REVIEW OF THE NATIONAL AMBIENT AIR QUALITY STANDARDS FOR OZONE
PRELIMINARY ASSESSMENT OF SCIENTIFIC AND TECHNICAL INFORMATION
OAQPS STAFF PAPER
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Strategies and Air Standards Division
Office of A1r Quality Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, N.C. 27711
March 1986
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The cover Illustration is an air quality map of the U.S. which displays all
urban areas (104 SMSAs) and counties outside of SMSA's (14) which recorded
exceedances of the ozone standard based on 1982-84 data reported to
SAROAD. In each map, a spike 1s plotted at the city location on the map
surface. Each spike 1s also projected onto a backdrop facilitating comparl
with the dashed line correspondlng to 1.05 exceedances.
NOTE: Scale has been truncated at 40 exceedances/yr. L.A. sites had
approximately 160 exceedances/yr.
This document 1s an OAQPS staff draft that 1s being
circulated for technical review and comment. It has
not been fully reviewed within EPA and does not
represent Agency policy.
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REVIEW OF THE NATIONAL AMBIENT AIR QUALITY STANDARDS FOR OZONE
PRELIMINARY ASSESSMENT OF SCIENTIFIC AND TECHNICAL INFORMATION
OAQPS STAFF PAPER
Strategies and A1r Standards Division
Office of A1r Quality Planning and Standards
U.S. Environmental Protection Agency
Research Triangle Park, N.C. 27711
March 1986
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111
Page
List of Figures v11
List of Tables v111
Executive Summary x
I. Purpose 1-1
II. Background II-l
III. Approach III-l
IV. Ambient Ozone Concentrations 1n Urban and Rural Areas IV-1
V. Ozone Exposure Analysis V-l
A. Overview of the Ozone National Exposure Model V-l
B. A1r Quality Concentrations 1n M1croenv1ronments... V-2
C. Simulation of Population Movement V-5
0. Exposure Estimates for 10 Urban Areas V-6
E. Nationwide Extrapolations V-16
VI. Critical Elements 1n the Review of the Primary Standard for Ozone VI-1
A. Ozone Absorption and Mechanisms of Effects VI-1
B. Factors Affecting Susceptibility VI-4
1. Age VI-4
2. Sex VI-5
3. Smoking Status VI-6
4. Nutritional Status VI—7
5. Environmental Stress VI—8
6. Exercise VI —8
C. Potentially Susceptible Groups VI-10
1. Individuals Having Preexisting Disease VI-11
2. "Responders" VI-13
3. Exercising Individuals VI-17
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iv
Page
VII. Assessment of Health Effects and Related Health Issues
Considered in Selecting Primary Standard(s) for Ozone....... VII-1
A. Health Effects of Concern VII-1
1. Alterations in Pulmonary Function VII-2
2. Symptomatic Effects VII-12
3. Effects on Exercise Performance VII-15
4. Aggravation of Existing Respiratory Disease VII-16
5. Morphological Effects VII-19
6. Altered Host Defense Systems VII-21
7. Extrapulmonary Effects VII-24
B. Related Health Issues VI1-25
1. Attenuation of Acute Pulmonary Effects VII-26
2. Relationship Between Acute and Chronic Effects...... VII-28
3. Effects of Other Photochemical Oxidants VII-30
VIII. Staff Conclusions and Recommendations for Ozone Primary
Standard(s) VI11 -1
A. Pollutant Indicator VI11 -1
B. Form of the Standard VIII-4
C. Averaging Time(s). VI11-5
D. Level of the Ozone Primary Standard VI11-7
E. Summary of Staff Recommendations for Ozone Primary
Standards VI11-19
IX. Critical Elements 1n the Review of the Secondary Standard
for Ozone IX-1
A. Mechanisms of Action for Vegetation..... IX-1
1. Biochemical Response IX-2
2. Physiological Response IX-3
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V
fi2®
B. Factors Affecting Plant Response IX-6
1. Biological Factors IX—7
a. Plant Genetics IX-7
b. Development Factors IX-7
c. Pathogen and Pest Interactions IX-8
2. Physical Factors IX-8
3. Chemical Factors IX-9
a. Multiple Pollutants IX-10
b. Chemical Sprays IX-11
X. Assessment of Welfare Effects Considered in Selecting Secondary
Standard(s) for Ozone X-l
A. Vegetation Effects X-2
1. Types of Exposure Effects X-2
a. Visible Foliar Injury Effects X-2
b. Growth and Yield Effects X-6
1. Open Top Chamber Studies X-7
2. Greenhouse and Other Controlled Environment
Studies X-l 2
3. Ambient A1r Studies X-l4
2. Related Vegetation Issues X-19
a. Empirical Models Used To Develop Exposure
Response Relationships X-19
b. Statistics Used To Characterize Ozone
Exposures X-20
c. Effects of Peroxy Acetyl Nitrate X-22
B. Ecosystem Effects X-23
C. Materials Danage... X-38
D. Effects on Personal Comfort and Well Being X-42
XI. Staff Conclusions and Recommendations for Secondary
Standard(s) XI-1
A. Pollutant Indicator XI-1
B. Form of the Standard XI-3
C. Averaging T1me(s) XI-4
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vi
Page
D. Effect Levels of Concern XI-10
E. Summary of Recommendations for Ozone Secondary
Standards XI-15
Appendix A. Air Quality A-l
Appendix B. Risk Assessment B-l
Appendix C. Glossary of Pulmonary Terms and Symbols C-l
References
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vi i
LIST OF FIGURES
Figure Title Page
V-l Indoor-to-Outdoor Multiplicative Factor (bm) V-4
VI-1 Cumulative Frequency Distribution of
Percent Decrease in FEVi Due to O3 Exposure
in Healthy Exercising Males VI-15
VI-2 Cumulative Frequency Distribution of
Percent Decrease in Airway Resistance Due
to Ozone Exposure in Healthy Exercising
Males VI -16
VII-1 Group Mean Decrements in FEV^ During
2-hour Ozone Exposures with Different Levels
of Intermittent Exercise VII-5
X-l Examples of the Effects of O3 on the
Yield of Soybean and Wheat Cultivars X-8
X-2 Examples of the Effects of O3 on the
Yield of Cotton, Tomato, and Turnip X-9
A-l Cumulative Frequency Distribution of
Peak-to-Mean Ozone Indices in MSA Counties A-10
A-2 Cumulative Frequency Distribution of Short-Term
Ozone Air Quality Indicators in Non-MSA Areas A-14
A-3 Cumulative Frequency Distribution of the Ratios
of Short- to Long-Term Ozone Indices to the
Seasonal Average of Daily Daylight Values A-22
B-l Flow Chart of the EPA Ozone NAAOS Exposure
and Health Risk Assessment Projects B-2
B-2 Probabilistic Exposure-Response Relationship for
a Given Health Endpoint, and Its Derivation
from the Encoding Data 8-6
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vi ii
LIST OF TABLES
Table Title Page
V-l Estimates of Multiplicative Environmental
Factors (bm) V-3
V-2 The Cumulative Number of People in the
New York City Area Exposed to One-Hour Average
O3 Concentrations During the Ozone Season
for the "Current" Situation V-8
V-3 Estimates of the Cumulative Number of One-Hour
Average Person Occurrences of Exposure to
Ozone in the New York City Area in the Ozone
Season for the "Current" Situation V-9
V-4 Estimates of New York City Area People Exposed to
Their Highest One-Hour Ozone Concentration
Interval During the Ozone Season V-l0
V-5 "Best" Estimates of the Cumulative Number of People
in the New York City Area Exposed to One-Hour
Average Ozone Concentrations During the Ozone
Season Under Alternative NAAQS V-l 1
V-6 Estimate of the Cumulative Number of People
in the New York City Area Exposed to One-Hour
Daily Maximums During the Ozone Season When the
0.12 ppm O3 NAAQS is Just Attained V-l2
VI-1 Estimated Values of Oxygen Consumption and
Minute Ventilation Associated with
Respresentative Types of Exercise VI-9
VI-2 Prevalence of Chronic Respiratory
Conditions by Sex and Age for 1979 VI-12
VII-1 Lung Function Changes and Symptoms
Attributed to Ozone Exposures VI1-8
VII-2 Changes in Lung Function After Repeated
Dally Exposure to Ambient Ozone VI1-27
IX-1 Effects of O3 on Photosynthesis IX-4
X-l O3 Concentrations for Short-term Exposures that
Produce 5 or 20 Percent Injury to Vegetation
Growth Under Sensitive Conditions X-4
X-2 Compilation of O3 Concentrations Predicted to
Cause 10% and 30% Yield Losses as well as Yield
Losses Predicted to Occur at 7-hour Seasonal
Mean O3 Concentrations of 0.04 and 0.06 ppm X-l 1
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ix
LIST OF TABLES (continued)
Table Title Page
X-3 Ozone Concentrations at Which Significant
Yield Losses Have Been Noted for a Variety
of Plant Species Exposed Under Various
Experimental Conditions X-13
X-4 Effects of Ambient Oxidants on Yield of
Selected Crops X-15
X-5 The Effects of O3 on Crop Yield as Determined
by the Use of Chemical Protectants X-17
X-6 Continuum of Characteristic Ecosystem
Responses to Pollutant Stress X-25
X-7 Effects of Ozone Added to Filtered Air
on the Yield of Selected Tree Crops X-30
A-l Distribution of Expected Number of Exceedances
of the 0.12 ppm O3 Standard for Metropolitan
Statistical Areas (1982-1984 Data Base) A-3
A-2 Distribution of O3 Design Values for
Metropolitan Statistical Areas (1982-
1984 Data Base) A-5
A-3 Descriptive Statistics Associated with Long-Term
Daily Daylight Air Quality Indicators
in MSAs (1981-1983 Air Quality) A-8
A-4 Descriptive Statistics Associated with
Short-Term Ozone Air Quality Indicators in
Non-MSA Areas A-l 3
A-5 Descriptive Statistics Associated with
Short-Term Ozone Air Quality Indicators
in Argicultural and Remote Areas
(1982-1984 Data) A-16
A-6 Descriptive Statistics Associated with
Repeated Daily Peaks of Ozone Air Quality
in Non-MSA Areas (1981-1983 Data) A—17
A-7 Descriptive Statistics Associated with
Long-Term Ozone Daily Daylight Averages
in Non-MSA Areas (1981-1983 Data) A-19
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X
EXECUTIVE SUMMARY
This paper evaluates and interprets the available scientific and
technical information that the EPA staff believe is most relevant to the
review of primary (health) and secondary (welfare) national ambient air
quality standards (NAAQS) for ozone (O3) and presents staff recommendations
on alternative approaches to revising the standards. Periodic review of
the NAAQS is a process instituted to ensure the scientific adequacy of air
quality standards and is required by section 109 of the 1977 Clean Air
Act Amendments. The assessment in this staff paper Is intended to help
build a bridge between the scientific review contained in the EPA criteria
document "Air Quality Criteria for Ozone and Other Photochemical Oxidants"
and the judgments required of the Administrator in setting ambient standards
for O3. Therefore, the staff paper is an important element in the standards
review process and provides an opportunity for review by the Clean Air
Scientific Advisory Committee (CASAC) and the general public on proposed
staff recomendations before they are presented to the Administrator.
