A 1-27 6/29/84
-------
By far the most widely used technique for the quantitative determination
of ppb concentrations of PAN and its homologues is GC-ECD (Stephens, 1969).
With carbowax or SE30 as a stationary phase, PAN, peroxypropionyl nitrate (PPN),
peroxybenzoyl nitrate (PBzN), and other homologues (e.g., peroxybutyrl 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. Table 1-4 shows parameters used
by several investigators to determine trace levels of PAN by GC-ECD. Sample
injection into the GC is accomplished by means of a gas-sampling valve with a
gas-sampling loop of a few milliliters1 volume. Sample injection may be per-
formed manually or automatically. Typically, manual air samples are collected
in 50-200 ml ungreased glass syringes and purged through the gas-sampling valve.
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 Sal as (1983a, 1983b) on the measurement of PAN
in the free (unpolluted) troposphere (see Chapter 6) 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. Some
investigators have reported a reduced response to PAN calibration samples when
dry diluent gas is used, whereas others have not observed this effect. The
reduced response has been attributed to losses of PAN to surfaces within the
inlet system and the GC. Presumably, water vapor may deactivate surfaces. For
the present, if a moisture effect is suspected in a PAN analysis, the bulk
of this evidence suggests that humidification of PAN calibration samples (to a
range approximating the humidity of the samples being analyzed) would be advisa-
ble.
Conventional long-path infrared spectroscopy and Fourier-transform infrared
spectroscopy (FTIR) have been used to detect and measure atmospheric PAN. Sen-
sitivity is enhanced by the use of FTIR. The most frequently used IR bands
have been assigned and the absorptivities shown in Table 1-5 permit the quan-
titative analysis of PAN without calibration standards. The absorptivity of the
990 cm band of PBzN has been reported by Stephens (1969). Some recent simul-
taneous measurements of PAN and other atmospheric pollutants such as Q^> HNu3»
019GC1/A 1-28 6/29/84
-------
TABLE 1-4. SUMMARY OF PARAMETERS USED IN DETERMINATION OF PAN BY GC-ECD
Reference
Heuss and Glasson,
1968
Grosjean, 1983
Darley et al. ,
1963
Stephens and Price,
1973
Lonneman et al . ,
1976
Holdren and Spicer,
1984
Peake and Sandhu,
1982
Singh and Sal as,
1983b
Grosjean et al . ,
1984
Nielson et al. ,
1982
Column
dimensions
and material
4 ft x 1/8 in
Glass
6 ft x 1/8 in
Teflon
3 ft x 1/9 in
Glass
1.5 ft. x 1/8 in
Teflon
3 to 4 ft x 1/8 in
Glass
5 ft x 1/8 in
Teflon
3.3 ft x 1/8 in
Glass
1.2 ft x 1/8 in
Teflon
1.7 ft x 1/8 in
Teflon
3.9 ft x 1/12 in
Glass
Stationary
phase
SE30
(3.8%)
10% Carbowax 400
5% Carbowax 400
5% Carbowax E 400
10% Carbowax 600
60/80 Mesh
Carbowax 600
5% Carbowax 600
10% Carbowax 600
10% Carbowax 400
5% Carbowax 400
Column
Solid temperature,
support °C
80-100 25
Mesh
Diatoporte S
60/80 Mesh 30
Chromosorb P
100-200 Mesh 35
Chromosorb W
Chroraosorb 25
G 80/100
mesh treated
with dimethyl
dichlorosilane
Gas Chrom Z 25
Gas Chrom Z 35
Chromosorb W 33
80/100 Mesh 33
Supelcoport
60/80 Mesh 30
Chromosorb G
Chromosorb 25
W - AW - DCMS
Flow Elution
rate, Carrier time, Concentration
ml/min gas min range
N.A.a N.A.a N.A.a
40 N2 N.A.a
25 N2 2.17
60 N2 1.75
70 95% Ar 2.7
5% CH4
70 90% Ar 3.00
10% CH4
50 N2 N.A.a
30 95% AR N.A.3
5% CH4
40 N2 5.0
40 N2 6.0
ppb
range
ppb
range
3 to 5
ppb
37
ppb
0.1 to 100 ppb
ppb
0.2 to 20
ppb
0.02-0.10
ppb
2-400
ppb
11 ppb
a
'N.A. - not available in reference.
-------
TABLE 1-5. INFRARED ABSORPTIVITIES OF PEROXYACETYL NITRATE
CO
o
Absorptivity, ppm-1
Frequency
cm-1
1842
1741
1302
1162. 5
930
791.5
Mode
v(c=o)
vas(N02)
vs(N02)
v(c-o)
v(o-o)
6(N02)
Liquid PAN
(Bruckmann and
Wlllner, 1983)
12.4
32.6
13.6
15.8
N.A.a
13.4
PAN 1n air
(Stephens,
1969)
10.0
23.6
11.2
14.3
N.A.a
10.1
Frequency
cm-1
1830
1728
1294
1153
930
787
m-1 x 104
PAN In air
(Stephens and
Price, 1973)
10.0
23.6
11.4
13.9
1.8
10.3
PAN 1n octane
(Holdren and
Spicer, 1984)
9.44
26.5
9.44
9.66
N.A.a
10.1
Not available 1n reference.
-------
HCOOH, and HCHO have been made by long-path FTIR spectrometry during smog epi-
sodes in the Los Angeles Basin. Tuazon et al . (1978) describes an FTIR system
operable at pathlengths up to 2 km for ambient measurements of PAN and other
trace constituents. This system employed an eight-mirror multiple reflection
cell with a 22.5-m base path. Detection of PAN was by bands at 793 and 1162 cm .
The 793 cm band is characteristic of peroxynitrates, while the 1162 cm band
is reportedly attributable to PAN only (Hanst et al . , 1982). Tuazon et al . (1981)
reported a detection limit for PAN of 3 ppb at a 900-meter pathlength.
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 peroxybenzoyl nitrate (PbzN) was placed, based on observations in the
vicinity of the PBzN band at 990 cm ; the maximum PAN concentration observed
was 15 ppb.
Sampling may constitute one of the major problems in the analysis of trace
reactive species, such as PAN, by long-path FTIR spectrometry. The large inter-
nal surface area of the White cells may serve to promote the decomposition or
irreversible adsorption of reactive trace species. 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 purified PAN, calibration samples are not commercially available.
Each laboratory involved in making such measurements must prepare its own
standards. Calibration samples are usually prepared by various means at con-
centrations in the ppm range, and they must be analyzed by some absolute tech-
nique.
Earlier methods used to synthesize PAN have been summarized by Stephens
(1969). The photolysis of alky! 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 photol-
ysis chamber is purified by preparation-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 nitrogen cylinders at 100 psig and stored at reduced temperatures,
Gay et al . (1976) have used the photolysis of C12: aldehyde: N02 mixtures
in air or oxygen for the preparation of PAN and a number of its homologues at
019GC1/A 1-31 6/29/84
-------
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).
The other technique for PAN preparation in current use involves the nitra-
tion of peracetic acid. Several investigators have recently reported on a con-
densed-phase synthesis of PAN with peracetic acid that produces high yields 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). Most of these
procedures call for the addition of peracetic acid (40 percent in acetic acid)
to a hydrocarbon solvent (pentane, heptane, octane) maintained at 0°C in a dry-
ice acetone bath, followed by acidification with sulfuric acid and slow addition
of sodium nitrate. 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 absorptivities given in Table 1-5. Conventional IR
instruments and 10-cm gas cells can analyze gas standards of concentrations
>35 ppm. Liquid microcells can be used for the analysis of PAN in octane
solutions.
The alkaline hydrolysis of PAN to acetate ion and nitrite ion in quantita-
tive yield (Nicksic et al., 1967) provides a means independent of infrared for
the quantitative analysis of PAN. Following hydrolysis, nitrite ion may be
quantitatively analyzed by the Saltzman colorimetric procedure (Stephens, 1969).
The favored procedures now use ion chromatography to analyze for nitrite (Nielsen
et al., 1982) or acetate (Grosjean, 1983, 1984) ions. Another calibration pro-
cedure has been proposed that is based on the thermal decomposition of PAN in the
presence of excess NO (Lonneman et al., 1982). The peroxyradical, CH3C(0)02, and
its decomposition products rapidly oxidize NO to N02 with a stoichiometry that
has been experimentally measured. By the use of NO standard mixtures and the
measurement by chemiluminescence of the NO consumed, the absolute PAN concentra-
tion can be determined.
1.4.4.6 Methods for Sampling and Analysis of Hydrogen Peroxide. Hydrogen perox-
ide (H?0?), like ozone and PAN, is formed as a product of the photooxidation of
hydrocarbons and reaches maximum concentrations during daylight hours. There
are some early reports of H?0? concentrations as high as 180 ppb at an ozone
maximum of 650 ppb, but it now appears more likely that maximum H202 concentra-
tions are in the range of 10 to 50 ppb and are only a small fraction (< 10%)
019GC1/A 1-32 6/29/84
-------
of the corresponding ozone maximum. Applied and potentially useful techniques
for the measurement of ambient H»0p are summarized in Table 1-6.
With the exception of Fourier-transform infrared (FTIR) studies, all of
the techniques that have been used for atmospheric H^CL measurements have em-
ployed aqueous traps for sampling. Recent studies have indicated that this
approach leads to interference from ozone, which will always be present at
higher concentrations. Absorbed 0- has been observed to promote both the for-
mation and destruction of H?CL in aqueous media (Zika and Saltzman, 1982).
Therefore, an obvious research need in HpO- measurements is a clear delinea-
tion of the nature of any 0» interferences and the development of means for
their prevention.
Of the procedures given in Table 1-6, only the titanium colorimetric,
enzyme-catalyzed, and FTIR methods have been used for atmospheric sampling.
The other procedures do not appear promising for ambient air analysis. The
titanium sulfate-8-quinolinol reagent has been used in several earlier studies
on atmospheric H202 (Bufalini et al., 1972; Gay et al., 1972a; Gay et al., 1972b;
Kok et al., 1978a). Hydrogen peroxide in air is scrubbed in a coarse-fritted
bubbler containing aqueous titanium sulfate-ammonium sulfate-sulfuric acid solu-
tion. After sampling, the solution is extracted with an aliquot of 8-quinolinol
in chloroform. The absorbance at 450 nm of the titanium (IV)-H202-9-quinolinol
complex in chloroform is determined. A positive interference is expected from
any compound that can liberate H»0» via acid hydrolysis (Pobiner, 1961), e.g.,
t-butylhydroperoxide. Of the major atmospheric pollutants investigated (S02,
03, NOp, NO, and hydrocarbons), only S0? at high concentrations gave a small
(0.7 percent) negative interference (Gay et al., 1972b).
In the titanium tetrachloride method, samples are collected in a midget
impinger containing an aqueous TiCl.-HCl solution. A stable TiCl^-h^O,, complex
is formed immediately, and after the solution is diluted to a known volume, the
absorbance of the complex at 410 nm is determined. The principal difficulty
with this method is the formation of fine particles, presumably TiO^, which scat-
ter visible radiation and create an apparent absorption. In an intercomparison
of hL02 measurement methods, Kok et al. (1978a) reported rather poor agreement
between the two titanium reagents and between these and chemiluminescence.
A promising method for the measurement of hydrogen peroxide in the atmos-
phere at very low concentrations is based on the chemiluminescence obtained from
the Cu(II)-catalyzed oxidation of luminol (5-amino-2,3 dihydro-1,4-phthalazine-
dione) by H202 (Armstrong and Humphreys, 1965). The product of the reaction with
019GC1/A 1-33 6/29/84
-------
TABLE 1-6. MEASUREMENT METHODS FOR HYDROGEN PEROXIDE
Method
Titanium
colorimetry
Chemi 1 umi nescence
Enzyme- catalyzed
Enzyme-catalyzed
Enzyme- cata 1 yzed
Fourier- transform
infrared absorption
Electrochemical
H202-olefin
reactions
Mixed-ligand
complex reagents
Reagent(s)
(1) Titanium Sulfate
-8-Quinolinol
(2) Titanium Tetrachloride
Luminol, Cu(II)
basic solution
Scopoletin, horseradish-
peroxidase (HRP)
Leuco crystal violet,
HRP
3-(p-hydroxyphenyl )
propionic acid
None
Aqueous solutions
l,2-di-(4-pyridyl)
ethyl ene
Vanadium and
uranium hydroxamic
acid chelates
Limits of
detection
(1) 1.6 x 10-6 M
(2) ca 10-6 M
0.001 to 1 ppm
1.5 x 10-11 M
10-8 M
10-6 to 10-4 Mf
0.005 ppm (est.)
5 x 10-6 to 1 M
10-6 to 5 x 10-4 M
10-6 M
Interferences
Positive
Alkyl hydro-
peroxides
PANd
NA
NA
NA
NA9
NA
03
NA
Negative
S02C?
S026
NA
NA
NA
None
NA
NA
NA
Applications Primary reference
Atmospheric (1) Gay et al. (1972a, 1972b)
(2) Pilz and Johann (1974);
Kok et al. (1978a)
Atmospheric, Armstrong and Humphreys (1965);
rainwater Kok et al. (1978a,1978b)
Atmospheric, Andreae (1955); Perschke
rainwater and Broda (1961); Zika and
Saltzman (1982)
Mottola et al. (1970)
Zaitsu and Ohkura (1980)
Atmospheric*1 Hanst et al. (1982)
— Pisarevskii and Polozova (1980)
Hauser and Kolar (1968)
Csanyi (1981);
Meloan et al. (1961)
Except where noted, detection limits are in moles/1 iter(M) in aqueous solution.
03 may be both a positive and negative interference in all these procedures using aqueous sampling. See Text. NA = not available.
°The S02 interferences is reported to be small at high S02 concentrations (Gay et al., 1972b). Studies of potential positive and
negative interferences are incomplete for these methods.
The reported PAN interference is small (Kok et al., 1978b).
p
'The report of an S02 interference is undocumented.
fThe lower limit could presumably be reduced by the use of larger samples.
9With sufficient resolution, there should be no interferences. IR absorption by atmospheric water vapor is the major analytical
limitation.
VjOz bands have not been observed in any long-path FTIR studies. The estimated lower limit of detection in these studies is
approximately 0.005 ppm.
-------
H.CL is 3-amino-phthalic acid, a nitrogen molecule, and a photon of light at
450 nm. A small positive interference was reported for PAN (Kok et al., 1978b).
If 03 absorption leads to the formation of H-O^ as reported (Zika and Saltzman,
1982; Heikes et al. , 1982), then 0» is a major interference. There have also
been undocumented reports of a negative interference from SCL.
Perhaps the most promising chemical approach for the measurement of trace
concentrations of H^CL employs the catalytic acitivity of the enzyme, horse-
radish peroxidase (HRP), on the oxidation of organic substrates by H^O,,. This
general method involves three components: a substrate that is oxidizable, HRP,
and \\yQy. Three substrates that have been used are scopoletin (6-methoxy-7-
hydroxy-1,2-benzopyrone), 3-(p-hydroxyphenyl)propionic acid (HPPA), and leuco
crystal violet (LCV). The scopoletin reagent has recently been used in atmos-
pheric analysis. The disappearance of scopoletin fluorescence, upon oxidation
of scopoletin by HJ^?' 1S monitorecl anc' the fluorescence intensity is used to
obtain the concentration of H909 from a calibration curve. The most signifi-
-11
cant advantage of the scopoletin method is the sensitivity (ca. 16 M). The
chief disadvantage of the method is that the concentration of H?CL must be
within a narrow concentration range in order to obtain an accurately measurable
decrease in fluorescence. This limits the usefulness of the technique in
determining unknown H^Op concentrations over several orders of magnitude. With
the leuco crystal violet (LCV) substrate, intensely colored crystal violet is
formed from the reaction of hLCL with LCV, catalyzed by HRP. The absorbance is
measured at 596 nm, where the molar absorption coefficient of crystal violet is
10 M cm , a very high value and an inherent advantage of this method.
Finally, Zaitsu and Ohkura (1980) have tested a number of 4-hydroxy phenyl com-
pounds and found that 3-(p-hydroxyphenyl) propionic acid (HPPA) provided a sen-
sitive and rapid means for determining H?0?. A product is formed that fluo-
resces at 404 nm, and the intensity of this fluorescence is monitored as a func-
tion of HpOp concentration. The detection limit was reported to be 10 mole
HpOp with a test solution of only 0.1 ml volume used. The molar sensitivity
could presumably be improved by the use of large sample volumes.
The enzymatic methods appear to be the most promising colorimetric methods
of H^Op and have considerably greater sensitivity than the methods employing
titanium reagents. However, studies of potential atmospheric interferences
have apparently not been conducted for any of these three substrates.
019GC1/A 1-35 6/29/84
-------
Hydrogen peroxide can be monitored directly in the gas phase by FTIR absorp-
tion at 1250 cm , where the absorption coefficient is 8.4 cm atm at I cm
resolution (Hanst et al., 1981). One FTIR measurement of the possible presence
of 0.070 ppm HpO- was reported during an intense smog episode in Pasadena,
California (Hanst et al. , 1975). Unfortunately, minimum detection limits at
1 km pathlength are degraded to 0.040 ppm because of neighboring absorption
bands of H20 and CH4 (Hanst et al., 1981).
As with 0~, H907 calibration standards are not commercially available and
O tL £
are usually prepared at the time of use. The most convenient method for pre-
paring aqueous samples containing micromolar concentrations of H,,02 1S s^mP^
the serial dilution of commerical grade 30 percent H£02 (Fisher Analytical
Reagent). Techniques for the convenient generation of gas-phase standards are
not available. A technique often used for generating ppm concentrations of
H?0p in air involves the injection of microliter quantities of 30 percent H,^
solution into a metered stream of air that flows into a Teflon bag. Aqueous and
gas-phase samples are then standardized by conventional iodometric procedures
(Allen et al., 1952; Cohen et al., 1967).
Hydrogen peroxide liberates iodine from an iodide solution quite slowly,
but in the presence of a molybdate catalyst the reaction is rapid. The iodine
liberated can be determined by titration with standard thiosulfate at higher
concentrations or by photometric measurement of the tri-iodide ion at low con-
centrations. The molar absorption coefficient of the tri-iodide ion at 350 nm
has been determined to be 2.44 x 10 (Armstrong and Humphreys, 1965). The
stoichiometry is apparently 1 mole of iodine released per mole of H202- How-
ever, definitive studies of the stoichiometry have not been performed for H202
as they have for the iodometric determination of 03-
1.5 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 exposure of individuals; communities; the general
population and those subpopulations in communities that may be
especially susceptible to adverse effects from these oxidants;
natural ecosystems, managed ecosystems such as crops; and nonbiologi-
cal materials such as polymers and paints.
019XX/A 1-36 6/29/84
-------
2. Assessing whether levels of ozone and other photochemical oxidants
in ambient air are within or near the range of concentrations shown
to produce adverse effects in health and welfare effects studies.
3. Determining whether levels of ozone and other photochemical oxidants
are as high indoors as in the ambient air, for the purpose of asses-
sing actual, as opposed to potential, exposures of individuals in
the general population or susceptible subpopulations.
4. Assessing whether non-ozone photochemical oxidants occur in ambient
air at levels within or near the range of concentrations shown to
produce potentially adverse effects in health and welfare effects
studies.
5. Assessing whether concentrations of ozone plus the other photochemical
oxidants together occur at levels sufficient to produce adverse
effects in the general or susceptible subpopulations, or in vegetation
and ecosystems.
6. Evaluating the relationship(s) between ozone and the other photochemi-
cal oxidants, in order to determine whether ozone can function as a
control surrogate in the event that these other, non-ozone photochem-
ical oxidants are found to produce adverse effects on public health
and welfare.
1.5.1 Ozone Concentrations in Urban Areas
The current ozone standard is expressed in terms of a 1-hour value not to
be exceeded on more than 1 day per year. Thus, the second-highest value is a
concentration of significance, since it determines compliance with the standard
and is, thereby, an indicator of exposures having potential health and welfare
significance.
In Chapter 6, the second-highest 1-hour ozone concentrations reported
in each of 4 years have been given for the 80 most populous Standard Metropoli-
tan Statistical Areas (SMSAs) of the United States, i.e., those with popula-
tions > 0.5 million. In Table 1-7, 1982 ozone concentrations for the subset
of SMSAs with 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 measured in 1982 in those
38 SMSAs having populations of at least I million ranged from 0.09 ppm in the
Ft. Lauderdale, Florida, and Seattle, Washington, areas to 0.32 ppm in the Los
Angeles and Riverside, California, areas. The second-highest 1-hour ozone
concentrations for 32 of the 38 SMSAs in Table 1-7 equal or exceed 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
019XX/A 1-37 6/29/84
-------
TABLE 1-7. SECOND-HIGHEST 1-HR OZONE CONCENTRATIONS IN 1982 IN
STANDARD METROPOLITAN STATISTICAL AREAS WITH POPULATIONS
> I MILLION, GIVEN BY CENSUS DIVISIONS AND REGIONS3
Division
and region
SMSA
population,
SMSA millions
Second-highest
1982 03
concn. , ppm
NORTHEAST
New England
Boston, MA
Middle Atlantic Buffalo, NY
Nassau-Suffolk, NY
Newark, NJ
New York, NY/NJ
Philadelphia, PA/NJ
Pittsburgh, PA
SOUTH
South Atlantic
Atlanta, GA
Baltimore, MD
Ft. Lauderdale-Hollywood, FL
Miami, FL
Tampa-St. Petersburg, FL
Washington, DC/MD/VA
>2
1 to <2
>2
1 to <2
>2
>2
>2
>2
>2
1 to <2
1 to <2
1 to <2
>2
0.16
0.11
0.13
0.17
0.17
0.18
0.14
0.14
0.14
0.09
0.14
0.11
0.15
SOUTH
West South
Central
Dallas-Ft. Worth, TX
Houston, TX
New Orleans, LA
San Antonio, TX
>2
>2
1 to <2
1 to <2
0.17
0.21
0.17
0.14
NORTH CENTRAL
East North
Central
Chicago, IL
Detroit, MI
Cleveland, OH
Cincinnati, OH/KY/IN
Milwaukee, WI
Indianapolis, IN
Columbus, OH
>2
>2
1 to <2
1 to <2
1 to <2
1 to <2
1 to <2
0.12
0.16
0.12
0.13
0.13
0.12
0.13
West North
Central
St. Louis, MO/IL
Minneapolis-St. Paul
Kansas City, MO/KS
MN/WI
>2
>2
1 to <2
0.15
0.10
0.10
019XX/A
1-38
6/29/84
-------
TABLE 1-7 (cont'd). SECOND-HIGHEST 1-HR OZONE CONCENTRATIONS IN 1982 IN
STANDARD METROPOLITAN STATISTICAL AREAS WITH POPULATIONS > 1 MILLION
GIVEN BY CENSUS DIVISIONS AND REGIONS3
Division
and region SMSA
WEST
Mountain Denver-Boulder, CO
Phoenix, AZ
Pacific 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
'.MSA Sw,und-hlyh*il
population, 1982 03
millions concn. , ppm
1 to <2
1 to <2
>2
>2
1 to <2
1 to <2
1 to <2
I to <2
1 to <2
I to <2
1 to <2
0.14
0.12
0.32
0.14
0.18
0.21
0.09
0.32
0.14
0.12
0.16
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, SAROAD data file for 1982.
States), in the Gulf Coast area (West South Central states), and on the west
coast (Pacific states). Second-highest 1-hour concentrations in the SMSAs
within each of these three areas averaged 0.15, 0.17, and 0.19 ppm, respectively,
for 1982. 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 11 of the 16 SMSAs in the country with populations >_ 2 million are located in
these areas.
Sources of oxidant precursors are strongly correlated with population
(Chapter 3). In accord with this relationship, three population groups within
the 80 largest SMSAs had the following median values for their collective second-
highest 1-hour ozone concentrations in both 1981 and 1982: populations >^ 2 million,
0.15 ppm 0.,; populations of 1 to 2 million, 0.13 ppm 0,.; and populations of 0.5
C5 «3
to 1 million, 0.12 ppm 0.,.
019XX/A 1-39 6/29/84
-------
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 these stations reported second-highest 1-hour
values > 0.28 ppm (Figure 1-3).
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 equal or exceed levels near those known to
elicit responses. In addition, the number of days of respite between such
multiple-day periods of high ozone is of possible consequence. Data presented
in Chapter 6 show that the probabilities of prolonged exposures to (conse-
cutive days) or respites from (consecutive days) specified concentrations are
location-specific. In Pasadena, CA, a high-ozone area, there is a 42 percent
probability (based on 1979 through 1981 aerometric data) that an ozone concen-
tration of 0.18 ppm, once reached, is likely to persist for 3 days or longer.
Other, lower-ozone areas show lower probabilities of such multiday high ozone
concentrations. These and other data presented demonstrate the occurrence, at
least in some urban areas, of multiple-day exposures to relatively high concen-
trations of ozone.
1.5.2. Trends in Urban and Nationwide Ozone Concentrations
Discussion in Chapter 5 pointed out and substantiated that aerometric
data obtained by potassium iodide methods in earlier years are essentially
concentrations of ozone rather than "total oxidants." Comparison of concen-
trations of "total oxidants" in major urban areas for 1974 and 1975 (U.S. En-
vironmental Protection Agency, 1978) with ozone data for those same urban
areas for 1979 through 1982 (U.S. Environmental Protection Agency, SAROAD
file) shows that the more recent ozone concentrations are in the same general
range for many cities, have declined in some, and are somewhat higher in
others.
Trends in nationwide ozone concentrations, gauged by annual averages at
two subsets of stations reporting data from 1974 through 1981, show declines
of 15 to 20 percent. 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;
019XX/A 1-40 6/29/84
-------
2
g
99.99
0.45
0.40
0.35
0.30
0.25
99 9 99 8
99 98 95 90 80 70 60 50 40 30 20 10 5 21 0.5 0.2 0 1 0.05 0.01
o
2 0.20
O
o
LU
O 0.15
O
0.10
0.05
HIGHEST
2nd HIGHEST
3rd HIGHEST
I II I \/\
0.01 0.050.1 0.2 05 1 2 5 10 20 30 40 50 60 70 80 90 95 98 99 99.899.9 99.99
STATIONS WITH PEAK 1 hour CONCENTRATIONS < SELECTED VALUE, percent
Figure 1-3. Collective distributions of the three highest 1-hour ozone concentrations for 3
years (1979, 1980, and 1981) at valid sites (906 station-years).
-------
and (4) changes in precursor emission rates. When adjustments for the first
two factors are made, a portion of the decrease is real. 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 Chapter 5).
1.5.3. 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 on maximum 1-hour concentrations and
arithmetic mean 1-hour concentrations reveal that maximum (peak) 1-hour concen-
trations at nonurban sites classified as rural (SURE study, Martinez and
Singh, 1979; NAPBN studies, Evans et al., 1982) may exceed the concentrations
observed at nonurban 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. Arith-
metic 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 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.
Comparison of these data with data for nonurban and remote locations
during the 1973-1976 period show that mean concentrations at these various
nonurban locations are not dissimilar. Ranges of concentrations and the
maximum 1-hour concentrations at the NAPBN and SURE sites show the probable
influence, however, of ozone transported from urban areas. In one documented
case, for example, a 1-hour peak ozone concentration of 0.125 ppm at an NAPBN
site in Mark Twain National Forest, Missouri, was measured during passage of
019XX/A 1-42 6/29/84
-------
an air mass whose trajectory was calculated to have included Detroit, Cincinnati,
and Louisville in the preceding hours (Evans et al., 1982).
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 sustain higher ozone con-
centrations than those found in urban areas. Reasons for this phenomenon
include 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. Generally, however, lower ozone concentrations occur in
nonurban areas, as the data in Chapter 6 indicate.
1.5.4. Patterns in Ozone Concentrations
Since the photochemical reactions of precursors that result in ozone for-
mation are driven by sunlight, as well as emissions, the patterns of ozone
occurrence in ambient air depend on daily and seasonal variations in sunlight
intensity. The typical diurnal pattern of ozone in ambient air has a minimum
ozone level around sunrise (near zero in most urban areas), increasing through
the morning to a peak concentration in early afternoon, and decreasing toward
minimal levels again in the evening. 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 in
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 trans-
ported from an upwind area where high ozone levels have occurred earlier in the
day. As documented in Chapter 6, secondary peak concentrations may be higher
than concentrations resulting from the photochemical reactions of locally emit-
ted 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 succes-
sive 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).
019XX/A 1-43 6/29/84
-------
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
concentrations to occur outside the two quarters of highest average ozone
concentrations (cf. data for Tucson, Arizona, and data for the California
sites given in Chapter 6). Exceptions to seasonal patterns are important consi-
derations 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.
As data for different averaging times clearly demonstrate, averaging smooths
out and submerges the occurrence of peak concentrations. 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 expo-
sure that elicits untoward responses.
Certain spatial variations in ozone concentrations occur that are general-
ly of little consequence in exposure assessment. For example, ozone concentra-
tions increase with increasing altitude (e.g., Viezee and Singh, 1981). 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.
Spatial variations on a smaller scale assume more importance relative to
exposure assessment. Indoor-outdoor gradients in ozone concentrations are
known to occur even in structures ventilated by fresh air rather than air
conditioning (e.g., Sabersky et al., 1973; Thompson et al., 1973). Ozone
019XX/A 1-44 6/29/84
-------
reacts with surfaces inside buildings, so that decay occurs fairly rapidly.
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 composition of
interior surfaces all affect indoor ozone concentrations. Ratios (I/O) in the
literature thus vary from 80 ± 10 percent (Sabersky et al., 1973) in an air-
conditioned office building (but with 100 percent outside air intake) to 10 to
25 percent in air-conditioned residences (Berk et al., 1981).
On a larger scale, within-city variations in ozone concentrations can
occur, despite the commonly accepted maxim that ozone is a regional pollutant.
Data in Chapter 6 show, for example, relatively homogeneous ozone concentrations
in New Haven, Connecticut (U.S. Environmental Protection Agency, SAROAD files),
which is a moderately large city downwind of a reasonably well-mixed urban plume
(Cleveland et al., 1976). In a large metropolis such as New York City, however,
appreciable gradients in ozone concentration can exist from one side of the
city to the other (Smith, 1981). Such gradients must be taken into considera-
tion in exposure assessments.
1.5.5 Concentrations and Patterns of Other Photochemical Oxidants
1.5.5.1 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 Chapter 6 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 concentration data
have been presented are formic acid, peroxyacetyl nitrate (PAN), peroxypropionyl
nitrate (PPN), and hydrogen peroxide. Peroxybenzoyi nitrate has not been
clearly identified in ambient air in the United States.
Recent data indicate the presence in urban atmospheres of only trace
amounts of formic acid (5 15 ppb, measured by FTIR). 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).
019XX/A 1-45 6/29/84
-------
The measurement methods (IR and GC-ECD) for PAN and PPN are specific and
highly sensitive, and have been in use in air pollution research for nearly
two decades. Thus, the more recent literature on the concentrations of PAN
and PPN confirm and extend, but do not contradict, earlier findings reported
in the two previous criteria documents for ozone and other photochemical
oxidants (U.S. Department of Health, Education, and Welfare, 1970; U.S. Environ-
mental Protection Agency, 1978).
Concentrations of PAN have been reported in the air pollution literature
from about 1960 through the present. The highest concentrations reported over
this extended period were those found in the 1960s 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 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 recently measured PAN concentrations in
the Los Angeles Basin were in the range of 10 to 20 ppb. Average concentrations
of PAN in the Los Angeles Basin in the past 5 years ranged from 4 to 13 ppb
(Tuazon et al., 1981a; Grosjean, 1981; respectively). Only one published report
covering PAN concentrations outside California in the past 5 years is that of
Lewis et al. (1983) for New Brunswick, New Jersey. The average PAN concentra-
tion was 0.5 ppb and the maximum was 11 ppb during a study done there from Septem-
ber 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).
Reports of PPN concentrations appear in the literature from about 1963
through the present. The highest PPN concentration reported in early studies
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 concentrations at respective
sites ranged from 0.07 ppb in Pittsburgh, Pennsylvania, in 1981 (Singh et al.,
019XX/A 1-46 6/29/84
-------
1982) to 3.1 ppb at Staten Island, New York (Singh et a!., 1982). California
concentrations fell within this range. Average PPN concentrations at the respec-
tive 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,,02) concentrations have been reported
to range from < 0.5 ppb in Boulder, Colorado (Heikes et al., 1982) to < 180 ppb
in Riverside, California (Bufalini et al., 1972). In nonurban areas, reported
concentrations ranged from 0.2 ppb near Boulder, Colorado, in 1978 (Kelly
et al., 1979) to < 7 ppb 54 km southeast of Tucson, Arizona (Farmer and Dawson,
1982). These nonurban data were obtained by the luminol chemiluminescence
technique (see Chapter 5). The urban data were obtained by a variety of
methods, including the luminol chemiluminescence, the titanium (IV) sulfate
8-quinolinol, and other wet chemical methods (see Chapter 5).
The higher concentrations of H^O,, reported in the literature must be
regarded as especially problematic, since FTIR measurements of ambient air
have not demonstrated unequivocally the presence of H?0? 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 (Chapter 5); FTIR is capable of
measuring concentrations of H^O^ if it is present above the limit of detection.
1.5.5.2 Patterns. The patterns of formic acid (HCOOH), PAN, PPN, and HLO-
may be summarized fairly succinctly. They bear qualitative but not quantita-
tive resemblance to the patterns already summarized for ozone concentrations.
Qualitatively, diurnal patterns are similar, 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 the work of
Tuazon et al. (1981) at Claremont, California, demonstrates, ozone concentra-
tions return to baseline levels faster than the concentrations of PAN, HCOOH,
or H202 (PPN was not measured). The diurnal patterns of PAN were reported in
earlier criteria documents. Newer data merely confirm those patterns.
019XX/A 1-47 6/29/84
-------
Seasonally, winter concentrations (third and fourth quarters) of PAN are
lower than summer concentrations (second and third quarters). The winter
concentrations of PAN are proportionally higher, however, than the winter
concentrations of ozone; i.e., PAN-to-ozone ratios are higher in winter. Data
are not readily available on the seasonal patterns of the other non-ozone oxi-
dants.
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 for the
other non-ozone oxidants.
1.5.6 Relationship Between Ozone and Other Photochemical Oxidants
The relationship between ozone concentrations and the concentrations of
PAN, PPN, H202, and HCOOH is important only if these non-ozone oxidants are
shown to produce adverse health or welfare effects, singly, in combination
with each other, or in various combinations with ozone. If only ozone is
shown to produce adverse health or welfare effects, then only ozone needs to
be controlled. If any or all these other four oxidants is shown to produce
adverse health or welfare effects, then it, or they, will also have to be
controlled. Since ozone and all four of the other oxidants arise from reac-
tions 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 of this report document what is known about the
welfare effects of PAN (see Sections 1.6 through 1.8). No data are available
regarding the possible welfare effects of HCOOH, H202, or PPN. Chapters 10
through 13 document what is known about the health effects of PAN and H202
(see Sections 1.10 through 1.13). Formic acid is not covered because of
extremely limited aerometric data and no health effects data pertinent to the
trace quantities of formic acid measured in the ambient air. No health effects
data are available for PPN. One report that PBzN is a potent lachrymator is
not discussed in the health effects chapters since no reliable data indicate
its presence in ambient air, even in high-oxidant areas. The health effects
data reported in Chapter 10 on H202 show that all levels tested to date are
orders of magnitude above even the highest concentrations reported for ambient
019XX/A 1-48 6/29/84
-------
air; and, as noted above, the highest concentrations reported for ambient air
are not strongly documented. Thus, the brief discussion below focuses on the
relationship between ozone and PAN concentrations 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-0_ and, indirectly, of PAN-to-PPN ratios presented in the review of
Altshuller (1983) and summarized in Chapter 6. Ratios of PAN concentrations
to ozone concentrations, as derived by Altshuller (1983), show that PAN-to-peak
03 ratios vary from 1 to 12 across the country (PAN at time of CL peak);
ratios for average PAN to average 0_ concentrations vary from 2 to 20 across
the country. The correspondence between PAN and ozone concentrations is not
exact but is similar for most locations at which both pollutants have been
measured concurrently. Disparities between locations point up the lack of a
consistent quantitative relationship. Likewise, disparities between the ratio
of the average concentrations of the two pollutants 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 ozone and PAN. Not only are ozone-PAN 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 ratio 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 measured concurrently at three separate monitoring sites
in the same city. 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) demonstrated that PAN-to-03
ratios are considerably lower in nonurban than in urban areas. Thompson et al.
(1973) showed that PAN persists longer than ozone indoors. (This is to be
expected from its lower reactivity with surfaces and 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
019XX/A 1-49 6/29/84
-------
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).
Altshuller (1983) prepared for the U.S. Environmental Protection Agency a
comprehensive review and analysis of concentrations and relationships for
ozone and other smog components, including PAN. The smog components he reviewed
relative to ozone included aldehydes, aerosols, and nitric acid, as well as
the non-ozone oxidants covered in this chapter. It must be emphasized that
Altshuller examined the issue of whether ozone could serve as an abatement
surrogate for all photochemical products, not just oxidants and not just the
subset of photochemical oxidants of concern in this document. His conclusion
was that "the ambient air measurements indicate that ozone may serve direction-
ally, but cannot be expected to serve quantitatively, as a surrogate for the
other products" (Altshuller, 1983). He found a greater correspondence between
aldehydes and their organic precursors than between aldehydes and ozone. He
found also that the correspondence between ozone and PAN concentrations (as well
as PPN, H?02, and HCOOH) is greater by far than the ozone-aldehyde relationship.
In summary, the significance for public health or welfare of the imposition
of an additional oxidant burden from non-ozone oxidant rests on the answers to
three basic questions:
1. Do PAN, PPN, H202, or HCOOH, singly or in combination, elicit adverse
or potentially aaverse responses?
2. Do any or all of these non-ozone oxidants act additively or synergistically
in combination with ozone to elicit adverse or potentially adverse
responses? Do any or all act antagonistically with ozone?
3. Do the time course and magnitude of the concentrations of these non-ozone
oxidants parallel the time course and magnitude of ozone concentrations
in the ambient air?
Given the information on health and welfare effects presented in subsequent
chapters, coupled with the aerometric data presented in Chapter 6, the relation-
ship between ozone and PAN concentrations is the specific relationship of most
concern in this document.
019XX/A 1-50 6/29/84
-------
1.6 EFFECTS OF OZONE AND PEROXYACETYL NITRATE ON VEGETATION
1.6.1 EFFECTS OF OZONE ON VEGETATION
1.6.1.1 Introduction. Foliar injury to vegetation is one of the earliest and
most obvious manifestations of ozone injury to vegetation. The effects of ozone
are not limited, however, to visible injury. Although plant foliage is the pri-
mary site of injury, secondary effects from ozone can occur. They include re-
duced plant growth of both roots and foliage, decreased yield, changes in crop
quality, and alterations in susceptibility to biotic and abiotic stresses.