Ozone is an air pollutant formed in the ambient air as a result of a
series of complex chemical reactions involving hydrocarbons and nitrogen
oxides emitted from mobile and stationary sources, atmospheric oxygen,
and sunlight. At ambient concentrations often measured during warmer
months O3 can adversely affect human health, agricultural crops, forests,
ecosystems, and materials. Interactions of O3 with nitrogen oxides and
sulfur oxides may also contribute to the formation of acidic precipitation.
Typical short-term (1-hour) O3 levels range from 0.01 ppm in some isolated
rural areas to as high as 0.35 ppm 1n one of the nation's most heavily
populated metropolitan areas. Daily daylight seasonal averages in some
rural areas have been reported to be 0.06 ppm O3 and higher.
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xi
Primary Standard
The staff have reviewed scientific and technical information on the
known and potential health effects of ozone cited in the criteria document.
The information includes respiratory tract absorption and deposition of
ozone, studies of mechanisms of O3 toxicity, effects of exposure to O3
reported in controlled human exposure, field, epidemiological and animal
toxicology studies, as well as air quality information. Based on this
review, the staff derives the following conclusions.
1) The mechanisms by which inhaled O3 may pose health risks involve
(a) penetration into and absorption of O3 in various regions
of the respiratory tract, (b) pulmonary response resulting
from chemical interactions of O3 along the respiratory tract,
and (c) extrapulmonary effects caused indirectly by effects of
O3 1n the lungs.
2) The risks of adverse effects associated with absorption of O3
in the tracheobronchial and alveolar regions of the respiratory
tract are much greater than for absorption in the extrathoraclc
region (head). Increased exercise levels are generally
associated with higher ventilation rates and increased oronasal
or oral (mouth) breathing. Thus, maximum penetration and exposure
of sensitive lung tissue occurs when heavily exercising individuals
are exposed to O3.
3) Factors which have been demonstrated to affect susceptibility
to O3 exposure are activity level and environmental stress (e.g.,
humidity, high temperature). Those factors which either have not
been adequately tested and remain uncertain Include age, sex,
nutrition, and smoking status.
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xil
The major subgroups of the population that appear likely to be
at greatest risk to the effects of O3 include: (a) individuals
with preexisting respiratory disease (e.g., asthmatics and
persons with chronic obstructive lung disease or allergies),
(b) "responders" who are otherwise healthy individuals, both
adults and children, but experience significantly greater than
group mean lung function response to 03 exposure, and (c) any
individual exercising heavily during exposure to O3.
The major effects categories of concern associated with exposures
to O3 in approximate order of strength of data base includes:
(a) alterations in pulmonary function
(b) symptomatic effects
(c) effects on work performance
(d) aggravation of preexisting respiratory disease
(e) morphological effects (lung structure damage)
(f) altered host defense systems (increased susceptibility to
respiratory infection)
(g) extrapulmonary effects (e.g., effects on blood enzymes,
central nervous system, liver, endocrine system).
The most useful exposure-response information is from
controlled human exposure and field studies which provide a
quantitative relationship between alterations in pulmonary
function and O3 exposure concentrations. Of less certain
quantitative use are the epidemiological studies which associate
ambient O3 exposures with lung function decrements, symptoms,
and aggravation of existing respiratory disease. Finally, animal
toxicology data provide acute and chronic exposure effects
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xf 1-f
information on increased susceptibility to respiratory infection,
lung structure damage, and extrapulmonary effects, but possible
differences 1n human vs. animal dosimetry and species sensitivity
produce large uncertainty in the use of these data.
Based on the scientific and technical reviews as well as policy
considerations, the staff makes the following recommendations with respect
to primary ozone standards.
1) O3 should remain as the surrogate for controlling ambient
concentrations of photochemical oxidants.
2) The existing form of the standard should be retained (i.e.,
that the NAAQS is attained when the expected number of days per
calendar year with maximum hourly average concentrations above the
level of the standard is equal to or less than one).
3) The 1-hr averaging time of the standard should be retained.
4) The range of 1-hour O3 levels of concern for standard-setting
purposes is 0.08 to 0.14.
5) Insufficient quantitative data are currently available to support
the basis for a long-term primary standard, but concern for
serious chronic exposure effects suggests a need to set a 1-hr
standard which protects against multiple peak and elevated
chronic exposures.
Secondary Standard
The staff have reviewed the scientific and technical information
on the known and potential welfare effects of ozone cited in the criteria
document. This information includes impacts on vegetation, natural
ecosystems, materials and symptomatic effects in humans. Based on this
review the staff dervies the following conclusions:
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1) The mechanisms by which O3 may injure plants and plant communities
include (a) absorption of O3 into leaf through stomata followed by
diffusion through the cell wall and membrane, (b) alteration of cell
structure and function as well as critical plant processes, resulting
from the chemical interaction of O3 with cellular components, (c)
occurrence of secondary effects including reduced growth and yield
and altered carbon allocation.
2) The magnitude of the O3 induced effects depends upon the physical
and chemical environment of the plant as well as various biological
factors (including genetic potential, developmental age of plant
and interaction with plant pests).
3) Effects of O3 on vegetation and ecosystems have been demonstrated
to occur from both short-term and long-term exposures. Although
there are a limited number of studies in which short-term (1-2 hour)
exposures have resulted in growth and yield reduction, there is a
growing body of evidence that repeated peaks above a given level
are important in eliciting plant response.
4) In regard to long-term exposures, the bulk of the evidence indicates
that growth and yield losses occur in several plant species exposed
to seasonal concentrations of O3, typically characterized as the
daily daylight mean over the growing season. In addition, evidence
indicates that forests experience cummulatlve stress as a result of
chronic exposure to O3.
5) There appears to be no threshold level below which material damage
will not occur; the slight acceleration of the aging processes
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XV
of materials which occurs at the level of the proposed NAAQS is not
judged to be significant or adverse.
6) Effects on personal comfort and well-being, as defined by human
symptomatic effects, have been associated with ambient photochemical
oxidant levels of >0.10 in children and adults. If these effects
should be determined not to constitute adverse health effects in
setting the primary standard, they should be considered effects on
personal comfort and well-being and used in developing a basis for
the secondary standard for O3.
Based on the scientific and technical reviews as well as policy
considerations, the staff makes the following recommendations with respect
to secondary standards:
1) O3 should remain as the surrogate for controlling ambient
concentrations of photochemical oxidants
2) The statistical form of the standard should be retained (i.e.,
a number of expected exceedances allowed per year)
3) A 1-hour standard in the range of 0.08-0.12 ppm should be considered
as a surrogate for repeated peak exposures
4) Serious consideration should be given to setting a long-term
standard in the range of 0.04-0.06 ppm to protect cops as well
as trees and other native vegetation. The level of such a standard
will be influenced by the protection from long-term exposures
of concern afforded by the 1-hour standard.
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Review of the National Ambient Air Quality Standards for Ozone
Preliminary Assessment of Scientific and Technical Information
Draft Staff Paper
I. Purpose
The purpose of this draft staff paper is to evaluate and interpret
scientific information contained in the draft EPA document "Air Quality
Criteria for Ozone and Other Photochemical Oxidants" (CD, U.S. EPA,
1985) and to identify critical elements to be considered in selecting
primary (health based) and secondary (welfare based) national ambient air
quality standards (NAAQS) for ozone (O3). Staff conclusions and recommen-
dations will integrate critical elements of the review of standards with
other factors such as averaging times, form of standards, and margin of
safety considerations.
II. Background
Since 1970 the Clean Air Act as amended has provided authority and
guidance for the listing of certain ambient air pollutants which may
endanger public health or welfare and the setting and revising of NAAQS
for those pollutants. Primary standards must be based on health effects
criteria and provide an adequate margin of safety to ensure protection of
public health. As several judicial decisions have made clear, the economic
and technological feasibility of attaining primary standards are not to
be considered in setting them, although such factors may be considered in
the development of state plans to implement the standards (Lead Industries
Association v. EPA, 1980; American Petroleum Institute v. EPA, 1981).
Further guidance provided in the legislative history of the Act indicates
that the standards should be set at "the maximum permissible ambient air
level . . . which will protect the health of any (sensitive) group of the
population" (U.S. Senate, 1974). Also, margins of safety are to be
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11-2
provided such that the standards will afford "a reasonable degree of
protection . . . against hazards which research has not yet identified"
(U.S. Senate, 1974). In the final analysis, the EPA Administrator must
make a policy decision in setting the primary standard based on a judgment
regarding the implications of all the health effects evidence and the
requirement that the standards provide an adequate margin of safety.
Secondary ambient air quality standards must be based on welfare
effects and must be adequate to protect the public welfare from any known
or anticipated adverse effects associated with the presence of a listed
ambient air pollutant. Welfare effects, which are defined in section
302(h) of the Act, include effects on vegetation, visibility, water,
crops, man-made materials, animals, economic values and personal comfort
and wel1-bei ng.
On April 30, 1971, the Environmental Protection Agency (EPA) published
in the Federal Register (36 FR 8186) primary and secondary national
ambient air quality standards (NAAQS) for photochemical oxidants. Roth
standards were set at an hourly average level of 0.08 ppm not to be
exceeded more than once per year.
In accordance with the provisions of sections 108 and 109 of the Clean
Air Act as amended, EPA reviewed and revised the criteria upon which the
original photochemical oxidants NAAQS were based. On February 8, 1979,
revised standards were published (44 FR 8202) with the following changes:
(1) changing the primary and secondary standards to 0.12 ppm, (2) changing
the chemical designation of the standards from photochemical oxidants to
ozone (O3), (3) changing to a daily maximum standard rather than an
"all-hours" standard, and (4) changing the definition of the point at which
the primary and secondary standards are attained to "when the expected number
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11-3
of days per calendar year with maximum hourly average concentrations above
0.12 ppm is equal to or less than one."
Several factors were cited as a basis for revising the primary standard
for O3 in 1979. Among these were: (1) an adverse health effect threshold
for oxidants could not be identified with certainty, (2) O3 is a pulmonary
irritant that affects respiratory mucous membranes as well as other lung
tissue and impairs respiratory function at levels as low as 0.15 ppm for
exercising persons (Delucia and Adams, 1977), (3) evidence suggests an
elevated number of asthma attacks when peak hourly oxidant concentrations
reach about 0.25 ppm (Schoettlin and Landau, 1961), (4) several studies
show increased susceptibility to bacterial infection in laboratory animals
exposed to O3 plus a bacterial challenge, (5) premature aging symptoms
reported in animals and (6) apparent synergistic effects on pulmonary
function from exposure to 0.37 ppm O3 and 0.37 ppm sulfur dioxide. EPA
concluded that a primary standard of 0.12 ppm (one-hour average) not to be
exceeded more than one day per year on average would protect public health
with an adequate margin of safety.
EPA based its decision on the secondary standard on the limited
information that was available on growth and yield •"eduction ln commercially
important crops and indigenous vegetation exposed to ozone under field
conditions. These studies indicated that growth and yield responses we^e
related to long-term (growing season) exposure of plants. Rased on an
examination of this Information and available air quality data, EPA
concluded that there was no evidence indicating that a significant decrease
in growth and yield would result from long-term average concentrations
expected to occur when the primary standard was attained. Consequently,
a secondary standard more stringent than the primary standard was deemed
unnecessary on the basis of ozone-related yield reduction effects on
vegetation.
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III-l
III. Approach
This is the first draft staff paper to be provided during current
review of the NAAQS for O3; judgments contained herein are based on scientific
evidence reviewed in the CD. Subsequent staff paper draft(s) will incorporate
the results of a health risk assessment and will include benefits analysis
for alternative NAAQS.
This paper identifies the critical elements that the staff believe
should be considered in a review of the primary and secondary standards.
Particular attention is drawn to those judgments that must be based on the
careful interpretation of incomplete or uncertain evidence. In such instances,
the paper states the staff's evaluation of the evidence as it relates to a
specific judgment, sets forth alternatives that the staff believe should he
considered, and recommends a course of action. To facilitate the review,
this paper is organized into sections as outlined below.
Section IV provides an overview of the ambient levels of O3 currently
being experienced in various portions of the U.S. This section is intended
to set the stage for the remaining discussion by identifying the present
air quality situation so the reader can relate the available health and
welfare information to O3 levels occurring in the real world.
Section V summarizes preliminary results of the O3 exposure analysis.
The NAAQS Exposure Model (NEM) will be used to estimate nationwide human
exposure to O3 given attainment of alternative standards. The preliminary
results presented in this section will be refined and updated in subsequent
draft(s) of the O3 staff paper.
Section VI addresses elements related to the health effects evidence
examined in reaching conclusions regarding the primary standards; these
include the following:
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° most probable mechanisms of toxicity by which health effects occur,
0 discussion of factors potentially affecting susceptibility to O3
exposure,
0 description of the most sensitive population groups and estimates
of the size of those groups.
Section VII, which is a preliminary assessment of health effects and
related health issues, provides:
0 identification of health effects which have been attributed to O3
and other photochemical oxidant exposures,
0 identification and evaluation of scientific uncertainties with
regard to the health effects evidence as well as staff judgments
concerning which effects are most important for the Administrator to
consider in reviewing and setting primary standard(s), and
0 discussion of issues related to health effects attributed to ozone
and other photochemical oxidants.
Drawing from the discussions in Sections IV, V, VI, and VII, Section
VIII identifies and assesses the factors that the staff believes should
be considered in selecting a pollutant indicator, averaging time, form,
and level of primary standards, including margin of safety considerations.
Preliminary staff recommendations also are presented in this section.
In Section IX, the effects of O3 and other photochemical oxidants on
vegetation, personal comfort, natural ecosystems, and man-made inaterials
are identified. The elements addressed in this section include the following:
0 description of the physiological and biochemical alterations associated
with welfare effects which result from exposure to O3 and other
photochemical oxidants
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111-3
° identification of welfare effects of O3 and other photochemical
oxidants
0 discussion of factors affecting plant response
Section X is a discussion of welfare effects to be considered in
selecting secondary standard(s). It consists of:
0 description of the scientific evidence on welfare effects attributed
to O3 and other photochemical oxidant exposures, and
0 identification and evaluation of scientific uncertainties related
to welfare effects evidence in addition to staff judgments concerning
which welfare effects are important for the Administrate to consider
in reviewing and setting secondary standard(s).
Drawing from discussions in Sections IX and X, Section XI identifies
and assesses the factors that the staff believes should be considered in
selecting averaging time(s), level(s) and form of secondary standards.
Preliminary staff recommendations also are presented in this section.
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IV-1
IV. Ambient Concentrations of Ozone and Other Photochemical Oxidants in
Urban and Rural Areas
This section provides a capsule summary of ambient O3 air quality
in urban and non-urban areas. More information on the topic appeals in
Appendix A. The data base used here generally is 1981-1984 SAPOAD air
quality data, but data are presented for other time periods also. Urban
areas are interpreted to be Metropolitan Statistical A--eas (MSAs) as
defined by the U.S. Bureau of Census.
A. Urban Areas
There are 319 MSAs in the 50 states. Using 1982-1984 data--the most
recent available—216 (68%) of them have enough O3 air quality data to
ascertain attainment status. Of these, 119 areas (55%) have more than
one expected exceedance per year of the current O3 standard of 0.12 ppm.
Thus, more than one-half of the SMSAs with sufficient data violate the
standard. Approximately 115 million people, slightly over one-half of
the total U.S. population, live in these areas which exceed the standard.
(However, this does not mean that everyone in these areas are exposed to
O3 concentrations at or above the standard. See Section V.)
About 14% (34) of MSAs with sufficient data have a characteristic
highest concentration (CHC; See Appendix A) of 0.16 ppm O3 or higher;
over 4% (11) of MSAs have a CHC above 0.20 ppm O3. There is no clear
temporal trend in O3 concentration levels in MSAs around the country,
although 1982—and to a lesser extent, 1981—had generally lower levels
than other years during the 1979-1984 time period.
Generally, third quarter (July-Sept.) and seasonal (April-Sept.)
averages of 8am - 4pm daily daylight values are both in the range of 0.043
0.050 ppm O3. There are statistically significant, but modest, ^elation-
ships among peak and longer-term mean indices of O3 air quality in urban
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IV — 2
areas. These relationships can be used to estimate the impact that alterna-
tive short-term peak O3 standards will have on long-term average levels of
°3-
B. Non-MSA Areas
Air quality data indicate that non-MSAs have a lower CHC than do MSA
areas and that the CHC is often associated with 03 transported into non-MSA
areas after 4pm. About 10% of all days exceed a 0.08 ppm O3 daily maximum
on average in non-MSA areas.
Generally, longer-term O3 averages of 7-hours or 12-hours daily daylight
time periods in non-MSAs are similar to those seen in MSA areas. The
seasonal average ranges between 0.021 and 0.050 ppm O3 in non-MSAs, with a
mean of 0.044 ppm O3. The highest monthly means vary between 0.023 and
0.071 ppm O3, with an average of 0.053 ppm O3. The highest month in non-MSA
areas is usually either May, July, or August.
There are fairly stable and narrow relationships between monthly
(and other longer-term) ai" quality indicators and the O3 seasonal average.
However, the relationship between the 2nd high daily maximum and O3 seasonal
average is broad and unstable. Thus, in non-MSAs there is no assurance
that reducing one will reduce the other in the same proportion.
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V. O3 Exposure Analysis
Analysis of population exposure under alternative NAAQS requires that
all significant factors contributing to total human exposure be taken into
account. These factors include the temporal and spatial distribution of
people and O3 concentrations throughout an urban area as people go through
their typical daily pattern of life. To the maximum extent possible with
existing data, this has been done in the NAAQS Exposure Model (NEM), a
simulation model designed to estimate human exposure in selected urbanized
areas under user-specified regulatory scenarios (Biller et al., 1981).
A. Overview of the Ozone NEM
There are two basic versions of NEM, a "neighborhood" version and
a "district" version. The O3 NEM model utilizes the district version.
In it, land areas within a selected urban area are represented by large
"exposure districts." Population living within each exposure district, as
estimated by the U.S. Census in 1980, is assigned to a single discrete
point, the population centroid. The air quality level within each exposure
district is represented by air quality at the population centroid, which is
estimated for each hour of the year by monitoring data from nearby monitoring
sites. Because pollutants in the ambient air are generally modified considerably
when entering a building or vehicle, outdoor air quality estimates are
adjusted to account for five different microenvironments: indoors at home,
indoors other (all other indoor locations), inside a transportation vehicle,
outdoors near a roadway, and all other outdoor locations. The air quality
adjustments are made by using microenvironmental transformation factors
(explained below).
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V-2
Because degree of exposure and susceptibility to effects of pollution
vary with age, occupation, and intensity of exercise, the total population
of each study area is divided into age-occupation (A-0) groups. Each A-0
group is further subdivided into three or more subgroups. A typical pattern
of activity through the five microenvironments is established for each
subgroup and an exercise level (high, medium, or low) for each is also
speci fied.