Ozone exerts a phytotoxic effect only if a sufficient amount reaches the
sensitive cellular sites within the leaf. Ozone diffuses from the ambient
air into the leaf through the stomata, which can exert some control on ozone up-
take, to the active sites within the leaf. Ozone injury will not occur (1) if
the rate of ozone uptake is low enough that the plant can detoxify or metabolize
ozone or its metabolites; or (2) if the plant is able to repair or compensate for
the effects of ozone (Tingey and Taylor, 1982). This is analogous to the response
of plants to sulfur dioxide (S02) (Thomas et al., 1950). Cellular disturbances
that are not repaired or compensated for are ultimately expressed as visible
injury to the leaf or as secondary effects that can be expressed as reduced root
growth, reduced yield of fruits or seeds, or both.
Plant growth and yield are the end products of a series of biochemical and
physiological processes related to uptake, assimilation, biosynthesis, and
translocation. Sunlight drives those processes that convert carbon dioxide into
the organic compounds (photosynthesis) necessary for plant growth and development.
The mineral nutrients and water necessary for plant growth are extracted by the
plant from the soil. Plant organs then convert these raw materials into a wide
array of compounds required for plant growth and yield. A disruption or reduc-
tion 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: (1) if it directly affected the plant process that
was limiting plant growth; or (2) if it affected another step sufficiently such
that this process became the step limiting plant growth (Tingey, 1977). Conversely,
ozone will not limit plant growth if the process affected is not or does not
become rate-limiting. This implies that not all the effects of ozone on plants
are reflected in growth or yield reductions. This also suggests that there are
combinations of ozone concentration and exposure duration that the plant can
experience that will not result in visible injury or reduced plant growth and
019XX/A 1-51 6/29/84
-------
yield. Indeed, numerous studies have demonstrated combinations of concentration
and time that did not cause a significant detectable effect on plant growth or
yield.
Ozone induces a diverse range of effects on plants and plant communities.
These effects are usually classified as either injury or damage. Injury
encompasses all plant reactions such as reversible changes in plant metabolism
(e.g., altered photosynthesis), leaf necrosis, altered plant quality, or
reduced growth that do not impair yield or intended use of the plant
(Guderian, 1977). In contrast, damage or yield loss includes all effects that
reduce the intended use or the value of the plant, such as a reduction in the
quantity or in aesthetic value; or any impairment in the intended use of the
plant. 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 it is not always classi-
fied as damage, the occurrence of foliar injury is an indication that phytotoxic
concentrations of ozone are present. In areas displaying foliar injury, addi-
tional studies should be conducted to assess the risk of ozone to vegetation and
to determine if the intended use or value of the plants is being impaired.
1.6.1.2 Limiting Values of Plant Response. Several approaches have been used
to estimate the ozone concentrations and exposure durations that induce foliar
injury. Most of these studies have used short-term exposures (less than 1 day)
and have measured visible injury as the response variable. In one approach to
estimating the concentrations and durations that would induce specific amounts
of visible injury, plants were exposed to a range of ozone concentrations and
exposure durations and the resulting data were evaluated by regression analysis
(Heck and Tingey, 1971). Data for several species were summarized to illustrate
the range of concentrations required to induce foliar injury (5 and 20 percent)
on sensitive, intermediate, and less sensitive species (Table 1-8).
An alternative approach for estimating the ozone concentrations and exposure
durations that induce foliar injury is to use limiting-value analysis (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 are
likely to induce foliar injury (U.S. Environmental Protection Agency, 1978).
019XX/A 1-52 6/29/84
-------
TABLE 1-8. OZONE CONCENTRATIONS FOR SHORT-TERM EXPOSURES THAT PRODUCE 5 OR 20
PERCENT INJURY TO VEGETATION GROWN UNDER SENSITIVE CONDITIONS3
Exposure
time, hr
0.5
1.0
2.0
4.0
8.0
Sensitive plants
0.35 to 0.50
(0.45 to 0.60)
0.15 to 0.25
(0.20 to 0.35)
0.09 to 0.15
(0.12 to 0.25)
0.04 to 0.09
(0.10 to 0.15)
0.02 to 0.04
Intermediate plants
0.55 to 0.70
(0.65 to 0.85)
0.25 to 0.40
(0.35 to 0.55)
0.15 to 0.25
(0.25 to 0.35)
0.10 to 0.15
(0.15 to 0.30)
0.07 to 0.12
Less
sensitive plants
SO. 70 (0.85)
£0.40 (0.55)
£0.30 (0.40)
£0.25 (0.35)
£0.20 (0.30)
The concentrations in parenthesis are for the 20% injury level. Table from
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
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 both approaches estimate concentrations and exposure
durations that might induce visible injury but that they cannot be used to pre-
dict impacts on crop yield or intended use. It should also be emphasized that
both approaches are still considered valid.
The concept of limiting values has also been used to estimate the ozone
concentrations 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 the appraoch of Jacobson (1977)
(Figure 1-4). In Figure 1-4 the line bounds mean ozone concentrations and ex-
posure durations below which effects on plant growth and yield were not detected.
019XX/A 1-53 6/29/84
-------
1.0
OL
a
O
LU
O
I
Z
O
N
O
0.1
0.01
1 I I I I 1111
21D 11Q
\ 44 • 19O18 *45 *46 •48-52
10
XO24 ' *" Q31 7QQ20
\ J514 30 59
• •42430Q9
* 1213 41 ,
\ 26 '
\ 1C* CD29
\ 39
\
33
34-
53
EXPOSURE, hr/day
A < 1.99
D 2 TO 3.99
O 4 TO 5.99
• 3* 6
IMOS. = REF. NOS. ON TABLE 11-4
I I II I I I I I I I I II
57
8 10
20 40 60 80 100
EXPOSURE PERIOD, days
200
400
Figure 1-4. Relationship between O3 concentration, exposure dura-
tion, and a reduction in plant growth or yield (see Table 7-18; also
U.S. EPA, 1978).
Source: U.S. Environmental Protection Agency (1978).
1-54
-------
This graphical analysis used data from both greenhouse and field studies and
indicates that the lower limit for reduced plant performance is a mean ozone
concentration of 0.05 ppm for several hours per day for exposure periods greater
than 16 days. The 03 response threshold increases to about 0.10 ppm at 10 days
and to about 0.30 ppm at 6 days.
1.6.1.3 Methods for Determining Ozone Yield Losses. Diverse experimental
procedures have been used to study the effects of ozone on plants, including
studies under highly controlled conditions, exposures in open-top chambers, and
field exposures without chambers. In general, the more controlled conditions
are most appropriate for investigating specific responses and for providing
the scientific basis for interpreting and extrapolating results. These systems
are powerful tools by which to gain increased understanding of the biological
effects of air pollutants. To assess the impact of ozone on plant yield, however,
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 03 (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 eco-
nomic 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 0-; and
3. To advance the understanding of the cause and effect relation-
ships 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 at these sites approximate typical agronomic practices and
open-top field exposure chambers are used to minimize perturbations of the plant
environment during the exposure. The investigators involved have attempted to
019XX/A 1-55 6/29/84
-------
use realistic 03 concentrations and sufficient replication to permit the develop-
ment of exposure-response models. The data have been analyzed using regression
approaches. The exposures are characterized by a 7-hr (9:00 a.m. to 4:00 p.m.)
seasonal mean 03 concentration. This is the time period during which 0, is added
to the exposure chambers.
1.6.1.4 Estimates of Yield Loss. Studies, frequently using open-top exposure
chambers, have been conducted to estimate the effects of 03 on the yield of
various crop species. These studies can be grouped into two types, depending
on the experimental design and statistical methods used to analyze the data:
(1) studies in which predictive equations relating 03 exposure to plant
response were developed; and (2) studies in which discrete treatment levels were
compared to a control. The advantage of the regression approach is that exposure-
response models can be used to interpolate results between treatment levels.
Both types of experimental design, however, provide useful data for determining
the effects of 03 on plants.
In the NCLAN studies, ozone was added to either charcoal-filtered or ambient
air to create the range of 03 concentrations that is required when the regression
approach is used to estimate Og-induced yield loss. In summarizing the data, 03~
induced yield loss was derived from comparing performance of 0_-exposed plants
to that of plants in charcoal-filtered air. Various regression techniques have
been used to derive exposure-response functions. The use of regression approaches
permits the estimation of the effects of 03 on plant yield over the range of con-
centrations, not just at the treatment means, as is the case with analysis of
variance methods. Examples of graphs of exposure-response equations and the data
used to derive them show the fit of the various models to the experimental data
(Figure 1-5).
Linear regression equations have been used to estimate yield loss but for
some species and cultivars there appear to be systematic deviations from the
2
data even though the equations had high coefficients of determination (r ).
The use of plateau-linear or polynomial equations appeared to fit the data
better. More recently, a Weibull model has been used that yields a curvilinear
response line providing a reasonable fit to the data. This model has also been
used to develop yield response equations, combining the responses for several
cultivars of a species (Figure 1-6). Statistical analysis indicates that for
most crops the model fits the combined data, as well as the data for the indivi-
dual cultivars. Yield losses for some major crop species were estimated
using the combined models. It appears that 03 affects the yield of corn and
wheat much less than it does the yields of cotton, soybeans, and peanuts.
019XX/A 1-56 6/29/84
-------
CO
lj>
3000
2500
2000
1500
1000
1 \
CORSOY SOYBEAN
(A)
Y = 3099.3 -15135.0 ±03 R2 = .975
I I I I
0.00 0.05 0.10 0.15
O3 CONCENTRATION, ppm
0.20
160
^ 120
JS
.0.
"
80
Q
O
a.
40
PEANUT (NC-6)
RALEIGH, 1980
(B)
1. Y = 173-1046 + 03 R2 = .96
2. Y = 142.3 IF 03^.037
Y= 184.6-1160 ± 03 IF 03 >.037 R2 = .99
I I I
0.00 0.05 0.10 0.15
O3 CONCENTRATION, ppm
0.20
X
O
UJ
a
Hi
Ul
v>
260
240
220
200
180
160
OJ
I I
CORN (COKER 16)
RALEIGH, 1976
Y = 222.91 + 331.11 ± 03-3511.99 ± 032
Y = 247.8 - 260 ± 03 R2 = .65
J_
I
I
00 0.05 0.10 0.15
O3 CONCENTRATION, ppm
0.20
_CD
_a
"Si
Q
u
m
CO
WINTER WHEAT (HOLLY)
RALEIGH, 1977
- (D)
1. Y = 4.5333 + 19.31 ± 03-215.1 ± 032
2. Y = 5.7 16 + 03 R2 = .82
3. Y = 4.9 IF 03 < .087
Y = 8.2 - 38 ± 03 IF 03 > .087 R2 = .99
I
I
0.00 0.05 0.10 0.15 0.20
O3 CONCENTRATION, ppm
Figure 1-5. Examples of effects of O3 exposure on yield of various plants. O3
concentration (ppm) is expressed as 7-hr seasonal mean. Soybean (A) data from
Kress and Miller (1983); peanut (B) data from Heagle et al., (1983) and Heck et
a!., (1982); corn (C) and wheat (D) data from Heagle and Heck (1980) and Heck et
al., (1982).
1-57
-------
1.0
01
g 0.8
(0
LU
oc
111
> 0.6
g
QC
O 0.4
Q.
O
OC
Q.
0.2
0.0
WHEAT
SOYBEANS
PEANUTS
0.0
0.02 0.04 0.06 0.08
O3 CONCENTRATION, ppm
0.10
Figure 1-6. Relative O3-induced yield reduction of selected crops
as predicted by the Weibull model (Heck et al., 1983).
1-58
-------
The yield response models can be used to estimate the 0, concentrations
that induce losses (e.g., 10 and 30 percent losses) in various plant species and
cultivars (Table 1-9). In general, when several models were fit to the data they
tended to predict similar concentrations that induced yield losses. In the case
of corn, turnip, and winter wheat, however, the linear model tended to underesti-
mate the 0- concentrations that would cause 10 or 30 percent yield reductions.
The similarity among the estimated concentrations for a given cultivar suggests
that the predicted values are influenced to a greater extent by the original
data than by the model used to describe the data. A brief review of the data
(Table 1-9) indicates that for several species, mean yield reductions of 10 per-
cent were predicted when the 7-hr seasonal mean 0~ concentration exceeded 0.04
to 0.05 ppm.
In addition to the studies in which regression approaches were used,
various other approaches have been used to investigate the effects of 0~
treatments that were different from the control, rather than to develop
exposure-response equations. In general, these data were analyzed using
analysis of variance. Table 1-10 summarizes concentrations of 0., reported to
produce a loss of 10 percent in the yield of a number of crops. To summarize
the data from studies that used discrete treatments, the lowest 0_ concentration
that significantly reduced yield was determined from the analyses of the authors
(Table 1-10). 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 level. 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 weeks generally caused
significant yield reductions. Although it appears from this analysis that a
higher 0- concentration was required to cause an effect than 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 1-10) the 0.10 ppm concentration frequently induced
mean yield losses of 10 to 50 percent.
The data from the previous criteria document (U.S. Environmental Protection
Agency, 1978) were used to develop limiting values that suggested that 0_ concen-
trations of 0.04 to 0.06 ppm for 4 hours or more were likely to injure plant
foliage. The growth data summarized in that document indicated that plant growth
and yield can be reduced at 0- concentrations of 0.05 to 0.08 ppm for several
019XX/A 1-59 6/29/84
-------
TABLE 1-9. SEASONAL 7-hour OZONE CONCENTRATIONS (ppra) AT WHICH YIELD
LOSSES OF 10 PERCENT OR 30 PERCENT ARE PREDICTED FROM EXPOSURE-RESPONSE MODELS
i
en
o
Plants
Grains/Seeds
Soybean
(Corsoy)
(Corsoy)
(Davis)
(Davis)
(Essex)
(Hodgson-F)*
(Hodgson-P)*
(Williams)
Peanut - 1979+
Peanut - 1980
Peanut - 1980
Peanut - 1980
Kidney bean
Kidney bean
Field Corn
(Coker 16)
(Coker 16)
(Coker)
(PAG 397)
(Pioneer 3780)
Winter wheat
(Blueboy II)
(Blueboy II)
(Blueboy II)
(Coker 47-27)
(Coker 47-27)
(Coker 47-27)
(Holly)
(Holly)
(Holly)
(Holly)
Model
Kg/ha = 3099.3 - 15135 x 03
g/plant = 15.6 exp [-(03/0.129)1'70]
seed wt/« = 534.5 - 3988. 6x03-H0960xO§
g/plant = 31.1 exp [-(03. 0.129)0'91]
g/plant = 18.7 exp [-(03/0.309)0'76]
g/plant = 15.2 exp [-(03/0.207)0' so]
g/plant = 15.5 exp [-(Og/O.lSS)1'57]
g/plant = 19.4 exp [-03/0. 243)°' 94]
pod wt/plant = 112 - 563 x 03
pod wt/plant = 173 - 1046 x 03
pod wt/plant = 142.3 if 03 £ 0.037;
if 03 > 0.037 PW/P = 184.6 - 1160 x 03
g/plant - 148 exp [-(03/0.186)3'20]
seed wt/plant = 17.44 - 35.51 x 0,
g/plant = 16.5 exp [-(03/0.287)1-"]
g/plant 247.8 - 260 x 03
g/plant = 222.91-t-331.ll x 03-
3511.99 x 0§
g/plant = 240 exp [-(03/0.221)4'46]
g/plant = 166 exp [-(03/0.160)4'28]
g/plant = 149 exp [-(03/0.155)3' J1]
g/plant = 6.6 - 18 x 03
g/plant = 5.908 + 3.958 x 03 -
137.7 x 0§
g/plant = 5.88 exp [-(03/0.175)3'22]
g/plant = 5.8 - 21 x 03
g/plant = 5.765 - 18.79 x 03 -
20.00 x 0§
g/plant 5.19 exp - [-(03/0. 171)2'06]
g/plant = 5.7 - 16 x 03
g/plant = 4.533 + 19.31 x 03-
215.1 x 0§
g/plant = 4.95 exp [-(03/0. 1564'95]
g/plant = 4.9 if x S 0.087
if 03 > 0.087 g/p =8.2 -38 03
Control 03
Concentration
0.022
0.022
0.025
0.025
0.014
0.017
0.017
0.014
0.026
0.025
0.025
0.025
0.025
0.025
0.02
0.02
0.02
0.15
0.15
0.03
0.03
0.03
0.03
0.03
0.03
0.03
0.03
0.03
0.03
Yield
10%
0.040
0.043
0.038
0.038
0.037
0.039
0.043
0.038
0.043
0.039
0.049
0.046
0.072
0.086
0.113
0.132
0.133
0.095
0.075
0.063
0.0187
0.088
0.055
0.055
0.064
0.063
0.095
0.099
0.100
Loss
30%
0.077
0.076
0.070
0.071
0.109
0.096
0.084
0.098
0.078
0.067
0.073
0.073
0.165
0.164
0.300
-
0.175
0.126
0.111
0.131
0.129
0.127
0.104
0.103
0.107
0.128
0.129
0.127
0.126
Reference
Kress and Miller, 1983
Heck et al., 1983
Heagle et al . , 1983
Heck et al. 1983
Heck et al. 1983
Heck et al. 1983
Heck et al. 1983
Heck et al. 1983
Heagle et al. , 1983
Heagle et al . , 1983
Heck et al . , 1982
Heck et al . , 1983
Kohut and Lawrence, 1983
Heck et al., 1983
Heck et al. , 1982
Heagle & Heck, 1980
Heck et al . , 1983
Heck et al., 1983
Heck et al . , 1983
Heck et al . , 1982
Healge and Heck, 1980
Heck et al . , 1983
Heck et al. , 1982
Heagle and Heck, 1980
Heck et al., 1983
Heck et al., 1982
Heck et al., 1982
Heck et al . , 1983
Heck et al., 1982
-------
TABLE 1-9. SEASONAL 7-hour OZONE CONCENTRATIONS (ppra) AT WHICH YIELD
LOSSES OF 10 PERCENT OR 30 PERCENT PREDICTED FROM EXPOSURE-RESPONSE MODELS (continued)
cr,
Plants
(Oasis)
(Oasis)
(Oasis)
Cotton
Root Crops
Turnip
(Just Right)
(Just Right)
(Just Right)
(Purple Top
White Globe)
(Purple Top
White Globe)
(Purple Top
White Globe)
(Shogoin)^
(Shogoin)
(Tokyo Cross)
(Tokyo Cross)
(Tokyo Cross)
Foliage Crops
Lettuce
Lettuce
Spinach
(America)
(Winter
Bloomsdale)
(Winter
Bloomsdale)
(Hybrid 7)
(Hybrid 7)
(Viroflay)
(Viroflay)
Model
g/plant = 4.9 - 12 x 03
g/plant = 4.475 + 3.320 x 03 -
93.49 x 0§
g/plant = 4.88 exp [-(03/0. 186)3'20]
g/plant = 41.5 exp [-(03/0. 197)1' 12]
edible rt wt/plant = 12.9 - 94 x 03
edible rt wt/plant = 10.7 if 03 SO. 038
if 03 > 0.038 = 15.5 - 127 x 03
g/plant = 10.89 exp [-(03/0.090)3'05]
edible rt wt/plant = 7.2 - 49 x 03
edible rt wt/plant = 6.0 if 03 SO. 034
if > 0.034 ERW/P =8.1 -60 x 03
g/plant = 6.22 exp [-(03/0.095)2' S1]
edible rt wt/plant = 5.3 - 36 x 03
g/plant = 4.68 exp (-(03/0.096)2- 12]
edible rt wt/plant = 18.1 - 116 x 03
edible rt wt/plant = 14.8 if 03 S 0.054
if 03 > 0.054 ERW/P = 27.0 - 226 x 03
g/plant = 15.25 exp [-(03/-.094)3'94]
fresh hd wt/plant = 1065.7 - 5978 x 03
g/plant = 1245 exp [-(03/0.098)1- 22]
g/plant =22.7 - 106 03
if 03 > 0.087 g/p =8.2 -38 03
g/plant = 23.3 - 121 x 03
g/plant = 20.8 exp [-(03/0.127)2-°7]
g/plant = 42.1 - 193 x 03
g/plant = 36.6 exp [-(03/0. 139)2' 68]
g/plant = 46.1 - 238 x 03
g/plant = 41.1 exp [-(O-j/0.129)1' "]
Control 03
Concentration
0.03
0.03
0.03
0.018
0.014
0.014
0.014
0.014
0.014
0.014
0.014
0.014
0.014
0.014
0.014
0.043
0.043
0.024
0.024
0.024
0.024
0.024
0.024
0.024
Yield
10*
0.068
0.088
0.093
0.041
0.026
0.046
0.043
0.027
0.045
0.040
0.027
0.036
0.028
0.061
0.053
0.057
0.053
0.043
0.041
0.049
0.043
0.060
0.041
0.048
Loss
30%
0.143
0.138
0.135
0.092
0.051
0.063
0.064
0.054
0.065
0.064
0.054
0.060
0.057
0.074
0.072
0.084
0.075
0.081
0.075
0.080
0.082
0.095
0.075
0.080
Reference
Heck et al.
Heagle and
Heck et al.
Heck et al.
Heck et al.
Heck et al.
Heck et al.
Heck et al .
Heck et al.
Heck et al.
Heck et al.
Heck et al.
Heck et al.
Heck et al.
Heck et al.
Heck et al.
Heck et al .
Heck et al.
Heck et al.
Heck et al.
Heck et al .
Heck et al.
Heck et al.
Heck et al.
, 1982
Heck, 1980
, 1983
, 1983
, 1982
, 1982
, 1983
, 1982
, 1982
, 1983
, 1982
, 1983
, 1982
, 1982
, 1983
, 1982
, 1983
, 1982
, 1982
, 1983
, 1982
, 1983
, 1982
, 1983
*The Hodgson data were obtained from two designs in 1981; a full harvest (F) and a partial plot harvest (P),
where some plants were removed prior to harvest.
*This model did not fit the data well and tended to underestimate the 03 concentrations which cause yield losses.
-------
TABLE 1-10. OZONE CONCENTRATIONS AT WHICH SIGNIFICANT YIELD LOSSES HAVE BEEN NOTED FOR A VARIETY OF
PLANT SPECIES EXPOSED TO 03 UNDER VARIOUS EXPERIMENTAL CONDITIONS
i
01
IX)
Plant species
Alfalfa
Alfalfa
Pasture grass
Ladino clover
Soybean
Sweet corn
Sweet corn
Wheat
Radish
Beet
Potato
Pepper
Cotton
Carnation
Coleus
Begonia
Exposure duration
Yield reduction,
% of control
03 concentration,
ppm
Reference
7 hr/d, 70 d
2 hr/d, 21 d
4 hr/d, 5d/wk, 5 wk
6 hr/d, 5 d
6 hr/d, 133 d
6 hr/d, 64 d
3 hr/d, 3 d/wk, 8 wk
4 hr/d, 7 d
3 hr
2 hr/d, 38 d
3 hr/d, every 2 wk, 120 d
3 hr/d, 3 d/wk, 11 wk
3 hr/d, 2 d/wk, 13 wk
24 hr/d, 12 d
2 hr
4 hr/d, once every 6 d for
a total of 4 times
51, top dry wt 0.10
16, top dry wt 0.10
20, top dry wt 0.09
20, shoot dry wt 0.10
55, seed wt/plant 0.10
45, seed wt/plant 0.10
13, ear fresh wt 0.20
30, seed yield 0.20
33, root dry wt 0.25
40, storage root dry wt 0.20
25, tuber wt 0.20
19, fruit dry wt 0.12
62, fiber dry wt 0.25
74, no of flower buds 0.05-0.09
20, flower no. 0.20
55, flower wt 0.25
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
Actedipe and Ormrod, 1974
Ogata and Maas, 1973
Pel 1 et al., 1980
Bennett et al., 1979
Oshima et al., 1979
Feder and Campbel1, 1968
Adedipe et al., 1972
Reinert and Nelson, 1979
Ponderosa pine
6 hr/d, 126 d
21, stem dry wt
0.10
Wilhour and Neely, 1977
-------
TABLE 1-10. OZONE CONCENTRATIONS AT WHICH SIGNIFICANT YIELD LOSSES HAVE BEEN NOTED FOR A VARIETY OF
PLANT SPECIES EXPOSED TO 03 UNDER VARIOUS EXPERIMENTAL CONDITIONS (continued)
1
en
CO
Plant species
Western white
pine
Loblolly pine
Pitch pine
Poplar
Hybrid poplar
Hybrid poplar
Red maple
American
sycamore
Sweetgum
White ash
Green ash
Willow oak
Sugar maple
Exposure duration
6
6
6
12
12
8
8
6
6
6
6
6
6
hr/d,
hr/d,
hr/d,
hr/d
hr/d
hr/d,
hr/d,
hr/d,
hr/d,
hr/d,
hr/d,
hr/d,
hr/d,
126 d
28 d
28 d
, 5 mo
, 102 d
5 d/wk, 6 wk
6 wk
28 d
28 d
28 d
28 d
28 d
28 d
Yield reduction,
% of control
9,
18,
13,
stem dry wt
height
height
growth
growth
+1333, leaf abscission
58,
50,
37,
9,
29,
17,
24,
19,
12,
height
shoot
height
height
height
total
height
height
height
growth
dry wt
growth
growth
growth
dry weight
growth
growth
growth
03 concentration,
ppm Reference
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
0.
10
05
10
041
15
15
25
05
10
15
10
15
15
Wilhour and Neely
Wilhour and Neely
Wilhour and Neely
Wilhour and Neely
Patton, 1981
Patton, 1981
, 1977
, 1977
, 1977
, 1977
Dochinger and Townsend, 1979
Kress and Skelly,
Kress and Skelly,
Kress and Skelly,
Kress and Skelly,
Kress and Skelly,
Kress and Skelly,
1982
1982
1982
1982
1982
1982
-------
hours per day. These concentrations are similar to the concentrations (0.04
to 0.07 ppm) shown in this document to reduce plant yield in field studies
(using various approaches) and in ambient air studies.
1.6.1.5 Effects on Crop Quality. Although only a few studies have been
reported, 0,. can also 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 a!., 1977); and increased reducing sugars in potatoes,
which are associated with undesirable darkening when potatoes are used to make
potato chips (Pell et al., 1980).
1.6.1.6 Yield Loss from Ambient Exposures. Of the studies done to determine
the impact of ambient air oxidants (primarily 0_) on plant yield, most have
compared the yield differences between plants grown in ambient air and those
grown in charcoal-filtered air. Early research documented that ambient oxidants
reduced the yield and quality of citrus, grape, tobacco, cotton, and potato
(U.S. Environmental Protection Agency, 1978). More recent studies have sub-
stantiated the effects of ambient oxidants on plant yield. Ozone has been
shown to induce significant yield reductions in tomato and bean (Maclean and
Schneider, 1976), soybean (Howell et al., 1979), two sweet corn cultivars
(Thompson et al., 1976), and in native plants (forbes, grasses, and sedges)
(Duchelle et al., 1983). In a study conducted over several years, bean yields
varied from a 5 percent increase to a 22 percent decrease in response to 03
concentrations in excess of 0.06 ppm (Heggestad et al., 1980). Studies con-
ducted on eastern white pine in the southern Appalachian mountains have shown
that exposure to 0, in ambient air has reduced the radial growth of sensitive
«j
individual trees 30 to 50 percent annually over the last 15 to 20 years (Mann
et al., 1980; Benoit et al. , 1982). Field studies in the San Bernardino
National Forest have shown that during the last 30 years exposure to ambient
air 0-. reduced height growth of ponderosa pine by 25 percent, radial growth by
37 percent, and the total wood volume produced by 84 percent (Miller and
Elderman, 1977).
1.6.1.7 Statistics Used to Characterize Ozone Exposures. The characteriza-
tion and representation of plant exposures to 0_ has been, and continues to
be, a major problem. Research has not yet clearly identified which components
019XX/A 1-64 6/29/84
-------
of the pollutant exposure cause the plant response. Most studies have charac-
terized the exposure by the use of mean 0, concentrations, although various
averaging times have been used. Some studies have also used cumulative 0-
dose. The difficulty of selecting an appropriate statistic by which to charac-
terize plant exposure has been summarized by Heagle and Heck (1980). Ambient
and experimental 03 exposures have been presented in published studies 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 have adequately characterized the
relationship among 0_ concentration, exposure duration, interval between
«3
exposures, and plant response. The use of a mean concentration implies that
all concentrations of 0- are equally effective in causing plant responses and
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 exposures. Most of the reported exposure statistics are not directly
correlated with each other and it is difficult to relate them to ambient air
measurements of 0~, which are usually reported as 1-hr means. Also it is
difficult to transform one exposure statistic to another without reanalyzing
the original air monitoring data.
Studies with beans and tobacco (Heck et a!., 1966) showed that a dose
(concentration x time) over a short period induced more injury than the same
dose distributed over a longer period. Tobacco studies showed that the 0_
concentration was approximately twice as important as exposure duration in
causing foliar injury (Tonneijck, 1984). In beans, foliar injury was shown to
-2
occurred when the internal 0- flux exceeded 5500 ug m in 1 hr (Bennett,
1979). A single 3-hr exposure, however, at approximately half the concentration
(0.27 compared with 0.49 ppm) required a 64 percent greater internal flux of
0~ to produce the same amount of foliar injury as the 1-hr exposure. The
greater importance of concentration compared to exposure duration has been
reported by numerous authors (e.g., Heck and Tingey, 1971; Henderson and
Reinert, 1979; Reinert and Nelson, 1979).
Not only are concentration and time important, but also the dynamic
nature of the 0- exposure; i.e., is the exposure at a constant or variable
concentration? Musselman et al. (1983) recently showed that constant concen-
trations of 0- caused the same kinds of effects in plants as variable concen-
trations at equivalent doses; but, the variable concentration exposures caused
a greater effect than the constant exposures. Studies with radishes exposed
019XX/A 1-65 6/29/84
-------
to ambient air ozone showed that significant yield reductions occurred when
the daily maximum 0- concentration exceeded 0.06 ppm at least 10 percent of
the days or more (Ashmore, 1984). In soybeans, reduced yield (weight/seed)
was most closely correlated with the number of 0~ peaks in excess of 0.10 ppm
•3
(Pratt, 1982). Studies with SO- have also shown that plants exposed to variable
concentrations exhibited a greater plant response than those exposed to a
constant concentration (Mclaughlin et al., 1979; Male et a!., 1983).
1.6.1.8 Relation Between Yield Loss and Foliar Injury. Because plant growth
and production depends 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 signifi-
cant foliar injury did not always cause a yield loss (Heagle et al., 1974;
Oshima et al., 1975). The relative sensitivities of two potato cultivars were
reversed when judged by foliar injury versus yield reductions (Pell et 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).
1.6.1.9 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, assimilation, biosynthesis, and
trans!ocation. Am impairment in these processes may lead to reduced plant
yeild if the process is limiting.
For growth to occur, plants must assimilate carbon dioxide and convert it
into organic substances; thus, an inhibition in carbon assimilation (photosyn-
thesis) may be reflected in altered plant growth or yield. In several species
03 (at 0.05 ppm and higher) inhibited photosynthesis, as measured by gas-
exchange (e.g., U.S. Environmental Protection Agency, 1978; Coyne and Bingham,
1978; Black et al., 1982). Biochemical studies showed that 03 (0.12 ppm for
2 hr) inhibited an enzyme that catalyzes the assimilation of carbon dioxide
(Pell and Pearson, 1983).
In addition to decreasing the total amount of carbon dioxide that is
assimilated, ozone alters the pattern by which the reduced amount of assimilate
019XX/A 1-66 6/29/84
-------
is partitioned throughout the plant. There is generally less photosynthate
translocated to the roots and to the reproductive organs (e.g., Tingey et al. ,
1971; Jacobson, 1982; Oshima et al., 1978, 1979; Bennett et al., 1979). This
reduces root size and vigor as well as marketable yield.
Reproductive capacity (flowering and seed set) is reduced by 0~ in orna-
mental plants, soybean, corn, wheat, and some other plants (Adedipe et al.,
1972a, Feder and Campbell, 1968; Heagle et al., 1972, 1974; Shannon and Mulchi,
1974). These data suggest that 0~ impairs the fertilization process in plants.
This suggestion has been confirmed in tobacco and corn studies using low
concentrations (0.05 to 0.06 ppm) of 03 (Feder, 1968; Mumford, 1972).
Ozone both in field and 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 O^induced yield
reductions have been attributed to premature senescence. The premature leaf
drop and senescence decrease the amount of photosynthate that a leaf can
contribute to plant growth and yield and also the time during which the leaf
contributes.
1.6.1.10 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,
although some studies have measured yield and a few have examined the physiolo-
gical basis for such influences. The factors studied include environmental
factors, biological factors, and interactions with other air pollutants.
1.6.1.10.1 Environmental conditions. Environmental conditions before and
during plant exposure are more influential in determining the magnitude of the
plant response than 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, in most, foliar injury
was the plant response measured. 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 permitting
the plant to absorb pollutants.
019XX/A 1-67 6/29/84
-------
2. No consistent pattern relating plant response to temperature
has been observed (U.S. Environmental Protection Agency, 1978),
although plants do not appear to be sensitive at extremely high
or low temperatures.
3. Plant injury tends to increase with increasing relative humidity
(U.S. Environmental Protection Agency, 1978). The relative
humidity affect 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 difference has been attri-
buted 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. Environ-
mental Protection Agency, 1978). The reduced CL sensitivity is
apparently related to stomatal closure, which reduces CU uptake
(U.S. Environmental Protection Agency; Olszyk and Tiboits,
1981; Tingey et al. , 1982). Water stress does not confer a
permanent tolerance to 0-; once the water stress is alleviated
the plants regain their sensitivity to CL (Tingey et al. ,
1982).
1.6.1.10.2 Interaction with plant diseases. Ozone affects the development of
disease in plant populations. Most laboratory evidence suggests that 03 (at
ambient concentrations or greater for 4 or more hours) inhibits infection by
pathogens and subsequent disease development (Laurence, 1981; Heagle 1982;
U.S. Environmental Protection Agency, 1978). Increases, however, in diseases
from "stress pathogens" have been noted. For example, plants exposed to 03
were more readily injured by Botrytis spp. than plants not exposed to 03
(Manning et al., 1970a,b; Wukasch and Hofstra 1977a,b; Biseassar, 1982). Both
field and laboratory studies have confirmed that the roots and cut stumps of
0--injured ponderosa and Jeffrey pines are more readily colonized by a root
•J
rot (Heterobasidion annosum). The degree of infection was correlated with the
foliar injury (James et al., 1980a; Miller et al., 1982). Studies in the San
Bernardino National Forest showed that Og-injured trees were predisposed to
attack by bark beetles and that fewer bark beetles were required to kill an
03-injured tree (Miller et al. , 1982).
1.6.1.10.3 Interaction of ozone with other air pollutants. The report of
Menser and Heggestad (1966) provided the initial impetus for studying the
interaction of 0, with SO-. They showed that Bel W-3 tobacco plants exposed
«3 <-
to 0, (0.03 ppm) or S0? (0.24 to 0.28 ppm) were uninjured but that substantial
O £•
019XX/A 1-68 6/29/84
-------
foliar injury resulted when the plants were exposed to both gases simultane-
ously. Subsequent studies (both greenhouse and field) have confirmed and
extended the observation that combinations of 0, and SO,, frequently cause more
O C,
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, indivi-
dually, is small. At higher concentrations, or when extensive injury occurs,
the effects of the individual gases tends to be less than additive (antagonis-
tic). The effects of pollutant combinations has also been investigated in
relation to other plant effects besides foliar injury, and these have been
discussed in several reviews and numerous individual reports (e.g., Reinert
et a!., 1975; Ormrod, 1982; Jacobson and Colavito, 1976; Heagle and Johnston,
1979; Olszyk and Tibbitts, 1981).
There have been fewer studies of the effects of 0, and S0» on plant yield
than on visible injury (Flagler and Younger, 1982a; Foster et al. , 1983;
Heggestad and Bennett, 1981; Heagle et al., 1983a). In field studies, the
addition of SCL to 03 generally did not influence the 0- response unless the
concentrations and exposure frequencies were greater than those of S0? that
typically occur in the ambient air of 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, 10 or
fewer periods of co-occurrence occurred during the growing season (Lefohn and
Tingey, 1984). Co-occurrence was defined as the simultaneous occurrence of
hourly-average 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
cominations (03 and SO-) on plant yield have used a higher frequency of expo-
sure duration and pollutant co-occurrence than occurs in the ambient air.
Only a few studies have investigated the effects of 0- with other pollu-
tants and no clear trend is available. Preliminary studies using three-pollu-
tant mixtures (0~, S0», N0») showed that the addition of S02 and NCL (at low
concentrations) caused a greater growth reduction than 03 alone.
1.6.1.11 Economic Assessment of Ozone Effects Ozone has been identified as
the most important air pollutant in terms of spatial distribution and impacts
on agricultural yields. Given the importance of United States agricultural
products to both domestic and world consumption of food and fiber, significant
reduction in their supply would have substantial economic consequences.
019XX/A 1-69 6/29/84
-------
Various methods have been used to assess the economic impact of 0^, many of
which have been simplistic. Reliable assessment procedures should use theo-
retically justified economic methodologies that consider the effects to both
the producer and consumer. These methods usually address price changes result-
ing from adjustments in production and the role of producer input and output
substitution strategies. The resulting estimates more accurately assess the
true economic impact than other procedures.
Numerous studies have attempted to assess the dollar losses to crop
production that result from exposures to ozone in ambient air. The quality
of these various estimates is variable. For example, the economic loss data
cited in the previous criteria document (U.S. Environmental Protection Agency,
1978) used simplistic traditional approaches that were not well-based theoreti-
cally. Therefore, the previous estimates should be viewed with caution. Most
of the economic assessments of agricultural losses since the last criteria
document (U.S. Environmental Protection Agency, 1978) have focused on regional
losses. Crop loss estimates for southern California ranged from 45 million
(Adams et a!., 1982) to approximately 100 million dollars (Leung et a!.,
1982). These studies used different assessment methodologies and considered
the effects of ozone on different crops. The economic impact of ozone on
corn, wheat, and soybeans for the "Corn Belt" was estimated at 688 million
dollars (Adams and McCarl, 1984), while for Illinois alone the losses were
estimated at 55 to 200 million dollars (Mjelde et al., 1984).
Only a few studies have attempted to assess the national economic conse-
quences of ambient ozone. Nationwide economic losses have been estimated to
be between approximately 2 billion (SRI, 1981; Adams and Crocker, 1982b) and 3
billion dollars (Shriner et al., 1982). These estimates include more complete
dose-response information for an increasing number of major commodities and
better air quality data than previous national estimates (U.S. Environmental
Protection Agency, 1978). These estimates should be considered preliminary,
however, since two of the three studies used simple traditional approaches.
In summary, the current dollar estimates of crop damage are useful primari-
ly as indicators of the magnitudes of impact. A full accounting of the economic
mechanisms underlying agricultural production is required to provide definitive
estimates of the extent of agricultural losses. Such accounting should include
both annual and perennial crops (agronomic and horticultural) and the associated
dynamic adjustments of agricultural production. It must consider the effects
019XX/A 1-70 6/29/84
-------
on intermediate consumers, such as livestock growers and food processors, and
final consumers, both domestic and foreign. The effect of 0,, on ornamentals,
both physically and economically, has also never been addressed.
1-6-2 Effects of Peroxyacetyl Nitrate on Vegetation
1.6.2.1 Introduction. Peroxyacetyl nitrate (PAN) is an extremely phytotoxic
air pollutant that is produced by photochemical reactions similar to those
that produce ozone. The sequence of events within the plant leading to the
effects of PAN is conceptually similar to that described for 0.,, except that
the pollutants apparently have different reactive sites within the cells. 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.
1.6.2.2 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 (Taylor, 1969; Davis, 1975,
1977).
There is an absolute requirement for light before, during, and after
exposure or visible PAN injury will not develop (Taylor et a!., 1961). Field
observations have shown that crops growing under moisture stress developed
little or no injury during photochemical oxidant episodes while, adjacent to
them, recently irrigated crops were severely injured (Taylor, 1974).
Only a few studies have investigated the effects of PAN and 0_ 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).
1.6.2.3 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.
019XX/A 1-71 6/29/84
-------
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).
1.6.2.4 Effects of PAN on Plant Yield. Only limited studies have been con-
ducted to determine the effects of PAN on plant growth and yield. In green-
house 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 evi-
dence 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 concentra-
tions below the injury threshold can cause significant yield losses in sensi-
tive 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
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 the measured ambient concentrations (Chapter 6) indicates
that it is unlikely that PAN effects will occur to plants in the United States
except in some areas of California and in possibly a few other localized areas.
1.7 EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS ON NATURAL ECOSYSTEMS
1.7.1 Introduction
Temperate forest ecosystems within the United States currently are exper-
iencing declines. Tree responses, unless they are the result of a specific
biotic disease or an acute pollutant exposure, are cumulative and frequently
the culmination of a number of chronic stresses (Figure 1-7). Among chronic
stresses to which trees are exposed is air pollution.
019XX/A 1-72 6/29/84
-------
r~
ABIOTIC AGENTS
OF DISEASE
AIR POLLUTION
HIGH
TEMPERATURES
FREEZING
TEMPERATURES
PESTICIDES
DROUGHT
SALT
POOR SOIL
AERATION
MINERAL
DEFICIENCY
SOIL
POLLUTION
MECHANICAL
DAMAGE
DECLINE DISEASES
OF COMPLEX ORIGIN
FUNCTIONAL PARTS
OF A TREE
REDUCED
GROWTH <
SHOOT
BLIGHT
PHOTOSYNTHESIS
TRANSPIRATION
SHOOTS:^
CHLOROSIS OF
FOLIAGE
^-HEIGHT GROWTH
FOLIAGE DISEASES
VASCULAR WILTS
&
SAP ROT
BRANCHES AND STEM:
TRANSLOCATSON
STRUCTURE
STORAGE
SECONDARY GROWTH
CANKER GALL
TRANSLOCATION
STRUCTURE
STORAGE
ROOTLET^
NECROSIS
MYCORRHIZAE (FUNGUS ROOTS)
BIOTIC AGENTS
OF DISEASE
FUNGI
BACTERIA
MYCOPLASMAS
RICKETTSIA
SPIROPLASMA
VIRUSES
INSECTS
MITES
NEMATODES
HIGHER PLANTS
WATER AND MINERAL
ABSORPTION
PROTECTION
ROOT PATHOGENS
Figure 1-7. Summation of abiotic and biotic agents involved in diseases of trees, given by
types of diseases and functional parts of the tree. Decline diseases are caused by a com-
bination of biotic and abiotic agents.
Source: Manion (1981).
1-73
-------
The mixed-conifer forests of the San Gabriel and San Bernardino mountain
ranges east of Los Angeles have been exposed to oxidant air pollution since
the early 1950s (Miller, 1973). Ozone was first identified as the agent
responsible for the slow decline and death of ponderosa pine (Pinus ponderosa
Laws) trees in these forests (Miller et al., 1963). Later, Jeffrey pine
(Pinus jeffreyi Grev. & Balf.) was also found to be injured by 03 exposure.
Oxidant injury of eastern white pine (Pinus strobus L.) has been observed for
many years in the eastern United States. It was first reported as needle
blight in the early 1900s but in 1963 was shown to be the result of acute and
chronic ozone exposure (Berry and Ripperton, 1963). More recently, oxidant
injury of eastern white pine in the Blue Ridge Mountains of Virginia has been
reported by Hayes and Skelly (1977) and on the Cumberland Plateau of east
Tennessee by Mann et al. (1980). In addition, ozone injury in natural plant
communities has been reported by Treshow and Stewart (1973) and by Duchelle et
al. (1983).
1.7.2 Oxidant-induced Effects on a Western Coniferous Forest Ecosystem
One of the most thoroughly studied ecosystems in the United States is the
mixed coniferous forest ecosystem in the San Bernardino Mountains of southern
California. The San Bernardino Forest is located at the eastern end of the
80-mile-long South Coast Air Basin, where a severe air pollution problem has
been created by the last three decades of extensive urban and industrial
development (Miller and Elderman, 1977). Oxidants carried by the marine air
flow probably entered the forest in the early 1940s or soon after when vegeta-
tion injury was first recognized near the coast. Sensitive plant species in
the National Forest, such as ponderosa pine, began showing unmistakable injury
in the early 1950s (Miller and Elderman, 1977), but the source of the injury
was not identified as QS until 1962 (Miller et al., 1963). Extensive visible
injury and concern about the possible adverse effects of chronic 03 exposure
on an important forest ecosystem led to an interdisciplinary study. From 1973
to 1978, a study was conducted to determine the response of the organisms and
biological processes of the conifer forest to chronic oxidant exposures and to
interpret responses within the ecosystem context (Miller et al., 1982).
The ecosystem processes analyzed were: (1) carbon flow (the movement of
carbon dioxide into the plant; its incorporation into green plant organic
matter; and then its partitioning among consumers, litter, decomposers, and
the soil; and its return to the atmosphere); (2) the movement of water in the
019XX/A 1-74 6/29/84
-------
soil-piant-atmosphere continuum; (3) mineral nutrient flow through the green
plant litter and soil-water compartments; and (4) the shift in diversity
patterns in time and space as represented by changes in composition of tree
species in stands, age, structure, and density.
All of the ecosystem processes mentioned above were shown by the study to
be affected directly or indirectly. Foliar injury of sensitive ponderosa and
Jeffrey pine was observed when 03 concentrations ranged from 0.05 to 0.06 ppm.
During the period of study, average 24-hr 03 concentrations during the months
May through September ranged from a background of 0.03 to 0.04 ppm to a maximum
of 0.10 to 0.12 ppm.
Less sensitive trees, in decreasing order of sensitivity, were white fir
(Abies concolor Lindl.), black oak (Quercus kelloggii Newb.), incense cedar
( Libocedrus decurrens Torr.), and sugar pine (Pinus lambertiana Doug!.).
Associated with foliar injury were a decrease in photosynthesis, a reduction
in tree growth (both height and diameter), and a reduction in seed production
in ponderosa and Jeffrey pine. Foliar injury, premature needle fall, and
senescence decreased the amount of foliage capable of conducting photosynthesis
and a reduction in carbohydrates decreased the capacity of the remaining
foliage. Carbon flow in the form of carbohydrates diminished as stressed
trees retained smaller amounts of assimilated carbon after transpiration
losses. The amounts of mineral nutrients in the living foliage of injured
ponderosa pines were lower than in needles on healthy trees. The store of
carbon and mineral nutrients accumulated in the thick needle layers under
stands of 0~-injured trees and their movement back into the trees was cur-
tailed. Nutrient availability was influenced 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, because the usual increase
that occurs with age was prevented by premature needle senescence and abscis-
sion (Miller et al. , 1982). Stressed trees showed a decrease in the number of
mycorrhzial rootlets and their replacement by small saprophytic fungi in the
small rootlets of stressed trees (Parmeter et al., 1962). Mycorrhizae are
very sensitive to the photosynthetic capacity of the host and to the capacity
of the host to translocate carbon compounds to the roots (Hacskaylo, 1973).
A comparison of the radial growth of ponderosa pine during years (1910 to
1940) of low pollution (<0.03 ppm) with years (1941 to 1971) of high pollution
(0.03 to 0.12 ppm) indicate that 0., exposure reduced the average annual radial
growth by approximately 40 percent, height by 25 percent, and wood volume by
019XX/A 1-75 6/29/84
-------
84 percent in trees less than 30 years of age. The marketable volume of trees
30 years of age was reduced by 83 percent in the areas with the highest 0~
concentrations.
Stressed pines also became more susceptible to root rot (Heterobasidion
annosum) and pine beetle (Dendroctonus brevicomis), as the result of weakening
of the host by photochemical oxidants. Photochemical oxidant injury of pon-
derosa pines results in reduced oleoresin yield, rate of flow and exudation
pressure, moisture of phloem and sapwood, and phloem thickness. All of these
are believed to be important in the defense of the tree against bark beetles
(Stark and Cobb, 1969). Studies also indicate that a disease-insect relation-
ship exists between root-infecting fungi and bark beetles. Approximately 80
percent of the ponderosa pines infested with bark beetles had been infected by
root-disease fungi prior to beetle infestation (Stark and Cobb, 1969). Ver-
ticicladiella wagenerii was the major fungus attacking the roots. The fungus
moves from tree to tree via the roots. Heterobasidion annosum was likewise
found to have infected conifer roots prior to beetle attack. Heterobasidion
usually does not become a serious problem in California forests, however, until
disturbances by humans, such as logging, have occurred (Stark and Cobb, 1969).
Mortality rate of the trees reached 2 to 3 percent in some years. Injured
ponderosa and Jeffrey pines older than 130 years produced significantly fewer
cones per tree than uninjured trees of the same age (Luck, 1980). Heavy
litter accumulation occurred in stands with the most severe needle injury and
defoliation. Pine seed establishment was hindered by litter depth, but the
growth of oxidant-tolerant understory species was encouraged. Buildup of
litter and the presence of easily ignited foliage on smaller trees could lead
to destructive fires. Removal by 0- and by fires of the pine-dominated forest
and the reduction of competition among remaining trees leads to a dominance in
these forests of self-perpetuating, fire-adapted, 0~-tolerant shrub and oak
species mixtures that provide fewer commodity and amenity values than the former
pine forest and that inhibit reestablishment of pines and other conifers.
Any mature natural community transfers 10 to 20 percent of the energy
fixed by plants to herbivores (Woodwell, 1974). Consumer organisms constitute
an extremely diverse group, and only a limited amount of information on their
response to pollutants is available (Newman, 1979). The influence of oxidants
on these organisms is assumed to be mainly through the food webs. At this
time, studies have not indicated a direct impact of 0_ on the organisms them-
selves. The breakdown, however, of the processes of energy flow and nutrient
019XX/A 1-76 6/29/84
-------
cycling resulting from the disruption of photosynthesis, reproduction, or a
structural change among the producers within ecosystems can affect consumers
by removing their shelter and food source.
1.7.3 Effects of Ozone on Other Ecosystems
The responses that have been observed in the San Bernardino Forest eco-
system from 0~-associated stress have also been observed in other ecosystems
within the United States that have been exposed to the same or lower ranges of
0, concentrations.
Studies made along the Blue Ridge Parkway and on the Cumberland Plateau
of east Tennessee support the view that exposure to CL reduces growth in
sensitive trees (Benoit et al., 1982). Eastern white pine of reproducing age
located in experimental plots situated along the Blue Ridge Parkway from the
Shenandoah National Park in the north to the southernmost end of the Parkway
in Virginia were studied to determine the radial increment during the 1955 to
1978 period. Growth of trees classified as sensitive was 25 percent less; and
in trees classified as intermediate in sensitivity, growth was 15 percent less
than in tolerant trees. Mean radial increments for all trees during the last
10 years of the study were smaller than for the previous 24 years. Comparison
of growth during 1974 to 1978 with radial growth during 1955 to 1959 indicated
a decrease in growth of 26, 37, and 51 percent for tolerant, intermediate, and
sensitive trees. During the period of the study, concentrations of 0.05 to
0.07 ppm of 03 were recorded on a recurring basis, with episodic peaks of
0.12 ppm or higher occurring (Benoit et al., 1982). Steady decline in annual
ring increments of sensitive white pine was also observed on the Cumberland
Plateau during the years 1962 to 1979 (Mclaughlin et al., 1982). A reduction
of 70 percent in average annual growth and 90 percent in average bole growth
was observed in sensitive white pine when compared to both tolerant trees and
trees of intermediate sensitivity. Annual occurrences of 0, at hourly concen-
«3
trations of 0.08 ppm or greater were associated with the growth reductions.
Reduction in growth of sensitive white pine on the Blue Ridge Parkway and on
the Cumberland Plateau, as in the case of the San Bernardino Mountains, was
correlated with the predisposing symptoms of chronic decline, which includes the
following sequence of events and conditions: (1) premature senescence and loss
of older needles at the end of the growing season; (2) reduced storage capacity
of carbohydrates in the fall and resupply capacity in the spring to support new
needle growth; (3) increased reliance of new needles on self-support during growth;
019XX/A 1-77 6/29/84
-------
(4) shorter new needles, resulting in lower gross photosynthetic productivity;
(5) higher retention of current photosynthate by foliage resulting in reduced
availability of photosynthate for external usage (including repair of chroni-
cally stressed tissues of older needles); and (6) premature casting of older
needles (Mclaughlin et al., 1982). Degeneration of feeder roots and mycorrhi-
zae usually precedes the onset of above-ground symptoms (Manion, 1981). De-
creases in nutrient and water uptake may also occur. These changes produce
weakened trees. Weakened trees are, in turn, predisposed to attack by root-
rot fungi such as Heterobasidion annosum, Verticicladella wagenerii, and
V. procera, to defoliation by insects, and to attack by the pine beetle,
Dendroctonus breviconn's.
Injury by 03 to native herbaceous vegetation growing in the Virginia
mountains was also observed (Duchelle et al., 1983). Ambient 0_ concentrations
were shown to reduce growth and productivity of graminoid and forb vegetation
in the Shenandoah National Park. For each year of the study, biomass production
was greatest for vegetation grown in filtered-air chambers. The total 3-year
cumulative dry weight for the filtered chambers was significantly (P <0.05)
different from non-filtered and open-air plots. Common milkweed (Ascelepias
syrica L.) and common blackberry (Rubus allegheniensis Porter) were the only
two native species to develop visible injury. Milkweed has been previously
shown to be quite sensitive to 03 (Duchelle and Skelly, 1981). Ozone episodes
occurred several times each year during the period of the study. Peak hourly
concentrations ranged from 0.08 to 0.12 ppm; however, monthly hourly average
concentrations ranged from 0.03 to 0.06 ppm. The effects of 0, in altering
the natural vegetation of the Virginia mountains was not assessed. Lower
biomass production could result in selection for vegetation better able to
cope with the 03 stress. As in California, 0_ is transported from distant
sources to the Virginia mountains. In the Blue Ridge and Appalachian Mountains,
these sources include the industrial midwest, eastern Virginia, and the Washing-
ton, D.C., area.
In Utah, Treshow and Stewart (1973) conducted one of the few studies
concerned with the impact of air pollution on natural plant communities.
Grassland, oak, aspen, and conifer communities in the Salt Lake Valley and
Wasatch Mountains were studied. Some dominant species considered keys to
community integrity were found to be sensitive. Bromus tectorum L. (cheatgrass),
the most prevalent species in the grassland community, was also the most
sensitive to 0». Other grasses and forbs were not as sensitive (Table 1-11);
O
however, in those grasses with visible injury, carbohydrate production was
019XX/A 1-78 6/29/84
-------
TABLE 1-11. INJURY THRESHOLDS FOR 2-HOUR EXPOSURES TO OZONE
Species
Injury threshold,
ppm 03 for 2 hr
Species
Injury threshold,
ppm 03 for 2 hr
i
~~j
vo
Grassland-oak community species:
Trees and shrubs:
Acer grandidentatum Nutt. over 0.40
Acer negundo L. over 0.25
Arteresia tridentata Nutt. 0.40
Mahonia repens G. Don over 0.40
Potentilla frutlcosa L. 0.30
Quercus gambelii Nutt. 0.25
Toxicodendron radicans (L.) Kuntze over 0.30
Perennial forbs:
Achillea millefolium L. over 0.30
Ambrosia psilostachya DC. over 0.40
Calochortus nuttallii Torr. over 0.40
Cirsium arvense (L. ) Scop. 0.40
Coniurn maculaturn L. over 0.25
Hedysarum boreale Nutt. 0.15
Helianthus anuus L. over 0.30
Medocago sativa L. 0.25
Rumex crispus L. 0.25
Urtica gracilis Ait. 0.30
Vicia americana Muhl. over 0.40
Grasses:
Bromus brizaeformis Fish. & Mey. 0.30
Bromus tectorum L. 0.15
Poa pratensis L. 0.25
Aspen and conifer community species:
Trees and shrubs:
Abies concolor (Gord. & Glend.) Lindl. 0.25
Amelanchier alnifolia Nutt. 0.20
Pachystima myrsinites (Pursh) Raf. over 0.30
Populus tremuloides Michx. 0.15
Perennial forbs:
Alii urn acuminatum Hook 0.25
Angelica pinnata S. Wats. under 0.25
Aster engelmanni (Eat.) A. Gray 0.15
Carex siccata Dewey 0.30
Cichorium intybus L. 0.25
Cirsium arvense (L. ) Scop. under 0.40
Epilobium angustifolium L. 0.30
Epilobium watsoni Barbey 0.30
Eriogonum heraclioides Nutt. 0.30
Fragaria ovalis (Lehm.) Rydb. 0.30
Gentiana amarella L. over 0.15
Geranium fremontii Torr. under 0.40
Geranium richardsonii Fisch. & Traut. 0.15
Juncus sp. over 0.25
Lathyrus lanzwertii Kell. over 0.25
Lathyrus pauciflorus Fern. 0.25
Mertensia arizonica Greene 0.30
Mimulus guttatus DC. over 0.25
Mimulus moschatus Dougl. under 0.40
Mitel la stenopetala Piper over 0.30
Osmorhiza occidental is Torr. 0.25
Phacelia heterophylla Pursh under 0.25
Polemonium foliosissiraum A. Gray 0.30
Rudbeckia occidental is Nutt. 0.30
Saxifraga arguta D. Don under 0.30
Senecio serra Hook. 0.15
Taraxacum officinale Wiggers over 0.25
Thalictrum fendleri Engelm. over 0.25
Veronica anagallis-aquatica L. 0.25
Vicia americana Muni. over 0.25
Viola adunca Sm. over 0.30
Annual forbs:
Chenopodium fremontii Wats. under 0.25
Callomia linean's Nutt. under 0.25
Ribes hudsonianum Richards. 0.30
Rosa woodsii Lindl. over 0.30
Sambucus melanocarpa A. Gray over 0.25
Symphoricarpos vaccinioiders Rydb. 0.30
Perennial forbs:
Actaeu arguta Nutt. 0.25
Agastache urticifolia (Benth.) Kuntze 0.20
Source: Treshow and Stewart (1973).
Descurainia californica (Gray) 0.E. Schulz 0.25
Galium bifolium Wats. over 0.30
Gayophytum racemosura T. & G. 0.30
Polygonum douglasii Greene over 0.25
Grasses:
Agropyron caninum (L.) Beauv. over 0.25
Bromus carinatus Hook. & Arn. under 0.25
-------
significantly reduced. Aspen (Populus tremuloides Michx) was the most sensi-
tive member of the aspen community. In both cases single 2-hr exposures to
0.15 ppm of 03 caused severe injury. Removal of the dominant species (cheat-
grass) from plant communities could result in a shift to another species.
Decline in or removal of aspen could affect the growth of white fir because
seedlings require the shade provided by aspen for optimal juvenile growth.
Loss of aspen populations could influence forest succession by restricting
white fir development, causing a shift from a forest to a grassland or forb
vegetation community (Treshow and Stewart, 1973). In a companion study con-
ducted in chambers in the greenhouse, 0, exposures of 0.15 to 0.3 ppm for 2 hr
per day reduced root and top growth, and fewer seeds were produced (Harwood
and Treshow, 1975).
It is apparent that in natural communities exposed to 0_, the tolerant
O
species would soon become the dominants. The authors concluded that 0, must
O
be considered a significant environmental parameter that influences the composi-
tion, diversity, and stability of natural plant communities.
The foregoing studies indicate that the impact of 0, changes the composi-
O
tion and succession patterns of plant communities. The more mature stages of
ecosystems use nutrients and energy more efficiently. Mature systems are
tight; disturbances cause leakage. The leakage may be large enough under
certain circumstances to in time reduce the potential of the site to support
life (Woodwell, 1974). Changes that cause reductions in biotic structure are
destabilizing and retrogressive. The entire array of plants is changed by
disturbance from one in which large-bodied, long-lived species occur to one in
which small-bodied, short-lived, rapidly reproducing plants predominate (Woodwell,
1974). This pattern is exemplified by the San Bernardino National Forest,
where the mixed conifer forest is being replaced by low-growing shrubs and
annual herbs. It is also occurring in the eastern United States, where the
degradation of the Appalachian forests from North Carolina to Maine is
currently taking place as the red spruce (Picea rubens Sarg. ) and other large,
long-lived species are being removed by at-present unknown forces (Johnson
and Siccama, 1983). Also associated with the loss of stable ecosystems is the
maintenance of normal water and climatic conditions, protection from wind and
erosion, and protection from noise pollution (Guderian, 1977).
1.7.4 Interrelated Ecosystems
1.7.4.1 Aquatic Ecosystems. It is extremely important to consider that an
adverse impact on a forest or agricultural ecosystem may in turn adversely affect
019XX/A 1-80 6/29/84
-------
adjacent aquatic systems. A variety of linkages for energy and nutrient exchange
exist. Disruptions induced by air pollution stress on terrestrial ecosystems
often trigger dysfunctions in neighboring aquatic ecosystems, such as streams,
lakes, and reservoirs. Sediments resulting from erosion can change the physical
character of stream channels, causing changes in bottom deposits, erosion of
channel banks, obstruction of flow, and increased flooding. They can fill in
natural ponds and reservoirs. Finer sediments can reduce water quality,
affecting public and industrial water supplies and recreational areas. Turbid-
ity caused by increased erosion can also reduce the penetration of light into
natural waters. This, in turn, can reduce plant photosynthesis and lower
supplies of dissolved oxygen, leading to changes in the natural flora and
fauna (Bormann and Smith, 1980). Significant forest alterations, therefore,
may have a regional impact on nutrient cycling, soil stabilization, sedimenta-
tion, and eutrophication of adjacent or nearby aquatic systems. Interfacing
areas, such as wetlands and bogs, may be especially vulnerable to impact.
1.7.4.2 Agricultural Ecosystems. Natural and agricultural ecosystems possess
the same basic functional components, require energy flow and mineral cycling
for maintenance, and are subject to the dominating influences of climate and
substrate. Natural ecosystems vary in diversity from simple systems with few
species to complex systems with many species. Their populations also vary in
genetic composition, age, and species diversity. They are self-regulating and
self-perpetuating. Agroecosystems, on the other hand, are highly manipulated
monocultures of similar genetic and age composition and are unable to maintain
themselves without the addition of nutrients, energy, and human effort; oppor-
tunistic native and imported species may invade the sites. The manipulation
of monocultures is designed to concentrate ecosystem productivity into a
particular species to maximize its yield (e.g., corn, wheat, soybeans) for the
benefit of humans (Cox and Atkins, 1979). If any of the species, varieties,
or cultivars is very sensitive to C- , its market value is destroyed. When
O
this occurs, efforts are made to find a resistant cultivar, as with tobacco,
or to grow a crop less sensitive to 0- stress. Cost alone would prevent
replacement of the variety of species in a natural ecosystem.
1.7.5 Ecosystem Responses to Stress
Ecosystems, because of their complexity, respond to stress in a manner
different from individuals (Figure 1-8). Ecosystems respond to stress through
the response of the organisms that compose them. Three main levels of interac-
tion are involved: between the individual and its environment, the population
019XX/A 1-81 6/29/84
-------
BIOCHEMICAL LEVEL
CELLULAR LEVEL
WHOLE PLANT LEVEL POPULATION LEVEL
CHRONIC OR ACUTE EXPOSURES
COMMUNITY LEVEL
I
oo
BREAKDOWN OF
METABOLIC PATH
» t
CHANGES IN
CELLULAR CONSTITUENTS
REDUCED VIGOR.
ADAPTABILITY.
GROWTH, YIELD.
PRODUCT QUALITY
Figure 1-8.Conceptual sequence of levels showing continuum of plant responses.
Source: Adapted from Heck (1973).
-------
Apparently no research has been done on the potential effects on materials of
the peroxyacyl nitrates or of hydrogen peroxide. In spite of the research
focus on ozone, however, the amount of damage from ozone to actual in-house
materials remains poorly characterized.
The materials known to be most susceptible to ozone attack are elastomers,
textile fibers and dyes, and certain types of paints. Ideally, the nature and
amount of ozone damage to the materials can be approximated by physical damage
functions in combination with ambient air concentrations. The economic impact
from ozone-related damage can then be estimated by using accelerated replace-
ment and repair costs or increased avoidance costs. None of these areas is
sufficiently defined in the literature, however, to assess the amount and cost
of oxidant-related damage.
1.8.2 Effects and Damage Functions
1.8.2.1 Elastomers. Virtually all the available literature on photochemical
oxidant research focuses on ozone and its effects on economically abundant or
important materials. The effects of ozone on elastomers are the best docu-
mented. Natural rubber and synthetic polymers such as polymers of styrene,
butadiene, and isoprene, make up most of the elastomer production in the
United States. These chemicals are used for formulating automotive tires and
for protective electrical coverings. The mechanism of ozone degradation on
elastomers shares similarities and differences with simple oxidation from
atmospheric oxygen. Ozone damage is mainly a surface phenomenon, whereas
damage from simple oxidation occurs internally. Ozone cracks occur at right
angles to the direction of stress (Mueller and Stickney, 1970). Over time,
the elastomer becomes hard and brittle, losing its physical integrity. In the
absence of ozone and other photochemical oxidants, oxidation from atmospheric
oxygen still occurs, but at a much slower rate and apparently by different
mechanisms.
High humidity and mechanical stress greatly affect the formation, depth
of cracking, and, in automotive tires, the adhesion between plies (Davies,
1979; Wenghoefer, 1974). Ozone affects natural rubber and other elastomers in
a dose-related fashion.
Dose is defined in materials research as the product of concentration and
duration of exposure. The importance of ozone dose was demonstrated by Bradley
and Haagen-Smit (1951), who used a specially formulated ozone-sensitive natural
rubber (NR). Samples exposed to ozone at a concentration of 20,000 ppm cracked
019XX/A 1-84 6/29/84
-------
almost instantaneously, and those exposed to lower concentrations took a
proportionately longer time to crack. At concentrations of 0.02 to 0.46 ppm,
and under 100-percent strain, the cracking rate was 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 styrene-butadiene rubber (SBR) elastomers to ozone at a concentration of
0.25 ppm for 19 to 51 hr under 100-percent strain. With ozone doses of 4.75
ppm-hr to 12.75 ppm-hr, a proportional rate in cracking depth was observed,
averaging 2.34 pm/hr for cold SBR and 4.01 pm/hr for hot SBR. When antiozonants
were added to the compounds, the reduction in cracking depth rate was propor-
tional to the amount added. Haynie et al. (1976) exposed samples of a tire
sidewall to ozone at concentrations of 0.08 and 0.5 ppm for 250 to 1000 hr
under 10 and 20 percent-strain. Under 20-percent strain, the mean cracking
rate for 0.08 ppm was 1.94 um/hr. From these and other data, they estimated
that at the ozone standard of the time (0.08 ppm, 1-hr average), and at the
annual NO standard of 0.05 ppm, it would take 2.5 years for a crack to pene-
trate cord depth.
In addition to stress, factors affecting the cracking rate include atmos-
pheric pressure, humidity, sunlight, and other atmospheric pollutants. Veith
and Evans (1980) found a 16-percent difference in cracking rates reported from
laboratories located at various geographic elevations.
Ozone has been found to affect the adhesion of plies (rubber-layered
strips) in tire manufacturing. Exposure to ozone concentrations of 0.05 to
0.15 ppm for a few hours significantly decreased adhesion in an NR/SBR blend,
causing a 30-percent decrease at the highest ozone level. This adhesion prob-
lem worsened at higher relative humidities. When fast-blooming waxes and
antiozonants or other antioxidants were added, only a combination of protec-
tive measures allowed good adhesion and afforded protection from attack by
ozone and sunlight. Wenghoefer (1974) showed that ozone (up to 0.15 ppm),
especially in combination with high relative humidity (up to 90 percent),
caused greater adhesion losses than heat and NO- did, with or without high
relative humidity.
1.8.2.2 Textile Fibers and Dyes. 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 0.1 ppm ozone and noted fading, which until
that time had been thought to be caused by N0_. Subsequent work by Schmitt
019XX/A 1-85 6/29/84
-------
(1960, 1962) confirmed the fading action of ozone and the importance of rela-
tive humidity in the absorption and reaction of ozone in vulnerable dyes. The
acceleration in fading of certain dyes by high relative humidity was noted
later by Beloin (1972, 1973) at an ozone concentration of 0.05 ppm and a
relative humidity of 90 percent. Kamath et al. (1982) also found that a slight
rise in relative humidity (85 to 90 percent) caused a 20-percent dye loss in
nylon fibers.
Both the type of dye and the material in which it is incorporated are
important factors in the resistance a fabric has 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
versus 50 percent) on royal blue rayon-acetate, red rayon-acetate, or plum
cotton. On the other hand, Haylock and Rush (1976, 1978) showed that anthra-
quinone dyes on nylon fibers were sensitive to fading from ozone at a concen-
tration of 0.2 ppm at 70 percent relative humidity and 40°C for 16 hr. More-
over, 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 Huevel et al. (1978) and Salvin (1969), Haylock and Rush (1976,
1978) noted the importance of surface area in relation to the degree of fading.
In explaining this relationship, Kamath et al. (1982) found that ozone pene-
trated 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 at various relative humid-
ities. 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 for quantifying the amount of damage to
fibrous materials 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 such as modacrylic and polyester are rela-
tively resistant; and cotton, nylon, and acrylic fibers show variable sensiti-
vities 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
019XX/A 1-86 6/29/84
-------
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.
1.8.2.3 Paints. The effects of ozone on paint are small in comparison with
those of other factors (Campbell et al., 1974). Past studies have shown that,
of various paints, only vinyl and acrylic coil coatings are affected (Haynie
et al., 1976), 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 final results are needed before conclusions can be drawn.
Pigments in artists' paints have also been tested under controlled condi-
tions for 3 months at an average exposure level of 0.4 ppm of ozone. While
fading occurred in anthraquinone-based pigments, no quantitative information
on dose-response relationships is available.
1.8.3 Economic Assessment of Effects of Ozone or Oxidants on Materials
Damage to nonbiological materials from ozone is usually expressed in terms
of one or both of the following two general classes of costs to producers
and consumers: (1) ozone accelerated replacement and repair costs, as when
the service life and/or aesthetics of a material are impaired; and (2) in-
creased avoidance costs, as when certain industries (e.g., manufacturers of
tires, plastics, paints, dyes, and fabrics) are obligated to incur expenditures
for antiozonant research and development, substitute processes and materials,
additives and formulations, product packaging, advertising, etc., in order to
offset sales losses that would otherwise occur.
In theory, the approach selected should depend on the observed behavior
of the producers and consumers of the materials in question, and the type of
damage to which they are reacting. In practice, the existing empirical esti-
mates of ozone damage to materials are far from reliable for the reasons
presented in the following paragraphs:
First, in some studies, coverage is limited to one or two classes of
materials, and to restricted geographical regions. Other studies are entirely
too aggregative, suffering deficiencies because of (1) broad and vague notions
of materials exposure and ozone concentrations; (2) little or no data on the
019XX/A 1-87 6/29/84
-------
spatial and temporal distributions of the exposed materials; (3) unverified
guesses regarding the incidence and level of cost increases and production
adjustments incurred by ozone-affected industries; and (4) inadequate attention
to economic trade-offs among different industries and different regions, and
between producers versus consumers.
Second, the engineering and economic estimates are not well related to
the scientific literature in this area, and tend to be far too simplistic to
meet the concerns of the scientist. Third, most of the cost assessments were
conducted in the early 1970s. Few recent studies exist. Moreover, these
earlier studies cite extensively from each other and there are few independent
analyses that do not merely rework old data.
As a consequence of the third item above, many of the ozone-related costs
reported in the early 1970s for research and development, product substitu-
tion, etc., are no longer appropriate. Some of these were presumably once-only
costs that are no longer charged against current production. Because the
literature is dated, there may also be some current research and development
and substitution attempts that are not reflected at all in the studies cited
in Chapter 9. In addition, studies are outdated because the supply-demand
relationships that prevailed when the studies were conducted may no longer be
valid. In sum, the cost estimates largely reflect technologies, ozone or
oxidant concentrations, and economic conditions that prevailed some 10 to 20
years ago.
Finally, most of the so-called economic studies of ozone damage to mate-
rials have been conducted using an engineering approach. That approach focuses
on the classification and quantification of the various kinds of costs in-
curred by the producers and users of the ozone-sensitive materials. Economic
theory would argue, however, that this is merely the first step in the assess-
ment process, and that supply-demand relationships are then needed in order to
proceed with the calculation of social net benefits (i.e., changes in producer
and consumer surpluses). In practice, however, it appears that almost all of
the damage assessments conducted to date stop short of obtaining an econometric
measure of economic surplus. As such, the studies reported in Chapter 9 of
this document must be interpreted accordingly.
Despite the shortcomings of the quantitative economic assessments that are
available, the data indicate that, among the various materials studied, those
most likely to affect the economy as the result of ozone exposure include
elastomers and textile fibers and dyes. Among these, natural rubber used for
019XX/A 1-88 6/29/84
-------
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. McCarthy et al.
(1983) calculated the cost of antiozonants in automobile and truck tires for
protection against ozone. While limitations in this study preclude the reliable
estimation of damage costs, the figures ($163 million in 1984 dollars) indicate
the magnitude of potential damage from exposure to ozone in ambient air.
Research has shown that house paint and certain textile fibers and dyes are
also damaged by ozone; but the absence of reliable damage functions makes
accurate economic assessments impossible. Thus, while damage to these mate-
rials is undoubtedly occurring, the actual damage costs cannot be estimated
confidently.
1.9 INTRODUCTION TO HEALTH EFFECTS
The purpose of the health effects of chapters of this document is to
describe the known biomedical effects of ambient levels of 0- and other photo-
chemical oxidants. Reports of animal, clinical, and epidemiological research
are available for this purpose. They are reviewed in the following sections
of this chapter. The primary goal of the review process is to describe and
assess concentration-response relationships, particularly for concentrations
at or near those found in ambient air, for both humans and laboratory animals.
Such information is integral to the standard-setting process.
1.9.1 Organization of Health Effects Information
Reasons for the inclusion in this criteria document of Chapters 10 through
13 may not be self-evident to those who have never been involved in the pre-
paration or review of criteria documents. Thus, the basic reasons are briefly
noted below:
1. Chapter 10: Toxicologic Effects of Ozone and Other Photochemical
Oxidants. Jji vitro studies on isolated cells and tissues and i_n
vivo studies on laboratory animals permit the measurement of effects
under circumstances that are not permissible in clinical research.
Such studies in animals are useful for identifying mechanisms of
effects; for determining concentration-response relationships over a
wide range; for studying responses that require invasive procedures,
such as tissue sampling and surgery; and for sorting out and testing
hypotheses as a prelude to clinical investigations and as an aid in
0190GC/A 1-89 6/28/84
-------
the design of epidemiologies! studies. This information can be used
to understand possible linkages between acute and chronic effects;
and correlations of biochemical, functional and structural changes
with growth, development and aging of the lung as the result of
exposure to ozone. The chief weakness of animals studies lies in
the difficulties and associated uncertainties of extrapolating
results to humans.
2. Chapter 11: Controlled Human Studies - Studies on humans provide
information about sensitive populations, dose-response relationships
and responses to a limited number of repeated exposures. Such
studies are necessarily restricted to ethically and legally accept-
able pollutant concentrations and exposure regimes, as well as
restricted to techniques for measurement of effects that are similarly
constrained. The emphasis in human studies found in the literature
is, therefore, on pulmonary function, with less on clearance, resist-
ance to infection and even less on cytological effects. The chief
weaknesses of controlled human exposure studies are: (a) small
sample size; (b) the necessary absence of chronic exposure studies;
(c) limitations on the range of pollutant concentrations and type of
subjects studied; and (d) use of synthetic, simplified atmospheres,
usually at unvarying concentrations, and usually without the changes
in temperature, humidity, and pressure that occur in ambient condi-
tions. The latter (d) also constitutes a strength of such studies,
however, since it permits determination of concentration-response
functions relative to a specific pollutant and specific end points.
3. Chapter 12: Field and Epidemiological Studies of the Effects of
Ozone and Other Photochemical Oxidants - Epidemiological studies
attempt to associate various characteristics of human health and
function with ambient air concentrations of photochemical oxidants.
Epidemiology involves the study of real-world human populations in
their normal setting; of human responses to short-term and long-term
oxidant exposure; and of sensitive subgroups within the population.
Investigations within the normal setting are not, of course, without
their drawbacks. The information gathered on exposure-effect rela-
tions and results may be confounded by the presence of factors such
0190GC/A 1-90 6/28/84
-------
as variations in the time spent out of doors, variations in activity
levels, cigarette smoking, poor hygiene, coexisting pollutants, and
socioeconomic status. Nevertheless, associations (or lack of them)
can be drawn between health indicators and oxidant exposure. These
associations may complement or extend the findings of clinical and
toxicological research.
4. Chapter 13: Evaluation of Integrated Health Effects Data for Ozone
and Other Photochemical Oxidants - The extensive body of data on the
effects of ozone on the respiratory system was reported and discussed
in particular detail in Chapters 10, 11, and 12. Chapter 13 provides
a vehicle for evaluating this collective body of data for its signi-
ficance to public health and for assessing the certainties and
uncertainties associated with the data. Since the purpose of a
criteria document is to provide a scientific basis for the deriva-
tion and promulgation of standards, this chapter also addresses
specific issues and questions that are important in standard-setting.
Paramount among the issues considered in standard-setting is the
identification of the population or subpopulation to be protected by
the regulation, that is, one that is at particular risk from exposure
to ozone and other photochemical oxidants. The identification of
such a population or subpopulation presupposes the identification of
one or more effects that are in and of themselves adverse, or that
are indicators of other effects that are adverse but that not measur-
able in man because of ethical constraints.