Units of population analyzed by NEM are called cohorts. Each cohort
is identified by exposure district of residence, by exposure district of
employment or school attendance, by A-0 group, and by activity-pattern
subgroup. During each ten minute period of the day, each cohort is assigned
to a particular exposure district and a particular microenvironment. The
assignment is based upon (1) data regarding human activity patterns gathered
by EPA and university "time budget" researchers, and (2) home-to-work
transportation data gathered by the U.S. Census Bureau. Using these sources
of information, NEM simulates ten minute movements of cohorts through
different districts of the urban area and through different microenvironments,
combines the movements with hourly averaged air quality data, and accumulates
the resulting exposures over a period of one year.
B. Air Quality Concentrations in Microenvironments
NEM requires that hourly air quality estimates be available for
each microenvironment that every cohort passes through. The estimates are
obtained by using a simple linear function relating outdoor air quality
concentrations to microenvironment levels via a "transformation" relating
outdoor-to-indoor levels and then adding to this the pollutant concentration
associated with the microenvironment itself. For O3, the transformation
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V-3
is essentially a multiplicative ratio derived from a review of the O3
exposure literature (Ferdo, 1985).
The relationship is:
xm,t 3 am,t + * x^-)
where xm>t = air quality in microenvironment m during hour t
am,t = hourly-averaged pollutant concentration due to sources
located in the microenvironment
bm = multiplicative ratio of the microenvironment concentration
value to the monitored air quality value
X£ = monitor-derived air quality value
Because no significant sources of ozone were identified with any of the
microenvironments, = 0 for all environments. Estimated bm values
obtained from the literature are shown in Table V-l. A cumulative frequency
distribution of the indoor microenvironment values is depicted in Figure V-l.
TABLE V-l
ESTIMATES OF MULTIPLICATIVE MICROENVIRONMENTAL FACTORS (hm)
Estimated Value
(Unitless)
Low Best High
Mi croenvi ronment Estimate Estimate Estimate
Indoors-residential 0.36 0.58 0.70
Indoors-other 0.40 0.52 0.62
Motor vehicle 0.00 0.11 0.30
Outdoors-near roadway 0.13 0.18 0.28
Outdoors-other 1.00 1.00 1.00
Source: Ferdo, 1985
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V-4
100
—I—J.-1—1—
90
80
70
INDOOR-OTHER
(n = 84)
3 60
50
INDOOR-RESIDENTIAL
(n = 40)
40
30
20
10
0.0 0.2 0.4 0.6 0.8 1.0 1.2 1.4 1.6
INDOOR-TO-OUTDOOR MULTIPLICATIVE FACTOR (bm)
Figure V-l. Cumulative frequency distribution of the indoor-to-outdoor
multiplicative factor.
1.8
Source: Ferdo (1985).
-------
V-5
The xt values are actual monitored values for the current (or "as is")
situation. The monitored values are adjusted to represent a future situation
when air quality in the study area just meets the O3 NAAQS being analyzed.
By definition, a NAAQS is attained when all monitors in an area have less
than one expected exceedances of the standard concentration value (currently
it is .12 ppm) in a year. The exposure analysis is based on a "just attains"
scenario, where air quality levels at the monitor currently having the
highest number of expected exceedances is reduced to where that monitor
just attains the standard being analyzed. The other monitors are adjusted
using a complex non-linear approach described in Johnson et al. (1986).
EPA's Empirical Kinetic Modeling Approach (EKMA) model is used to
determine future characteristic largest O3 concentrations at monitors used
in NEM. EKMA results are used in conjunction with a Wei bull distribution
analytic procedure to derive hour-by-hour concentrations for future air
quality simulations. In addition, a time series model based upon a Fourier
transformation is used to generate a complete air quality data set when
there are missing values. These procedures are described in more detail in
Johnson and Paul, 1983; Johnson and Capel, 1985; and Johnson et al., 1986.
C. Simulation of Population Movement
Population movement in NEM is based upon information gathered by
the U.S. Census Bureau regarding householders' commuting patterns to their
work place (Bureau of the Census, 1982). The information includes SMSA-
specific data on the census tract level, which itself is based upon actual
location information regarding the sampled population's home and workplace.
The census tract information is aggregated for exposure districts used in
the NEM analysis to obtain district-to-district trip information for those
cohorts that work. (Otherwise, cohorts are assumed to stay in their home
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V-6
districts.) Because of lack of travel data for non-work activities, we
assume that all shopping is done in each cohort's residential district.
The same assumption is also made regarding school-related activities.
There is no trip information available from the U.S. Census Bureau
regarding weekend inter-district travel in SMSAs. (There is information
available regarding weekend recreational travel, but it is not locationally
specific nor is it systematic.) Consequently, all cohorts are assigned to
their home districts on weekends in NEM analysis.
D. Ozone Exposure Estimates for the New York City Area
Results of the NEM analyses of human exposure associated with
attainment of four alternative ozone NAAQS are presented in this section.
Because of uncertainty surrounding availability of air quality data for all
of the SMSAs that will be evaluated,* results for the New York City area
only will be discussed in this draft of the Staff Paper. (Subsequent drafts
will include results for the other areas.) This area encompasses parts of
four MSAs: New York City, Newark (NJ), Jersey City (NJ), and Paterson-
C1ifton-Passaic (NJ). The area investigated includes 11,514,362 people out
of a total population for the four MSAs of 11,540,445 (1980 census data).
The four alternative NAAQS evaluated are: 0.08 ppm, 0.10 ppm, 0.12 ppm,
and 0.14 ppm--all for a one hour daily maximum standard not to be exceeded
on average more than one day per calendar year. This is the current form
of the ozone NAAQS.
*Ten to 12 MSAs will be used in the final exposure analysis. The ten
areas that definitely will be modeled are:
Chicago Los Angeles Philadelphia
Denver Miami St. Louis
Houston New York Tacoma
Washington, O.C.
An additional 2 MSAs will be modeled if resources permit. They are:
Birmingham (AL) and Cincinnati (OH).
-------
V-7
Results of applying the O3-NEM in the New York City Area appear
in Tables V-2 through V-6. Table V-2 presents estimates for the cumulative
number of people exposed to one-hour O3 averages throughout the ozone season.
For New York, the ozone season is April through October.
The first column indicates air quality concentrations in ppm that
are equalled or exceeded by the number of people noted in the body of the
table. These measures of the number of people exposed correspond to "low,"
"best," and "high" exposure estimates. These different estimates are
intended to portray some of the uncertainty inherent in modeling exposures
to ambient ozone air quality. Additional work will be undertaken to more
completely describe uncertainty of our exposure estimates. It should be
noted that two types of notation are used in the body of Table V-2 (and
subsequent tables in this section). The estimate is shown in standard
integer format if the high estimate in a row is less than ten million
persons and in scentific notation for a high estimate greater than or equal
to 10 million persons. For example, the total population modeled is approxi-
mately 11,510,000 people. In the table, this is given as 1.151 + 007,
equal to 1.151 x 107. The same convention
The above overall population level of the study area coincides with the
number of people exposed at or above 0.0 ppm ozone in all three types of
estimates in Table V-2. The numbers of people exposed at or above 0.121 ppm,
however, varies widely in the three estimates, from 3.7 million people in the
low estimate to 9.9 million people in the high estimate. Note that the
highest level of exposure occurred at or above 0.261 ppm (but not above
0.281 ppm) and that 5,056 people were exposed according to the three
estimates. High exposures most frequently occur outdoors where the
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V-8
TABLE V-2
ESTIMATES OF THE CUMULATIVE NUMBER OF PEOPLE IN THE NEW YORK CITY AREA
EXPOSED TO ONE-HOUR AVERAGE O3 CONCENTRATIONS DURING
THE OZONE SEASON FOR THE CURRENT" SITUATION
(1983 Air Quality Data)
AQ Level
Equalled or
Exceeded
(ppm)
Low
Type of Estimate
Best
High
0.281
0
0
0
0.261
5,056
5,056
5,056
0.241
33,900
33,900
132,104
0.221
34,528
37,649
489,449
0.201
160,482
160,482
2,491,358
0.181
812,216
812,216
3,063,846
0.161
1,664,378
1,904,080
4,324,267
0.141
2,337,708
2,861,096
9,173,504
0.121
3,703,324
5,577,211
9,921,829
0.101
5.901E+006
9.027E+006
1.095E+007
0.081
8.964E+006
1.081E+007
1.140E+007
0.061
1.072E+007
1.140E+007
1.151E+007
0.041
1.129E+007
1.151E+007
1.151E+007
0.021
1.151E+007
1.151E+007
1.151E+007
0.001
1.151E+007
1.151E+007
1.151E+007
0.000
1.151E+007
1.151E+007
1.151E+007
Source: Paul et al., 1986.
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V-9
TABLE V-3
ESTIMATES OF THE CUMULATIVE NUMBER OF ONE-HOUR AVERAGE PERSON-
OCCURRENCES OF EXPOSURE TO OZONE IN THE NEW YORK CITY AREA
IN THE OZONE SEASON FOR THE "CURRENT" SITUATION
AQ Level
Equalled or
Exceeded
(ppm)
(1983 Air
Low
Quality Data)
Type of Estimate
Best
High
0.281
0
0
0
0.261
5,056
5,056
5,056
0.241
33,900
33,900
132,104
0.221
34,824
37,945
562,322
0.201
163,746
163,746
2,594,000
0.181
897,679
897,715
3,836,804
0.161
2,809,152
3,078,907
8,418,559
0.141
4.934E+006
6.000E+006
2.601E+007
0.121
1.856E+007
2.303E+007
7.512E+007
0.101
4.643E+007
5.977E+007
2.657E+008
0.081
1.252E+008
2.085E+008
1.300E+009
0.061
3.383E+008
9.020E+008
3.272E+009
0.041
9.623E+008
4.091E+009
8.843E+009
0.021
4.066E+009
1.238E+010
2.304E+010
0.001
5.426E+010
5.426E+010
5.426E+010
0.000
5.914E+010
5.914E+010
5.914E+010
Source: Paul
et al., 1986.
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V-10
TABLE V-4
ESTIMATES OF NEW YORK CITY AREA PEOPLE EXPOSED TO THEIR HIGHEST
ONE-HOUR OZONE CONCENTRATION INTERVAL DURING THE OZONE SEASON
(1983 Air Quality Data)
Air Quality Type of Estimate
Interval
(ppm)
Low
Best
Hi gh
0.281
-
0.300
0
0
0
0.261
_
0.280
5,056
5,056
5,056
0.241
-
0.260
28,844
28,844
127,048
0.221
-
0.240
628
3,749
357,345
0.201
-
0.220
125,954
122,833
2,001,909
0.181
-
0.200
651,734
651,734
572,488
0.161
_
0.180
852,162
1,091,864
1,260,421
0.141
-
0.160
673,330
957,016
4,849,237
0.121
-
0.140
1,365,616
2,716,115
748,325
0.101
-
0.120
2,197,227
3,450,117
1,028,766
0.081
-
0.100
3,063,024
1,777,747
446,072
0.061
0.080
1,756,172
595,108
117,695
0.041
-
0.060
570,309
114,179
0
0.021
-
0.040
224,306
0
0
0.001
-
0.020
0
0
0
0,
.000
0
0
0
Source: Paul et al., 1986.
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V-ll
TABLE V-5
"BEST" ESTIMATES OF THE CUMULATIVE NUMBER OF PEOPLE IN THE NEW YORK CITY
AREA EXPOSED TO ONE-HOUR AVERAGE O3 CONCENTRATIONS DURING THE OZONE
SEASON UNDER ALTERNATIVE NAAQS
Ai r Qua!ity
Level Equalled
or Exceeded
(ppm)
0.08
Alternative NAAQS (in ppm)
0.10 0.12
0.14
O.I61
0
0
0
0
0.141
0
0
0
320
0.121
0
0
5,056
16,665
0.101
0
320
45,898
276,831
0.081
5,056
175,379
2,100,140
2,798,555
0.061
1,592,056
3.961E+006
7.864E+006
8.824E+006
0.041
9.813E+006
1 .045E+007
1 .087E+007
1 .087E+007
0.021
1.151E+007
1.151E+007
1.151E+007
1.151E+007
0.001
1.151E+007
1.151E+007
1.151E+007
1 .151E+007
0.000
1.151E+007
1.151E+007
1.151E+007
1.151E+007
Source: Paul et al., 1986.
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V -12
TABLE V-6
ESTIMATE OF THE CUMULATIVE NUMBER OF PEOPLE IN THE NEW YORK CITY AREA
EXPOSED TO ONE-HOUR DAILY MAXIMUMS DURING THE OZONE SEASON WHEN THE
0.12 PPM 03 NAAQS IS JUST ATTAINED
AQ Level Equalled Number of Days When Exposure Occurred
or Exceeded
(ppm) 12 3 4 5
0.141
0
0
0
0
0
0.121
5,056
0
0
0
0
0.101
34,251
0
0
0
0
0.081
1 ,463,319
300,869
80,925
35,854
2,077
0.061
2,226,020
1,725,339
561,145
545,136
709,489
0.041
2,859,629
2,111,432
1,311,697
747,024
2,910,445
0.021
3,210,336
2,430,160
1,887,013
1,082,493
4,612,936
0.001
3,840,569
2,843,805
1 ,923,431
1,097,975
4,612,936
0.000
3,840,569
2,843,805
1,923,431
1,097,975
4,612,936
Notes: (T) Daily maxima 1-hour average ozone levels always occur
outdoors away from roadways.
(2) Only one estimate for daily maxima because no (variable)
microenvironment factors used.
Source: Paul et al., 1986.
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V -13
multiplicative factor is unity (See Table V-1); therefore, high exposures
are frequently the same in all three types of estimates.
Table V-3 presents estimates of cumulative occurrences of exposure to
one-hour average ozone levels during ozone season. As in the previous
table, the first column Indicates the air quality level equalled or exceeded
and the other three columns show cumulative distributions for low, best, and
high estimates respectively. Note that there are 24 occurrences of one-hour
average exposure each day and 214 days in the ozone season for New York
City. Since there are 11.5 million people in the study area, there are
5.9 x 10lO occurrences (24 x 214 x 11.5 x 10®) of exposure at or above
0.0 ppm for each of the three estimates.
Table V-4 shows estimates of highest exposures to one-hour average
ozone during ozone season. Unlike the previous two tables, the first
column of this table shows intervals of air quality. The lowest value in
each interval 1s the air quality level in the corresponding row in Tables
V-2 and V-3. Note that 0.0 ppm is treated separately. Hourly average
ozone values of 0 are not missing data, but are very low ozone levels
(usually below the detection limit of the instrument) that are reported to
EPA as 0 ppm.
Following the first column of Table V-4 are three columns showing
(non-cumulative) distributions for the low, best, and high estimates. Each
entry in the table represents the sum of the populations of all cohorts who
reached their highest exposure during the NEM simulation in the indicated
air quality interval. Considerable variation may be noted in the three
distributions of highest exposures. For example, the numbers of people
experiencing their highest one-hour average exposure in the interval 0.221
-------
V-14
to 0.240 ppm were 628; 3,749; and 357,345 for the low, best, and high
estimates respectively.
The next table, V-5, focuses on only one estimate, the "best" one,
for the hypothetical situation where the ambient standard for ozone would
just be attained. Each of the alternative NAAQS investigated was expressed
as a specified level of a characteristic longest daily maximum (CLDM)
value at the ozone monitor having the highest ozone "design" value in the
New York City area. Using the adjusted air quality procedure mentioned
earlier, new air quality data sets are developed to simulate the just-
attaining situation. The other data sets used in NEM do not change.
New exposure estimates are then obtained for the new air quality data;
they appear in Table V-5.
As can be seen, exposures are greatly reduced under any of the
alternative NAAQS compared to the current situation. Among the four
alternatives investigated, the highest exposures occur at or near the
level of the NAAQS, which is to be expected. (Particulary so when the
micro-environmental transforms are all less than 1.0). Thus, higher
exposures are seen for the 0.14 ppm O3 NAAQS than for the 0.12 ppm
NAAQS, etc.
There are fairly large differences among the four alternatives for
intermediate exposure levels, say 0.081 ppm or above. The number of people
estimated to experience that level or higher is about 5 thousand under
a 0.08 ppm standard and about 2.8 million for a 0.14 ppm NAAQS. The
final table to be discussed is an estimate of the number of days (between
1 and 5) that people see various daily maximum ozone concentrations. This
measure might be important if repeated peak exposures to the pollutant
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V-15
are of interest. The data for the 0.12 ppm NAAQS alternative appear in
Table V-6. Note that almost 1.5 million people see a daily maximum O3
concentration of 0.081 or higher on one day, while only 2 thousand
people would see it on 5 or more days (when the 0.12 ppm standard is
just attained, of course).
Other output measures are possible; the ones discussed above are just
a sampling of the different types of results available from the O3 NEM.
For additional results, see Paul et al., 1986.
E. Nationwide Extrapolation
[As has been our practice in the past (e.g., see Johnson and Paul,
1983), we will extrapolate results of the 10- or 12-urban area exposure analyses
to the nation as a whole. The extrapolation scheme still is being developed;
when it is completed, national exposure estimates for the urban U.S. population
will be provided for just-attaining the four standards mentioned above.]
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VI-1
VI. Critical Elements in the Review of the Primary Standard(s) for Ozone
Of primary concern in this section are the health effects associated
with levels of O3 and other photochemical oxidants that are observed
in ambient air of the U.S. Of the photochemical oxidants, only O3 has
been reported to exist in cities a-t sufficiently high concentrations to
be of significant concern for human health. Since other photochemical
oxidants such as hydrogen peroxide (H2O2) and peroxyacetyl nitrate (PAN)
exhibit health effects only at concentrations much higher than those found in
ambient air, this section will focus on the mechanisms of toxicity for O3
and documented evidence of pulmonary and extrapulmonary effects of O3.
The approach will rely primarily on available human data but also will
include consideration of animal data and mechanistic studies to support
the possibility of health effects caused by O3 1n the absence of human data.
In addition, factors affecting susceptibility and potentially susceptible
groups will be discussed.
A. Ozone Absorption and Mechanisms of Effects
Ozone enters the human body through the respiratory system. During
inhalation and exhalation, O3 is removed from air by airway surfaces
through a process of dissolution and chemical reaction. The rate, amount,
and sites of O3 uptake and removal largely determine the extent to which
exposure of an individual to a particular concentration of O3 will evoke
adverse health effects.
Numerous studies have provided Information which helps to explain
the quantity and sites of O3 uptake 1n mammalian respiratory tracts.
Nasopharyngeal removal studies reviewed in the CO (p. 1-90) suggest that:
1) the fraction of O3 uptake depends Inversely on the flow rate,
2) tracheal and exposure chamber concentrations of O3 are positively
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VI-2
correlated (Yokoyama and Frank, 1972; Moorman, et al., 1973; and Miller
et al., 1979) and 3) approximately 50 percent of inhaled O3 (> 72% for
dogs and > 50% for rabbits) is removed in the nasopharyngeal region of
animals exposed to between 0.1 and 0.2 ppm O3 thereby indicating the role
of the nasopharynx in removing O3 before it reaches the more sensitive
lung tissues. Only one study measured O3 uptake in the lower respiratory
tract and reported 80 to 87% uptake by the lower respiratory tract of
dogs (Yokoyama and Frank, 1972). There are, however, no published data
currently available for human nasopharyngeal or lower respiratory tract
absorption.
Inhaled O3 not absorbed in the nasopharyngeal region can be deposited
along the entire respiratory tract. Penetration into the lower respiratory
tract increases as inhaled O3 concentrations Increase from 0.2 to 0.8 ppm
(Dungworth et al., 1975). Models have been developed to estimate lower
respiratory uptake (Miller et al., 1978b, 1985; McJUton et al. 1972).
One O3 deposition model has predicted that similar patterns of O3 deposition
occur in humans, rabbits, and guinea pigs and that the junction of the
conducting airways and gas exchange region receives the maximal dose
(Miller et al., 1978b; 1985). This prediction is consistent with location
of 03-induced lesions as indicated by pathology data from several species
of 03-exposed animals. Recently the Miller dosimetry model has been used
to estimate the sensitivity of the uptake of O3 in the human lung to
lower respiratory tract secretions and exercise (Miller et al., 1985).