Three issues are not broached at all in the health effects chapters,
inasmuch as they are regulatory issues that by law rest with the Administrator
and by precedent are addressed for the Administrator by the Agency's Office of
Air Quality Planning and Standards. These issues are: (1) determination of
what constitues an "adverse effect;" (2) assessment of risk; and (3) determi-
nation of a margin of safety. While scientific data contribute significantly
to decisions regarding them, the resolution of these issues cannot be achieved
solely on the basis of experimentally acquired scientific information. Conse-
quently, these issues are among the more problematic or difficult concepts and
issues involved in protecting the public from the untoward effects of exposure
to air pollutants.
0190GC/A 1-91 6/28/84
-------
1.9.2 Literature Coverage and Selection
The number of scientific reports on the biomedical effects of photochemi-
cal oxidants has grown substantially in recent years. To provide a comprehen-
sive yet manageable review to satisfy the objectives of the criteria document,
the most pertinent references must be identified for in-depth examination.
Guidelines were developed to facilitate this process.
The material selected for review and comment in the text generally comes
from the more recent literature, with emphasis on studies conducted at or near
pollutant concentrations found in ambient air. Older literature that was
cited in the previous criteria document for ozone and other photochemical
oxidants (U.S. Environmental Protection Agency, 1978) has often been summar-
ized and presented briefly. An attempt has been made, however, to discuss at
greater length in the text older studies (1) judged significant because of
their usefulness in deriving the 1979 standards; (2) open to reinterpreted on
because of newer data; or (3) potentially useful in deriving subsequent stand-
ards. The newer information on oxidants now available may in some instances
make possible a better understanding of the earlier studies, such that a more
detailed and comprehensive picture of health effects is emerging on several
issues. An attempt has been made to discuss key literature in the text and
present it in tables as well. Reports of lesser importance to the purposes of
this document may appear in tables only.
Generally, only published material that has undergone scientific peer re-
view is included. In the interest of admitting new and important information,
however, the health effects chapters may also include some other materials
that is thought to meet the standards of scientific reporting.
Studies cited in the chapters on toxicologic (Chapter 10) and clinical
research (Chapter 11) are generally confined to those employing ozone at
concentrations of I ppm or less. This concentration cutoff was chosen because
ozone concentrations in ambient air rarely exceed 0.4 ppm (averaged over 1
hour) and then in only a few urban areas on rare occasions (Chapter 6).
Typically, 1-hr maximum ozone levels are well below 0.2 ppm. Application of
the concentration cutoff of I ppm eliminates discussions of studies on mor-
tality and sublethal effects. Higher concentrations are cited, however, when
(1) they have been used to extend the range of concentration-response relation-
ships, as in multiple-concentration studies; (2) they elucidate mechanisms of
effect; or (3) their use has resulted in the discovery of previously unreported
effects.
0190GC/A 1-92 6/28/84
-------
In selecting studies for consideration, each paper was reviewed in detail.
Technical considerations for inclusion of a specific study included, but were
not restricted to, an analysis of the exposure method; specificity or appropri-
ateness of the analytical method used to monitor the oxidant concentration;
information on oxidant monitoring practices such as location, calibration, and
sampling time; characteristics of the subjects; techniques used for obtaining
cohorts; and the appropriateness of the technique used to measure the effect.
Interpretation of the results included consideration of the following factors:
the end results of the statistical analysis; the degree to which the results
are plausible in the context of other extant data; the appropriateness of the
hypothesis developed; and the agreement between the hypothesis and the results
reported. No additional statistical analyses beyond those reported by the
authors have been undertaken. Unless otherwise stated, all statements in the
text, positive or negative, are statistically significant at p < 0.05 or less.
1.10 TOXICOLOGIC EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS
1.10.1 Introduction
The biological effects of ozone have been studied extensively in animals
and a wide array of toxic effects has been ascribed to ozone inhalation.
Although much has been accomplished to improve the existing data, refine the
concentration-response relationships, and better interpret the mechanisms of
ozone effects, many of the present data were not accumulated for the purpose
of making quantitative comparisons across animal studies or deriving concen-
tration-response functions. In many cases, only qualitative comparisons can
be made. To maximize the extent that animal toxicological data can be used to
estimate the human health risk of exposure to ozone, the qualitative as well
as quantitative similarities between the toxicity of ozone to animals and to
man must be considered. Significant advances have been made in understanding
the toxicity of ozone through appropriate animal models. This summary high-
lights the results of selected studies that will provide data useful for
predicting and assessing, in a scientifically sound manner, possible human
responses to ozone.
Summary figures and tables are presented in the following sections.
Studies were selected for inclusion in these figures and tables on the basis
of specific criteria presented below:
0190GC/A 1-93 6/28/84
-------
1. Studies have been cited only if the reported effects are clearly due
to CL exposure. Studies involving mixtures of 0-, and other pollutants
or tnose involving exercise, diet deficiencies, or other possible
modifiers of response to 0^ 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
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. Specific responses can
be found in the accompanying tables.
4. Only pulmonary function effects were divided by short-term (<14
days) and long-term (>14 days) exposures to follow the discussion in
the text.
1.10.2 Respiratory Transport and Absorption of Ozone
The respiratory system is the route of entry for ozone and other oxidizing
air pollutants, just as it is for air itself. Throughout inhalation and
exhalation, ozone undergoes transfer from the gas phase to the airway surfaces
and parenchyma. Not all of the gas is taken up, however; a variable fraction
is expelled with exhalation. Following contact with the respiratory tract,
ozone or its transformation products can react with both extra- and intracellu-
lar elements.
The amount of ozone acting at a given site in the lung is related to the
airway luminal concentration at that level. Thus, ozone 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 here that ozone is quite reactive chemically. Reactions with
components of this layer result in an increase in total absorption of ozone in
the upper airways and reduces the amount of ozone reaching sensitive tissues.
The site at which uptake and subsequent interaction occur and the local dose
(quantity of ozone absorbed per unit area), along with cellular sensitivity,
will determine the type and extent of the injury. For this reason, a thorough
knowledge of the complex process of gas transport and absorption within the
respiratory tract is crucial to understanding the effects of ozone and other
oxidants in humans.
Measurements of the regional uptake of ozone and other oxidants that are
reactive and metabolized by body tissue and fluids are just beginning. Com-
parative uptake studies between man and animals have not yet appeared in the
0190GC/A 1-94 6/28/84
-------
literature. Studies with aerosols, however, have shown similarities in deposi-
tion in both the total respiratory tract and in the pulmonary region in guinea
pig, rabbit, rat, and man. Nevertheless, some interspecies differences,
especially in regional deposition and uptake, may be expected. Such differences
may be imposed by modes of breathing. For example, rodents breathe only by
nose, while humans may breathe nasally, oronasally, or orally, depending on a
variety of factors. Differences may also result from differences among species
in anatomic and morphometric structures. For example, respiratory bronchioles
are absent or primordial in rats, but are well developed in primates. Similarly,
the capacity for responding to a specific dose may vary between animals and
humans because of dissimilarities in detoxification systems, pharmacokinetics,
metabolic rates, genetic makeup, or other factors. Such differences must be
accounted for when extrapolating the results of animal studies to the human
population.
The animal studies that have been conducted are beginning to indicate the
quantity and site of ozone uptake in the respiratory tract. For example,
experiments conducted to determine the nasopharyngeal removal of ozone in
animals have demonstrated (1) that the fraction of ozone taken up is inversely
related to the flow rate and ozone concentration, (2) that uptake is greater
for nose than for mouth breathing, and (3) that trachea! and exposure chamber
concentrations are positively correlated (Yokoyama and Frank, 1972; Moorman
et al., 1973; Miller et al., 1979). The limited data available indicate that
at concentrations of ozone ranging from 0.1 to 2.0 ppm, removal of ozone in
the nasopharyngeal region would be expected to be approximately 50 percent of
the inhaled ozone.
Morphological studies have provided substantiating data that ozone is
absorbed along the entire respiratory tract, penetrating further into the
peripheral nonciliated airways and the respiratory bronchioles as inhaled
ozone concentration increases from 0.2 ppm to 0.8 ppm (Dungworth et al. ,
1975). From animal studies, it has been predicted that in man, rabbit, and
guinea pig the pattern of ozone deposition is similar, with one specific area
of the lung, the junction of the conducting airways and the gas-exchange region,
receiving the maximal dose (Miller et al., 1978). This prediction correlates
well with reported histopathological data of Dungworth et al. (1975) and Stephens
et al. (1974).
To date, there has been only one study (Yokoyama and Frank, 1972) that
attempted to measure ozone uptake in the lower respiratory tract. These data
0190GC/A 1-95 6/28/84
-------
indicate that in dogs, 80 to 87 percent of the inhaled ozone was taken up by
the lower respiratory tract. It should be noted that this estimates the
uptake as applied to the total lung and does not describe the uptake of ozone
by individual airways or airway generations.
Three models appear to have merit for estimating ozone uptake in the
respiratory tract (Aharonson et al., 1974; McJilton et al. , 1972; Miller
et al., 1978).
The model of Aharonson et al. (1974) is useful in analyzing nasopharygeal
uptake data. Applied to ozone data, the model indicates that the average mass
transfer coefficient is the nasopharygeal region increases with increasing air
flow.
The McJilton model (McJilton et al., 1972) and the Miller model (Miller
et al., 1978) for lower respiratory tract ozone uptake are similar in their
treatment of ozone in the airways, taking into account convection, diffusion,
wall losses, and ventilatory patterns; and in their use of morphological data
for defining the dimensions of the airways and their liquid lining. The
Miller model is more realistic, however, because it accounts for chemical
reactions of ozone with constituents of the mucous-serous layer. Tissue dose
is predicted by the Miller model 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. Comparison of the Miller
results with morphological data indicates qualitative agreement in the pulmonary
region. Comparison in the tracheobronchial region indicates, however, that
further research is needed to define the relevant toxic chemical and physical
mechanisms.
Ozone dosimetry modeling is in its formative stages, and at present there
are few experimental results that are useful for judging the validity of the
modeling efforts. With experimental confirmation, models can become practical
tools for understanding respiratory tract transport and absorption of ozone
and for understanding ozone dosimetry in respective species.
1.10.3 Effects of Ozone on the Respiratory Tract
1.10.3.1 Morphological Effects. Morphological studies of the effects of
ozone have indicated that the pattern and distribution of tissue lesions are
similar in the respective species studied. They depend, however, upon (1) the
location of the sensitive cells and (2) the location of the junction between
the conducting airways and the gas-exchange region of the lung, both of which
0190GC/A 1-96 6/28/84
-------
are species-specific. Damage to all parts of the respiratory tract can occur
in animals, depending on the ozone concentration. At low concentrations of
ozone (< 1960 (jg/m ; 1 ppm), damage is principally confined to the junction
between the alveoli and the conducting airways. Dogs, monkeys, and man have
respiratory and nonrespiratory bronchioles, while respiratory bronchioles are
either absent or poorly developed in mice, rats, and guinea pigs. The location
of the ozone lesion thus differs according to the species examined (Plopper
et al., 1979; Castleman et al., 1977, 1980; Dungworth et a!., 1975a; Eustis
et al., 1981). In both types of lungs, the effects of ozone have been found at
concentrations as low as 392 |jg/m (0.2 ppm) and for exposure times as short
as 2 hr (Stephens et al., 1974a).
In the upper and lower conducting airways, ciliated cells appear to be
the most sensitive cell type; they are damaged by exposures to ozone at concen-
trations as low as 392 to 1568 ug/m (0.2 to 0.8 ppm) for 8 or 24 hr for 7
days in rats (Schwartz et al., 1976), bonnet monkeys (Castleman et al., 1977),
Rhesus monkeys (Dungworth et al. , 1975b; Mellick et al., 1977), and mice
(Ibrahim et al., 1980). When Moore and Schwartz (1981) and Boorman et al.
(1980) extended these exposures to 180 days at the same concentrations, similar
changes in these ciliated cells were observed. Uniform damage was not always
noted; most often shortened and less dense cilia occurring in random patches
were reported. Electron microscopy revealed severe cytoplasmic changes and
condensed nuclei. Damage is present in both trachea and bronchi (Eustis et
al., 1981; Mellick et al., 1977; Castleman et al., 1977). The damaged cilia
are replaced by nonciliated clara cells that become hyperplasic (Evans et al.,
1976a; Lum et al., 1978).
3
In mice, ozone levels of 980 and 1568 |jg/m (0.5 and 0.8 ppm) elicited a
pronounced hyperplasia of these nonciliated cells that persisted for 10 days
after cessation of the exposure (Zitnik et al., 1978; Ibrahim et al., 1980).
In a number of species, ozone damage is clearly evident at the centriacinar
region, which includes the terminal bronchiole region, portions of the respira-
tory bronchioles, and possibly the alveolar ducts, depending on the species
(Stephens et al., 1973, 1974a,b; Schwartz et al., 1976; Mellick et al., 1977).
Type 1 epithelial cells are significantly affected (Stephens et al.,
1974a; Evans et al., 1976a; Castleman et al., 1980; Eustis et al. , 1981; Barry
3
et al., 1983; Boorman et al. , 1980). In monkeys, for example, at 1764 |jg/m
(0.9 ppm), death of type 1 cells reaches a maximum at 12 hr after continuous
exposure (Castleman et al. , 1980). With the destruction of these cells, there
0190GC/A 1-97 6/28/84
-------
is a hyperplasia of type 2 alveolar epithelial cells, which re-covers the
denuded basal lamina (Stephens et al., 1974a,b; Sherwin et al., 1983; Eustis
et al., 1981). Type 2 cells are relatively resistant to ozone exposure.
Following and during continued exposures, these type 2 cells begin to
proliferate, which is a hallmark of ozone injury regardless of species. In
rats, DNA synthesis in type 2 cells was reported as early as 4 hr after expo-
3
sure to 0- to 392 pg/m (0.2 ppm) (Stephens et al., 1974a) and reached a
J 3
maximum at 2 days following continuous exposure to 686 or 980 ng/m (0.35 or
0.5 ppm) (Evans et al., 1976a,b), or 1568 ug/m (0.8 ppm) (Boorman et al.,
1980). Although type 2 cells proliferated in the ozone-exposed lung, complete
maturation of type 2 cells to type 1 cells did not occur, even as late as 180
days of exposure (Moore and Schwartz, 1981). In the normal progression, type
2 cells would have matured into type 1 cells. Continued ozone exposure inhibits
both ciliagenesis and type 2 cell maturation.
Inflammation occurs in all species examined so far. The inflammatory
3
response is seen as early as 4 hr after exposure to 1568 ug/m (0.8 ppm) in
monkeys (Castleman et al., 1980). In rats and monkeys, inflammation persists
with continued exposure, although at reduced levels. The inflammatory exudate
includes both fibrin and various leukocytes in the initial phase. In the
later phase the inflammatory cells are predominantly macrophages (Castleman et
al., 1980; Brummer et al. , 1977; Boorman et al., 1980; Moore and Schwartz,
1981). Quantitative estimates of the degree of inflammation are, however,
lacking at present. The contribution of the inflammatory response to sub-
sequent long-term features of ozone toxicity has not been studied in detail,
even though techniques are available. A number of studies have reported that
3
exposure to 980 ug/m (0.5 ppm) and above thickens the interalveolar septa of
centriacinar alveoli (Schwartz et al. , 1976; Castleman et al., 1980; Boorman
et al., 1980). Thickness could be caused by interstitial fibrosis.
Although some delay has been observed between an exposure to ozone and
the maximum manifestation of morphological changes, the shortest time required
for ozone exposure to result in significant morphological changes is 2 hr, at
392 or 980 ug/m3 (0.2 or 0.5 ppm) in rats (Stephens et al., 1973, 1974a,b) or
4.7 or 6.6 hr of exposure by endotracheal tube in cats to 510, 980, or
1960 ug/m3 (0.26, 0.5, or 1 ppm) (Boatman et al., 1974). Most of these morpho-
logical studies were specifically designed, however, to look at long-term
(i.e., days, months, years) exposures rather than acute effects. The data
from acute studies are in agreement with molecular theories that ozone acts
0190GC/A 1-98 6/28/84
-------
rapidly to oxidize some critical tissue component. Little difference in
severity was noted by Schwartz et al. (1976) between exposure to 8 hr/day or
24 hr/day when the exposure was continued for 7 days. Quantitative studies of
different exposure regimens are lacking but are technically feasible. The
sequence in which the anatomic sites are affected appears to be a function of
concentration rather than of exposure duration. Increasing the concentrations
of ozone not only results in more severe lesions, but also extends the lesion
to higher generations of the respiratory structure.
Morphological studies of vitamin E-deficient or supplemented rats have
been undertaken to correlate the biochemical findings with morphological
alterations (Plopper et al., 1979; Stephens et al., 1983; Chow et al., 1981;
Schwartz et al., 1976; Sato et al . , 1976a,b, 1978, 1980). Despite the pre-
sence of vitamin E in the diets of these animals, however, the morphological
lesion resulting from ozone exposure was unchanged.
When comparisons are made at analogous anatomical sites, the morphol-
ogical effects of ozone on the lungs of a number of species of animals are
seen to be remarkably similar. Despite the inherent differences in anatomy
between most experimental animals and man, the junction between the conducting
airways and the gas exchange region is the site affected most by ozone.
Studies on the morphologic effects of ozone exposures of experimental
animals are summarized in Figure 1-9 and Table 1-12 (see Section 1.10.1 for
criteria used to summarize the studies).
1.10.3.. 2 Pul monary Funct i on . One of the limitations of animal studies is
that many pulmonary function tests comparable to those conducted after acute
exposure of human subjects are difficult to interpret. Methods exist, however,
for obtaining similar measurements of many variables pertinent to understanding
the effects of ozone on the respiratory tract, particularly after longer exposure
periods. A number of newer studies reported here reflects recent advances in
studying pulmonary function in small animals.
Changes in lung function following ozone exposure have been studied in
mice, rats, guinea pigs, rabbits, cats, dogs, sheep, and monkeys. Short-term
3
exposure for 2 hr to concentrations of 431 to 980 vg/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
0190GC/A 1-99 6/28/84
-------
I£N
,0
O
o
xx .**• e«* *$f' ^ ^
^° ^ V** V<°N V* ^0
0. 1 -
E 0.2-
a
a
% 0.3-
c
0
~ 0.4-
0
L
-^ 0.5-
(D
U
c 0.6-
0
U
<
• i
i
i i
i
» i
i . — — i
i i
i
i i
<
» (
» i
i
> i
> 1
i
i
1 4
i 1
<
i <
i <
i I
t
I <
i
i (
1
1
(
i
1 {
I
I
i I
i
I
> (
1
I
»
t
i
i
»
i
>
0
Figure 1-9. Summary of morphological effects in experimental animals exposed
to ozone. See Table 1-12 for reference citations for studies
summarized here.
-------
TABLE 1-12. MORPHOLOGICAL EFFECTS OF OZONE IN EXPERIMENTAL ANIMALS
Effect/response
03 concentration, ppm
References
Abnormal cilia 0.2, 0.35, 0.5, 0.8
0.2
0.2, 0.35
0.2, 0.5, 0.8
0.8
0.26, 0.5, 1.0
0.3
0.5, 0.8
0.5, 0.8
0.54, 0.88
0.7
0.8
0.8
0.8
0.85
Dungworth et al. (1975b)
Plopper et al . (1979)
Castleman et al . (1977)
Schwartz et al. (1976)
Boorman et al . (1980)
Boatman et al . (1974)
Sato et al. (1976a)
Eustis et al. (1981)
Mellick et al . (1975, 1977)
Stephens et al . (1974a)
Evans et al. (1976a)
Ibrahim et al . (1980)
Lum et al. (1978)
Plopper et al. (1978)
Stephens et al . (1978)
Increased number of
alveolar macrophages
(AM)
Increased evidence of
collagen, fibrosis
Increased lung weight,
edema
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
0.54, 0.88
1.0
1.0
0.5, 1.0
0.54, 0.88
1.0
0.4
0.35
0.5, 0.8
Plopper et al. (1979)
Dungworth et al. (1975b)
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)
Last et al. (1979)
Freeman et al. (1974)
Stokinger et al. (1957)
Freeman et al. (1973)
Fukase et al. (1978)
Freeman et al. (1974)
Cavender et al. (1977)
P'an et al. (1972)
Castleman et al. (1977)
0190GC/A
1-101
6/28/84
-------
TABLE 1-12. MORPHOLOGICAL EFFECTS OF OZONE IN EXPERIMENTAL ANIMALS
(continued)
Effect/response
Decreased weight
gain
Altered type 1 and
2 cells
03 concentration, ppm
0.2, 0.5, 0.8
0.5, 1.0
0.25
0.26, 0.5, 1.0
0.3
0.35, 0.5, 0.7, 1.0
0.5
0.5
0.5, 0.8
0.54, 0.88
0.5, 0.8
0.5, 1.0
0.54, 0.88
0.7, 0.8
0.8
0.85
References
Schwartz et. al . (1976)
Fukase et al. (1978)
Barry et al. (1983)
Boatman et al. (1974)
Sherwin et al. (1983)
Evans et al . (1976b)
Stephens et al. (1974b)
Zitnik et al. (1978)
Eustis et al. (1981)
Stephens et al . (1974a)
Mellick et al. (1975, 1977)
Cavender et al. (1977)
Freeman et al . (1974)
Castleman et al. (1973,
(1980)
Plopper et al . (1978)
Stephens et al. (1978)
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).
The effects of short-term exposures to ozone on pulmonary function and
airway reactivity in experimental animals are summarized in Figure 1-10 and
Table 1-13 (see Section 1.10.1 for criteria for selecting studies summarized).
Long-term exposure of 4 to 6 weeks to ozone concentrations of 392 to
490 ug/m (0.2 to 0.25 ppm) increases lung distensibility at high lung volumes
in young rats (Bartlett et al., 1974; Raub et al., 1983a). Similar increases
3
in lung distensibility were found in older rats exposed to 784 to 1568 ug/m
(0.4 to 0.8 ppm) for up to 180 days (Moore and Schwartz, 1981; Costa et al. ,
1983; Martin et al. , 1983). Three to twelve months of exposure to 0_ concen-
3
trations of 1176 to 1568 ug/m (0.6 to 0.8 ppm) increased pulmonary resistance
and caused impaired stability of the small peripheral airways in both rats
and monkeys (Costa et al., 1983; Wegner, 1982). The effects in monkeys were
not completely reversed by 3 months following exposure; lung distensibility
had also decreased in the postexposure period, suggesting the development of
lung fibrosis.
0190GC/A 1-102 6/28/84
-------
^ o°V
-,0
.0
. e>
o
CO
0. 1 -
£ 0.2-
a
a
v 0.3-
c
0
0
L
-£ 0.5-
4
k
i 1
>
1
<
\
t
b 1
»
1
>
1
k . 4
>
1
<
) «
1 1
4
|
1 4
(
I —i
>
»
ft
Figure 1-10. Summary of effects of short-term ozone exposures on pulmonary
function in experimental animals. See Table 1-13 for reference
citations for studies summarized here.
-------
TABLE 1-13. EFFECTS ON PULMONARY FUNCTION
OF SHORT-TERM EXPOSURES TO OZONE
Effect/response
03 concentration, ppm
References
Increased breathing
frequency
Decreased tidal volume
Decreased lung
compliance
Increased residual
volume (RV),
closing capacity
(CC), and closing
volume (CV)
Decreased diffusion
capacity
Increased pulmonary
resistance
Increased airway
reactivity
0.22, 0.41, 0.8
0.34, 0.68, 1.0
0.5
0.34, 0.68, 1.0
0.4, 0.8
0.26, 0.5, 1.0
1.0
0.24 - 1.0
0.26, 0.5, 1.0
0.26, 0.5, 1.0
1.0
0.5
1.0
0.5
0.7
1.0
Amdur et al. (1978)
Murphy et al. (1964)
Yokoyama (1969)
Murphy et al. (1964)
Amdur et al. (1978)
Watanabe et al. (1973)
Yokoyama (1969)
Inoue et al. (1979)
Watanabe et al. (1973)
Watanabe et al. (1973)
Gertner et al. (1983a, b)
Yokoyama (1969)
Yokoyama (1974)
Abraham et al. (1980)
Lee et al. (1977)
Holtzman et al. (1983)
0190GC/A
1-104
6/28/84
-------
The effects of long-term exposures to ozone on pulmonary function and
airway reactivity in experimental animals are summarized in Figure 1-11 and
Table 1-14 (see Section 1.10.1 for criteria for summary).
Studies of airway reactivity following ozone exposure in experimental
animals show that ozone increases the reactivity of the lung to mechanical and
chemical stimulation partly by increased sensory neural activity travelling in
the vagus nerve and partly by a local action of ozone on the tissues. Aerosolized
ovalbumin can reach immunologic receptors in the lungs of mice preexposed to 980
3
or 1568 M9/ra (0-5 or 0.8 ppm) continuously for 3 to 5 days (Osebold et al.,
1980), resulting in an increased incidence of anaphylaxis. Increased sensiti-
vity to histamine or cholinomimetic drugs by aerosol or injection has been
noted in several species. Easton and Murphy (1967) showed that the lethal
dose of histamine in guinea pigs was reduced in those animals preexposed to
3
concentrations as low as 980 or 1960 ug/m (0.5 or 1 ppm) of ozone for 2 hr.
The pulmonary resistance due to subcutaneous injection of histamine increased
3
in guinea pigs exposed to 1568 ug/m (0.8 ppm) of ozone for 1 hr (Gordon and
3
Amdur, 1980). Similarly, dogs exposed to 1372 and 1960 ug/m (0.7 and 1.0 ppm)
of ozone for 2 hr had greater changes in pulmonary resistance following histamine
aerosol inhalation (Lee et al., 1977; Holtzman et al., 1983a). Sheep exposed
3
to 980 ug/m (0.5 ppm) of ozone for 2 hr experienced increased pulmonary
resistance for the cholinomimetic drug, carbachol (Abraham et al. , 1980).
The time course of ozone-induced airway hyperreactivity suggests a possi-
ble association with inflammation (Holtzman et al., 1983a,b; Sielczak. et al.,
1983; Fabbri et al., 1984), but responses are variable and not very well
understood. Additional studies that demonstrate increased collateral resistance
following 30-min local exposure of ozone or histamine in sublobar bronchi of
dogs (Gertner et al., 1983a,b,c) suggest that other mechanisms, along with am-
plification of reflex pathways, may contribute to changes in airway reactivity.
1.10.3.3 Biochemical Effects of Ozone in the Lung of Experimental Animals.
The lung is metabolically active, and several key steps in metabolism have been
studied after 0-, exposure. Since the procedures for such studies are invasive,
this research has been conducted only in animals. Effects, to be summarized
below, have been observed on antioxidant metabolism, oxygen consumption,
proteins, lipids, and xenobiotic metabolism.
The lung contains several compounds (e.g., vitamin E, sulfhydryls, gluta-
thione) and enzymes (e.g., glutathione peroxidase, glutathione reductase,
0190GC/A 1-105 6/28/84
-------
\f
-------
TABLE 1-14. 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
0.8
0.4
0.2, 0.8
0.64
0.5, 0.8
0.64
0.12, 0.25
0.64
0.8
Raub et al. (1983)
Bartlett et al. (1974)
Costa et al. (1983)
Martin et al. (1983)
Costa et al. (1983)
Wegner (1982)
Eustis et al. (1981)
Wegner (1982)
Raub et al. (1983)
Wegner (1982)
Costa et al. (1983)
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 ozone since exposure to ozone causes numerous effects on lung
structure, function, and biochemistry. Acute exposure to high ozone levels
(2920 pg/m , 2 ppm) typically decreases antioxidant metabolism, whereas repeated
exposures to lower levels (< 1568 ug/m , 0.8 ppm) increases this metabolism
(DeLucia et al., 1975). In rats maintained on normal diets, this response
has been observed after a week of continuous or intermittent exposure to
392 ug/m3 (0.2 ppm) 03 (Mustafa, 1975; Mustafa and Lee, 1976; Plopper et al.,
1979). Similar responses are seen in monkeys and mice, but at higher concen-
trations (980 ug/m , 0.5 ppm; Fukase et al., 1978; Mustafa and Lee, 1976).
The effects of ozone 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,
~ ~ 3
oxygen consumption); repeated exposure to lower levels (> 1568 (jg/m , 0.8 ppm)
0190GC/A
1-107
6/28/84
-------
increases oxygen consumption (Mustafa et al. , 1973; Schwartz et al., 1976;
Mustafa and Lee, 1976). Effects in rats on normal diets have been observed
3
after a short-term exposure to ozone levels as low a*s 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).
Similar patterns of response for both antioxidant metabolism and oxygen
consumption are observed after exposure to ozone. A 7-day exposure to ozone
produces linear concentration-related increases in activities of glutathione
peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, and
succinate oxidase (Mustafa and Lee, 1976; Chow et al., 1974; Schwartz et al.,
1976; Mustafa et al., 1973). Rats on a vitamin E-deficient diet experience an
increase in enzyme activities at 196 pg/m (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).
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 4 a plateau is reached
(Mustafa and Lee, 1976; DeLucia et al., 1975). Recovery from these effects
occurs by 6 days post-exposure (Chow et al., 1976), This apparent tolerance
is not long-lasting. 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., 1975).
Studies in which monkeys have been compared to rats did not include, however,
a description of appropriate statistical considerations applied (if any).
Thus, no definitive conclusions about responsiveness of monkeys versus rats
can be made.
0190GC/A 1-108 6/28/84
-------
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, which are rich 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 (jg/m (0.1 ppm) ozone
(Chow et a!., 1981). Higher levels caused a similar response in rats, but not
in monkeys, on normal diets (Chow et al., 1974, 1977). This enzyme is frequent-
ly used as a marker of cellular damage because it is released upon cytotoxicity.
It is not known, however, whether the increase in this enzyme is a direct
reflection of cytotoxicity or whether it is an indicator of an increased
number of type 2 cells and macrophages in the lungs.
An increase in a few of the measured activities of lysosomal enzymes has
3
been shown in the lungs of rats exposed to > 1372 ug/m (0.7 ppm) ozone (Oillard
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 jji vivo or j_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
observed, with 980 ug/m (0.5 ppm) 0- 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
0190GC/A 1-109 6/28/84
-------
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.
Although the ability of 0- to initiate peroxidation of unsaturated fatty
acids i_n vitro is well established, few i_n vivo studies of lung lipids have
been conducted. Generally, ozone decreases unsaturated fatty acid content of
the lungs (Roehm et al., 1972) and decreases incorporation of fatty acids into
lecithin (a saturated fatty acid) (Kyei-Aboagye et al., 1973). These altera-
tions, however, apparently do not alter the surface-tension-lowering properties
of lung lipids that are important to breathing (Gardner et al., 1971; Huber
et al., 1971).
One of the earliest demonstrated effects of ozone was that very high
concentrations caused mortality as a result of pulmonary edema. As more
sensitive techniques were developed, lower levels (510 ug/m , 0.25 ppm) were
observed to increase the protein content of the lung (Hu et al., 1982).
Since some of the excess protein could be attributed to serum proteins, the
interpretation was that edema had occurred. This effect was more pronounced
several hours after exposure ceased. At higher concentrations, a loss of
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 poten-
tial physiological activities across the alveolar walls.
The biochemical effects observed in experimental animals exposed to ozone
are summarized in Figure 1-12 and Table 1-15 (see Section 1.10.1 for criteria
used in developing this summary).
1.10.3.4 Effects of Ozone in Altering Host Defense Against Microbes. Reports
over the years have presented substantial evidence that exposure to ozone
significantly increases the ability of an inhaled infectious microorganism to
colonize and to proliferate within the lung, resulting in significant increases
in mortality. This response is dose-related and is significant at concentra-
tions of ozone as low as 0.08 to 0.1 ppm (Coffin et al., 1968; Ehrlich et al.,
1977; Miller et al., 1978; Aranyi et al., 1983). The biological basis for
this response appears to be that ozone or one of its reactive products can
impair the normal bactericidal pulmonary defenses, which results in prolonging
the life of the infectious agent, permitting its multiplication, and ultimately,
0190GC/A 1-110 6/28/84
-------
.,^v
A°
&
&
-<"* rt
0. 1 -
£
Q_ r> o
CL 8'2
C 0.3-
0
-^ 0.4-
D
L
-£ 0.5-
0
1 0.6-
0
u
0.7-
c
Q
N 0-8
O
0.9-
1 d
I
1
1
1
\
p
(
<
1
(
I
1 <
>
1
» (
<
1
I 1
1 (
(
\
\ «
1
(
1
» (
1 <
1 (
1
1
1 <
1
\ {
1 1
(
{
1
b 1
1 1
1 1
» 1
1 1
1 1
k 1
1 (
<
1 (
1 (
1 1
> (
h 1
1
1
t
t
> <
1
<
{
<
»
\
(
»
Figure 1-12. Summary of biochemical changes in experimental animals exposed to ozone. See Table
1-15 for reference citations for studies summarized here.
-------
TABLE 1-15. BIOCHEMICAL CHANGES IN EXPERIMENTAL ANIMALS
EXPOSED TO OZONE
Effect/response
03 concentration, ppm
References
Increased 02
consumption
Increased lysosomal
activities
Increased lung
hydroxyproline and
prolylhydroxylase
activity
Altered collagen and
elastin levels
Altered glycoprotein
secretions
Increased alveolar
protein and
permeability changes
Increased LDH
activity
Increased NADPH -
cytochrome -C-
reductase activity
Increased succinate
oxidase
Increased GSH
0.1, 0.2
0.1, 0.2, 0.8
0.2, 0.5, 0.8
0.8
0.7,
0.7,
0.8
0.8
0.5, 0.8
0.5
0.2, 0.8
0.5
0.45
0.8
0.8
0.5, 0.6, 0.8
0.5, 0.6, 0.8
0.6, 0.8
0.26, 0.51, 1.0
0.5, 1.0
0.6, 1.0
1.0
0.1
0.5
0.8
0.2, 0.35, 0.8
0.2, 0.5, 0.8
0.2, 0.5, 0.8
0.35, 0.5, 0.8
0.2, 0.5, 0.8
0.45
0.8
0.8
0.1
0.5,
0.2,
0.8
0.32
0.45
0.5
1.0
0.5, 1.0
Mustafa (1975)
Mustafa and Lee (1976)
Mustafa et al. (1973)
Chow et al. (1974)
Dillard et al. (1972)
Castleman et al. (1973)
Hussain et al. (1976a,b)
Last and Greenberg (1980)
Costa et al. (1983)
Last et al. (1979)
Bhatnagar et al. (1983)
Hesterberg and Last (1981)
Hussain et al. (1976a,b)
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, 1975)
Mustafa and Lee (1976)
Schwartz et al. (1976)
Mustafa et al. (1982)
Chow et al. (1976)
Elsayed et al. (1982a)
Chow et al. (1981)
Fukase et al. (1978)
Fukase et al. (1975)
DeLucia et al. (1975)
Moore et al. (1980)
Mustafa et al. (1982)
Chow et al. (1975)
0190GC/A
1-112
6/28/84
-------
TABLE 1-15. BIOCHEMICAL CHANGES IN EXPERIMENTAL ANIMALS
EXPOSED TO OZONE (continued)
Effect/response
Increased GSH
peroxidase
Increased GSH
reductase
Increased G-6-PD
Increased 6-P-GD
Increased NPSH
03 concentration, ppm
0.1
0.1, 0.2
0.2, 0.5, 0.8
0.2, 0.5, 0.8
0.5, 1.0
0.45
0.5
0.7, 0.75
0.8
0.9
0.9
0.8
0.1
0.1, 0.2
0.2, 0.5, 0.8
0.2, 0.5, 0.8
0.5, 1.0
0.2, 0.5, 0.8
0.45
0.5
0.7, 0.75
0.9
0.9
0.8
0.8
0.7, 0.75
0.1
0.1, 0.2
0.2, 0.35, 0.5, 0.8
0.5, 0.8
0.2, 0.5, 0.8
0.5, 1.0
0.2, 0.5, 0.8
0.32
0.45
0.5
0.45
0.75, 0.8
0.8
0.1, 0.2
0.2, 0.5, 0.8
0.45
0.8
References
Chow et al. (1981)
Plopper et al. (1979)
Mustafa and Lee (1976)
Chow et al . (1974)
Fukase et al. (1975)
Mustafa et al. (1982)
Chow et al. (1975)
Chow and Tappel (1972, 1973)
Chow et al. (1976)
Tyson et al. (1982)
Tyson et al . (1982)
Chow et al. (1976)
Chow et al. (1981)
Plopper et al. (1979)
Mustafa and Lee (1976)
Chow et al. (1974)
Fukase et al. (1975)
DeLucia et al. (1975)
Mustafa et al. (1982)
Chow et al. (1975)
Chow and Tappel (1972, 1973)
Lunan et al. (1977)
Tyson et al. (1982)
Elsayed et al. (1982a)
Chow et al. (1976)
Chow and Tappel (1972, 1973)
Chow et al. (1981)
Plopper et al . (1979)
Mustafa and Lee (1976)
Chow et al. (1974)
Schwartz et al . (1976)
Fukase et al. (1975)
DeLucia et al . (1972, 1975)
Moore et al. (1980)
Mustafa et al. (1982)
Chow et al. (1975)
Mustafa et al . (1982)
Chow and Tappel (1973)
Elsayed et al. (1982a,b;
1983)
Plopper et al. (1979)
DeLucia et al. (1975)
Mustafa et al. (1982)
Chow et al. (1976)
0190GC/A
1-113
6/28/84
-------
in this animal model, resulting in death. Such infections occur because of a
breakdown in a complex host defense system involving tissue morphology, transport
mechanisms, phagocytic ability, and various immune factors.
The data obtained in various experimental animal studies indicate that
short-term ozone exposure can reduce the effectiveness of several vital defense
systems including (1) the ability of the lung to inactivate bacteria and
viruses (Coffin et al., 1968; Coffin and Gardner, 1972a,b; Goldstein et al.,
1974, 1977; Hurst et al., 1970; Hurst and Coffin, 1971; Ibrahim et al., 1976;
Nakajima et al., 1972; 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; Thomas et al., 1981;
Aranyi et al., 1983; and (4) the pulmonary macrophage (Dowell et al., 1970;
Goldstein et al., 1971; Hadley et al., 1977; McAllen et al., 1981; Witz et al.,
1983; Amoruso et al., 1981). Studies have also indicated that the activity
level of the test subject and the presence of other airborne chemicals are
important variables that can influence the determination of the lowest effective
concentration of the pollutant (Gardner et al., 1977; Aranyi et al., 1983;
Ehrlich, 1980, 1983; Grose et al., 1980, 1982; Phalen et al., 1980; Goldstein
et al., 1974; 111 ing et al., 1980).
A major problem remains in assessing the relevance of these animal data
to humans. If this animal model is to be used to reflect the toxicological
response occurring in humans, then the endpoint for comparison of such studies
should not be mortality, since today few individuals die of bacterial pneumonias.
A better comparison in humans would be the increased prevalence of respiratory
illness in the community. Such a comparison is proper since both mortality
from respiratory infections (animals) and morbidity from respiratory infections
(humans) result from a loss in pulmonary defenses.
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, present knowledge of the physiology, metabo-
lism, 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. The
effects seen in animals represent alterations in basic biological systems.
One would not expect to see an equivalent response (e.g., mortality) in man,
0190GC/A 1-114 6/28/84
-------
but 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 ozone at which
effects become evident can be influenced by a number of factors, such as
preexisting disease, dietary factors, concurrent exposure to other pollutants,
or the presence of other environmental stresses, or a combination of these.
Thus, one could hypothesize that humans exposed to ozone could experience
similar effects. 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 ozone on host defense mechanisms in experimental animals
are summarized in Figure 1-13 and Table 1-16 (see Section 1.10.1 for criteria
used in developing this summary).
1.10.3.5 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 low levels of exposure to 0, will certainly protect
against subsequent lethal doses and the development of edema (Stokinger et al.,
1956; Fairchild, 1967; Coffin and Gardner, 1972a). The delay in mucociliary
activity (i.e., clearance reported for 0,) can also be eliminated by pre-
exposure to a lower concentration. This effect is only 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 CL, 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 prevented by prior treatment with low levels of 0^.
Dungworth et al. (1975b) and Castleman et al. (1980) have attempted to explain
tolerance by careful examination of the morphological changes that occur with
repeated 0- exposures. These investigators suggest that during continuous
exposure to 03 the injured cells attempt to initiate early repair of the
specific lesion. This repair thus results in a reduction of the effect first
observed. 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;
0190GC/A 1-115 6/28/84
-------
..v^
00-- ^
v^ . \J
0.1-
0.2-
e
a
a 0.3-
, -v
i C
s ; 0.4-
0
i 0.5-
c
Q)
g 0.6-
0
u
a, 0-7-
c
0
£ 0.8-
0.9-
1 R
\
i
i
<
•
i i
p
i
i
i
( 1
•
»
. <
i
i
i
i 1
i
i
i
4
1
1
1
I
(
1 1
1
I
|
1
|
{
»
1
Figure 1-13. Summary of effects of ozone on host defense mechanisms in experi-
mental animals. See Table 1-16 for reference citations for studies
summarized here.
-------
TABLE 1-16. EFFECTS OF OZONE ON HOST DEFENSE
MECHANISMS IN EXPERIMENTAL ANIMALS
Effect/response
03 concentration, ppm
References
Inhibited bactericidal
activity
0.5
0.99
0.62
0.7
0.7
0.4
0.4
Delayed mucociliary 0.4, 0.8, 1.0
clearance; accelerated 1.0
alveolar clearance 0.8
Altered macrophage
membrane
Decreased macrophage
function
Altered no. of defense
cells
Increased suscepti-
bility to infection
0.1, 1.0
0.5
0.5
0.5, 1.0
0.25, 0.5
0.5
0.5, 0.67
0.5, 0.67
0.8
1.0
1.0
0.2
0.2, 0.35, 0.5, 0.8
0.2, 0.35
0.2, 0.5, 0.8
0.25
0.5
0.5, 0.88
0.5
0.54, 0.88
0.8
1.0
1.0
0.5, 0.88
0.5, 0.8
0.2
0.2
0.08
0.08,
0.1
0.
0.
0.
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, E., et al. (1972)
Kenoyer et al. (1981)
Abraham et al. (1980)
Phalen et al. (1980)
Gardner et al. (1971)
Dowel 1 et al. (1970)
Hadley et al. (1977)
Goldstein et al. (1977)
Hurst et al. (1970, 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. (1975b)
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)
0.4,
0.3
0.7
Coffin et al.
Miller et al.
Ehrlich et al
Aranyi et al.
Illing et al.
Bergers et al
(1968)
(1978)
(1977)
(1983)
(1980)
(1983)
0190GC/A
1-117
6/28/84
-------
TABLE 1-16. EFFECTS OF OZONE ON HOST DEFENSE
MECHANISMS IN EXPERIMENTAL ANIMALS (continued)
Effect/response
03 concentration, ppm
References
Increased suscepti-
bility (cont'd)
Altered immune
activity
0.3
0.7,
1.0
0.1
0.5,
0.5,
0.59
0.9
0.8
0.8
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)
Bhatnagar et al. , 1983). 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 routes, depending on the
specific response measured. Tolerance does not imply complete or absolute
protection, because continuing injury does still occur, which could potentially
lead to nonreversible pulmonary changes.
1-10-4 Extrapulmonary Effects of Ozone
It was formerly believed that 03, on contact with respiratory system
tissue, immediately reacted and thus was not absorbed or transported to extra-
pulmonary sites. However, several studies suggest that either 03 or products
formed by the interaction of 0- and respiratory system tissue produce effects
in lymphocytes, erythrocytes, and serum, as well as in the parathyroid gland,
the myocardium, 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 QS causes extrapulmonary
changes is unknown. Mathematical models of 0~ dosimetry predict that very little
0~ penetrates to the blood of the alveolar capillaries. Whether these effects
J
result from 0, or a reaction product of 03 which penetrates to the blood and is
transported is the subject of speculation.
1.10.4.1 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
0190GC/A
1-118
6/28/84
-------
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 O, exposure concentra-
3
tions (490 pg/m , 0.25 ppm) an increase in activity is observed after exposure
3
ends. Higher 0., concentrations (980 pg/m , 0.5 ppm) produce a decrease in
O
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
3
atmosphere containing greater than 980 |jg/m (0.5 ppm) (Peterson and Andrews,
1963, Tepper et al., 1983). These studies suggest that the aversive effects
of 0,, may be due to lung irritation. It is unknown whether lung irritation,
odor, or a direct effect on the CNS causes change in rodent behavior at lower
0., concentrations.
1.10.4.2 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. Structural changes in the cell membranes and nuclei of
the myocardium muscle fibers in mice were found after 3 weeks of exposure to
3
392 pg/m (0.2 ppm) (Brinkman et al., 1964), and these effects were reversible
in clean air. The exposure of rats to 0- alone or in combination with cadmium
3
(1176 pg/m , 0.6 ppm 03) 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?
3
decreased 30 min following exposure of dogs to 588 pg/m (0.3 ppm) of 0~
(Friedman et al., 1983). The decrease in pulmonary capillary blood flow per-
sisted for as long as 24 hr following exposure.
1.10.4.3 Hematological and Serum Chemistry Effects. The data base for the
effects of CL on the hematological system is extensive and indicates that 03
or one of its reactive products can cross the blood-gas barrier, causing
changes in the circulating erythrocytes (RBC) as well as significant differ-
ences in various components of the serum.
0190GC/A 1-119 6/28/84
-------
Effects of 03 on the circulating RBCs can be readily identified by exa-
mining either morphological and/or biochemical endpoints. These cells are
structually and metabolically well understood and are available through rela-
tively non-invasive methods, which makes them ideal candidates for both human
and animal studies. A wide range of structural effects have been reported in
a variety of species of animals, including an increase in the fragility of
RBCs isolated from monkeys exposed to 1470 ug/m (0.75 ppm) of 0_ 4 hr/day for
^
4 days (Clark et al., 1978). A single 4-hr exposure to 392 ng/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
3
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
3
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 uniquely 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
3
had a decrease in RBC GSH after exposure to 1568 |jg/m (0.8 ppm) for 7 days
(Chow and Kaneko, 1979). Animals with a vitamin E-supplemented diet did not
have any changes in glucose-6-phosphate dehydrogenase (G-6-PD), superoxide
3
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
3
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
3
exposure of 627 ug/m (0.32 ppm) of 0~ for 6 hr. Decreases observed in AChE
activity occurred in both groups (Moore et al., 1980).
Other blood changes are attributed to Ov Rabbits exposed for 1 hr to
3
392 ug/m (0.2 ppm) of 0, showed a significant drop in total blood serotonin
3
(Veninga, 1967). Six- and 10-month exposures of rabbits to 784 ug/m (0.4 ppm)
0190GC/A 1-120 6/28/84
-------
of 0., produced an increase in serum protein esterase and in serum trypsin
«3
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; and 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 interim't-
3
tent (8 hr/day, 7 days). The CL concentration in both studies was 1568 |jg/m
(0.8 ppm) of 03.
Short-term exposure to low concentrations of 03 induced an immediate
change in the serum creatine phosphokinase level in mice. In this study, the
0 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 jjn 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 i_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.
1.10.4.4 Cytogenetic and Teratogenic Effects
Uncertainty still exists regarding possible reproductive, teratogenic,
and mutational effects of exposure to ozone. Based on various vn 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, 1977b, 1978; Hamelin and Chung, 1975, 1978; Scott and
Lesher, 1963; Erdman and Hernandez, 1982; Guerrero et al., 1979; Dubean and
Chung, 1979, 1982). The interpretation, relevance, and predictive values of
such studies to human health are questionable since (1) the concentrations
used were many-fold greater than what is found in the ambient air (see
0190GC/A 1-121 6/28/84
-------
Chapter 10); (2) attempts to extrapolate jm vitro exposure concentrations to
human exposure dose is not yet possible; and (3) direct exposure of isolated
cells to ozone is highly artifactual since it bypasses all the defenses of the
host that would normally be functioning in protecting the individual from the
inhaled gas. Furthermore, the direct exposure of isolated cells i_n vitro to
ozone may result in chemical reactions between ozone and culture media that
might not occur j_n vivo.
Important questions still exist regarding jm vivo cytogenetic effects of
ozone in rodents and humans. In 1971, Zelac et al. reported chromosomal
abnormalities in peripheral leukocytes of hamsters exposed to CL (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 et al. , 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.
1.10.4.5 Other Extrapulmonary Effects. A series of studies was conducted to
show that 0 increases drug-induced sleeping time in a number of species of
O
animals (Gardner et al., 1974; Graham, 1979; Graham et al., 1981, 1982a,b,
3
1983a,b). At 1960 ug/m (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
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
0190GC/A 1-122 6/28/84
-------
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., 1983a).
Several investigators have attempted to elucidate the involvement of the
endocrine system in 0_ toxicity. Most of these studies were designed to
investigate the hypothesis that the survival rate of mice and rats exposed to
lethal concentrations of 0, could be increased by use of various thyroid
blocking agents or by thyroidectomy. To follow up these findings, demons and
Garcia (1980a,b) investigated the effects of a 24-hr exposure to 1960 ng/m
(1.0 ppm) of 03 on the hypothalamo-pituitary-thyroid system of rats. These
three organs regulate the function of each other through various hormonal
feedback mechanisms. Ozone caused decreases in serum concentration of thyroid
stimulating hormone (TSH), in circulating thyroid hormones (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. The thyroid
O
gland itself was altered (e.g., edema) by 0,. The authors interpreted these
findings as an 0~~induced lowering of the hypothalamic set point for the
pituitary-thyroid axis and a simultaneous reduction of the activity of pro-
lactin inhibiting factor in the hypothalamus. The anterior pituitaries had
fewer cells but more TSH per cell. These cells also released a greater amount
of TSH into the culture medium.
The extrapulmonary effects of ozone in experimental animals are summarized
in Figure 1-14 and Table 1-17. Criteria used in developing the summary were
presented in Section 1.10.1
1.10.5 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. The few toxicological
studies on PAN indicate that it is much less acutely toxic than 0_. When the
effects seen after exposure to 03 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 pul-
monary defense system (Campbell et al., 1967; Dungworth et al. , 1969; Thomas
et al., 1979, 1981a). The concentrations of PAN required to produce these
effects are many times greater than what has been measured in the atmosphere
(0.037 ppm).
0190GC/A 1-123 6/28/84
-------
-------
TABLE 1-17. EXTRAPULMONARY EFFECTS OF OZONE IN EXPERIMENTAL ANIMALS
Effect/response
03 concentration, ppm
References
CNS effects
Hematological effects
Chromosomal, reproduc-
tive, teratological
effects
Liver effects
Endocrine system
effects
0.05, 0.5
0.1 - 1.0
0.12 - 1.0
0.2, 0.3, 0.5, 0.7
0.5
0.5
0.5
0.6
1.0
1.0
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
0
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
1.0
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. (1983a)
Brinkman et al. (1964)
Veninga (1967, 1970)
Veninga et al. (1981)
Moore et al. (1980; 1981a,b)
Jegier (1973)
P'an and Jegier (1972, 1976)
Menzel et al. (1972)
Larkin et al. (1983)
Clark et al. (1978)
Chow and Kaneko (1979)
Chow et al. (1974)
Menzel et al. (1975a)
Schlipkoter and Bruch (1973)
Dorsey et al. (1983)
Mizoguchi et al. (1973)
Christiansen and Giese (1954)
Brinkman et al. (1964)
Veninga (1967)
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)
demons and Garcia (1980a,b)
0190GC/A
1-125
6/28/84
-------
Similarly, most of the investigations reporting H?0? toxicity have involved
concentrations much higher than those found in the ambient air (0.1 ppm), or
the investigations were conducted by using various iji vitro techniques for
exposure. Very limited information is available on the health significance of
inhalation exposure to gaseous H-O^. Because H-C" 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.
A few jj} vitro studies have reported cytotoxic, genotoxic, and biochemical
effects of H?0? 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 adverse 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 et al. , 1972; Hueter et al. , 1966). Certain
other biological responses were observed in both treatment groups, including a
decrease in spontaneous activity, a decrease in infant survival rate, 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
X.
had relatively good correlation with structural changes (Hyde et al., 1978;
Gillespie, 1980; Lewis et al. , 1974). There were no significant differences
0190GC/A 1-126 6/28/84
-------
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
s\
manner.
1.11 EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS IN CONTROLLED EXPOSURES
1.11.1 Pulmonary Function Effects in Controlled Human Studies: Mechanical
Function of the Lung
Controlled human exposure (clinical) studies typically evaluate much
smaller numbers of subjects for shorter periods of time compared with large-
scale population studies. A major advantage of these studies is that exposures
to either single pollutants or combinations of pollutants are usually carried
out in environmentally controlled chambers in which relative humidity, tempera-
ture, and pollutant concentrations are well defined and carefully controlled.
Exposure conditions are designed to approximate representative ambient air
exposure conditions, especially those thought to be associated with the induc-
tion of acute effects. Inherent in the design, however, of controlled human
exposure studies are limitations on the range of pollutant exposures, types of
subjects studied, and types of effects studied. Conditions are strictly
monitored by human rights and medical ethics committees to assure that the
experimental exposures to the pollutants being tested will not lead to serious
morbidity or irreversible illness. Consequently, the types of acute pulmonary
responses assessed in controlled exposure studies could be considered as
"transient" and "reversible." Depending, however, upon the population at risk,
the method of exposure, and the level of subject activity, the so-called mild
and reversible health effects measured in controlled human exposure studies
may be indicators of other more serious health effects likely to occur if
prolonged or repeated ambient exposures to the same concentrations of pollutants
were encountered by study subjects. In addition, relatively small changes in
lung function of no particular concern for healthy, non-sensitive adults may
be medically important for sensitive individuals or for those having compromised
pulmonary functions.
1.11.1.1 General Population. A number of controlled human studies have
reported significant decrements in pulmonary function associated with ozone
exposure, including the presence of respiratory symptoms. The increased
severity of reported symptoms generally parallels the observed impairment in
pulmonary function. Table 1-18 summarizes pertinent studies on controlled
human exposure to ozone.
0190GC/A 1-127 6/28/84
-------
TABLE 1-18. SUMMARY TABLE: RESULTS OF CONTROLLED HUMAN EXPOSURES TO OZONE
Ozone3
concentration Measurement 'c Exposure
ug/m5
HEALTHY
627
1960
980
980
1470
ppm method duration
ADULT SUBJECTS AT REST
0.32 MAST, NBKI 2 hr
1.0
0.5 CHEM, NBKI 2 hr
0.50 CHEM, NBKI 2 hr
0.75
Activity
level (VE) Observed effect(s)
R Specific airway resistance increased with
acetylchol ine 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
392
686
0.12 CHEM, UV 2.5 hr
0.18
0.24
0.30
0.40
0.20 UV, UV 1 hr
0.35 (mouth-
piece)
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 s 0.24 ppm.
IE (77.5) @ vari- Decrement in forced expiratory volume and
able competitive flow with IE and CE; subjective symptoms
intervals increased with 03 concentration and may
CE (77.5) limit performance; respiratory frequency
increased and tidal volume decreased with
CE.
135 male McDonnell et al . ,
(divided into six 1983
exposure groups)
10 male Adams and Schelegle,
(distance runners) 1983
-------
TABLE 1-18 (cont'd) SUMMARY TABLE: RESULTS OF CONTROLLED HUMAN EXPOSURES TO OZONE
Ozone3
concentration Measurement ' Exposure
ug/m3
392
823
980
412
588
__, 980
I
ro
<^>
725
980
1470
784
784
ppm method duration
0.2 UV, UV 2 hr
0.42
0.50
0.21 UV, UV 1 hr
0.3 CHEM, NBKI 2 hr
0.5
0.37 MAST, NBKI 2 hr
0.50
0.75
0.4 UV, NBKI 2 hr
0.4 CHEM, NBKI & 3 hr
MAST, UV
Activity
level (VE)
IE (30 for male,
18 for female
subjects)
@ 15-min intervals
CE (81)
R (10), IE (31,
50, 67)
@ 15-min intervals
R (11) & IE (29)
@ 15-min intervals
IE (2xR)
@ 15-min intervals
IE (4-5xR)
for 15 min
Observed effect(s)
Repeated daily exposure to 0.2 ppm did not
affect response at higher exposure concen-
trations (0.42 or 0.50 ppm); large inter-
subject variability but individual
pulmonary function responses were highly
reproducible.
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 Q3 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 VE) 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 was
greatest on the 2nd of 5 exposure days;
attenuated response by the 4th day of
exposure.
No. and sex
of subjects
8 male
13 female
6 male
1 female
(distance cyclists)
40 male
(divided into four
exposure groups)
20 male
8 female (divided into
six exposure groups)
12 male
7 female
(divided into three
exposure groups)
10 male
4 female
Reference
Gliner et al . , 1983
Fol insbee et al . ,
1984
Fol insbee et al . ,
1978
Silverman et al. ,
1976
Dimeo et al . , 1981
Farrell et al . , 1979
-------
TABLE 1-18 (cont'd). SUMMARY TABLE: RESULTS OF CONTROLLED HUMAN EXPOSURES TO OZONE
Ozone3 b c
concentration Measurement ' Exposure
ug/m3 ppm method duration
784 0.4 CHEM, UV 3 hr
Activity
level (VE)
IE (4-5xR)
for 15 min
Observed effect(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 bronchial reactivity with
methacholine 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
I
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
2 hr
IE (3xR)
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.
8 male
3 female
Linn et al . , 1982b
1176 0.6 UV, NBKI
2 hr
(noseclip)
IE (2xR)
@ 15-min intervals
Specific airway resistance increased in 7
nonatopic subjects with histamine and
methacholine and in 9 atopic subjects
with histamine.
11 male
5 female (divided
by history of atopy)
Holtzman et al . ,
1979
1470
0.75
MAST, NBKI
2 hr
IE (2xR)
@ 15-min intervals
Decrements in spirometric variables
(20%-55%); residual volume and closing
capacity increased.
12 male
Hazucha et al.,
1973
-------
TABLE Irl8 (cont'd). SUMMARY TABLE: RESULTS OF CONTROLLED HUMAN EXPOSURES TO OZONE
Ozone3
concentration Measurement >c Exposure
ug/m3
ppm method duration
Activity
level (VE)
Observed effect(s)
No. and sex
of subjects
Reference
ASTHMATICS
392
490
SUBJECTS
235
353
490
392
588
784
0.2 CHEM, NBKI 2 hr
0.25 CHEM, NBKI 2 hr
WITH CHRONIC OBSTRUCTIVE LUNG DISEASE
0.12 UV, NBKI 1 hr
0.18 UV, NBKI 1 hr
0.25
0.2 CHEM, NBKI 2 hr
0.3
0.41 UV, UV 3 hr
IE (2xR)
@ 15-min intervals
R
IE (variable)
@ 15-min intervals
IE (variable)
@ 15-min intervals
IE (28) for
7.5 min each
half hour
IE (4-5xR)
for 15 min
No significant changes in pulmonary func-
tion. Small changes in blood biochemistry.
Increase in symptom frequency reported.
No significant changes in pulmonary func-
tion.
No significant changes in forced expiratory
performance or symptoms. Decreased arterial
oxygen saturation during exercise was
observed.
No significant changes in forced expiratory
performance or symptoms. Group mean arterial
oxygen saturation was not altered by 03
exposure.
No significant changes in pulmonary function
or symptoms. Decreased arterial oxygen
saturation during exposure to 0.2 ppm.
Small significant decreases in FVC and FEV3.0.
20 male
2 female
5 male
12 female
18 male
7 female
15 male
13 female
13 male
17 male
3 female
Linn et al. , 1978
Silverman, 1979
Linn et al . , 1982a
Linn et al . , 1983
Solic et al. , 1982
Kehrl et al. , 1983
Kulle et al. , 1984
Ranked by lowest observed effect level.
Measurement method: MAST = Kl-Coulometric (Mast meter); CHEM = gas phase chemiluminescence; UV = ultraviolet photometry.
Calibration method: NBKI = neutral buffered potassium iodide; UV = ultraviolet photometry.
Minute ventilation reported in L/min or as a multiple of resting ventilation. R = rest; IE = intermittent exercise; CE = continuous exercise.
-------
Studies employing at-rest (no exercise) exposures to ozone have shown
that ozone concentrations > 0.5 ppm produce significant decrements in pulmonary
function. Subsequent studies have employed various levels of exercise will
enhance to modify the change in function during ozone exposure. The severity
of exercise is expressed in terms of minute ventilation (VV). (See Volumes IV
and V for a glossary of terms.) Increased minute ventilation accompanying
exercise will enhance pulmonary decrements during ozone exposure. While the
most recent reports include actual measurements of minute ventilation obtained
during exposure, earlier publications often included only a description of the
exercise regimen. Table 1-19 presents estimates of the minute ventilation
associated with given exercise regimens. This table compares the level of
exercise with the work performed (watts or kg-m/min), the minute ventilation
required, and representative activities of individuals for that level of work
(exercise).
Based on reported studies of 1 to 3 hr duration, significant pulmonary
function impairment (decrement) occurs when exercise is combined with exposure
to ozone:
1. Light exercise (V£ < 25 L/min) - Effects at > 0.37 ppm 03;
2. Moderate exercise (V£ = 26-43 L/min) - Effects at > 0.30 ppm 03;
3. Heavy exercise (V£ = 44-63 L/min) - Effects at > 0.24 ppm 03; and
4. Very heavy exercise (VV > 64 L/min) - Effects at > 0.18 ppm 03,
with suggestions of decrements at 0.12 ppm 0.,.
For the majority of these studies, 15-min intermittent exercise alternated
with 15-min rest was employed for the duration of the exposure. Whether the
exercise is intermittent or continuous does not appear to affect the pulmonary
function response at a given concentration and ventilation.
Experimental design factors that influence the level of pulmonary function
changes observed, in terms of group means associated with an exposure study,
include the number of subjects tested, timing of the pulmonary function measure-
ments, and the ozone measurement and calibration techniques. A critical
minimum number of subjects is required to determine the significance of pulmonary
function changes associated with a given ozone exposure. For example, individual
responses in males versus females have been difficult to analyze because of
the limited number of females in the reported studies. In virtually all of
the reported studies, pulmonary function measurements have been made at the
0190GC/A 1-132 6/28/84
-------
TABLE 1-19. ESTIMATED VALUES OF OXYGEN CONSUMPTION AND MINUTE VENTILATION ASSOCIATED WITH REPRESENTATIVE TYPES OF EXERCISE3
Level of work
Light
Light
-
CO
co
Light
Moderate
Moderate
Moderate
Heavy
Heavy
Very heavy
Very heavy
Severe
Work perforned .
watts kg-m/min
25
50
75
100
125
150
175
200
225
250
300
150
300
450
600
750
900
1050
1200
1350
1500
1800
02 consumption,
L/mi n
0.
0.
1.
1.
1.
2.
2.
2.
3.
3.
4.
65
96
25
54
83
12
47
83
19
55
27
Minute
ventilation,
L/min
13
19
25
30
35
40
55
63
72
85
100+
Representative activities
Level walking at 2 mph; washing clothes
Level walking at 3 mph; bowling; scrubbing floors
Dancing; pushing wheelbarrow with 15- kg load;
simple construction; stacking firewood
Easy cycling; pushing wheelbarrow with 75- kg load;
using sledgehammer
Climbing stairs; playing tennis; digging with spade
Cycling at 13 mph; walking on snow; digging trenches
Cross-country skiing; rock climbing; stair climbing
with load; playing squash and handball; chopping
with axe
Level running at 10 raph; competitive cycling
Competitive long distance running; cross-country
skiing
aSee text for discussion.
kg-m/min = work performed each minute to move a mass of 1 kg through a vertical distance of 1 m against the force of gravity.
cAdapted from Astrand and Rodahl (1977).
-------
beginning and end of exposure. Intermittent exercise protocols during exposures
would permit pulmonary function to be measured shortly after the completion of
each exercise period (during the intervening rest period), but few investigators
have included them in their design protocol. The precise timing of this
measurement, however, does not appear to be as critical for ozone exposures as
it is for sulfur dioxide exposures.
Other variables have not been adequately addressed in the available
clinical studies. Information derived from the exposure of smokers and non-
smokers to ozone is sparse and somewhat inconsistent, perhaps partly because
of undocumented variability in smoking histories. Although some degree of
attenuation appears to occur in smokers, a definite conclusion is not yet
possible. Further and more precise studies are required to answer the complex
problems associated with personal and ambient pollutant exposures. While a
few studies have investigated sex differences in responses to ozone, they have
not conclusively demonstrated that men and women respond differently to ozone.
Furthermore, gender differences in pulmonary capacities have not been adequately
considered in the response evaluation. Environmental conditions such as heat
and relative humidity may enhance subjective symptoms and physiological impair-
ment following ozone exposure, but the results to date indicate that the
effects are no more than additive. Other variables, such as seasonal effects
and age, need to be considered. In particular, responses in the very young and
the aged need to be examined. In addition, there may be interactions between
and among these variables that may modify the response to CL, but such informa-
tion is generally lacking.
In the majority of the studies reported, assessment of the significance
of results was typically based on the mean ± variance of changes in lung
function resulting from exposure to ozone as compared to exposure to control
i
clean air. Decrements in pulmonary function can be expressed as a function of
the effective dose of ozone, where effective dose is defined as the product of
ozone concentration, minute ventilation, and exposure duration. The relative
contribution of these variables to pulmonary decrements is greater for ozone
concentration than for minute ventilation, which is greater than that for
exposure duration. Figure 1-15 uses the pulmonary function measurement FEV,
for relating group mean decrements in lung function to ozone concentration and
ventilation. Other measures of spirometric pulmonary function (volumes and
flows) are consistent with FEV, and hence are not depicted here. Although
mean changes are useful for making statistical inferences about homogeneous
0190GC/A 1-134 6/28/84
-------
8
ui
5
3
EC
O
S
CC
Z
X
LJU
Q
UJ
O
cc
O
a.
O
UJ
Ifl
120
110
100
90
80
70
60
50
40
LIGHT
EXERCISE
MODERATE
VERY HEAVY
EXERCISE
EXERCISE
'HEAVY \.
EXERCISE
X _
0.1 0.2 0.3 0.4 0.5
OZONE CONCENTRATION, ppm
0.6
0.7
0.8
Figure 1-15. Group mean decrements in 1-sec forced expiratory volume during 2-hr
ozone exposures with different levels of intermittent exercise: light (Vg <25 L/min);
moderate (V^ = 26-43 L/min); heavy (Vg = 44-63 L/min); and very heavy (Vg ^64
L/min). (Concentration-response curves are taken from Figures 13-2 to 13-5 in
Chapter 13, Volume V).
1-135
-------
populations, they may not be adequate for describing differences in responsive-
ness to ozone among individuals. While the significant mean changes observed
demonstrate that the differences in response between ozone and clean air
exposures are not the result of chance, the variance of responses was quite
large in many studies. Characterization of reports of individual responses to
ozone is pertinent since it permits the assessment of a segment of the general
population or special subpopulations that are potentially at-risk to 03 exposure.
Since there is good intrasubject reproducibility, the response of a given
individual to a single ozone exposure is probably a reliable estimate of the
intrinsic responsiveness of that individual to ozone. Sensitive individuals
in any given study group apparently weight the group mean response of that
study, such that the mean decrement is the result of a greater contribution
from a small proportion of the group rather than more or less equal contribu-
tions across the entire study group. In any given study, it is desirable to
have a sufficiently large overall subject group in order to be able to perform
either post hoc categorization of subjects or determine a distribution of both
group and individual responses.
1.11.1.2 Subjects with Preexisting Disease. In the past, individuals with
compromised lung function have been considered to be potentially at-risk to
ozone exposure compared to healthy nonsmokers (U.S. Environmental Protection
Agency, 1978). Significant decrements in pulmonary function are not observed,
however, in mild asthmatic subjects exposed to <0.25 ppm 03 for 2 hr at rest
or with intermittent light exercise. In patients with chronic obstructive
lung disease (COLD) performing light intermittent exercise, no decrements in
pulmonary function are observed for 1- and 2-hr exposures to <0.30 ppm 03-
Although these results which are derived from spirometric tests suggest that
asthmatics and patients with COLD may not be more sensitive to ozone than are
healthy subjects, experimental-design considerations in reported studies
suggest that this issue is still unresolved. Ethical concern with triggering
adverse reactions in these individuals dictates that experimental protocols
use only low ozone concentrations and light-to-moderate exercise levels. In
one study, however, subjects with mild chronic bronchitis were exposed to 0.4
ppm ozone and were found to be less sensitive than healthy nonsmokers.
In addition to overt changes in pulmonary function, enhanced nonspecific
bronchial reactivity has been observed following exposures to ozone concentra-
tions > 0.3 ppm. Exposure to 0.2 ppm of ozone with intermittent light exercise
does not affect nonspecific bronchial reactivity.
0190GC/A 1-136 6/28/84
-------
1.11.1.3 Intersubject Variability. Group mean decrements in pulmonary function
can be predicted with some degree of accuracy when expressed as a function of
effective dose of ozone, defined, again, as the product of ozone concentration,
minute ventilation, and exposure duration. The relative contribution of these
variables to pulmonary decrements, as noted in section 1.11.1.1, is greatest
for ozone concentration, followed by minute ventilation and exposure duration,
in order. A greater degree of predictive accuracy is obtained if the contribu-
tion of each of these variables is appropriately weighted. Several additional
factors, however, make the interpretation of prediction equations more difficult.
Intrasubject variability is relatively small, and the responses of a given
individual to a given ozone concentration are quite reproducible. There is
considerable intersubject variability, however, in the magnitude of pulmonary
function changes with ozone exposure. The data clearly indicate that some
individuals in the general population are more responsive than others to
ozone. No information is available to account for these differences. Consider-
ing the great variability among individuals in their pulmonary responses to
ozone exposure, prediction equations that use some form of effective dose may
not be adequate for predicting differences in responsiveness to 0, among
O
individuals.
1.11.1.4 Attenuation with Repeated Exposures. During repeated daily exposures
to ozone, decrements in pulmonary function (spirometric variables) are greatest
on the second exposure day; thereafter, pulmonary responsiveness to ozone is
attenuated, with smaller decrements occurring on each successive day until the
fourth or fifth exposure day, when very small or even no changes are observed.
Following a sequence of repeated daily exposures, there is a gradual time-
related return of susceptibility of pulmonary function to ozone exposure
similar to that observed prior to repeated exposures. This attenuated pulmonary
responsiveness usually persists for 3 to 7 days, but apparently can last up to
3 weeks in sensitive individuals.
The following general observations appear appropriate: (1) the time
required to abolish pulmonary response to ozone is directly related to the
magnitude of the initial response; (2) the longer the period required for
attenuation of pulmonary response to ozone, the longer the attenuation persists;
and (3) the severity of symptomatic responses is associated with the magnitude
of functional changes during repeated exposures.
0190GC/A 1-137 6/28/84
-------
Attenuation of bronchial reactivity has also been observed in response to
ozone. The time for attenuation of the initial enhancement in bronchial reac-
tivity is reported to be equivalent to that for decrement in pulmonary function;
however, this attenuation appears to last longer.
In studies exposing healthy nonsmokers and subjects with chronic bronchi-
tis to 0.4 ppm ozone, those with chronic bronchitis were less sensitive to
ozone, showed attenuation of the initial pulmonary function response earlier,
and lost the attenuated response sooner than the healthy nonsmokers.
Repeated daily exposure to a given low (0.20 ppm) concentration of ozone
does not affect the magnitude of decrement in pulmonary function resulting
from exposure at higher (0.40 to 0.50 ppm) ozone concentrations. This finding
is consistent with the proposition that functional adaptation may not occur in
the airways of individuals living in communities where the ambient ozone
levels do not exceed 0.2 ppm. The difficulty, however, of drawing such infer-
ences on the basis of narrowly defined laboratory studies is that under ambient
conditions a number of uncontrollable factors will modify the response. Most
notably, other pollutants may interact with ozone to modify changes in the
host at lower concentrations during generally more protracted exposures. The
evidence suggesting that Los Angeles residents exhibit functional adaptation
is sparse and requires confirmation.
Some evidence suggests that exercise performance may be limited by exposure
to ozone. Decrements in forced expiratory flow occurring with ozone exposure
•
during prolonged heavy exercise (VV = 65 to 81 L/min) along with increased
respiratory frequency and decreased tidal volume might be expected to produce
ventilatory limitations at near maximal exercise. Results from exposure to
ozone during high exercise levels (68 to 75 percent of max V0?) indicate that
discomfort associated with maximal ventilation may be an important factor in
limiting performance. There are not enough data available, however, to address
this issue adequately.
An issue that merits attention and needs resolution is whether attenuated
pulmonary responsiveness is beneficial or detrimental. It may possibly reflect
the presence or development of underlying changes in neural responses that are
protective and do not exact a physical penalty or it may reflect progressive
injury to lung tissues.
1.11.2 Other Effects of Ozone in Controlled Human Exposures
No consistent cytogenetic or functional changes have been demonstrated in
circulating lymphocytes from human subjects exposed to ozone concentrations as
0190GC/A 1-138 6/28/84
-------
high as 0.4 to 0.6 ppm. Chromosome or chromatid aberrations would therefore
be unlikely at lower ozone levels. Limited data have indicated that ozone can
interfere with biochemical mechanisms in blood erythrocytes and sera, but the
physiological significance of these studies is questionable.
1.11.3 Effects of Peroxyacetyl Nitrate and Mixtures in Controlled Human
Exposures ' ~~~~~~
No significant enhancement of respiratory effects has been consistently
demonstrated for combined exposures of ozone with sulfur dioxide, nitrogen
dioxide, 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 a series of studies on the effects of peroxyacetyl
nitrate (PAN) on healthy young and middle-aged males during intermittent
exercise on a treadmill. No significant effects were observed at PAN concentra-
tions of 0.25 to 0.27 ppm, which are an order of magnitude higher than the
daily maximum concentrations of PAN reported for relatively high oxidant areas
of the country (0.047 ppm). Two additional studies at 0.24 and 0.30 ppm of
PAN have suggested a possible limitation on forced expiratory volume and flow,
but there are not enough data yet for evaluating the significance of this
effect. Further studies are also required on the more complex mixtures of
pollutants found in the natural environment.
1.12 FIELD AND EPIDEMIOLOGICAL STUDIES OF THE EFFECTS OF OZONE AND OXIDANTS
1.12.1 Introduction
Field and epidemiological studies, when properly executed, offer a unique
view of health effects research because they involve the real world, i.e., the
study of human populations in their natural setting. However, these studies
also have attendant limitations that must be considered in a critical evaluation
of their results. One major problem in singling out the effects of one pollu-
tant in field studies of either morbidity or mortality in populations has been
the interference of other critical variables in the environment. Limitations
also exist for epidemiological research on the health effects of oxidants,
including interference or interaction between oxidants and other pollutants;
meteorological factors such as temperature; proper exposure assessments includ-
ing individual activity patterns and location of pollutant monitors; difficulty
0190GC/A 1-139 6/28/84
-------
in identifying oxidant species responsible for observed effects; and charac-
teristics of the populations such as hygiene practices, smoking habits, and
socioeconomic status.
Investigative approaches comparing communities with high 0_ concentra-
O
tions to those with low 0- concentrations have usually been unsuccessful,
often because actual pollutant levels have not differed enough during the
study and other important variables have not been adequately controlled. The
terms "oxidant" and "ozone" and their association with health effects are
often insufficiently clarified. Moreover, our knowledge about the measurement
and calibration methods used is still lacking. Also, as our knowledge and
skills in epidemiology improve, the incorporation of new key variables into
the analyses is required. Thus, the incorporation of individual exposure data
(e.g., from the home and workplace) becomes more of a necessity.
Both acute and chronic exposure situations have been reported in the
literature on photochemical oxidants. Relevant studies providing quantitative
information on effects associated with acute exposure include those on irrita-
tive symptoms, pulmonary function, and aggravation of existing respiratory
disease (Table 1-20). A few studies, of limited quality, have been reported
on morbidity, mortality, and chromosomal effects from chronic exposures.
1.12.2 Field and Epidemiological Studies of Effects of Acute Exposure
Studies on the irritative effects of CL have been complicated by the
3
presence of other photochemical oxidants and their precursors in the ambient
environment. That 0_ causes the eye irritation normally associated with smog
is doubtful. Nevertheless, studies indicate that eye irritation is likely to
occur at oxidant levels of about 0.10 ppm. A shown in Table 1-20, associations
between oxidant levels and symptoms such as eye, nose, 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). Zagraniski et al. (1979) also reported an association
3
of these symptoms with approximately 157 ug/m (0.08 ppm) ozone in adults with
asthma and allergies. Discomfort caused by irritative symptoms may be respon-
sible for the impairment of athletic performance reported in high school
students during cross-country track meets in Los Angeles (Wayne et al., 1967;
Herman, 1972). Although several additional studies have shown respiratory
irritation apparently related to ambient exposure in community populations,
none of these studies provide satisfactory quantitative data on acute respira-
tory illnesses.
0190GC/A 1-140 6/28/84
-------
TABLE 1-20. SUMMARY TABLE: ACUTE EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS IN POPULATION STUDIES
Lowest
estimated
effect level ,
ppm
Average maximum
hourly concentration
range during study,
ppm
Observed effect(s)
Subjects
Reference
OXIDANTS
b
0.10
0.10C
0,03-0.15
0.02-0.21
<0.23
Daily asthma attack rates increased on days
with high oxidant and particulate levels and
on cool days during a 34-week period in Los
Angeles.
Eye irritation incidence rates increased with
oxidant concentration.
Symptoms of eye irritation, sore throat,
headache, and cough related to oxidant
concentration and temperature but not
S02, N02, or NO.
Juvenile and adult
asthmatics
Adolescents
Children and
adolescents
Whittemore and Korn, 1980
Okawada et al . , 1979
Makino and Mizoguchi, 1975
0.10-0.15
<0.04-0.50
Symptoms of eye irritation, cough, chest
discomfort, and headache related to oxidant
concentration but not carbon monoxide,
nitrogen dioxide, or daily minimum
temperature.