The Miller dosimetry model is also an important tool used in assessing
animal toxicology data. Chapter 10 of the CO provides a detailed discussion
of the use and comparison of O3 dosimetry models.
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VI—3
Biologically important functional groups which react relatively
rapidly with O3 include the alkenic groups (carbon-carbon double bonds),
amino groups, and sulfhydryl groups. Alkenic bonds are found in essential
fatty acids and polyunsaturated fatty acids (PUFA) which are important
components of the lipids in cell membranes. Oxidation of amino and
sulfhydryl groups can result in protein denaturation with concomitant
loss of structural and functional integrity for the affected protein.
Although there is general agreement that toxic effects of O3 are
caused by its oxidative properties, the precise molecular mechanism of
toxicity- remains unclear. Several theories which have been proposed include:
1. Oxidation of polyunsaturated lipids contained mainly in cell
membranes;
2. Oxidation of sulfhydryl, alcohol, aldehyde, or amine groups in
low molecular weight compounds or proteins;
3. Formation of toxic compounds (ozonides and peroxides) through
reaction with polyunsaturated lipids;
4. Formation of free radicals, either directly or Indirectly,
through lipid peroxidation; and
5. Injury mediated by some pharmacologic action, such as via a
neurohormonal mechanism or release of histamine (CD, p. 10-100).
Molecular targets (i.e., carbon - carbon double bond, sulfhydryl
groups, etc.) are shared across all species. Therefore, if O3 initiates
mechanisms in an animal which ultimately result in lung structural damage,
there is reason for concern that the same mechanisms may be activated in
man with similar outcomes. This assumption is limited by differences in
human and animal dosimetry which produce different doses of O3 for equivalent
exposures. Also defense and repair mechanisms are likely to provide
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VI —4
quantitative differences in the display of toxicity resulting from
equivalent doses. Nonetheless, mechanism information strongly supports
the hypothesis that equivalent effects may occur in man and animals,
albeit not necessrily at the same concentrations.
B. Factors Affecting Susceptibility to Ozone
Numerous factors are believed to affect susceptibility to O3
exposure and to alter physiological responsiveness. These factors include
such individual characteristics as age, sex, smoking status, and nutritional
status. In addition, environmental stresses (e.g., humidity and temperature)
and exercise level during exposure can influence the extent and level of
an individual's response to O3 by increasing the volume of inhaled O3 and
by promoting penetration deeper into the lungs.
1. Age
It has been postulated that age-related changes in lung growth and
development are among the factors responsible for altering individual
susceptibility to O3 and thus extent of damage may be dependent on stage
of lung development. Supporting information for this hypothesis has come
from both human and animal studies. Definitive evidence, however, is
unavailable due to a lack of a sufficient number of studies which test
adequately for O3 effects between age groups.
Several clinical, field, and epidemiology studies have provided
evidence of pulmonary function and symptomatic response in younger persons
exposed to less than 0.15 ppm O3 (McDonnell et al., 1985b,c; Avol et
al., 1985a,b; Kagawa and Toyama, 1975; Kagawa et al., 1976; Kagawa, 1983;
Lebowitz et al., 1982, 1983; Lebowitz, 1984; Lippmann et al., 1983; Lioy
et al., 1985; Bock et al., 1985). In addition, symptoms have been reported
for children exposed to oxidant concentrations of 0.10 ppm and higher
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VI -5
(Okawada et al., 1979; Maklno and Mizoguchi, 1975). Although it has been
suggested that older Individuals are less susceptible to O3 exposure than
younger persons, age differences 1n response to O3 have not yet been investigated
systematically 1n controlled human studies. Conclusions regarding age as a
susceptibility factor in humans, therefore, will remain uncertain until
additional research 1s available.
Animal research is also relatively inconclusive due to the very few
studies in which age comparisons have been made within the same study.
While some studies have suggested that neonates and adult rats are about
equally responsive to O3 (Raub et al., 1983; Barry, 1983; Barry et al.,
1983), other studies report that stage of development at initiation of O3
exposure may be an important determinant of age responsiveness (Stephens
et al., 1978; Lunan et al., 1977; Tyson et al., 1982; Elsayed et al.,
1982). Interpretation of these animal studies may be confounded by
exposure techniques used, but it appears that 35 day old rats respond
equivalently to adult rats.
Although some clinical, field, and epidemiology studies provide suggestive
evidence of differential age effects, "sufficient numbers of studies have
not been performed to provide any sound conclusions for effects of O3 in
different age groups" (CD, p. 13-80).
2. Sex
Due to the small number of female subjects in controlled human
studies, no definitive conclusions can be drawn regarding sex differences
in response to O3 exposures. Those human studies which have evaluated lung
function differences report that forced expiratory volume for 1-sec
(FEVi.q) appears to be affected more in females than in males for similar
exposure concentrations and exercise levels, but the results are not conclusive
-------
VI —6
(CD, p. 13-35). Only three studies gave enough information for limited
comparative evaluation (Horvath et al., 1979; GUner et al., 1983; Delucia
et al., 1983). Most O3 research on animals has been performed using only
males. When females were used, sex comparisons were not usually made.
An exception is the study by Graham et al. (1981) which reports increased
pentobarbltal-induced sleeping time in all females but not in male mice
or rats after 5 hour exposure to 1.0 ppm O3. Although reasons for sex
differences have not yet been elucidated, these differences have been
indicated in some research and thus require further investigation (CO, p.
13-35).
3. Smoking Status
Results of studies comparing effects of O3 on smokers versus non-
smokers are Inconclusive. Several studies report greater pulmonary
function changes for non-smokers than for smokers at rest during exposure
to lower O3 levels (0.37 to 0.5 ppm). This is reversed for higher O3
levels (0.75 ppm) with smokers showing greater response (Hazucha et al.,
1973; Bates and Hazucha, 1973; Kerr et al., 1975; Delucia et al., 1983).
Effects of O3 were greater for resting non-smokers than for resting
smokers at 0.5 than for 0.3 ppm (Kagawa and Tsuru, 1979a), but exercising
non-smokers showed a greater response than exercising smokers at 0.15 ppm
O3 (Kagawa, 1983). Exercising smokers showed slower and smaller spirometric
variable changes than non-smokers at 0.5 and 0.75 ppm O3 (Shephard et
al., 1983). While none of these studies have examined the effects of
different amounts of smoking, available data generally supports the
contention that smokers are less responsive to O3 than non-smokers, at
least at O3 levels found in ambient air. Further study of the respiratory
effects of O3 in smokers and non-smokers is needed, however, before firm
-------
VI — 7
conclusions can be drawn regarding the apparently greater responsiveness
of non-smokers.
4. Nutritional Status
Results of studies investigating nutritional status as a factor
affecting susceptibility to O3 are inconclusive. Some inconsistencies
between human and animal data are apparent but have been explained based on
different experimental approaches.
Human subjects receiving 4 to 8 times the recommended daily allowance
of vitamin E showed no statistically significant differences in blood bio-
chemistry or agglutination compared to unsupplemented subjects after 2-hour
exposures to 0.5 ppm O3 (Posin et. al., 1979; Hamburger et. al., 1979a,b).
Animal studies show that vitamin E deficiency makes rats more susceptible
to 03-induced enzymatic changes (Chow et. al., 1981; Plopper et. al.,
1979; Chow and Tappel, 1972) and that vitamin E alters the rate and
extent of O3 toxicity but not the centriacinar lesion itself (Stephens
et al., 1974; Schwartz et al., 1976). "Lesions were generally worse,
however, in vitamin E deficient or marginally supplemented rats when
compared to highly supplemented rats (Plopper et al., 1979; Chow et al., 1981),
supporting the finding from mortality (Donovan et al., 1977) and biochemical
studies that vitamin E is protective" (CD, pp. 13-37).
Since redistribution of vitamin E from extrapulmonary stores to
the lungs is slow, it is possible that protective effect does not occur over
short-term exposures to O3 in human studies. Animal studies in which
effects have been reported were conducted with a vitamin E deficient
group for comparison and for long-term exposures (Sato et al., 1976,
1978, 1980), neither of which is possible in human studies. Although
laboratory animal studies of vitamin E support the hypothesis that lipid
-------
VI -8
peroxidation is involved in O3 toxicity, benefits to be derived from
human dietary vitamin E supplementation in connection with O3 exposure
have not yet been demonstrated.
5. Environmental Stresses
Subjective symptoms and physiological impairment caused by O3
exposure can be substantially worsened by environmental stresses such as
heat and high relative humidity (rh). High temperatures (31 to 40°C)
and/or humid conditions (85% rh) when combined with exercise during O3
exposure have been shown to reduce FEVj more than similar O3 exposures at a
more moderate temperature (25°C) and humidity (50% rh) (Folinsbee et. al.t
1977a,b; Gibbons and Adams, 1984). Enhanced effects of O3 caused by high
temperatures and humidity may be the result of higher ventilation which
increases the volume of inhaled O3 and promotes deeper penetration into the
lungs. There may also be an Independent effect of elevated body temperature
on pulmonary function (CD, p. 13-34). Since many urban areas around the
U.S. tend to experience the highest O3 levels during periods of high
temperatures and humidity, environmental stess should be considered a
factor of concern in assessing potential effects from O3 exposure.
6. Exercise
Exercise stresses respiratory, cardiovascular, and musculoskeletal
systems and increases ventilation and, therefore, total dose to the lungs.