Young adults
Hammer et al. , 1974
0.12L
0.06-0.37
Impaired athletic performance related to
oxidant concentration but not nitrogen
oxide, carbon monoxide, or particulate
levels 1 hr before cross-country track
meets in Los Angeles.
Adolescents
Wayne et al., 1967
Herman, 1972
-------
TABLE 1-20. SUMMARY TABLE: ACUTE EFFECTS OF OZONE AND OTHER PHOTOCHEMICAL OXIDANTS IN POPULATION STUDIES (continued)
Lowest Average maximum
estimated hourly concentration
effect level, range during study,
ppm ppm
Observed effect(s)
Subjects
Reference
OZONE
0.08 0.004-0.235
0.08 0.01-0.12
^ 0.08 0.01-0.12
ro
0.15 0.01-0.30
0.16e 0.16-0.17
Increased daily prevalence rates for cough,
eye, and nose irritation in smokers and
patients with predisposing illnesses; pH of
particulate was associated with eye, nose, and
throat irritation while suspended sul fates were
not associated with any symptoms.
Daily peak flows decreased 12.2 to 14.8% with
ozone and total suspended particulate matter.
Decreased daily peak flows and increased pre-
valence rate for acute symptoms associated
with ozone, low temperature, and high total
suspended particulate matter.
Increased airway resistance associated with
ozone, sulfur dioxide, and temperature.
Small decrement in forced expiratory function
and increased symptoms with exercise in both
normals and asthmatics.
Asthma and allergy
patients; normal
adults
Children and
young adults
Adult asthmatics
Adolescents
Normal and
asthmatic adults
Zagraniski et al . , 1979
Lebowitz et al., 1982a, 1983
Lebowitz, 1984
Lebowitz et al . , 1982a, 1983
Lebowitz, 1984
Kagawa and Toyoma, 1975
Kagawa et al. , 1976;
Kagawa, 1983
Linn et al . , 1980, 1983
Ranked by lowest estimated effect level for oxidant or ozone.
Not determined.
CU.S. Environmental Protection Agency, 1978.
dHasselblad et al. , 1976.
eDaily mean concentration of ozone was monitored by ultraviolet photometry inside a mobile laboratory; Linn et al., 1980, report concentrations
multiplied by 1.25 that correspond to the neutral buffered potassium iodide (KI) method.
-------
Acute epidemiological studies in children and young adults have suggested
that decreased peak flow and increased airway resistance occur over the range
3
of 0, concentrations from 157 to 294 pg/m (0.08 to 0.15 ppm) (Kagawa and
O
Toyoma, 1975; Kagawa et al., 1976; Kagawa, 1983; Lebowitz et al., 1982a, 1983;
Lebowitz, 1984). Qualitative studies support this finding (McMillan et al.,
1969; Lebowitz et al. , 1974; Fabbri et al., 1979). No controlled human expo-
sure studies in children are presently available for comparison, although
3
studies in adults appear to show no effect below 235 |jg/m . (0.12 ppm) 03
(Chapter 11).
In studies of exacerbation of asthma and chronic lung diseases, the major
problems in most of the studies have been the lack of information on the
possible effects of medications, the absence of records for all days on which
symptoms could have occurred, and the possible concurrence of symptomatic
attacks. Investigators who have been able to control some of these variables
have found consistent effects of 0~ on asthma (Table 1-20). Their findings
have been in accordance with those of some of the earlier, more qualitative
studies. Whittemore and Korn (1980) found small increases in the probability
of asthma attacks associated with increases of 0.10 ppm in oxidant levels.
Zagraniski et al. (1979) reported an increased prevalence rate for respiratory
3
symptoms with approximately 157 (jg/m (0.08 ppm) 03 in patients with asthma.
Linn et al. (1980, 1983) found decreased pulmonary function and increased
symptoms in lightly exercising asthmatics exposed to 314 to 333 pg/m (0.16 to
0.17 ppm) 0., or greater, regardless of other pollutants. With increased
3
exercise levels, small effects were found at 235 ng/m (0.12 ppm) 0~. Lebowitz
et al. (1982a, 1983) and Lebowitz (1984) showed effects in asthmatics, related
also to temperature, at 03 levels of 102 to 235 ng/m (0.052 to 0.12 ppm).
There have been no consistent findings of symptom aggravation or changes in
lung function in patients with other chronic lung diseases besides asthma.
1.12.3 Epidemiological Studies of Effects of Chronic Exposure
Apparent adaptations have been observed under controlled conditions with
humans, but this effect would be difficult to demonstrate in community popula-
tions. Recent work with animals suggests that the processes involved in
adaptation may lead to other, perhaps adverse effects, but no implications for
human health can yet be drawn.
0190GC/A 1-143 6/28/84
-------
Although animal studies indicate that 0., impairs defenses against infec-
tion (Chapter 10), this impairment has not been examined in clinical studies.
No positive studies of 0~ effects on acute respiratory illnesses have been
reported in human populations. In addition, most studies have yet to address
the hypothesis that years or decades of air pollution exposures beginning in
childhood, especially among the sensitive, may increase the risk of developing
chronic illness (U.S. Environmental Protection Agency, 1978).
The lack of quantitative measures of oxidant levels limits the usefulness
of many studies of pollution exposure and mortality. In addition, properly
designed studies have not been conducted to address the effects of oxidants on
the growth and development of the lung or on the progression of chronic diseases,
although the available evidence is consistent with toxicological data indicating
that 0 is not a strong mutagen or a demonstrable carcinogen at ambient concen-
trations. Most long-term studies have employed average annual levels or have
involved broad ranges of pollution; others have used a simple high-oxidant/low-
oxidant dichotomy and compared mortality results. Failure to relate mortality
to specific levels (and types) of oxidant pollutants makes formulation of
exposure-response relationships impossible. Epidemiological identification of
chronic effects of air pollution generally requires well-conducted replicated
studies of large, well-defined populations over long periods of time, which
are not available at this time for 0- or other photochemical oxidants.
Studies using quantitative measures find that "ozone alerts" occur fre-
quently in association with high temperature. The latter may mask 0- effects
*5
or by itself produce excess mortality in susceptible elderly cardiopulmonary
patients. When attempts have been made to distinguish the effects of CL, no
O
positive relationship has been found with mortality; rather, the effect corre-
lates most closely with elevated temperature.
1.13 SUMMARY OF THE EVALUATION OF INTEGRATED HEALTH EFFECTS DATA
1.13.1 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 03- Airway resistance was not changed at these 0., concen-
trations. Breathing 0~ at rest at concentrations < 0.5 ppm did not significantly
impair pulmonary function although the occurrence of some 03~related pulmonary
symptoms has been suggested in a number of studies.
0190GC/A 1-144 6/28/84
-------
One of the principal modifiers of the magnitude of response to 0., is
minute ventilation (VF), 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 VL not only increase the overall volume of inhaled pollutant, but
such ventilatory patterns also promote a deeper penetration of ozone into the
peripheral lung, which is the region most sensitive to ozone and where a
greater absorption of ozone will occur. These processes are further enhanced
*
at high work loads (V_ > 35 L/min), since the mode of breathing will most
likely change at that VV from nasal to oronasal.
Even in well-controlled experiments on a homogeneous group of subjects,
physiological responses to the same work and pollutant loads will vary widely
among individuals. Despite such large interindividual variability, the magni-
tude 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, significant pulmonary function impairment (decrement) occurs
when exercise is combined with exposure to ozone:
1. Light exercise (V£ < 25 L/min) - Effects at > 0.37 ppm 03;
2. Moderate exercise (V£ = 26 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 (VV > 64 L/min) - Effects at > 0.18 ppm 0^, with
suggestions of decrements at 0.12 ppm 0».
O
For the majority of the controlled studies, 15-min intermittent exercise
alternated with 15-min rest was employed for the duration of the exposure.
Continuous exercise equivalent in duration to the sum of intermittent exercise
periods at comparable ozone concentrations (0.2 to 0.4 ppm) and minute ventila-
tion (60 to 80 L/min) seems to elicit about the same changes in pulmonary
function. The maximum response to 0, exposure can be observed within 5 to
10 min following 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
functional recovery, other regulatory systems may still exhibit abnormal
responses when stimulated; e.g., airway hyperreactivity might persist for
days.
0190GC/A 1-145 6/28/84
-------
A close association has been observed between changes in pulmonary function
and the occurrence of respiratory symptoms in response to acute exposure to
0~. This association holds for both the time-course and magnitude of effects.
The symptoms found in association with clinical exposure to 0., alone and with
exposure to photochemical air pollution are similar but not identical. Eye
irritation, one of the most common complaints associated with photochemical
pollution, is not characteristic of clinical exposures to 0^, even at concen-
trations several times higher than any likely to be encountered in ambient
air. There is also evidence to suggest that other symptoms, indicative of
either upper or lower respiratory tract irritation, are more likely to occur
in populations exposed to ambient air pollution than in subjects exposed to 0^
alone in chamber studies. For example, cough has been reported at 0.08 ppm 0^
and at 0.10 ppm oxidants in epidemiological studies and during clinical exposure
to 0.12 ppm 0.3; nose and throat irritation have been reported in community
studies in association with 0.10 ppm oxidants but not at or below 0.15 ppm 0^
in laboratory studies. Between 0.15 and 0.30 ppm, a variety of both respira-
tory and nonrespiratory symptoms have been reported in controlled exposures.
They include throat dryness, difficulty or pain during deep inspiration, chest
tightness, substernal soreness or pain, wheezing, lassitude, malaise, and
nausea. Symptoms are therefore considered to be useful adjuncts in assessing
the effects of 0, and photochemical pollution, particularly if combined with
O
objective measures of lung function.
Only a few studies have been designed to examine the effects of 03 on
exercise performance. In one study, very heavy exercise (V^ > 64 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 inconsistent. 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 enhance
subjective symptoms and physiological impairment following 03 exposure.
Modification of the effects of 0_ by these factors may be attributed to in-
creased ventilation which, like exercise, increases the overall volume of
inhaled pollutant and promotes greater penetration into peripheral areas of
the lung.
0190GC/A 1-146 6/28/84
-------
Additional factors suspected of altering sensitivity to ozone are numerous.
For example, age differences, especially between the very young and the very
old; gender differences, especially for children; personal habits such as
cigarette smoking; and possibly social, cultural, or economic factors such as
differences in nutritional status or differences in immunological status may
predispose individuals to susceptibility to ozone. 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 CL. The
following briefly summarizes what is actually known from the data regarding
the importance of these factors:
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^, studies have not been designed to test adequately for effects of
0- 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, „,
appears to be affected more than that of men under similar exercise and expo-
sure conditions, but the differences have not been analyzed systematically.
Further research is needed to determine whether differences in lung volumes or
differences in exercise capacity during exposure may lead to sex differences
in responses to CL.
O
3. Smoking Status. Differences between smokers and nonsmokers have
been studied often, but the data are not documented well and are often confusing.
Published results indicate a discrepancy in findings. There is some evidence,
however, to suggest that smokers may be less sensitive to CL.
O
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 hematological
effects from CL exposure.
0190GC/A 1-147 6/28/84
-------
Successive daily brief exposures of healthy human subjects to 0_ (<0.7 ppm
O
for approximately 2 hr) induce a typical temporal pattern of response. 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 effects are, on the average, 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 its
concentration. In addition, concentrations of 0_ that have no detectable
effect appear not to invoke changes in response to subsequent exposures at
higher CL concentrations. 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 symptomatic response is
generally related to the magnitude of the functional response, partial sympto-
matic attenuation 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. While there is limited information obtained
from controlled laboratory studies to support this hypothesis, additional
information is required.
Responses to 0~, whether functional, biochemical, or morphological, have
the potential for altering responses in both man and laboratory animals during
repeated or continuous exposure. At present, the underlying mechanisms for
this response are poorly understood and the effectiveness of such mitigating
forces in protecting the long-term health of the individual against 0^ is
still uncertain. Therefore, hyperresponsiveness to CL, including changes in
bronchial reactivity, and the subsequent attenuation of responsiveness may be
viewed as sequential states in a continuing process.
1.13.2 Health Effects in Potentially Susceptible Individuals
Currently available evidence indicates that individuals with preexisting
disease respond to 0~ 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
O
indication from epidemiological studies that asthmatics may be symptomatically
and possibly functionally more sensitive than healthy individuals to ambient
0190GC/A 1-148 6/28/84
-------
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 CL can be
O
adequately determined. None of these factors has been sufficiently studied
in relation to 0 exposures to give definitive answers. Thus, estimates of
at-risk populations are difficult to assess with any precision.
1.13.3 Extrapolation of Effects Observed in Animals to Human Populations
Several animal experiments have demonstrated increased susceptibility to
respiratory infections following CL exposure. Thus, it could be hypothesized
that humans exposed to CL could experience decrements in their host defenses
against infection. At the present time, however, these effects have not been
described in humans exposed to CL, 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
CL, including cardiovascular, reproductive, and teratological effects, along
with changes in endocrine function. The implications of these findings for
human health are difficult to judge at the present time. In addition, central
nervous system effects, alterations in red blood cell morphology and enzymatic
activity, as well as chromosomal effects on circulating lymphocytes, have been
observed in man and laboratory animals following exposure to high concentra-
tions of 0^. It is unlikely, however, that these changes would have any
functional significance in humans when exposure schedules are used that are
representative of exposures that the population at large might actually expe-
rience.
Despite wide variations in study techniques and experimental designs,
acute and subchronic exposures of animals to levels of ozone < 0.5 ppm produce
similar types of responses in all species examined. A characteristic inflamma-
tory lesion occurs at the junction of the conducting airways and the gas-
exchange regions of the lung after acute CL exposure. Dosimetry model Simula-
O
tions predict that the maximal tissue dose of CL occurs in this region of the
O
lung. Continuation of the inflammatory process during longer CL exposures is
*3
especially important since it appears to be correlated with increased lung
collagen content and remodeling of the centriacinar airways. There is no
evidence of emphysema, however, in the lungs of animals exposed to 0, for
prolonged periods of time.
0190GC/A 1-149 6/28/84
-------
Since substantial animal data exists for 0_-induced changes in lung
«5
structure 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 concentra-
tions at which man might experience similar effects.
1.13.4 Health Effects of Other Photochemical Oxidants and Pollutant Mixtures
Controlled human and animal exposures have not consistently demonstrated
any enhancement of respiratory effects for combined exposures of 0, with S0_,
N0?, CO, or HLSO. and other particulate aerosols. Ozone alone is considered
to be responsible for the observed effects of those combinations or of multi-
ple mixtures of these pollutants. In addition, there have been far too few
controlled toxicological studies with other oxidants, such as peroxyacetyl
nitrate or hydrogen peroxide, to permit any sound scientific evaluation of
their contribution to the toxic action of photochemical oxidant mixtures.
Nevertheless, there is still some concern that combinations of oxidant pollu-
tants with other pollutants may contribute to the symptom aggravation and
decreased lung function described in epidemiological studies on individuals
with asthma and in children and young adults. For this reason, the effects of
interaction between inhaled oxidant gases and other environmental pollutants
on the lung need to be systematically studied using exposure regimens that are
more closely representative of ambient air ratios of peak concentrations,
frequency, duration, and time intervals between events.
1.13.5 Identification of Potentially At-Risk Populations or Subpopulations
Despite uncertainties that may exist in the data, it is possible to
identify three major subpopulations that may be at particular risk from expo-
sure to ozone, based on known health effects, activity patterns, personal
habits, and actual or potential exposures to ozone.
The first major subpopulation that appears to be at particular risk from
exposure to ozone is that subgroup of the general population characterized as
having preexisting disease. Available data on actual differences in sensiti-
vity between these and healthy, normal members of the general population
indicate that under the exposure regimes used to date individuals with pre-
existing disease may not be more sensitive to ozone than normal individuals.
0190GC/A 1-150 6/28/84
-------
Nevertheless, two considerations place these individuals among subpopulations
at potential risk from exposure to ozone. First, it must be noted that concern
with triggering untoward reactions has necessitated the use of low concentra-
tions and low exercise levels in most studies on subjects with preexisting
disease. Therefore, few or no data on responses at higher concentrations and
higher exercise levels are available for comparison with responses in normal
subjects. Thus, definitive data on responses in individuals with preexisting
disease are not available and may not ever become 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 aller-
gies, 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.
A second major subpopulation at apparent special risk from exposure to
ozone consists of individuals ("responders") in the general population, not
yet characterized medically except for their responses to ozone, who experience
greater decrements in lung function from exposure to ozone than those observed
in the remainder of the general population. As yet no means 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 major
subpopulation 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 individuals with preexisting 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
subgroups may be considered to be potentially at risk, depending upon other
determinants of total ozone dose, 0_ concentration, and exposure duration.
0190GC/A 1-151 6/28/84
-------
Other biological and nonbiological factors are suspected of influencing
responses to ozone. Data remain inconclusive at the present, however, regard-
ing the importance of age, gender, and other factors in influencing response
to ozone. Thus, at the present time, no other subpopulations 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" populations are
both the domain of the Administrator.
0190GC/A 1-152 6/28/84
-------
1.14 REFERENCES
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. M. ; Januszkiewicz, A. J. ; Mingle, M. ; Welker, M. ; Wanner, A.;
Sackner, M. A. (1980) Sensitivity of bronchoprovocation and trachea!
mucous velocity in detecting airway responses to CL. J. Appl. Physio!.
Respir. Environ. Exercise Physio!. 48: 789-793.
Adams, W. C. ; Schelegle, E. S. (1983) Ozone toxicity effects consequent to
prolonged, high intensity exercise in trained endurance athletes. J.
Appl. Physio!. Respir. Environ. Exercise Physio!. 55: 805-812.
Adedipe, N. 0.; Barrett, R. E.; Ormrod, D. P. (1972) Phototoxicity and growth
responses of ornamental bedding plants to ozone and sulfur dioxide. J.
Am. Soc. Hort. Sci. 97: 341-345.
Adedipe, N. 0.; Ormrod, D. P. (1974) Ozone induced growth suppression in
radish plants in relation to pre- and post-fumigation temperatures. Z.
Pflanzen Physiol., 71: 281-287.
Aharonson, E. F.; Menkes, H.; Gurtner, G.; Swift, D. L.; Proctor, D. F. (1974)
Effect of respiratory airflow rate on removal of soluble vapors by the
nose. J. Appl. Physio!. 27: 654-657.
Allen, A. 0.; Hochanadel, C. J.; Ghormley, J. A.; Davis, T. W. (1952) Decomposi-
tion of water and aqueous solutions under mixed fast-neutron and y-radia-
tion. J. Phys. Chem. 56: 575-586.
Alpert, S. M. ; Gardner, D. E. ; Hurst, D. J. ; Lewis, T. R. ; Coffin, D. L.
(1971b) Effects of exposure to ozone on defensive mechanisms of the lung.
J. Appl. Physiol. 31: 247-252.
Alpert, S. M.; Schwartz, B. B.; Lee, S. D.; Lewis, I. R. (1971a) Alveolar
protein accumulation. A sensitive indicator of low level oxidant toxi-
city. Arch. Intern. Med. 128: 69-73.
Altshuller, A. P. (1983) Measurements of the products of atmospheric photo-
chemical reactions in laboratory studies and in ambient ail—relation-
ships between ozone and other products. Atmos. Environ. 17: 2383-2427.
Altshuller, A. P.; McPherson, S. P. (1963) Spectrophotometric analysis of
aldehydes in the Los Angeles atmosphere. J. Air Pollut. Control Assoc.
13:109-111.
Amdur, M. 0.; Ugro, V.; Underhi!!, D. W. (1978) Respiratory response of guinea
pigs to ozone alone and with sulfur dioxide. Am. Ind. Hyg. Assoc. J. 39:
958-961.
Amoruso, M. A.; Witz, G. ; Goldstein, B. D. (1981) Decreased superoxide anion
radical production by rat alveolar macrophages following inhalation of
ozone or nitrogen dioxide. Life Sci. 28: 2215-2221.
019COR/B 1-153 6/30/84
-------
Andreae, W. A. (1955) A sensitive method for the estimation of hydrogen peroxide
in biological materials. Nature (London) 175: 859-860.
Aranyi, C. , Vana, S. C.; Thomas, P. T.; Bradof, J. N.; Renters, J. D. ; Graham,
J. A.; Miller, F. J. (1983) Effects of subchronic exposure to a mixture
of 0.,, SO- and (NH.)?SO., on host defenses of mice. J. Toxicol. Environ.
Health 12: 55-71. * * *
Armstrong, W. A.; Humphreys, W. G. (1965) A L.E.T. independent dosimeter based
on the chemiluminescent determination of H?0,,. Can. J. Chem. 43: 2576.
Atkinson, R.; Aschmann, S. M.; Fitz, D. R. ; Winer, A. M. ; Pitts, J. N. , Jr.
(1982) Rate constants for the gas-phase reactions of Q~ with selected
organics at 296 K. Int. J. Chem. Kinet. 14: 13-18.
Atkinson, R. ; Aschmann, S. M.; Winer, A. M.; Pitts, J. N. , Jr. (1981) Rate
constants for the gas-phase reactions of 0- with a series of carbonyls at
296 K. Int. J. Chem. Kinet. 13: 1133-1142.
Atkinson, R.; Aschmann, S. M.; Winer, A. M.; Pitts, J. N., Jr. (1984c) Kinetics
of the gas phase reactions of NO- radicals with a series of dialkenes,
cycloalkenes and monoterpenes at ^95 ± 1 K. Environ. Sci. Technol. (in
press).
Atkinson, R.; Carter, W. P. L. (1984) Kinetics and mechanisms of the reactions
of ozone with organic compounds in the gas phase, submitted to Chem. Rev.
Atkinson, R. ; Carter, W. P. L. ; Plum, C. N. ; Winer, A. M.; Pitts, J. N., Jr.
(1984d) Kinetics of the gas phase reactions of N0« radicals with a series
of aromatics at 296 ± 2 K. Int. J. Chem. Kinet. fin press).
Atkinson, R.; Darnall, K. R. ; Lloyd, A. C. ; Winer, A. M. ; Pitts, J. N. , Jr.
(1979) Kinetics and mechanisms of the reactions of the hydroxyl radical
with organic compounds in the gas phase. Adv. Photochem. 11: 375-488.
Atkinson, R. ; Darnall, K. R.; Pitts, J. N., Jr. (1978) Rate constants for the
reactions of OH radicals and ozone with cresols at 300 ± 1 K. J. Phys.
Chem. 82: 2759-2761.
Atkinson, R. ; Lloyd, A. C. (1984) Evaluation of kinetic and mechanistic data
for modeling of photochemical smog. J. Phys. Chem. Ref. Data (in press).
Atkinson, R.; Pitts, J. N. , Jr.; Aschmann, S. M. (1984b) Tropospheric reactions
of dimethyl sulfide with NO- and OH radicals. J. Phys. Chem. (in press).
Atkinson, R. ; Plum, C. N. ; Carter, W. P. L. ; Winer, A. M.; Pitts, J. N., Jr.
(1984a) Rate constants for the gas phase reactions of N03 radicals with a
series of organics in air at 298 ± 1 K. J. Phys. Chem. (in press).
Atwal, 0. S. ; Pemsingh, R. S. (1981) Morphology of microvascular changes and
endothelial regeneration in experimental ozone-induced parathyroiditis.
Am. J. Pathol. 102: 297-307.
019COR/B 1-154 6/30/84
-------
Atwal, 0. S. ; Samagh, B. S. ; Bhatnagar, M, K. (1975) A possible autoimmune
parathyroiditis following ozone inhalation. II. A histopathologic,
ultrastructural, and immunofluorescent study. Am. J. Pathol. 80: 53-68.
Atwal, 0. S. ; Wilson, T. (1974) Parathyroid gland changes following ozone
inhalation. A morphologic study. Arch. Environ. Health 28: 91-100.
Barry, B. E. ; Miller, F. J. ; Crapo, J. D. (1983). Alveolar epithelial injury
caused by inhalation of 0.25 ppm of ozone. In: Lee, S. D. ; Mustafa,
M. G. ; Mehlman, M. A. , eds. International symposium on the biomedical
effects of ozone and related photochemical oxidants; March 1982; Pinehurst,
NC. Princeton, NJ: Princeton Scientific Publishers, Inc; pp. 299-309.
(Advances in modern environmental toxicology: v. 5.)
Bartlett, D. ; Faulkner, C. S. II; Cook, K. (1974) Effect of chronic ozone
exposure on lung elasticity in young rats. J. Appl. Physio!. 37: 92-96.
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; January. Volume I.
Research Triangle Park, NC: U.S. Environmental Protection Agency; pp.
13-17; EPA report no. EPA-600/3-77~001a.
Beloin, N. J. (1972) A field study: fading of dyed fabrics by air pollution.
Text. Chem. Color. 4: 77-78.
Beloin, N. J. (1973) Fading of dyed fabrics by air pollutants: a chamber
study. Text. Chem. Color. 5: 128-133.
Bennett, J. H. (1979) Foliar exchange of gases. Ln: Heck, W. W.; Krupa, S.
K. ; and Linzon, S. N. , Eds. Handbook of Methodology for the Assessment
of Air Pollution Effects on Vegetation. Air Pollution Control Association,
Pittsburgh, pp. 10-1 to 10-29.
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.
Benoit, L. F. ; Skelly, J. M. ; Moore, L. D. ; Dochinger, L. S. (1982) Radial
growth reductions in 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.
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.
Bergers, W. W. A.; Gerbrandy, J. L. F. ; Stap, J. G.; Dura, E. A. (1983) Influ-
ence of air polluting components viz. ozone and the open air factor on
host-resistance towards respiratory infections. In: Lee, S. D.; Mustafa,
M. G. ; Mehlman, M. A. , eds. International symposium on the biomedical
effects of ozone and related photochemical oxidants; March 1982; Pinehurst,
NC. Princeton, NJ: Princeton Scientific Publishers, Inc.; pp. 459-467.
(Advances in modern environmental toxicology: vol. 5).
019COR/B 1-155 6/30/84
-------
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 the 74th Annual Meeting of the Air Pollution Control Assoc-
ciation; June; Philadelphia, PA. Berkeley, CA: University of California,
Lawrence Berkeley Laboratory; report no. LBL-12189. Cited in: Yocom, J.
E. (1982).
Berliner, J. A.; Kuda, A.; Mustafa, M. G. ; Tierney, D. F. (1978) Pulmonary
morphologic studies of ozone tolerance in the rat (a possible mechanism
for tolerance). Scanning Electron Microsc. 2: 879-884.
Berry, C. R. ; Ripperton, L. A. (1963) Ozone, a possible cause of white pine
emergence tipburn. Phytopathology 53: 552-557.
Bhatnagar, R. S.; Hussain, M. Z. ; Sorensen, K. R.; Mustafa, M. G.; von Dohlen,
F. M. ; Lee, S. D. (1983) Effect of ozone on lung collagen biosynthesis.
In: Lee, S. D. ; Mustafa, M. G. ; Mehlman, M. A. , eds. International
symposium on the biomedical effects of ozone and related photochemical
oxidants; March 1982; Pinehurst, N.C. Princeton, NO: Princeton Scientific
Publishers, Inc.; pp. 311-321. (Advances in modern environmental toxi-
cology: vol. 5).
Billings, W. D. (1978) Plants and the ecosystem. 3rd Edition. Belmont, CA:
Wadsworth Publishing Company, Inc.; pp. 1-62.
Blum, U. T.; Smith, G. R.; and Fites, R. C. (1982) Effects of multiple (k
exposures on carbohydrate and mineral contents of Ladino clover. Environ.
Exp. Bot., 22: 143-154.
Boatman, E. S. ; Sato, S. ; Frank, R. (1974) Acute effects of ozone on cat
lungs. II. Structural. Am. Rev. Respir. Dis. 110: 157-169.
Boche, R. D. ; Quilligan, J. J. , Jr. (1960) Effects of synthetic smog on spon-
taneous activity of mice. Science (Washington, DC) 131: 1733-1734.
Bogaty, H.; Campbell, K. S.; Appel, W. D. (1952) The oxidation of cellulose by
ozone in small concentrations. Text. Res. J. 22: 81-83.
Bellinger, M. J. ; Parrish, 0. D.; Hahn, C.; Albritton, D. L. ; Fehsenfeld, F.
C. (1982) NO measurements in clean continental air. In: Proceedings of
2nd Symposium on Composition of the Nonurban Troposphere; May; Williamsburg,
VA.
Boorman, G. A.; Schwartz, L. W. ; Dungworth, D. L. (1980) Pulmonary effects of
prolonged ozone insult in rats. Morphometric evaluation of the central
acinus. Lab. Invest. 43: 108-115.
Boorman, G. A.; Schwartz, L. W. ; McQuillen, N. K. ; Brummer, M. E. (1977)
Pulmonary response following long-term intermittent exposure to ozone:
structural and morphological changes. Am. Rev. Respir. Dis. 115: 201.
Bormann, F. H. ; Smith, W. H. (1980) Effects of air pollution on forest eco-
systems. In: Energy and the fate of ecosystems. Washington, DC:
National Academy of Sciences; pp. 308-318.
019COR/B 1-156 6/30/84
-------
Bowman, L. D. ; Horak, R. F. (1972) A continuous ultraviolet absorption ozone
photometer. Anal. Instrum. 10: 103-108.
Bradley, C. E. ; Haagen-Smit, A. J. (1951) The application of rubber in the
quantitative determination of ozone. Rubber Chem. Technol. 24: 750-775.
Bradley, M. 0.; Erickson, L. C. (1981) Comparison of the effects of hydrogen
peroxide and x-ray irradiation on toxicity, mutation, and DNA damage/
repair in mammalian cells (V-79). Biochim. Biophys. Acta 654: 135-141.
Bradley, M. 0.; Hsu, I.C.; Harris, C.C. (1979) Relationships between sister
chromatid exchange and mutagenicity, toxicity, and DNA damage. Nature
(London) 282: 318-320.
Breeding, R. J. ; Lodge, J. P., Jr.; Pate, J. B.; Sheesley, D. C.; Klonis, H.
B. ; Fogle, B.; Anderson, J. A.; Englert, T. R.; Haagenson, P. L.; McBeth,
R. B. ; Morris, A. L. ; Pogue, R. ; Wartburg, A. F. (1973) Background trace
gas concentration in the central United States. J. Geophys. Res. 78: 7057-
7064.
Brewer, A. W. ; Milford, J. R. (1960) The Oxford Kew ozone sonde. Proc. R.
Soc. London Ser. A256: 470-495.
Brinkman, R.; Lamberts, H.; Veninga, T. (1964) Radiomimetic toxicity of ozonized
air. Lancet I: 133-136.
Bruckmann, P. W. ; Willner, H. (1983) Infrared spectroscopic study of peroxy-
acetyl nitrate (PAN) and its decomposition products. Environ. Sci.
Technol. 17: 352-357.
Brummer, M. E. G. ; Schwartz, L. W. ; McQuillen, N. K. (1977) A quantitative
study of lung damage by scanning electron microscopy. Inflammatory cell
response to high-ambient levels of ozone. Scanning Electron Microsc. 2:
513-518.
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.
EF76-111R, Systems Applications, Inc., San Rafael, CA. August.
California Air Resources Board. (1976) A study of the effect of atmospheric
humidity on analytical oxidant measurement methods. Presented at the
15th Conference on Methods in Air Pollution Studies, J. J. Wesolowski,
Chairman, California Air Resources Board, Air and Industrial Hygiene
Laboratory, Berkeley, CA.
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.
019COR/B 1-157 6/30/84
-------
Campbell, G. G. ; Schurr, G. G. ; Slawikowski, D. E. ; Spence, J. W. (1974)
Assessing air pollution damage to coatings. J. Paint Techno!. 46: 59-71.
Campbell, K. I.; Clarke, G. L. ; Emik, L. 0.; Plata, R. L. (1967) The atmos-
pheric contaminant peroxyacetyl nitrate. Arch. Environ. Health 15:
739-744.
Campbell, K. I.; Hilsenroth, R. H. (1976) Impaired resistance to toxin in
toxoid-immunized mice exposed to ozone on nitrogen dioxide. Clin. Toxicol.
9: 943-954.
Carter, W. P. L. ; Winer, A. M. ; Pitts, J. N. , Jr. (1981) Major atmospheric
sink for phenol and the cresols. Reaction with the nitrate radical.
Environ. Sci. Technol. 15: 829-830.
Castleman, W. L.; Dungworth, D. L.; Schwartz, L. W.; Tyler, W. S. (1980) Acute
respiratory bronchiolitis: an ultrastructural and autoradiographic study
of epithelial cell injury and renewal in rhesus monkeys exposed to ozone.
Am. J. Pathol. 98: 811-840.
Castleman, W. L. ; Dungworth, D. L.; Tyler, W. S. (1973) Cytochemically detec-
ted alterations of lung acid phosphatase reactivity following ozone
exposure. Lab. Invest. 29: 310-319.
Castleman, W. L.; Tyler, W. S.; Dungworth, D. L. (1977) Lesions in respiratory
bronchioles and conducting airways of monkeys exposed to ambient levels
of ozone. Exp. Mol. Pathol. 26: 384-400.
Cavender, F. L. ; Steinhagen, W. H. ; Ulrich, C. E.; Busey, W. M. ; Cockrell, B.
Y. ; Haseman, J. K.; Hogan, M. D. ; Drew, R. T. (1977) Effects in rats and
guinea pigs of short-term exposures to sulfuric acid mist, ozone, and
their combination. J. Toxicol. Environ. Health 3: 521-533.
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.
Chow, C. K. (1976) Biochemical responses in lungs of ozone-tolerant rats.
Nature (London) 260: 721-722.
Chow, C. K. ; Cross, C. E. ; Kaneko, J. J. (1977) Lactate dehydrogenase activity
and isoenzyme pattern in lungs, erythrocytes, and plasma of ozone-exposed
rats and monkeys. J. Toxicol. Environ. Health 3: 877-884.
Chow, C. K. ; Oil lard, C. J. ; Tappel, A. L. (1974) Glutathione peroxidase
system and lysozyme in rats exposed to ozone or nitrogen dioxide. Environ.
Res. 7: 311-319.
Chow, C. K. ; Hussain, M. Z. ; Cross, C. E.; Dungworth, D. L.; Mustafa, M. G.
(1976) Effect of low levels of ozone on rat lungs. I. Biochemical respon-
ses during recovery and reexposure. Exp. Mol. Pathol. 25: 182-188.
Chow, C. K. ; Kaneko, J. J. (1979) Influence of dietary vitamin E on the red
cells of ozone-exposed rats. Environ. Res. 19: 49-55.
019COR/B 1-158 6/30/84
-------
Chow, C. K.; Mustafa, M. G.; Cross, C. E.; Tarkington, B. K. (1975) Effects of
ozone exposure on the lungs and the erythrocytes of rats and monkeys:
relative biochemical changes. Environ. Physiol. Biochem. 5: 142-146.
Chow, C. K.; Plopper, C. G. ; Chiu, M.; Dungworth, D. L. (1981) Dietary vitamin E
and pulmonary biochemical and morphological alterations of rats exposed
to 0.1 ppm ozone. Environ. Res. 24: 315-324.
Chow, C. K. ; Tappel, A. L. (1972) An enzymatic protective mechanism against
lipid peroxidation damage to lungs of ozone-exposed rats. Lipids 7:
518-524.
Chow, C. K. ; Tappel, A. L. (1973) Activities of pentose shunt and glycolytic
enzymes in lungs of ozone-exposed rats. Arch. Environ. Health 26:
205-208.
Christensen, E.; Giese, A. C. (1954) Changes in absorption spectra of nucleic
acids and their derivatives following exposure to ozone and ultraviolet
radiation. Arch. Biochem. Biophys. 51: 208-216.
Clark, K. W. ; Posin, C. I.; Buckley, R. D.. (1978) Biochemical response of
squirrel monkeys to ozone. J. Toxicol. Environ. Health 4: 741-753.
demons, G. K. ; Garcia, J. F. (1980a) Endocrine aspects of ozone exposure in
rats. Arch. Toxicol. Suppl. (4): 301-304.
demons, G. K. ; Garcia, J. F. (1980b) Changes in thyroid function after short-
term ozone exposure in rats. J. Environ. Pathol. Toxicol. 4: 359-369.
Cleveland, W. S. ; Graedel, T. E.; Kleiner, B. (1976) Photochemical air pollu-
tion: transport from the New York City area into Connecticut and Massa-
chusetts. Science (Washington, DC) 191: 179-181.
Coffin, D. L. ; Blommer, E. J. (1970) Alteration of the pathogenic role of
streptococci group C in mice conferred by previous exposure to ozone.
In: Silver, I. H., ed. Aerobiology: proceedings of the third interna-
tional symposium; September 1969; Sussex, England. New York: Academic
Press, Inc.; pp. 54-61.
Coffin, D. L. ; Gardner, D. E. (1972a) The role of tolerance in protection of
the lung against secondary insults. In: MEDICHEM: first international
symposium of occupational physicians of the chemical industry; April;
Ludwigshafen, West Germany. Ludwigshafen, West Germany: Badische Anilin-
und Soda-Fabrik (BASF); pp. 344-364.
Coffin, D. L. ; Gardner, D. E. (1972b) Interaction of biological agents and
chemical air pollutants. Ann. Occup. Hyg. 15: 219-235.
Coffin, D. L. ; Gardner, D. E.; Holzman, R. S.; Wolock, F. J. (1968) Influence
of ozone on pulmonary cells. Arch. Environ. Health 16: 633-636.
Cohen, I. R.; Purcell, T. C.; Altshuller, A. P. (1967) Analyses of the oxidant
in photooxidation reactions. Environ. Sci. Techno!. 1: 247-252.
019COR/B 1-159 6/30/84
-------
Costa, D. L. ; Kutzman, R. S.; Lehmann, J. R.; Popenoe, E. A.; Drew, R. T.
(1983) A subchrom'c multi-dose ozone study in rats. In: Lee, S. D. ;
Mustafa, M. G. ; Mehlman, M. A., eds. International symposium on the
biomedical effects of ozone and related photochemical oxidants; March
1982; Pinehurst, NC. Princeton, NJ: Princeton Scientific Publishers,
Inc.; pp. 369-393. (Advances in modern environmental toxicology: v. 5).
Cox, G. W. ; Atkins, M. D. (1979) Agricultural ecology: an analysis of world
food production systems. San Francisco, CA: W.H. Freeman and Co.; pp.
35-38.
Cronn, D. R. (1982) Monitoring of ambient halocarbons and natural hydrocarbons
in the Smoky Mountains. In: Proceedings from 2nd Symposium on Composi-
tion of the Nonurban Troposphere; May; Williamsburg, VA.
Csanyi, L. J. (1981) Analytical applications of mixed-ligand complexes. III.
Vanadium (V)-xylenol orange reagent mixture for the spectrophotometric
determination of traces of hydrogen peroxide. Microchem. J. 26: 10-16.
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, K. M. (1979) Influence of environmental factors on interply adhesion.
In: Proceedings of the International Rubber Conference; pp. 80-89.