Exercise thus should be considered an Important susceptibility factor
when O3 exposure occurs concurrently. The most apparent and well-studied
effects of O3 during exercise occur 1n the respiratory system. In particular,
pulmonary function decrements and respiratory symptoms caused by O3 exposure
are increased by a greater work load, which 1s characterized by Increased
frequency and depth of breathing (Folinsbee et al., 1979, 1984; McDonnell
-------
tmle vi-1. esrmreo values of m&tt commm Am mm mniATiOH
ASSOCIATED WITH REPRESENTATIVE TYPES OF EXERCISE3
Level of work
Work
watts
performed
kg-m/minb
02 consumption,
L/min
M1nute
ventilation
L/min
Representative activities0
Resti ng
5
Sleep
Light
25
150
0.65
13
Level walking at 2 mph; washing, clothes
Light
50
300
0.96
19
Level walking at 3 mph; bowling; scrubbing floors
Light
75
450
1.25
25
Dancing; pushing wheelbarrow with 15-kg load;
simple construction; stacking firewood;
walking quickly (4 mph)
Moderate
100
600
1.54
30
Easy cycling; pushing wheelbarrow with 75-kg
load; using sledgehammer
Moderate
125
750
1.83
35
Climbing 3 flights of stairs; playing tennis;
digging with spade
Moderate
150
900
2.12
40
Cycling at 13 mph; walking on snow; digging
trenches; light jogging
Heavy
Heavy
Very heavy
175
200
225
1050
1200
1350
2.47
2.83
3.19
55
63
72
Cross-country skiing; rock climbing; stair
climbing with load; playing squash and
handball; chopping with axe
Very heavy
250
1500
3.55
85
Level running at 10 mph; competitive cycling
Severe
300
1800
4.27
100+
Competitive long distance running; competitive
cross-country skiing
aSee text of Criteria Document (pp. 11-7 to 11-14) for discussion.
bkg-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).
-------
VI-10
et al., 1983, 1985a,b,c; Avol et al., 1984, 1985a,b). Representative
activities and associated ventilation rates are summarized in Table VI-l
(CD, pp 11-13). Higher ventilation increases total volume of O3 breathed
and could cause deeper penetration of O3 into peripheral areas of the
lung which tend to be most sensitive to injury. This is particularly
true for higher ventilation rates >35 L/min) when the mode of breathing
changes from nasal to oronasal or to oral only (N11n1maa et. al., 1980).
There is, however, variability between individuals regarding the ventilation
rates at which breathing becomes oronasal or nasal only.
Effects of O3 on cardiovascular and musculoskeletal systems may be
related to compensatory mechanisms which might modify the magnitude and
persistence of reaction to O3 during exercise. Of the few studies which
have Investigated these effects, very heavy exercise ($£>64 L/min) during
0.75 ppm O3 exposure reduced post-exposure maximal exercise capacity by
limiting maximal oxygen consumption; submaxlmal oxygen consumption
changes were not significant (Follnsbee et. al., 1977a). On the other hand,
resting subjects exposed to up to 0.75 ppm O3 show no effect on maximal
oxygen consumption (Horvath et al., 1979). The extent of ventilatory and
respiratory metabolic changes during or following exposure appears to
have been related to magnitude of pulmonary function impairment (CD, pp.
13-33). While the relationship between the metabolic changes and lung
mechanics is unclear at present, it 1s clear that exercise should be
considered a susceptibility factor 1n assessing health effects of O3.
C. Potentially Susceptible Groups
The Clean A1r Act requires EPA to set standards which protect the
health of Individuals who are potentially susceptible to O3 exposure. This
-------
VI-11
section identifies potentially susceptible groups or subpopulations and
provides a rationale for selecting these groups.
Susceptibility to any pollutant nay depend upon many factors such as
those previously discussed (age, sex, smoking, nutrition, environment, and
exercise) but also is influenced by individual sensitivity. Greater than
normal sensitivity to a particular pollutant may be conferred by numerous
individual characteristics Including (1) predisposition to pulmonary infec-
tion, (2) preexisting disease or nutritional deficiency, (3) some aspect
of growth or decline in lung development, (4) a prior infection or immunological
problem, (5) sensitization caused by prior pollutant exposure or challenge
with respiratory irritants and (6) genetic variability in the population.
These sensitivity and susceptibility factors should be considered in
identifying groups or subpopulations which may be susceptible to O3
exposure.
1. Individuals Having Preexisting Disease
The first major group identified in the CO (pp. 13-72) as
appearing to be at particular risk to O3 exposure Is that group characterized
as having preexisting disease. This Includes individuals with asthma,
allergy, and chronic obstructive lung disease (COLD) such as emphysema.
Asthmatics, who experience variable airway restriction and/or reactivity
and who may have altered immunological states (e.g., atopy) or cellular
function (e.g., eos1noph1l1a) may be expected to be potentially more sensitive
to O3 than non-asthmatics. Asthma, however, is not a specific homogeneous
disease and efforts to precisely define asthma have been unsuccessful.
Similarly, allergic individuals with predisposing atopy have altered
immunological response and also may be expected to be more sensitive to O3.
Susceptibllity to O3 of patients with COLD remains somewhat uncertain,
-------
TABLE VI-2. PREVALENCE OF CHRONIC RESPIRATORY CONDITIONS BY SEX AND AGE FOR 1979*
Number of persons, thousands
Conditionb
Total0
Male
Female
< 17
years old
17-44
years old
45-64
years old
_> 65
years old
% of U,
popular
Chronic bronchitis
7,474
3,289
4,175
2,458
2,412
1,547
1,060
3.5
Emphysema
2,137
1,364
770
12d
127<*
1,008
990
1.0
Asthmae
6,402
3,113
3,293
2,225
2,203
1,482
488
3.0
Hay fever and
15,620
7,027
8,584
3,151
8,278
3,012
1,181
1.7
other upper
respi ratory
allergies^
aU.S. Department of Health and Human Services, 1981.
Classified by type, according to the Ninth Revision of the International Classification of Diseases (World Health
Organization, 1977).
cReported as actual number in thousands; remaining subsets have been calculated from percentages and are rounded off.
^Does not meet standards of reliability or precision set by the National Center for Health Statistics (more than 30%
relative standard error).
ewith or without hay fever.
^Without asthma.
-------
VI-13
depending on their clinical and functional state. Table V1-2 provides
estimates of the number of individuals with these conditions (CD, pp.
13-77).
Although several controlled human exposure studies suggest that
adults with preexisting respiratory disease may not be more responsive to
O3 than healthy adults, two considerations place these subgroups at potentially
higher risk to O3 exposure. First, due to concern for the health of these
persons, higher concentrations of O3 and higher exercise levels have not been
used during controlled exposure studies, thus making comparisons with healthy
subjects difficult. A second consideration 1s that for individuals with
already compromised respiratory systems, any further decrement In pulmonary
function may be expected to impair the ability to perform normal activities.
The same decrement 1n a healthy individual may go unnoticed. Increases In
symptoms reported for asthmatics and allergic Individuals exposed to O3 may
also be expected to Interfere with normal function.
2. Responders
A second group in the population which 1s unusually susceptible to
O3 exposure has been referred to as "responders." These individuals have
not been characterized as having any particular medical problem but experience
significantly greater pulmonary function decrements than the average response
of the groups concurrently studied during O3 exposure. It 1s not known if
"responders" are a population subgroup with a specific disease history or
simply represent the upper 5 to 20 percent of the O3 response distribution.
As yet there 1s no means of identifying these highly responsive individuals
prior to O3 exposure.
Individual responsiveness to O3 of apparently healthy, homogeneous
groups has been shown to vary widely. For example, during heavy exercise
-------
VI —14
(Vf » 45-51 L/m1n) and exposure to 0.4 ppm O3, subjects showed FEV^
decrements ranging from below 10% to as much as 40% of control values for
those subjects with an average of 26% (Haak et al., 1984; Silverman et al.,
1976). Mode (oral versus nasal) and pattern (rapid shallow versus slow
deep) of breathing may contribute to Intersubject variability but cannot
fully explain 1t. Unsuccessful attempts have been made to determine which
factors are responsible for modifying Individual responslveness (Hazucha,
1981). Factors such as prior exposure to O3 or other pollutants, latent
Infections, and nutritional deficiencies may also contribute to differential
response (CD, p. 13-20). The potential for these contributions 1s biologically
plausible, but these have yet to be demonstrated 1n human subjects.
Although the specific factors which modify Individual response to O3 are
not yet Identified, It has been suggested that Intersubject variability 1n
the magnitude of effects Induced by O3 1s caused by large differences 1n
Intrinsic responsiveness to O3 (McDonnell et al., 1985a). These differences
are graphically Illustrated 1n Figures VI-1 and VI-2, the cumulative
frequency distributions of response (% change from baseline) 1n FEVj and
specific airway resistance (SRaw) for a total of 132 subjects exposed to
either air or one of five different O3 concentrations (McDonnell et al.,
1983). As measured by FEVj and FVC, Individual responses to O3 are highly
reproducible for at least the 10 month period of observation and for a
given Individual differences tend to be much smaller than differences
between subjects (McDonnell et al., 1985a; GUner et al., 1983). Hence,
some Intrinsic factor appears to be responsible for Individual responsiveness.
Changes 1n FEVj of exercising subjects exposed to clean air are small
and uniformly distributed 1n the subject population. As O3 concentrations
Increase this distribution widens and becomes skewed toward larger FEVj
-------
FIGURE VI-1. CUMULATIVE FREQUENCY DISTRIBUTION OF
PERCENT DECREASE IN FEV-1 DUE TO 03 EXPOSURE
IN HEALTHY EXERCISING MALES *
CUMULATIVE FREQUENCY
100 r
10 20 30
PERCENT DECREASE IN FEV-1
0.0 PPM
0.12 PPM
0.18 PPM
0.24 PPM
0.30 PPM
20
22
20 f
tfl
21
20
0.40 PPM
*S0URCE: McDonnell ,• et. al, 1983.
-------
FIGURE VI-2. CUMULATIVE FREQUENCY DISTRIBUTION OF PERCENT
INCREASE IN AIRWAY RESISTANCE DUE TO OZONE
EXPOSURE IN HEALTHY EXERCISING MALES *
CUMULATIVE FREQUENCY
100
0.0 PPM
0.12 PPM
0.18 PPM
0.24 PPM
0.30 PPM
0.40 PPM
-20 -10
0 10 20 30 40 50 60
PERCENT INCREASE IN RESISTANCE
19
22
19
22
20
28
I
I—i
iOO PERCENTILE VALUE FOR 0.40 PPM IS 261.39
*S0URCE: McDonnell, et. al, 1983.