DeLucia, A. J.; Hogue, P. M.; Mustafa, M. G.; Cross, C. E. (1972) Ozone inter-
action with rodent lung, effect on sulfhydryls and sulfhydryl-containing
enzyme activities. J. Lab. Clin. Med. 80: 559-566.
DeLucia, A. J. ; Mustafa, M. G. ; Cross, C. E. ; Plopper, C. G. ; Dungworth,
D. L. ; Tyler, W. S. (1975) Biochemical and morphological alterations in
the lung following ozone exposure. In: Rai, C.; Spielman, L. A., eds.
Air: I. pollution control and clean energy; 1973; New Orleans, LA;
Detroit, MI; Philadelphia, PA; Vancouver, British Columbia. New York,
NY: American Institute of Chemical Engineers; pp. 93-100. (AIChE sympo-
sium series: no. 147, v. 71).
Demore, W. B. ; Patapoff, M. (1976) Comparison of ozone determinations by
ultraviolet photometry and gas-phase titration. Environ. Sci. Techno!.
10: 897-899.
Demore, W. B. ; Romanovsky, J. C. ; Feldstein, M.; Hamming, W. J. ; Mueller, P.
K. (1976) Interagency comparison of iodometric methods for ozone determi-
nation. In: Calibration in Air Monitoring. Philadelphia, PA: American
Soceity for Testing and Materials; pp. 131-143; ASTM Special Technical
Publication 598.
Dietz, W. A. (1967) Response factors for gas chromatographic analyses. J. Gas
Chromatogr. 5:68-71.
Dillard, C. J. ; Urribarri, N.; Reddy, K.; Fletcher, B.; Taylor, S.; de Lumen,
B. ; Langberg, S. ; Tappel, A. L. (1972) Increased lysosomal enzymes in
lungs of ozone-exposed rats. Arch. Environ. Health 25: 426-431.
019COR/B 1-160 6/30/84
-------
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.
Dochinger, L. S.; and Townsend, A. M. (1979) Effects of roadside deicer salts
and ozone on red maple progenies. Environ. Pollut., 19: 229-237.
Dorsey, A. P.; Morgan, D. L. ; Menzel, D. B. (1983) Filterability of erythro-
cytes from ozone-exposed mice. In: Abstracts of the third international
congress on toxicology; September; San Diego, CA. Toxicol. Lett.
18(suppl. 1): 146.
Dowel 1, A. R. ; Lohrbauer, L. A.; Hurst, D.; Lee, S. D. (1970) Rabbit alveolar
macrophage damage caused by i_n vivo ozone inhalation. Arch. Environ.
Health 21: 121-127.
Dubeau, H. ; Chung, Y. S. (1979) Ozone response in wild type and radiation-
sensitive mutants of Saccharomyces cerevisiae. Mol. Gen. Genet. 176:
393-398.
Dubeau, H. ; Chung, Y. S. (1982) Genetic effects of ozone induction of point
mutations and genetic recombination in Saccharomyces cerevisiae. Mutat.
Res. 102: 249-259.
Duce, R. A.; Mohnen, V. A.; Zimmerman, P. R.; Grosjean, D.; Cautreels, W. ;
Chatfield, R. B.; Jaenicke, R.; Ogren, J. A.; Pellizzari, E. D.; Wallace,
G. T. (1983) Organic material in the global troposphere. Rev. Geophys.
Space Phys. 21: 921-952.
Duchelle, S. F. ; Skelly, J. M. (1981) Response of common milkweed to oxidant
air pollution in the Shenandoah National Park in Virginia. Plant Disease
65: 661-662.
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.
Dungworth, D. L. (1976) Short-term effects of ozone on lungs of rats, mice and
monkeys. EHP Environ. Health Perspect. 16: 179.
Dungworth, D. L. ; Castleman, W. L. ; Chow, C. K. ; Mellick, P. W. ; Mustafa, M.
G. ; Tarkington, B.; Tyler, W. S. (1975b) Effects of ambient levels of
ozone on monkeys. Fed. Proc. Fed. Am. Soc. Exp. Biol. 34: 1670-1674.
Dungworth, D. L.; Clarke, G. L.; Plata, R. L. (1969) Pulmonary lesions produced
in A-strain mice by exposure to peroxyacetylnitrates. Am. Rev. Respir.
Dis. 99: 565-574.
Dungworth, D. L. ; Cross, C. E. ; Gillespie, J. R.; Plopper, C. G. (1975a) The
effects of ozone on animals. In: Murphy, J. S.; Orr, J. R., eds. Ozone
chemistry and technology. A review of the literature: 1961-1974. Phila-
delphia, PA: The Franklin Institute Press; pp. 29-54.
019COR/B 1-161 6/30/84
-------
Easton, R. E. ; Murphy, S. D. (1967) Experimental ozone preexposure and hista-
mine. Arch. Env. Health 15: 160-166.
Eaton, W. C.; Decker, C. E.; Tommerdahl, J. B.; Dimmock, F. E. (1979) Study of
the nature of ozone, oxides of nitrogen, and nonmethane hydrocarbons in
Tulsa, Oklahoma. Research Triangle Park, NC: Environmental Protection
Agency; EPA report no. EPA-450/4-79-008a.
Edwards, D. C. ; Storey, E. B. (1959) A quantitative ozone test for small
specimens. Chem. Can. 11: 34-38.
Ehrlich, R. (1980) Interaction between environmental pollutants and respiratory
infections. EHP Environ. Health Perspect. 35: 89-100.
Ehrlich, R. (1983) Changes in susceptibility to respiratory infection caused
by exposure to photochemical oxidant pollutants. 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. 273-285.
(Advances in modern environmental toxicology: v.5).
Ehrlich, R.; Findlay, J. C.; Fenters, J. D.; Gardner, D. E. (1977) Health
effects of short-term inhalation of nitrogen dioxide and ozone mixtures.
Environ. Res. 14: 223-231.
Ehrlich, R.; Findlay, J. C.; Gardner, D. E. (1979) Effects of repeated exposures
to peak concentrations of nitrogen dioxide and ozone on resistance to
streptococcal pneumonia. J. Toxicol. Environ. Health 5: 631-642.
Elsayed, N. M. ; Hacker, A. D. ; Kuehn, K. ; Mustafa, M. G. ; Schrauzer, G. N.
(1983) Dietary antioxidants and the biochemical response to oxidant
inhalation. II. Influence of dietary selenium on the biochemical effects
of ozone exposure in mouse lung. Toxicol. Appl. Pharmacol. 71: 398-406.
Elsayed, N. M. ; Mustafa, M. G. ; Postlethwait, E. M. (1982a) Age-dependent
pulmonary response of rats to ozone exposure. J. Toxicol. Environ.
Health 9: 835-848.
Elsayed, N.; Hacker, A.; Mustafa, M.; Kuehn, K.; Schrauzer, G. (1982b) Effects
of decreased glutathione peroxidase activity on the pentose phosphate
cycle in mouse lung. Biochem. Biophys. Res. Commun. 104: 564-569.
Erdman, H. E.; Hernandez, T. (1982) Adult toxicity and dominant lethals induced
by ozone at specific stages in spermatogenesis in Drosophila virilis.
Environ. Mutagen. 4: 657-666.
Eustis, S. L. ; Schwartz, L. W. ; Kosch, P. C.; Dungworth, D. L. (1981) Chronic
bronchiolitis in nonhuman primates after prolonged ozone exposure. Am.
J. Pathol. 105: 121-137.
Evans, G. ; Finkelstein, P.; Martin, B. ; Possiel, N. ; Graves, M. (1982) The
National Air Pollution Background Network, 1976-1980. Research Triangle
Park, NC: U.S. Environmental Protection Agency; EPA report no.
EPA-600/4-82-058.
019COR/B 1-162 6/30/84
-------
Evans, M. J.; Johnson, L. V. ; Stephens, R. J.; Freeman, G. (1976b) Cell renewal
in the lungs of rats exposed to low levels of ozone. Exp. Mol. Pathol.
24: 70-83.
Evans, M. J. ; Johnson, L. V.; Stephens, R. J.; Freeman, G. (1976a) Renewal of
the terminal bronchiolar epithelium in the rat following exposure to NO-
or 03. Lab. Invest. 35: 246-257.
Evans, M. J. ; Mayr, W.; Bils, R. F.; Loosli, C. G. (1971) Effects of ozone on
cell renewal in pulmonary alveoli of aging mice. Arch. Environ. Health
22: 450-453.
Fabbri, L. M.; Aizawa, H.; Alpert, S. E.; Walters, E. H.; O'Byrne, P. M. ;
Gold, B. D. ; Nadel, J. A.; Holtzman, M. J. (1984) Airway hyperresponsive-
ness and changes in cell counts in bronchoalveolar lavage after ozone
exposure in dogs. Am. Rev. Respir. Dis. 129: 288-291.
Fabbri, L. ; Mapp, C. ; Rossi, A.; Sarto, F.; Trevisan, A.; De Rosa, E. (1979)
Pulmonary function changes due to low level occupational exposure to
ozone. Med. Lav. 70: 307-312.
Fairchild, E. J. (1967) Tolerance mechanisms: determination of lung responses
to injurious agents. Arch. Environ. Health 14: 111-126.
Farmer, J. C. ; Dawson, G. A. (1982) Condensation sampling of soluble atmos-
pheric trace gases. J. Geophys. Res. 87: 8931-8942.
Parrel!, 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.
Feder, W. A.; Campbell, F. J. (1968) Influence of low levels of ozone on
flowering of carnations. Phytopathology. 58: 1038-1039.
Ferman, M. A. (1981) Rural nonmethane hydrocarbon concentrations and composition.
In: Bufalini, J. J.; Arnts, R. R., eds. Atmospheric Biogenic Hydrocarbons.
Ann Arbor, MI: Ann Arbor Science Publishers, Inc.
Fetner, R. H. (1962) Ozone-induced chromosome breakage in human cell cultures.
Nature (London) 194: 793-794.
Flamm, D. L. (1977) Analysis of ozone at low concentrations with boric acid
buffered KI. Environ. Sci. Technol. 11: 978-983.
Fletcher, B. L.; Tappel, A. L. (1973) Protective effects of dietary alphatoco-
pherol in rats exposed to toxic levels of ozone and nitrogen dioxide.
Environ. Res. 6: 165-175.
Folinsbee, L. J.; Bedi, J. F.; Horvath S. M. (1984) Pulmonary function changes
in trained athletes following 1-hour continuous heavy exercise while
breathing 0.21 ppm ozone. J. Appl. Physiol. Respir. Environ. Exercise
Physiol. (In Press).
019COR/B 1-163 6/30/84
-------
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.
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.
Frager, N. B. ; Phalen, R. F. ; Kenoyer, J. L. (1979) Adaptations to ozone in
reference to mucociliary clearance. Arch. Environ. Health 34: 51-57.
Freeman, B. A.; Mudd, J. B. (1981) Reaction of ozone with sulfhydryls of human
erythrocytes. Arch. Biochem. Biophys. 208: 212-220.
Freeman, B. A. ; Sharman, M. C. ; Mudd, J. B. (1979) Reaction of ozone with
phospholipid vesicles and human erythrocyte ghosts. Arch. Biochem.
Biophys. 197: 264-272.
Freeman, G. ; Juhos, L. T. ; Furiosi, N. J. ; Mussenden, R. ; Stephens, R. J. ;
Evans, M. J. (1974) Pathology of pulmonary disease from exposure to
interdependent ambient gases (nitrogen dioxide and ozone). Arch. Environ.
Health 29: 203-210.
Freeman, G. ; Stephens, R. J. ; Coffin, D. L. ; Stara, J. F. (1973) Changes in
dog's lungs after long-term exposure to ozone. Arch. Environ. Health 26:
209-216.
Friberg, L. ; Holman, B. ; Rylander, R. (1972) Animal lung reactions after
inhalation of lead and ozone. Environ. Physio!. Biochem. 2: 170-178.
Fried, A. ; Hodgeson, J. A. (1982) Laser photoacoustic detection of nitrogen
dioxide in the gas-phase titration of nitric oxide and ozone. Anal.
Chem. 54: 278-282.
Friedman, M. ; Gallo, J. M.; Nichols, H. P.; Bromberg, P. A. (1983) Changes in
inert gas rebreathing parameters after ozone exposure in dogs. Am. Rev.
Respir. Dis. 128: 851-856.
Fukase, 0.; Isomura, K. ; Watanabe, H. (1975) Effect of ozone on glutathione
in vivo. Taiki Osen Kenkyu 10: 58-62.
Fukase, 0.; Watanabe, H. ; Isomura, K. (1978) Effects of exercise on mice
exposed to ozone. Arch. Environ. Health 33: 198-200.
Gardner, D. E. ; Graham, J. A. (1977) Increased pulmonary disease mediated
through altered bacterial defenses. In: Sanders, C. L. ; Schneider, R. P.;
Dagle, G. E. ; Ragen, H. A., eds. Pulmonary macrophage and epithelial
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: 43).
019COR/B 1-164 6/30/84
-------
Gardner, D. E. ; Illing, J. W.; Miller, F. J.; Coffin, D. L. (1974) The effect
of ozone on pentobarbital sleeping time in mice. Res. Commun. Chem.
Pathol. Pharmacol. 9: 689-700.
Gardner, D. E.; Lewis, T. R.; Alpert, S. M. ; Hurst, D. J.; Coffin, D. L.
(1972) The role of tolerance in pulmonary defense mechanisms. Arch.
Environ. Health 25: 432-438.
Gardner, D. E. ; Miller, F. J. ; Illing, J. W. ; Kirtz, J. M. (1977) Increased
infectivity with exposure to ozone and sulfuric acid. Toxicol. Lett. 1:
59-64.
Gardner, D. E.; Pfitzer, E. A.; Christian; R. T. ; Coffin, D. L. (1971) Loss of
protective factor for alveolar macrophages when exposed to ozone. Arch.
Intern. Med. 127: 1078-1084.
Gay, B. W., Jr.; Noonan, R. C. ; Bufalini, J. J.; Hanst, P. L. (1976) Photochem-
ical synthesis of peroxyacyl nitrates in gas phase via chlorine - aldehyde
reaction. Environ. Sci. Technol. 10: 82-85.
Gay, B. W., Jr.; Bufalini, J. J. (1972a) Photochemical smog and ozone reactions.
R. F. Gould, ed., Am. Chem. Soc., Adv. in Chem. Ser. 113: 225.
Gay, B. W., Jr.; Bufalini, J. J. (1972b) Hydrogen peroxide in the urban atmos-
phere. Environ. Lett. 3: 21-24.
Gershwin, L. J.; Osebold, J. W.; Zee, Y. C. (1981) Immunoglobulin E-containing
cells in mouse lung following allergen inhalation and ozone exposure.
Int. Arch. Allergy Appl. Immunol. 65: 266-277.
Gertner, A. ; Bromberger-Barnea, B. ; Dannenberg, A. M. , Jr. ; Traystman, R. ;
Menkes, H. (1983a) Responses of the lung periphery to 1.0 ppm ozone. J.
Appl. Physiol. Respir. Environ. Exercise Physio!. 55: 770-776.
Gertner, A.; Bromberger-Barnea, B.; Traystman, R.; Menkes, H. (1983c) Effects
of ozone in peripheral lung reactivity. J. Appl. Physiol. Respir. Environ.
Exercise Physiol. 55: 777-784.
Gertner, A. ; Bromberger-Barnea, B. ; Traystman, R. ; Berzon, D. ; Menkes, H.
(1983b) Responses of the lung periphery to ozone and histamine. J. Appl.
Physiol. Respir. Environ. Exercise Physiol. 54: 640-646.
Gillespie, J. R. (1980) Review of the cardiovascular and pulmonary function
studies on beagles exposed for 68 months to auto exhaust and other air
pollutants In: Stara, J. F. ; Dungworth, D. L. ; Orthoefer, J. C. ;
Tyler, W. S., eds. Long-term effects of air pollutants in canine species.
Cincinnati, Ohio: U.S. Environmental Protection Agency; pp. 115-154;
EPA 600/8-80-014.
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.
019COR/B 1-165 6/30/84
-------
Goldstein, B. D. ; Hamburger, S. J.; Falk, G. W.; Amoruso, M. A. (1977) Effect
of ozone and nitrogen dioxide on the agglutination of rat alveolar macro-
phages by concanavalin A. Life Sci. 21: 1637-1644.
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, E. ; Eagle, M. C.; Hoeprich, P. (1972) Influence of ozone on pulmonary
defense mechanisms of silicotic mice. Arch. Environ. Health 24: 444-448.
Goldstein, E. ; Tyler, W. S. ; Hoeprich, P. D.; Eagle, C. (1971a) Ozone and the
antibacterial defense mechanisms of the murine lung. Arch. Intern. Med.
128: 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
(London) 229: 262-263.
Gooch, P. C. ; Creasia, D. A.; Brewen, J. G. (1976) The cytogenetic effect of
ozone: inhalation and in vitro exposures. Environ. Res. 12: 188-195.
Gordon, T. ; Amdur, M. 0. (1980) Effects of ozone on respiratory response of
guinea pigs to histamine. J. Toxicol. Environ. Health 6: 185-195.
Graham, J. A. (1979) Alteration of hepatic xenobiotic metabolism by ozone.
Durham, NC: Duke University. Ph.D. Dissertation.
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,
rats, and hamsters. Toxicol. Appl. Pharmacol. 61: 64-73.
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.; Menzel, D. B. ; Miller, F. J.; Illing, J. W.; Ward, R.; Gardner,
D.E. (1983a) Influence of ozone on xenobiotic metabolism. In: Lee,
S. D. ; Mustafa, M. G. ; Mehlman, M. A., eds. International symposium on
the biomedical effects of ozone and related photochemical oxidants; March
1982; Pinehurst, NC. Princeton, NJ: Princeton Scientific Publishers,
Inc.; pp. 95-117. (Advances in modern environmental toxicology: v. 5).
Graham, J. A.; Menzel, D. B.; Mole, M. L.; Miller, F. J.; Gardner, D. E.
(1983b) Influence of ozone on pentobarbital pharmacokinetics in mice.
Toxicol. Lett. (In Press).
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.
Grose, E. C. ; Gardner, D. E. ; Miller, F. J. (1980) Response of ciliated epi-
theluim to ozone and sulfuric acid. Environ. Res. 22: 377-385.
019COR/B 1-166 6/30/84
-------
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.
Grosjean, D. (1981) 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, D. (1983) Distribution of atmospheric nitrogenous pollutants at a
Los Angeles area smog receptor site. Environ. Sci. Technol. 17: 13-19.
Grosjean, D.; Fung, K.; Collins, J.; Harrison, J.; Breitung, E. (1984) Portable
generator for on-site calibration of peroxyacetyl nitrate analyzers.
Anal. Chem. 56: 569-573.
Guderian, R. (1977) Air pollution: Phytotoxicity of acidic gases and its
significance in air pollution control. In: Ecological studies 22.
Chapter 4. Springer-Verlag, Berlin.
Guerrero, R. R. ; Rounds, D. E.; Olson, R. S.; Hackney, J. D. (1979) Mutagenic
effects of ozone on human cells exposed j_n vivo and i_n vitro based on
sister chromatid exchange analysis. Environ. Res. 18: 336-346.
Hacskaylo, E. (1973) The Torrey symposium on current aspects of fungal develop-
ment. IV. Dependence of mycorrhizal fungi on hosts. Bull. Torrey Bot.
Club 100: 217-223.
Hadley, J. G. ; Gardner, D. E. ; Coffin D. L. ; Menzel, D. B. (1977) Enhanced
binding of autologous cells to the macrophage plasma membrane as a 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:
Hamelin, C. ; Chung, Y. S. (1975) The effect of low concentrations of ozone on
Escherichia coli chromosome. Mutat. Res. 28: 131-132.
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 E 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.
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.
019COR/B 1-167 6/30/84
-------
Hanst, P. L. ; Gay, B. W. ; Spence, J. W. (1981) Atmospheric measurement 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.
Hanst, P. L. ; Wilson, W. E.; Patterson, R. K.; Gay, B. W., Jr.; Chaney, L. W.
(1975) A spectroscopic study of California smog. Research Triangle Park,
NC. Publication No. EPA-650/4-75-006.
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. ; Kolar, A. M. (1968) Anal. Chem. 40: 231.
Hayes, E. M. ; Skelly, J. M. (1977) Transport of ozone from the northeast U.S.
into Virginia and its effect on eastern white pines. Plant Dis. Rep.
61: 778-782.
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. Environmen-
tal Protection Agency; EPA Report No. EPA-600/3-76-015.
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.
Heagle, A. S.; Letchworth, M. B.; Mitchell, C. A. (1983) Injury and yield
responses of peanuts to chronic doses of ozone in open-top field chambers.
Phytopathology 73: 551-555.
Heagle, A. S. ; Philbeck, R. B. ; Knott, W. M. (1979a) Thresholds for injury
growth, and yield loss caused by ozone on field corn hybrids. Phypto-
pathology 69: 21-26.
Heagle, A. S.; Spencer, S. ; Letchworth, M. B. (1979b) Yield response of winter
wheat to chronic doses of ozone. Can. J. Bot., 57: 1999-2005.
Heagle, A. S., and Heck, W. W. (1980) Field methods to assess crop losses due
to oxident air pollutants. In: Teng, P. S. , and Krupa, A. V., Eds. Crop
Loss Assessment: Proceedings of E. C. Stakman Commemorative Symposium.
University of Minnesota, Agricultural Experimental Station; Miscellaneous
Publications No. 7, Minneaplolis. pp. 296-305
Heagle, A. S. , Body, D. E., and Pounds, E. K. (1972) Effect of ozone on yield
of sweet corn. Phytopathology 62: 683-687.
019COR/B 1-168 6/30/84
-------
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.
Phytopahtology. 64: 132-136.
Heck, W. W. (1973) Air pollution and the future of agriculture. In: Naegele,
J. A., ed. Air pollution damage to vegetation. Washington, D.C: Ameri-
can Chemical Society (Advances in Chemistry Series No. 122); pp. 118-129.
Heck, W. W.; Adams, R. M.; Cure, W. W.; Heagle, A. S.; Heggestad, H. E.;
Kohut, R. J. ; Kress, L. W.; Rawlings, J. 0.; Taylor, 0. C. (1983) A
reassessment of crop loss from ozone. Environ. Sci. Tech., 17: 573A-581A.
Heck, W. W.; Dunning, J. A.; Hindawi, I. J. (1966) Ozone: Non-linear relation
of dose and injury in plants. Science 151: 577-578.
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. ; Tingey, D. T. (1971) Ozone time-concentration model to predict
acute foliar injury. Jji: Proceedings of the Second International Clean
Air Congress. Englund, H. M. ; Beery, W. T.; Eds. Academic Press, New
York. pp. 249-255
Heggestad, H. E. ; Heagle, A. S.; Bennett, J. H.; Koch, E. J. (1980) The effects
of photochemical oxidants on the yield of snap beans. Atmos. Environ.
14: 316-326.
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.
Henderson, W. R. ; Reinert, R. A. (1979) Yield response of four fresh market
tomato cultivars after acute ozone exposure in the seedling stage. J.
Amer. Soc. Hortic. Sci., 104: 754-759.
Hendry, D. G. ; Kenley, R. A. (1977) Generation of peroxy radicals from peroxy
nitrates (RO?NO?). Decomposition of peroxyacyl nitrates. Atmos. Environ.
99: 3198-3199.
Herman, D. R. (1972) The effect of oxidant air pollution on athletic perfor-
mance. Chapel Hill, NC: University of North Carolina. Master's Thesis.
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.
Heuss, J. M.; Glasson, W. A. (1968) Hydrocarbon reactivity and eye irritation.
Environ. Sci. Technol. 2: 1109-1116.
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, Vol I. Research Triangle Park, NC: U.S. Environmental Pro-
tection Agency; EPA report no. EPA-600/3-77-001a; pp. 3-12.
019COR/B 1-169 6/30/84
-------
Hodgeson, J. A.; Krost, K. J. ; O'Keeffe, A. E.; Stevens, R. K. (1970) Chemi-
luminescent measurement of atmospheric ozone. Anal. Chem. 42: 1795-1802.
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.
Holdren, M. W. ; Spicer, C. W. (1984) Field compatible calibration procedure
for peroxyacetyl nitrate. Environ. Sci. Techno!. 18: 113-116.
Holdren, M. W. ; Westberg, H. H.; Zimmerman, P. R. (1979) Analysis of monoter-
pene hydrocarbons in rural atmospheres. JGR J. Geophys. Res. 84: 5083-
5088.
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.
Holtzman, M. J. ; Fabbri, L. M.; 0'Byrne, P. M.; Gold, B. D.; Aizawa, H.;
Walters, S. E. ; Alpert, S. E. ; Nadel, J. A. (1983b) Importance of airway
inflammation for hyperresponsiveness induced by ozone. Am. Rev. Respir.
Dis. 127: 686-690.
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. Physio!. Respir. Environ. Exercise
Physiol. 55: 1232-1236.
Horsman, D. C. ; Nocholls, 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.
Horvath, S. M. ; Gliner, J. A.; Folinsbee, L. J. (1981) Adaptation to ozone:
duration of effect. Am. Rev. Respir. Dis. 123: 496-499.
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. 40: 901-905.
Howell, R. K. ; Kock, E. J. ; and Rose, L. P. (1979) Field assessment of air
pollution induced soybean yield losses. Agron. J., 71: 285-288.
Hu, P. C.; Miller, F. J.; Daniels, M. J.; Hatch, G. E.; Graham, J. A.; Gardner,
D. E. ; Selgrade, M. K. (1982) Protein accumulation in lung lavage fluid
following ozone exposure. Environ. Res. 29: 377-388.
Huber, G. L. ; Mason, R. J. ; LaForce, M. ; Spencer, N. J. ; Gardner, D. E. ;
Coffin, D. L. (1971) Alterations in the lung following the administration
of ozone. Arch. Intern. Med. 128: 81-87.
Hueter, F. G. ; Contner, G. L. ; Busch, K. A.; Hinners, R. G. (1966) Biological
effects of atmospheres contaminated by auto exhaust. Arch. Environ.
Health 12: 553-560.
019COR/B 1-170 6/30/84
-------
Huevel, H. M. ; Huisman, R. ; Schmidt, J. M. (1978) Ozone fading of disperse
blue 3 on nylon 6 fibers. In: The influence of physical fiber properties.
Text. Res. J. 48: 376-384.
Hunt, W. F. ; 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.
Hurst, D. J. ; Coffin, D. L. (1971) Ozone effect on lysosomal hydrolases of
alveolar macrophages i_n 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. Res. J. Reticuloendothel.
Soc. 8: 288-300.
Hussain, M. Z. ; Cross, C. E. ; Mustafa, M. G.; Bhatnagar, R. S. (1976b) Hydroxy-
proline contents and prolyl hydroxylase activities in lungs of rats
exposed to low levels of ozone. Life Sci. 18: 897-904.
Hussain, M. Z. ; Mustafa, M. G. ; Chow, C. K.; Cross, C. E. (1976a) Ozone-induced
increase of lung proline hydroxylase activity and hydroxyproline content.
Chest 69 (Suppl. 2): 273-275.
Hyde, D. ; Orthoefer, J.; 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. (1976) The effects of ozone on the
respiratory epithelium and alveolar macrophages of mice. I. Interferon
production. Proc. Soc. Exp. Biol. Med. 152: 483-488.
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 N0? and 0,.. 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.
Jacobson, J. S. (1977) The effects of photochemical oxidants on vegetation.
pp. 163-173 In: Ozone und Begleitsubstanzen im Photochemischen Smog.
VDI BER. (270).
Japar, S. M. ; Niki, H. (1975) Gas-phase reactions of the nitrate radical with
olefins. J. Phys. Chem. 79: 1629-1632.
019COR/B 1-171 6/30/84
-------
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.
Jegier, Z. (1973) Ozone as an air pollutant. Can. J. Public Health 64:
161-166.
Johnson, A. H. ; Siccama, T. G. (1983) Acid deposition and forest decline.
Environ. Sci. Technol. 17: 294A-305A.
Johnson, D. F. ; Kok, G. L. ; Sonner, R. J. (1981) Improved chromotropic 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 prepared
for Coordinating Research Council, Atlanta, GA.
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. Paper No. 78-50.1.
Joshi, S. B. ; Bufalini, J. J. (1978) Halocarbon interferences in chemilumines-
cent measurements of NO . Environ. Sci. Technol. 12:597-599.
/\
Kagawa, J. (1983) Effects of ozone and other pollutants on pulmonary function
in man. 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. 411-422. (Advances in modern toxicology:
v .5).
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.
Kamath, Y. K.; Ruetsch, S. B.; Weigmann, H. D. (1982) Micro-spectrophotometric
study of ozone fading of disperse dyes in nylon. Text. Res. J.: in press.
Kavlock, R. J.; Meyer, E.; Grabowski, C. T. (1980) Studies on the developmental
toxicity of ozone: postnatal effects. Toxicol. Lett. 5: 3-9.
Kavlock, R. ; Daston, G. ; Grabowski, C. T. (1979) Studies on the developmental
toxicity of ozone. I. Prenatal effects. Toxicol. Appl. Pharmacol. 48:
19-28.
019COR/B 1-172 6/30/84
-------
Kehrl, H. R. ; Hazucha, M. J. ; Solic, J. ; Bromberg, P. A. (1983) Effects of
ozone exposure on humans with moderate irreversible chronic obstructive
lung disease. 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.)
Kelly, T. V.; Stedman, D. H.; Kok, G. L. (1979) Measurements of H 0 and HNO,
in rural air. Geophys. Res. Lett. 6: 375-378. ^ ^ 6
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.
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.
Kesner, L_. ;+Kindya, 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
adenosine triphosphatase. Biochim. Biophys. Acta 429: 608-615.
Kohut, R. ; Laurence, J. A. (1983) Yield response of red kidney bean to incre-
mental ozone concentrations in field. Environ. Pollut. (Ser A), 32: 233-
240.
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. Techno!. 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.
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.
Konigsberg, A. S. ; Bachman, C. H. (1970) Ozonized atmosphere and gross motor
activity of rats. Int. J. Biometeorol. 14: 261-266.
Koontz, A. E. ; Ijleajh, R. L. (1979) Ozone alteration of transport of cations
and the Na /K ATPase in human erythrocytes. Arch. Biochem. Biophys.
198: 493-500.
Kravetz, T. M.; Martin, S. W.; Mendenhall, G. D. (1980) Synthesis of peroxyacetyl
and peroxyaroyl nitrates. Complexion of peroxyacetyl nitrate with benzene.
Environ. Sci. Technol. 14: 1262-1264.
Kress, L. W. ; Miller, J. E. (1983) Impact of ozone on soybean yield. J.
Environ. Qua!., 12: 276-281.
019COR/B 1-173 6/30/84
-------
Kress, L. W. ; Skelly, J. M. (1982) Response to several eastern forest tree
species to chronic doses of ozone and nitrogen dioxide. Plant Dis. Rep. ,
66: 1149-1152.
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. (In Press).
Kulle, T. J.; Sauder, L. R.; Kerr, H. D.; Farrell, 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.
Kuntz, R. ; Lonneman, W.; Namie, G.; Hull, L. A. (1980) Rapid determination of
aldehydes in air analyses. Anal. Lett. 13:1409-1415.
Kyei-Aboagye, K. ; Hazucha, M. ; Wyszogrodski, I.; Rubinstein, D.; Avery, M. E.
(1973) The effect of ozone exposure iji vivo on the appearance of lung
tissue lipids in the endobronchial lavage of rabbits. Biochem. Biophys.
Res. Commun. 54: 907-913.
Larkin, E.G.; Goheen, S.C.; Rao, G.A. (1983) Morphology and fatty acid compo-
sition 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.; 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.; 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.; 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.; 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.; Kaizu, T. (1980) Mucus glycoprotein secretion by tracheal explants:
effects of pollutants. EHP Environ. Health Perspect. 35: 131-138.
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. ; Bendheim, P.; Cristea, G. ; Markowitz, D. ; Misiaszek, Jr.;
Staniec, M.; Van Wyck, D. (1974) The effect of air pollution and weather
on lung function in exercising children and adolescents. Am. Rev. Respir.
Dis. 109: 262-273.
019COR/B 1-174 6/30/84
-------
Lebowitz, M. D. ; Holberg, C. J. ; Dodge, R. R. (1983) Respiratory effects on
populations from low level exposures to ozone. Presented at: 34th
annual meeting of the Air Pollution Control Association; June; Atlanta,
GA. Pittsburgh, PA: Air Pollution Control Association; paper no. 83-12.5.
Lebowitz, M. D. ; O'Rourke, M. K.; Dodge, R.; Holberg, C. J. ; Corman, G.;
Hoshaw, R. W. ; Pinnas, J. L. ; Barbee, R. A.; Sneller, M. R. (1982) The
adverse health effects of biological aerosols, other aerosols, and indoor
microclimate on asthmatics and nonasthmatics. Environ. Int. 8: 375-380.
Lee, L.-Y.; Bleecker, E. R.; Nadel, J. A. (1977) Effect of ozone on bronchomotor
response to inhaled histamine aerosol in dogs. J. Appl. Physio!. Respir.
Environ. Exercise Physiol. 43: 626-631.
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.
Lewis, T. R.; Hueter, F. G.; Busch, K. A. (1967) Irradiated automobile exhaust:
its effects on the reproduction of mice. Arch. Environ. Health 15: 26-35.
Lewis, T. R.; Moorman, W. J.; Yang, Y.; Stara, J. F. (1974) Long-term exposure
to auto exhaust and other pollutant mixtures. Effects on pulmonary
function in the beagle. Arch. Environ. Health 29: 102-106.
Linn, W. S. ; Avol, £. 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).
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 respiratory effects
of 0.12 ppm ozone exposure in volunteers with chronic obstructive lung
disease. Am. Rev. Respir. Dis. 125: 658-663.
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.; Medway, D. A.; Anzar, U. T.; Valencia, L. M.; Spier, C. E.; Tsao,
F. S-0. ; Fischer, D. A.; Hackney, J. D. (1982b) Persistence of adaptation
to ozone in volunteers exposed repeatedly over six weeks. Am. Rev. Respir.
Dis. 125: 491-495.
Linn, W. S.; Shamoo, D. A.; Venet, T. G.; Spier, C. E.; Valencia, L. M. ;
Anzar, U. T. ; Hackney, J. D. (1983) Response to ozone in volunteers with
chronic obstructive pulmonary disease. Arch. Environ. Health 38: 278-283.
019COR/B 1-175 6/30/84
-------
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.
Logan, J. A. (1983) Nitrogen oxides in the troposphere: global and regional
budgets. JGR J. Geophys. Res. 88: 10785-10807.
Logan, J. A.; Prather, M. J.; Wofsy, S. C.; McElroy, M. B. (1981) Tropospheric
chemistry: a global perspective. JGR J. Geophys. Res. 86: 7210-7254.
Lonneman, W. A.; Bufalini, J. J. ; Namie, G. R. (1982) Calibration procedure
for PAN based on its thermal decomposition in the presence of nitric
oxide. Environ. Sci. Techno!. 16: 655-660.
Lonneman, W. A.; Bufalini, J. J.; Seila, R. L. (1976) PAN and oxidant measure-
ment in ambient atmospheres. Environ. Sci. Techno!. 10: 274-280.
Luck, R. F. (1980) Impact of oxidant air pollution on ponderosa and Jeffrey
pine cone production. In: Miller, P.R. , ed. Proceedings of the sympo-
sium on the effects of air pollutants on Mediterranean and temperate
forest ecosystems; June; Riverside, CA. Berkeley, CA: U.S. Department
of Agriculture, Forest Service; genl. tech. report no. PSW-43; p. 256.
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. L. (1977) Glucose-6-phosphate
dehydrogenase response of postnatal lungs to NO^ and 0.,. In: Sanders,
C. L.; Schneider, R. P.; Dagle, G. E.; Ragan, R. 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. 236-247. (ERDA
symposium series: 43).
MacLean, D. C. ; Schneider, P. E. (1976) Photochemcial oxidants in Yonkers,
New York. J. Environ. Qual., 5: 75-78.
MacRae, W. D. ; Stich, H. F. (1979) Induction of sister chromatid exchanges in
Chinese hamster ovary cells by Thiol and hydrazene compounds. Mutat.
Res. 68: 351-365.
Makino, K. ; Mizoguchi, I. (1975) Symptoms caused by photochemical smog.
Nippon Koshu Eisei Zasshi 22: 421-430.
Male, L.; Preston, E.; Neely, G. (1983) Yield response curves of crops exposed
to S02. Atmos. Environ., 17: 1589-1593.
Manion, P. (1981) Tree disease concepts. Englewood Cliffs, NJ: Prentice-Hall,
Inc.; pp. 12-16, 325-339.
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.
019COR/B 1-176 6/30/84
-------
Martin, C. J.; Boatman, E. S.; Ward, G. (1983) Mechanical properties of alveo-
lar wall after pneumonectomy and ozone exposure. J. Appl. Physio!.
Respir. Environ. Exercise Physiol. 54: 785-788.
Martinez, J. R. ; Singh, H. B. (1979) Survey of the role of NO in nonurban
ozone formation. Prepared by SRI International for U.S. Environmental
Protection Agency, Research Triangle Park, NC. EPA report no.
EPA-450/4-79-035.
Mast, G. M.; Saunders, H. E. (1962) Research and development of the instru-
mentation of ozone sensing. ISA Trans. I: 325-328.
Mayrsohn, H. ; Brooks, C. (1965) The analysis of PAN by electron capture gas
chromatography. Presented at the Western Regional Meeting of the American
Chemical Society, Los Angeles, CA.
McAllen, S. J. ; Chiu, S. P.; Phalen, R. F.; Rasmussen, R. E. (1981) Effect of
i_n vivo ozone exposure on ijn vitro pulmonary alveolar macrophage mobility.
J. Toxicol. Environ. Health 7: 373-381.
McBride, J. M.; McClenny, W. A. (1980) Analysis of NMOC by cryogenic preconcen-
tration and flame ionization detection. Draft Report. U. S. Environmen-
tal Protection Agency, Research Triangle Park, NC.
McCarthy, E. F. ; Stankunas, A. R. ; Yocum, J. E. ; Rae, D. (1983) Damage cost
models for pollutant effects on material. East Hartford, CT: TRC Environ-
mental Consultants, Inc.; TRC project no. 1574-J80. U.S. Environmental
Protection Agency; EPA report no. 600/3-84-012.
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.
McElroy, F. F. (1979) Transfer standards for calibration of ambient air moni-
toring analyzers for ozone: technical assistance document. Research
Triangle Park, NC. U.S. Environmental Protection Agency; EPA report no.
EPA-600/4-79-056.
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; EPA report no.
EPA-600/4-75-010.
McJilton, C.; Thielke, J.; Frank, R. (1972) Ozone uptake model for the respira-
tory system. In: Abstracts of technical papers: American industrial
hygiene conference; May 1972; San Francisco, CA. Am. Ind. Hyg. Assoc. J.
33(2): paper no. 45.
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.
019COR/B 1-177 6/30/84
-------
Mclaughlin, S. B. ; Shriner, D. S. ; McConathy, R. K. ; Mann, L. K. (1979) The
effects of SOp dosage kinetics and exposure frequency on photosynthesis
and transpiration of kidney beans (Phaseolus vulgaris L.). Environ. Exp.
Bot., 19: 179-191.
McMillan, R. S. ; Wiseman, D. H. ; Hanes, B. ; Wehrle, P. F. (1969) Effect of
oxidant air pollution on peak expiratory flow rates in Los Angeles school
children. Arch. Environ. Health 18: 94-99.
Mellick, P. W. ; Dungworth, D. L.; Schwartz, L. W.; Tyler, W. S. (1977) Short-
term morphologic effects of high ambient levels of ozone on lungs of
rhesus monkeys. Lab. Invest. 36: 82-90.
Mellick, P. W. ; Mustafa, M. G.; Tyler, W. S.; Dungworth, D. L. (1975) Morpho-
logic and biochemical changes in primate lung due to low-level ozone
exposure. Bull. Int. Union Against Tuberculosis 51: 565-567.
Meloan, C. E. ; Mauck, M.; Huffman, C. (1961) Spectrophotometric determination
of traces of hydrogen peroxide. Anal. Chem. 33: 104-106.
Menzel, D. B. ; Roehm, J. N.; Lee, S. D. (1972) Vitamin E: the biological and
environmental antioxidant. J. Agric. Food Chem. 20: 481-486.
Menzel, D. B. ; Slaughter, R. J.; Bryant, A. M.; Jauregui, H. 0. (1975a) Heinz
bodies formed in erythrocytes by fatty acid ozonides and ozone. Arch.
Environ. Health 30: 296-301.
Menzel, D. B.; Slaughter, R. J.; Bryant, A. M.; Jauregui, H. 0. (1975b) Preven-
tion of ozonide-induced Heinz bodies in human erythrocytes by vitamin E.
Arch. Environ. Health 30: 234-236.
Meyer, D. A.; Sommer, J. G. (1957) Final technical report: the development of
weather and aging resistant pneumatic tires and mechanical rubber goods.
Dayton, OH: Dayton Rubber Co.
Miller, F. J. ; Illing, J. W. ; Gardner, D. E. (1978) Effect of urban ozone
levels on laboratory-induced respiratory infections. Toxicol. Lett.
2: 163-169.
Miller, F. J. ; McNeal, C. A.; Kirtz, J. M.; Gardner, D. E.; Coffin, D. L. ;
Menzel, D. B. (1979) Nasopharyngeal removal of ozone in rabbits and
guinea pigs. Toxicology 14: 273-281.
Miller, P. R. (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, (Advances in chemistry series:
no. 122); pp. 101-117.
Miller, P. R.; Elderman, M. J., eds. (1977) Photochemical oxidant air pollutant
effects on a mixed conifer forest ecosystem: a progress report, 1976.
Corvallis, OR: U.S. Environmental Protection Agency; EPA report no.
EPA-600/3-77-104. Available from: NTIS, Springfield, VA; PB-274531.
019COR/B 1-178 6/30/84
-------
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. ; Taylor, 0. C.; Wilhour, R. G. (1982) Oxidant air pollution
effects on a western coniferous forest ecosystem. EPA-600/D-82-276.
U.S. Environmental Protection Agency, Corvallis, Oregon.
Miller, P. R.; Taylor, 0. C.; Wilhour, R. G. (1982) Oxidant air pollution
effects on a western coniferous forest ecosystem. Corvallis, OR: U.S.
Environmental Protection Agency; EPA-600/D-82/276; 10 pp.
Mizoguchi, I.; Osawa, M. ; Sato, Y. ; Makino, K. ; Yagyu, H. (1973) Studies on
erythrocyte and photochemical smog. I. Effects of air pollutants on
erythrocyte resistance. Taiki Osen Kenkyu 8: 414.
Moore, G. S.; Calabrese, E. J.; Grinberg-Funes, R. A. (1980) The C57L/J mouse
strain as a model for extrapulmonary effects of ozone exposure. Bull.
Environ. Contain. Toxicol. 25: 578-585.
Moore, G. S. ; Calabrese, E. J.; Labato, F. J. (1981a) Erythrocyte survival in
sheep exposed to ozone. Bull. Environ. Contam. Toxicol. 27: 126-138.
Moore, G. S. ; Calabrese, E. J. ; Schulz, E. (1981b) Effect of in vivo ozone
exposure to dorset sheep, an animal model with low levels of erythrocyte
glucose-6-phosphate dehydrogenase activity. Bull. Environ. Contam. Toxicol.
26: 273-280.
Moore, P. F.; Schwartz, L. W. (1981) Morphological effects of prolonged exposure
to ozone and sulfuric acid aerosol on the rat lung. Exp. Mol. Pathol.
35: 108-123.
Moorman, W. J. ; Chmiel, J. J. ; Stara, J. F.; Lewis, T. R. (1973) Comparative
decomposition of ozone in the nasopharynx of beagles. Acute vs. chronic
exposure. Arch. Environ. Health 26: 153-155.
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.
Mueller, P. K. ; Hidy, G. M. (1983) The sulfate regional experiment (SURE):
report of findings. Palo Alto, CA: Electric Power Research Institute;
report no. EA-1901.
Mueller, W. J.; Stickney, P. B. (1970) A survey and economic assessment of the
effects of air pollution on elastomers. Columbus, OH: Battelle Memorial
Institute; NAPCA contract no. CPA-22-69-146.
Murphy, S. D. (1964) A review of effects on animals of exposure to auto exhaust
and some of its components. J. Air Pollut. Control Assoc. 14: 303-308.
Murphy, S. D. ; Leng, J. K.; Ulrich, C. E.; Davis, H. V. (1963) Effects on
animals of exposure to auto exhaust. Arch. Environ. Health 7: 60-70.
019COR/B 1-179 6/30/84
-------
Murphy, S. D. ; Ulrich, C. E. ; Frankowitz, S. H.; Xintaras, C. (1964) Altered
function in animals inhaling low concentrations of ozone and nitrogen
dioxide. Am. Ind. Hyg. Assoc. J. 25: 246-253.
Musselman, R. C.; Oshima, R. J.; Gallavan, R. E. (1983) Significance of pollu-
tant concentration distribution on the response of red kidney beans to
ozone. J. Amer. Soc. Hort. Sci., 108: 347-351.
Mustafa, M. G. (1975) Influence of dietary vitamin E on lung cellular sensiti-
vity to ozone in rats. Nutr. Rep. Int. 11: 473-476.
Mustafa, M. G. ; 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.; Elsayed, N. M.; Quinn, C. L.; Postlethwait, E. M.; Gardner, D.
E. ; Graham, J. A. (1982) Comparison of pulmonary biochemical effects of
low level ozone exposure on mice and rats. J. Toxicol. Environ. Health
9: 857-865.
Mustafa, M. G. ; Hacker, A. D.; Ospital, J. J.; Hussain, M. Z.; Lee, S.D.
(1977) Biochemical effects of environmental oxidants pollutants in animal
lungs. In: Lee, S.D., ed. Biochemical effects of environmental pollu-
tants. Ann Arbor, MI: Ann Arbor Science Publishers, Inc.; pp. 59-96.
Mustafa, M. G.; Lee, S. D. (1976) Pulmonary biochemical alterations resulting
from ozone exposure. Ann. Occup. Hyg. 19: 17-26.
Mustafa, M. G.; Tierney, D. F. (1978) Biochemical and metabolic changes in the
lung with oxygen, ozone, and nitrogen dioxide toxicity. Am. Rev. Respir.
Dis. 118: 1061-1090.
Nakajima, T. ; Kusumoto, S.; Tsubota, Y. ; Yonekawa, E.; Yoshida, R. ; Motomiya,
K. ; Ito, K.; Ide, G.; Ostu, H. (1972). Histopathological changes in the
respiratory organs of mice exposed to photochemical oxidants and automo-
bile exhaust gas. Osaka-Furitsu Koshu Eisei Kenkyusho Kenkyu Hokoku Rodo
Eisei Hen 10: 35-42.
National Academy of Sciences, National Research Council. (1977) Ozone and
other photochemical oxidants. Washington, DC: National Academy Press;
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.
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. pp. 663-673 In: International Conference on Photochemical
Oxidant Pollution and its Control. Proceedings. Volumn II. B.
Dimitriades, ed. EPA-600/3-77-001b. U.S. Environmental Protection Agency,
Research Triangle Park, N.C.
Newman, J. R. (1979) Effects of industrial air pollution on wildlife. Biol.
Conserv. 15: 181-190.
019COR/B 1-180 6/30/84
-------
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 analysis.
Atmos. Environ. 16: 2447-2450.
Niki, H.; Maker, P. D.; Savage, C. M.; Breitenbach, L. P. (1983) Atmospheric
ozone-olefin reactions. Environ. Sci. Technol. 17: 312A-322A.
Nipe, M. R. (1981) Atmospheric contaminant fading. Text. Chem. Color. 13(6):
18-28.
Odum, E. P. (1971) Fundamentals of ecology, third edition. Philadelphia, PA:
W. B. Saunders; pp. 1-38.
Ogata, G.; Mass, E. V. (1973) Interactive effects of salinity and ozone on
growth and yield of garden beet. J. Environ. Qual., 2: 518-520.
Ogle, L. D.; Hall, R. C.; Crow, W. L.; Jones, A. E. (1982) Development of
preconcentration and chromatographic procedures for the continuous and
unattended monitoring of hydrocarbons in ambient air. Presented at the
184th National Meeting of the American Chemical Society; September;
Kansas City, MO.
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.
Ormrod, D. P. (1982) Air pollutant interactions in mixtures. Ln: Effects of
Air Pollution in Agriculture and Horticulture. Unsworth, M. H.; Ormrod,
D. P., eds. Butterworths, London, pp. 307-331.
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.
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.
Oshima, R. J. (1973) Effects of ozone on a commercial sweet corn variety.
Plant Dis. Resp., 57: 719-723.
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.
Oshima, R. J.; Taylor, 0. C.; Braegelmann, P. K.; Baldwin, D. W. (1975) Effects
of ozone on the yield and plant biomass of a commercial variety of tomato.
J. Environ. Qual., 4: 463-464.
019COR/B 1-181 6/30/84
-------
Oshima, R. ; Taylor, 0. C.; Cardiff, E. A. (1974) Severe air pollution episode
in South Coast Basin. Calif. Agric. 28: 12-13.
Osman, M. ; Hill, H. H. ; Holdren, M. W. ; Westberg, H. H. (1979) Vapor-phase
silylation of alcohols for air analysis. In: A. Zlatkis, ed. Advances
in Chromatography, Chromatography Symposium-University of Houston, Houston,
TX.
P'an, A. Y. S.; Beland, J.; Jegier, Z. (1972) Ozone-induced arterial lesions.
Arch. Environ. Health 24: 229-232.
P'an, A. Y. S.; Jegier, 2. (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.
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.
Pate, C. T. ; Atkinson, R.; Pitts, J. N., Jr. (1976) The gas phase reaction of
0- with a series of aromatic hydrocarbons. J. Environ. Sci. Health All:
1-10.
Patton, R. L. (1981) Effects of ozone and sulfur dioxide on height and stem
specific gravity of Populus Hybrids. For. Sci. Res. Paper NE-471.
Paur, R. J. ; Bass, A. M. (1983) Standard reference photometer for the assay of
ozone. Presented at the National Meeting of the American Chemical Society;
October; Washington, DC.
Paur, R. J.; McElroy, F. F. (1979) Technical assistance document for calibration
of ambient ozone monitors. Research Triangle Park, NC: U.S. Environmental
Protection Agency; EPA report no. EPA-600/4-79-057.
Peake, E.; Sandhu, H. S. (1982) The formation of ozone and peroxyacetyl nitrate
(PAN) in the urban atmospheres of Alberta. Presented at 65th Annual Con-
ference Chem. Inst. Canada; May 30 - June 2,1982; Toronto, Canada.
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.
Perschke, H.; Broda, E. (1961) Determination of very small amounts of hydrogen
peroxide. Nature (London) 190: 257-258.
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.
019COR/B 1-182 6/30/84
-------
Pilz, W.; Johann, I. (1974) Measurement of very small quantities of hydrogen
peroxide in air. Int. J. Environ. Anal. Chem. 3: 257-270.
Pisarevskii, A. M.; Polozova, I. P. (1980) Electrode for potentiometric deter-
minations of hydrogen peroxide in alkaline media. Zh. Anal. Khim. 35:
2187-2194.
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 reexposure. 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.
Pobiner, H. (1961) Determination of hydroperoxides in hydrocarbons by conversion
to hydrogen peroxide and measurement by titanium complexing. Anal. Chem.
33: 1423-1426.
Pratt, G. C. (1982) Effects of ozone and sulfur dioxide on soybeans. PhD
Thesis. University of Minnesota, Minneapolis.
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 III, G. K.; Brooks, J. K.; Rubin, R. J. (1979) Enrichment
of albumin and IgG in the airway secretions of dogs breathing ozone. J.
Environ. Sci. Health C13: 335-346.
Reckner, L. R. (1974) Survey of users of EPA-Reference Method for measurement
of non-methane hydrocarbons in ambient air. Research Triangle Park, NC:
U.S. Environmental Protection Agency, EPA report no. EPA-650/4-75-008.
Regener, V. H. (1960) On a sensitive method for the recording of atmospheric
ozone. JGR J. Geophys. Res. 65: 3975-3977.
Regener, V. H. (1964) Measurement of atmospheric ozone with the chemiluminescent
method. JGR J. Geophys. Res. 69: 3795-3800.
Rehme, K. A.; Puzak, J. C.; Beard, M. E. ; Smith, C. F. ; Paur, R. J. (1981)
Project summary: Evaluation of ozone calibration procedure. Research
Triangle Park, NC: U.S. Environmental Protection Agency; EPA report no.
EPA-600/S4-80-050.
Reinert, R. A.; Nelson, P. V. (1979) Sensitivity and growth of twelve elatior
begonia cultivars to ozone. HortScience 14: 747-748.
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.
019COR/B 1-183 6/30/84
-------
Revis, N. W. ; Major, T.; Dalbey, W. E. (1981) Cardiovascular effects of ozone
and cadmium inhalation in the rat. In: Northrop Services, Inc., ed.
Proceedings of the research planning workshop on health effects of oxidants;
January 1980; Raleigh, NC. Research Triangle Park, NC: U.S. Environmental
Protection Agency, Health Effects Research Laboratory; EPA-600/9-81-001;
pp. 171-179. Available from: NTIS, Springfield, VA; PB81-178832.
Reynolds, R. W. ; Chaffee, R. R. (1970) Studies on the combined effects of
ozone and a hot environment on reaction time in subhuman primates. In:
Project clean air: v. 2. Santa Barbara, CA: University of California;
8 pp; Research Project S-6.
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; EPA report no. EPA-450/4-83-017.
Roehm, J. N. ; Hadley, J. G.; Menzel, D. B. (1972) The influence of vitamin E
on the lung fatty acids of rats exposed to ozone. Arch. Environ. Health
24: 237-242.
Roose, M. L. ; Bradshaw, A. D. ; Roberts, T. M. (1982) Evolution of resistance
to gaseous air pollutants. In: Unsworth, M. H.; Ormrod, 0. P., eds.
Effects of gaseous air pollution in agriculture and horticulture. London:
Butterworth Scientific; pp. 379-409.
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.
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. 24: 571-
585.
Sato, S.; Kawakami, M.; Maeda, S.; Takishima, T. (1976a) Scanning electron
microscopy of the lungs of vitamin E-deficient rats exposed to a low
concentration of ozone. Am. Rev. Respir. Dis. 113: 809-821.
Sato, S. ; Kawakami, M.; Maeda, S.; Takishima, T. (1976b) Electron microscopic
studies on the effects of ozone on the lungs of vitamin E-deficient rats.
Nippon Kyobu Shikkan Gakkai Zasshi 14: 355-365.
Sato, S.; Shimura, S.; Hirosa, T.; Maeda, S.; Kawakami, M.; Takishima, T. ;
Kimura, S. (1980) Effects of long-term ozone exposure and dietary vitamin
E in rats. Tohoku J. Exp. Med. 130: 117-128.
Sato, S.; Shimura, S. ; Kawakami, M. ; Hirosa, T. ; Maeda, S.; Takishima, T. ;
Kimura, S.; Yashiro, M.; Okazaki, S. ; Ito, M. (1978) Biochemical and
ultrastructural studies on the effects of long-term exposure of ozone on
vitamin E-depleted rats. Nippon Kyobu Shikkan Gakkai Zasshi 16: 260-268.
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.
019COR/B 1-184 6/30/84
-------
Scheutzle, D. ; Rasmussen, R. A. (1978) The molecular composition of secondary
aerosol particles formed from terpenes. J. Air Pollut. Control Assoc.
28: 236-240.
Schlipkoter, H. ; Bruch, J. (1973) Functional and morphological alterations
caused by exposure to ozone. Zentralbl. Bakteriol. Parasitenkd. Infektion-
skr. Hyg. Abt. 1: Orig. Reihe B 156: 486-499.
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.
Schwartz, L. W.; Christman, C. A. (1979) Alveolar macrophage migration. Influ-
ence of lung lining material and acute lung insult. Am. Rev. Respir.
Dis. 120: 429-439.
Schwartz, L. W. ; Dungworth, D. L.; Mustafa, M. G.; Tarkington, B. K.; Tyler,
W. S. (1976) Pulmonary responses of rats to ambient levels of ozone:
effects of 7-day intermittent or continuous exposure. Lab. Invest. 34:
565-578.
Scott, D. B. M.; Lesher, E. C. (1963) Effect of ozone on survival and permea-
bility of Escherichia coli. J. Bacteriol. 85: 567-576.
Seila, R. L. (1981) Nonurban hydrocarbon concentrations in ambient air north
of Houston, TX. In: Bufalini, J. J. ; Arnts, R. R. , eds. Atmospheric
Biogenic Hydrocarbons. Ann Arbor, MI: Ann Arbor Science Publishers,
Inc.
Seiler, W. ; Fishman, J. (1981) The distribution of carbon monoxide and ozone
in the free troposphere. JGR J. Geophys. Res. 86: 7255-7265.
Sevcik, J. (1975) Detectors in Gas Chromatography. Amsterdam, The Netherlands:
Elsevier Scientific Publishing Company.
Sexton, F. W. ; McElroy, F. F. ; Michie, R. M., Jr.; Thompson, V. L. (1981) A
comparative evaluation of seven automatic ambient non-methane organic
compound analyzers. Research Triangle Park, NC: U.S. Environmental
Protection Agency; cited in: U.S. Environmental Protection Agency (1981),
EPA report no. EPA-600/4-81-015.
Sexton, K. ; Westberg, H. (1984) Nonmethane hydrocarbon composition of urban
and rural atmospheres. Atmos. Environ, (in press).
Shannon, J. G.; Mulchi, C. L. (1974) Ozone damage to wheat varieties at anthe-
sis. Crop Sci., 14: 335-337.
Sherwin, R. P.; Richters, V.; Okimoto, D. (1983) Type 2 pneumocyte hyperplasia
in the lungs of mice exposed to an ambient level (0, ppm) of ozone. In:
Lee, S. D.; Mustafa, M. G.; Mehlman, M. A., eds. International symposium
on the biomedical effects of ozone and related photochemical oxidants;
March 1982; Pinehurst, NC. Princeton, NJ: Princeton Scientific Publishers,
Inc.; pp. 289-297. (Advances in modern environmental toxicology: v. 5).
019COR/B 1-185 6/30/84
-------
Sielczak, M. W. ; Denas, S. M. ; Abraham, W. M. (1983) Airway cell changes in
trachea! lavage of sheep after ozone exposure. J. Toxicol. Environ.
Health 11: 545-553.
Silverman, F. (1979) Asthma and respiratory irritants (ozone). EHP Environ.
Health Perspect. 29: 131-136.
Silverman, F. ; Folinsbee, L. J. ; Barnard, J. ; Shephard, R. J. (1976) Pulmonary
function changes in ozone - interaction of concentration and ventilation.
J. Appl. Physio!. 41: 859-864.
Singh, H. B.; Sal as, L. J. (1983a) Peroxyacetyl nitrate in the free troposphere.
Nature (London) 302: 326-328.
Singh, H. B.; Salas, L. J. (1983b) Methodology for the analysis of peroxyacetyl
nitrate (PAN) in the unpolluted atmosphere. Atmos. Environ. 17: 1507-1516.
Singh, H. B.; Salas, L. J.; Smith, A. J.; Shigeishi, H. (1981) Measurements of
some potentially hazardous organic chemicals in urban atmospheres.
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. Report on EPA
Cooperative Agreement 805990. Research Triangle Park, NC: U.S. Environ-
mental Protection Agency, Environmental Sciences Research Laboratory.
Smith, R. L. (1980) Ecology and field biology, 3rd ed. New York, NY: Harper
and Row; pp. 11-199.
Smith, W. J. (1981) New York State Air Monitoring Data Report for the Northeast
Corridor Regional Modeling Project. Albany, NY: New York State Department
of Environment and Conservation.
Solic, J. J. ; Hazucha, M. J.; Bromberg, P. A. (1982) Acute effects of 0.2 ppm
ozone in patients with chronic obstructive pulmonary disease. Am. Rev.
Respir. Dis. 125: 664-669.
Speit, G. ; Vogel, W. ; Wolf, M. (1982) Characterization of sister chromatid
exchange induction by hydrogen peroxide. Environ. Mutagen. 4: 135-142.
Spicer, C. W.; Gemma, J. L; Joseph, D. W.; Sticksel, P. R.; Ward, G. F. (1976)
The transport of oxidant beyond urban areas. Prepared for U.S. Environ-
mental Protection Agency, Research Triangle Park, NC. Publication No.
EPA-600/3-76-018.
Standing Air Monitoring Work Group. (1977) Air Monitoring Work Group. Air
monitoring strategy for implementation plans. U.S. Environmental Protection
Agency, Office of Air Quality Planning and Standards. Research Triangle
Park, NC. June 1977.
Stark, R. W.; Cobb, F. W., Jr. (1969) Smog injury, root diseases and bark
beetle damage in ponderosa pine. Calif. Agric. 23: 13-15.
019COR/B 1-186 6/30/84
-------
Stephens, E. R. (1969) The formation, reactions, and properties of peroxyacyl
nitrates (PANs) in photochemical air pollution. In: Pitts, J. N.; Metcalf,
R. L. , eds. Advances in environmental sciences and technology: vol. 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.
Stephens, E. R. ; Price, M. A. (1973) Analysis of an important air pollutant
--peroxyacetyl nitrate. J. Chem. Educ. 50: 351-354.
Stephens, R. J. ; Buntman, D. J. ; Negi, D. S. ; Parkhurst, R. M. ; Thomas, D. W.
(1983) Tissue levels of vitamin E in the lung and the cellular response
to injury resulting from oxidant gas exposure. Chest 83: 37S-39S.
Stephens, R. J. ; Freeman, G. ; Stara, J. F.; Coffin, D. L. (1973) Cytologic
changes in dog lungs induced by chronic exposure to ozone. Am. J. Pathol.
73: 711-726.
Stephens, R. J. ; Sloan, M. F. ; Evans, M. J. ; Freeman, G. (1974a) Early response
of lung to low levels of ozone. Am. J. Pathol. 74: 31-58.
Stephens, R. J.; Sloan, M. F.; Evans, M. J.; Freeman, G. (1974b) Alveolar type
1 cell response to exposure to 0.5 ppm 0_ for short periods. Exp. Mol.
Pathol. 20: 11-23. d
Stephens, R. J. ; Sloan, M. F. ; Groth, D. G. (1976) Effects of long-term, low
level exposure of N0? or 0~ on rat lungs. EHP Environ. Health Perspect.
16: 178-179. ^ J
Stephens, R. J. ; Sloan, M. F.; Groth, D. G.; Negi, D. S.; Lunan, K. D. (1978)
Cytologic responses of postnatal rat lungs to 0., or N0_ exposure. Am. J.
Pathol. 93: 183-200. J ^
Stevens, R. K. ; Hodgeson, J. A. (1973) Application of chemiluminescent reactions
to the measurement of air pollutants. Anal. Chem. 45: 443A-446A, 449A.
Stewart, R. M. ; Weir, E. K. ; Montgomery, M.R.; Niewoehner (1981) Hydrogen
peroxide contracts airway smooth muscle: a possible endogenous mechanism.
Respir. Physiol. 45: 333-342.
Stokinger, H. E. ; Wagner, W. D. ; Oobrogorski, 0. J. (1957) Ozone toxicity
studies, III. Chronic injury to lungs of animals following exposure at
low level. AMA Arch. Ind. Health 16: 514-522.
Stokinger, H. E. ; Wagner, W. D.; Wright, P. G. (1956) Studies on ozone toxicity.
I. Potentiating effects of exercise and tolerance development. AMA
Arch. Ind. Health 14: 158-162.
Taylor, 0. C. (1969) Importance of peroxyacetyl nitrate (PAN) as a phytotoxic
air pollutant. J. Air Pollut. Control Assoc. 19: 347-351.
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.
019COR/B 1-187 6/30/84
-------
Tepper, J. L. ; Weiss, B.; Cox, C. (1982) Microanalysis of ozone depression of
motor activity. Toxicol. Appl. Pharmacol. 64: 317-326.
Tepper, J. L.; Weiss, B. ; Wood, R. W. (1983) Behavioral indices of ozone
exposure. In: Lee, S. D.; Mustafa, M. G.; Mehlman, M. A., eds. Inter-
national symposium on the biomedical effects of ozone and related photo-
chemical oxidants; March 1982; Pinehurst, NC. Princeton, NJ: Princeton
Scientific Publishers, Inc.; pp. 515-526. (Advances in modern environmental
toxicology: v. 5).
Thomas, G. B. ; Fenters, J. D.; Ehrlich, R.; Gardner, D. E. (1981a) Effects of
exposure to peroxyacetyl nitrate on susceptibility to acute and chronic
bacterial infection. J. Toxicol. Environ. Health 8: 559-574.
Thomas, G. B. ; Fenters, J. D.; Ehrlich, R.; Gardner, D. E. (1981b) Effects of
exposure to ozone on susceptibility to experimental tuberculosis. Toxicol.
Lett. 9: 11-17.
Thomas, G. ; Fenters, J. D. ; Ehrlich, R. (1979) Effect of exposure to PAN and
ozone on susceptibility to chronic bacterial infection. Research Triangle
Park, NC: U.S. Environmental Protection Agency, Health Effects Research
Laboratory; EPA report no. EPA-600/1-79-001. Available from: NTIS,
Springfield, VA; PB292267.
Thomas, M. D. ; Hendericks, R. H. ; Hill, G. R. (1950) Sulfur metabolism of
plants. Effects of sulfur dioxide on vegetation. Industrial and Engineer-
ing Chemistry, 42: 2231-2235.
Thompson, C. R.; Hensel, E. G. ; Kats, G. (1973) Outdoor-indoor levels of six
air pollutants. J. Air Pollut. Control Assoc. 19: 347-351.
Thompson, C. R.; Kats, G.; Camerson, J. W. (1976) Effects of ambient photochem-
ical oxidants on growth, yield, and ear characteristics of two sweet corn
hybrids. J. Environ. Qual., 5: 410-412.
Tingey, D. T. (1977) Ozone induced alterations in plant growth and metabolism.
In: Dimitriades, B. , ed. International Conference on Photochemical
Oxidant Pollution and its Control: Proceedings, Volume II, January 1977.
EPA-600/3-77-001b. U.S. Environmental Protection Agency, Research Triangle
Park, N.C. pp. 601-609
Tingey, D. T.; Heck, W. W.; Reinert, R. A. (1971) Effects of low concentrations
of ozone and sulfur dioxide on foliage, growth and yield of radish. J.
Am. Soc. Hort. Sci., 96: 369-371.
Tingey, D. T. ; Reinert, R. A. (1975) The effects of ozone and sulfur dioxide
singly and in combination on plant growth. Environ. Pollut., 9: 117-125.
Tingey, D. T. ; Taylor, G. E. (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 Agricultural and Horticul-
ture. Butterworths, London, pp. 113-138
019COR/B 1-188 6/30/84
-------
Tokiwa, Y. ; Twiss, S.; deVera, E. A.; Mueller, P. K. (1972) Atmospheric ozone
determination by amperometry and colorimetry. In: Mamantov, G.; Shults,
W. D. , eds. Determination of air quality. New York, NY: Plenum Pub-
lishing Co.; pp. 109-130.
Trams, E. G.; Lauter, C. J.; Brown, E. A. B.; Young, 0. (1972) Cerebral corti-
cal metabolism after chronic exposure to 0~. Arch. Environ. Health 24:
153-159.
Treshow, M.; Stewart, D. (1973) Ozone sensitivity of plants in natural commun-
ities. Biol. Conserv. 5: 205-214.
Tuazon, E. C. ; Carter, W. P. L.; Winer, A. M.; Pitts, J. N. , Jr. (1981) Reac-
tions of hydrazines with ozone under simulated atmospheric conditions.
Environ. Sci. Technol. 15: 823-828.
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. (1981a) Atmos-
pheric measurements of trace pollutants: long path Fourier transform
infrared spectroscopy. Prepared for U.S. Environmental Protection Agency,
Environmental Sciences Research Laboratory, Research Triangle Park, NC.
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.
Tyson, C. A.; Lunan, K. D.; Stephens, R. J. (1982) Age-related differences in
GSH-shuttle enzymes in N0_- or 0.,-exposed rat lungs. Arch. Environ.
Health 37: 167-176.
U.S. Congress. (1977) The Clean Air Act as Amended August 1977. P. L. 95-95.
Washington, DC; U.S. Government Printing Office.
U.S. Department of Commerce, Bureau of the Census. (1982) Statistical Abstract
of the United States, 1982-83. 103rd Ed. Washington, DC: U.S. Government
Printing Office.
U.S. Department of Health, Education, and Welfare. (1970) Air quality criteria
for photochemical oxidants. Washington, DC: National Air Pollution
Control Administration; publication No. AP-63.
U.S. Environmental Protection Agency. (1982b). Air quality criteria for
particulate matter and sulfur oxides. Research Triangle Park, NC: U.S.
Environmental Protection Agency; EPA report no. EPA-600/8-82-029a,b,c,d.
U.S. Environmental Protection Agency. SAROAD data file for 1982. Office of
Air Quality Planning and Standards, Research Triangle Park, NC 27711.
019COR/B 1-189 6/30/84
-------
U.S. Environmental Protection Agency. SAROAD data file for 1976. Office of
Air Quality Planning and Standards, Research Triangle Park, NC 27711.
U.S. Environmental Protection Agency. SAROAD data file for 1979. Office of
Air Quality Planning and Standards, Research Triangle Park, NC 27711.
U.S. Environmental Protection Agency. SAROAD data file for 1980. Office of
Air Quality Planning and Standards, Research Triangle Park, NC 27711.
U.S. Environmental Protection Agency. SAROAD data file for 1981. Office of
Air Quality Planning and Standards, Research Triangle Park, NC 27711.
U.S. Environmental Protection Agency. (1971) Reference Methods. Code of
Federal Regulations, Title 40, Part 50, Appendix D. Washington, DC:
U.S. Government Printing Office.
U.S. Environmental Protection Agency. (1975) Ambient air monitoring reference
and equivalent methods. Fed. Regist. 40: 7042-7070, February 18.
U.S. Environmental Protection Agency. (1976a). Ambient air monitoring refer-
ence and equivalent methods. Code of Federal Regulations, Title 40,
Part 53.
U.S. Environmental Protection Agency. (1976b). Nitrogen dioxide measurement
principle and calibration procedure. Notice of final rulemaking. Fed.
Regist. 41:52686-5294, December 1.
U.S. Environmental Protection Agency. (1977) Quality assurance handbook for
air pollution measurement systems. Research Triangle Park, NC: U.S.
Environmental Protection Agency; EPA report no. EPA-600/4-77-027.
U.S. Environmental Protection Agency. (1978) Air quality criteria for ozone
and other photochemical oxidants. Research Triangle Park, NC: U.S.
Environmental Protection Agency; EPA report no. EPA-600/8-78-004.
U.S. Environmental Protection Agency. (1979a) Fed. Regist. 44(92): 27558,
Thursday, May 10.
U.S. Environmental Protection Agency. (1979b) Fed. Regist. 44(219): 65069,
Friday, November 9.
U.S. Environmental Protection Agency. (1979c) Fed. Regist. 44(242): 72589,
Friday, December 14.
U.S. Environmental Protection Agency. (I979d) Calibration of ozone reference
methods. Fed. Regist. 44: 8221-8233, February 8.
U.S. Environmental Protection Agency. (1980). 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.
019COR/B 1-190 6/30/84
-------
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.
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.
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.
Veninga, T. S. (1967) Toxicity of ozone in comparison with ionizing radiation.
Strahlentherapie 134: 469-477.
Veninga, T. S. (1970) Ozone-induced alterations in murine blood and liver.
Presented at: Second international clean air congress; December;
Washington, DC. Washington, DC: International Union of Air Pollution
Prevention Associations; paper no. MB-15E.
Veninga, T. S. ; Wagenaar, J.; Lemstra, W. (1981) Distinct enzymatic responses
in mice exposed to a range of low doses of ozone. EHP Environ. Health
Perspect. 39: 153-157.
Verweij, H. ; Van Steveninck, J. (1980) Effects of semicarbazide on processes
in human red blood cell membranes. Biochim. Biophys. Acta 602: 591-599.
Verweij, H.; Van Steveninck, J. (1981) Protective effects of semicarbazide and
p-aminobenzoic acid against ozone toxicity. Biochim. Pharmacol. 30: 1033-
1037.
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 Project 6690 for Coordinating Research Council,
Atlanta, Georgia.
Warshauer, D.; Goldstein, E. ; Hoeprich, P. D. ; Lippert, W. (1974) Effect of
vitamin E and ozone on the pulmonary antibacterial defense mechanisms.
J. Clin. Med. 83: 228-240.
Watanabe, S. ; Frank, R. ; Yokoyama, E. (1973) Acute effects of ozone on lungs
of cats. I. Functional. Am. Rev. Respir. Dis. 108: 1141-1151.
Wayne, W. S. ; Wehrle, P. F. ; Carroll, R. E. (1967) Oxidant air pollution and
athletic performance. J. Am. Med. Assoc. 199: 902-904.
Wegner, C. D. (1982) Characterization of dynamic respiratory mechanics by mea-
surement of pulmonary and respiratory system impedance in adult bonnet
monkeys (Macaca radiata): including the effects of long-term exposure to
low-level ozone. Davis, CA: University of California; Ph.D. Dissertation.
019COR/B 1-191 6/30/84
-------
Weiss, B. ; Ferin, J. ; Merigan, W. ; Stern, S.; Cox, C. (1981) Modification of
rat operant behavior by ozone exposure. Toxicol. Appl. Pharmacol. 58: 244-
251.
Wenghoefer, H. M. (1974) Environmental effects on RFL adhesion. Rubber Chem.
Techno!. 47(5): 1066-1073.
Westberg, H. H.; Holdren, M. W.; Hill, H. H. (1980) Analytical methodology for
the identification and quantification of vapor phase organic pollutants.
CRC-APRAC Project No. CAPA-11-71, Coordinating Research Council, New
York, NY.
Westberg, H.; Allwine, K.; Robinson, R. (1978) Measurement of light hydrocarbon
and oxidant transport: Houston study, 1976. Research Triangle Park, NC:
U.S. Environmental Protection Agency, Environmental Sciences Research
Laboratory; EPA report no. EPA-600/3-78-662.
Westberg, H. ; Lamb, B. (1982) Milwaukee ozone study - 1981. Final Report for
Contract No. NRA 98571. Wisconsin Department of Natural Resources,
Madison, WI.
Westberg, H. ; Lamb, B. (1983) Ozone production and transport in the Atlanta,
GA region. Final report for EPA grant no. CR 809221; Environmental
Sciences Research Laboratory, U.S. Environmental Protection Agency;
Research Triangle Park, NC.
Whittemore, A. S. ; Korn, E. L. (1980) Asthma and air pollution in the Los
Angeles area. Am. J. Public Health 70: 687-696.
Wilhour, R. G. ; Neely, G. E. (1977) Growth response of conifers seedlings to
low ozone concentrations. In: International Conference of Photochemical
Oxidant Pollution and Its Control: Proceedings. Volume II. B. Dimitriades,
ed. EPA-600/3-77-001b. U.S. Environmental Protection Agency, Research
Triangle Park, N.C. pp. 635-645.
Williams, S. J. ; Charles, J. M.; Menzel, D. B. (1980) Ozone-induced altera-
tions in phenol red absorption from the rat lung. Toxicol. Lett. 6:
213-219.
Winer, A. M. ; Peters, J. M. ; Smith, J. P.; Pitts, J. N., Jr. (1974) Response
of commercial chemiluminescent N0-N0» analysis to other nitrogen-contain-
ing compounds. Environ. Sci. TechnoT. 8:1118-1121.
Witz, G. ; Amoruso, M. A.; Goldstein, B. D. (1983) Effect of ozone on alveolar
macrophage function: membrane dynamic properties. In: Lee, S. D. ;
Mustafa, M. G. ; Mehlman, M. A. , eds. International symposium on the
biomedical effects of ozone and related photochemical oxidants; March
1982; Pinehurst, NC. Princeton, NJ: Princeton Scientific Publishers,
Inc.; pp. 263-272. (Advances in modern environmental toxicology: v. 5).
Woodwell, G. M. (1970) Effects of pollution on the structure and physiology of
ecosystems. Science (Washington, D.C.) 168: 429-433.
019COR/B 1-192 6/30/84
-------
Woodwell, G. M. (1974) Success, succession, and Adam Smith. BioScience 24:
81-87.
Xintaras, C. ; Johnson, B. L. ; Ulrich, C. E. ; Terrill, R. E. ; Sobecki, M. F.
(1966) Application of the evoked response technique in air pollution
toxicology. Toxicol. Appl. Pharmacol. 8: 77-87.
Yokoyama, E. (1969) A comparison of the effects of SO-, N0~ and 0~ on the
pulmonary ventilation. Guinea pig exposure experiments. Sangyo Igaku
11: 563-568.
Yokoyama, E. (1974) On the maximal expiratory flow volume curve of rabbits
exposed to ozone. Nipon Kyobu Shikkan Gakkai Zasshi 12: 556-561.
Yokoyama, E. ; Frank, R. (1972) Respiratory uptake of ozone in dogs. Arch.
Environ. Health 25: 132-138.
Zagraniski, R. T.; Leaderer, B. P.; Stolwijk, J. A. J. (1979) Ambient sulfates,
photochemical oxidants, and acute health effects: an epidemiological
study. Environ. Res. 19: 306-320.
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.
Zelac, R. E.; Cromroy, H. L.; Bolch, Jr., W. E.; 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.
Zika, R. G.; Saltzman, E. S. (1982) Interaction of ozone and hydrogen peroxide
in water: implications for analysis of H?0? in air. Geophys. Res. Lett.
9: 231-234. * *
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.
019COR/B 1-193 6/30/84
------- |