-------
VI -1 7
decrements, the largest changes representing the most responsive subjects
(McDonnell et al., 1983; Kulle et al., 1985). Classification of subjects
into "responders" and "non-responders" has been somewhat arbitrary. Examples
of retrospective classification include identifying responders by using
medical history and exposure test results (Hackney et al. 1975} and selecting
those with greater than 10% post-exposure decrements (Horvath et al., 1981)
or with FEV} decrements greater than 2 standard deviations above control
(Haak et al., 1984). While there are no clearly established criteria for
identifying or selecting "responders," it has been suggested that between 5
and 20% of the healthy population should be considered most responsive and,
therefore, at higher risk to O3 exposures (CD, p. 13-20). Further discussion
of frequency distribution is in section VH.A.l.
3. Exercising Individuals
A third susceptible group potentially at higher risk to O3 exposure
1s that group of exercising healthy and unhealthy persons with preexisting
respiratory disease whose daily outside activities cause increased
minute ventilation. As stated in the CD (p. 13-70), "the most prominent
modifier of response to O3 in the general population is minute ventilation,
which increases proportionately with Increases in exercise workload."
The increased proportion of oral breathing with increased exercise also
contributes to the increase in effects since more O3 is delivered to the
lungs. Although individuals with preexisting disease may not exercise at
the same levels as healthy persons, any increases in activity over resting
levels will Increase O3 exposure and resultant effects. It is reasonable
to assume, however, that individuals with preexisting respiratory or
cardiovascular disease should achieve generally higher ventilation rates
than healthy individuals for a given work load.
-------
VI-18
Exercise has become recognized in numerous recent studies as a factor
which can predispose all Individuals to O3 health effects (McDonnell et
al., 1983, 1985a,b,c; Avol et al., 1983, 1984, 1985a,b; Follnsbee et al.,
1978, 1984; Kulle et al., 1985). Thus, activities which increase minute
ventilation out-of-doors will also increase the risk associated with exposure
to O3 of exercising Individuals.
-------
VII. Assessment of Health Effects and Related Health Issues Considered in
Selecting Primary Standards for Ozone
This assessment of health effects attributed to O3 and related health
Issues is based on the review and evaluation of health effects research
literature contained in Chapter 10 to 13 of the CD. In a future draft of
the staff paper, the evaluation and judgment provided by a risk assessment,
which is currently being developed (See Appendix 8), will be incorporated.
A. Health Effects of Concern
For purposes of this staff paper and review of the NAAOS for O3, the
staff recommends that the following health effects attributed to O3 exposure
be considered in developing the basis for the primary O3 standard:
1. Alterations in pulmonary function
2. Symptomatic effects
3. Exercise performance
4. Aggravation of existing respiratory disease
5. Morphological effects
6. Altered host defense systems
7. Extrapulmonary effects.
Based on review of the CD, the staff further suggests that the order of
effects listed above corresponds with the strength of the O3 health data
base for regulatory purposes. Respiratory effects thus provide the strongest
data base for considering adverse health effects of O3. Extrapulmonary
effects such as behavioral, blood chemistry, chromosomal, reproductive,
liver, and endocrine system modifications also have been associated with O3
exposure, but most are of uncertain functional importance at this time and,
thus, do not provide very strong evidence of adverse effects associated
with O3 exposures.
-------
VI1-2
Evidence for the above effects has come from both human and animal
studies. The strongest and most quantifiable data are provided by
controlled human exposure studies, but these studies are limited to acute
(short-term) exposures and non-invasive techniques. Field studies are
similarly limited, but permit investigation of the effects of oxidants in
ambient air and allow for better characterization of exposure than epidemio-
logical studies. Although use of most community studies has been hampered
by the difficulty in adequately characterizing exposure and numerous confounding
variables, these investigations provide important supporting evidence for
effects occurring in populations. Animal toxicology studies have provided
evidence of acute and chronic (long-term) exposure effects which can be
detected only with invasive procedures, but uncertainties inherent in
dosimetry and species sensitivity differences have limited quantitative
extrapolation to humans.
Assessment of health effects attributed to O3 requires consideration
of the data base in each of the above areas of study. This section integrates
research in each of these areas to provide an indication of the strength of
the data base for each effect. The order of review suggests a hierarchy of
importance for consideration of health effects of O3 for regulatory purposes.
A more thorough review and evaluation of individual studies is available in
chapters 10 to 13 of the CD.
1. Alterations in Pulmonary Function
The best documented and strongest evidence of human health effects of
O3 exposure are pulmonary function decrements. Controlled human exposure,
field, epidemiology, and animal toxicology studies have provided evidence
that exposure to O3 can modify such pulmonary measurements as forced expiratory
volume (FEV), forced expiratory flow (FEF), forced vital capacity (FVC),
-------
VII-3
functional residual capacity (FRC), vital capacity (VC), tidal volume (Vy),
peak expiratory flow rate (PEFR), inspiratory capacity (IC), residual
volume (RV), total lung capacity (TLC), airway resistance (Raw) and breathing
frequency {fg)• These and other terms are defined in Appendix C which is
an abbreviated version of the glossary found in the CD.
Early controlled experimental studies of resting human subjects exposed
to O3 levels up to 0.75 ppm for 2 hours demonstrated little or no change
in FVC (Silverman et al., 1976; Folinsbee et al., 1975;), FEVi, and FRC
(Silverman et al., 1976). Flow rate variables such as FEF 25% and FEF 50%
showed up to 30% decreases in some subjects exposed at rest to 0.75 ppm
O3 (Bates et al., 1972; Silverman et al., 1976), while only small increases
in Raw (< 17%) were reported for > 0.5 ppm O3 exposures (Bates et al., 1972;
Golden et al., 1978). More recent studies have reported occurrence
of FEV and FEF decrements during resting exposures to _> 0.5 ppm O3
(Folinsbee et al., 1978; Horvath et al., 1979); however, no statistically
significant changes in Raw and only suggestive changes in RV and TLC
have been reported for similar exposures (Shephard et al., 1982). Airway
resistance is not generally affected in resting subjects at these O3 levels.
Changes in pulmonary function do not occur in resting subjects exposed
to £0.3 ppm O3 (Folinsbee et al., 1978), though some subjects exhibit
03-irduced pulmonary symptoms during resting exposures (Konlg et al., 1980;
Golden et al., 197B). In general, however, because subjects were at rest
in most of the older studies, significant respiratory effects were not
reported even for higher O3 exposures.
Exercise, which causes increased minute ventilation C?e), enhances
individual and group mean response to O3 exposure. As discussed in
section VI.B.6. of this staff paper, exercise increases breathing frequency
-------
VI1-4
and depth of breathing resulting in greater total dose of O3 inhaled and
increased penetration to the most sensitive lung tissue. As exercise
levels Increase to the point where Vg exceeds approximately 35 L/min,
oronasal or oral breathing tends to predominate (Nlinimaa et al., 1980);
thus at higher exercise levels a greater portion of the inhaled O3 will
bypass the nose and nasopharynx (N11n1maa et al., 1981). Individual variability
will affect the Vf at which oral or oronasal breathing predominates. This
further increases the total dose of O3 to the lower airways and parenchyma.
The relationship between exercise and magnitude of response is illustrated
quite well by Figure VII-1 prepared for the CD (p. 13-27) showing group
mean decrements in FEVj caused by exposure of exercising subjects to various
O3 levels based on results from 25 different studies. The curves clearly
demonstrate that as exercise levels increase for a given O3 exposure there
1s a resultant Increase in the group mean FEV1 decrements. These curves
also provide estimates of group mean FEV^ decrements resulting from exposure
of subjects to O3 under light, moderate, heavy, and very heavy exercise
conditions. Individual curves presented in the CD (p. 13-23 to 13-26)
suggest an Increase in subject response variability as exercise levels
increase.
Pulmonary function decrements have been reported In controlled exposure
studies of healthy exercising human subjects exposed to O3 levels in the range
of 0.12 to 0.18 ppm. During 2 hours of intermittent very heavy exercise
(Vf « 64 L/m1n.), healthy subjects experienced group mean decrements in
FEVi of 4.5, 6.4, and 14.4% for O3 exposures of 0.12, 0.18, and 0.24 ppm,
respectively with greater FEVi decrements at higher O3 concentrations
(McDonnell et al., 1983). Positive associations between group mean magnitude
of FVC (3, 4, and 12%) and FEF (7.2, 12, and 23%) decrements and O3 exposures
-------
110
5 100
••••
••
UGHT EXERCISE
MODERATE
EXERCISE
HEAVY ^
EXERCISE
Ui
VERY HEAVY
EXERCISE
u.
70
60
0.4
0.8
0.2
0.6
0
OZONE CONCENTRATION, ppm
Figure V11 -4 .Group mean decrements in 1 -sec forced expiratory volume during 2-
hr ozone exposures with different levels of intermittent exercise: light (Og < 23
L/min); moderate (0^ = 24-43'L/min); heavy (vg = 44-63 L/min); and very heavy
(v£ ^ 64 L/min). Concentration-response curves are taken from Figures 13-2
through 13-5.
-------
VI1-6
of (.12, .18, and .24 ppm) also were reported in the McDonnell et al.
(1983) study; statistically significant increases in SRaw and fg did not
occur until O3 was _> 0.24 ppm. In a separate study, McDonnell et al.
(1985b) reported a statistically significant but small decline (-3.4%)
in FEVj of children (8-11 years) after 2 hours of exposure to 0.12 ppm O3
during intermittent heavy exercise (Vg = 39 L/min). Furthermore, these small
decrements in FEVj persisted for 16 to 20 hours after O3 exposure ceases.
Support for 03-induced pulmonary function changes also comes fi-om
other controlled exposure studies. Avol et al. (1984) report statistically
significant, small decreases (6.1%) in FEV^, at 0.16 ppm O3 with larger
decrements at j> 0.24 ppm O3. Decrements have been reported in FEVj, FVC,
and FEF for distance runners and distance cyclists exposed to 0.20 ppm
and 0.21 ppm O3 respectively, during 1 hour of continuous, heavy exercise
(Vf = 77.5 and 81 L/min) (Adams and Schelegle, 1983; Folinsbee et al.,
1984). In another study Involving O3 concentrations ranging between 0.10
and 0.25 ppm, exponential decreases in FVC, FEVj, ^25.75, SGaw, IC, and
TLC have been reported with exposure to increasing O3 concentration during
very heavy exercise (tff = 68 1/min); time of exposure was related to linear
decreases in FVC and FEV^ (Kulle et al., 1985).
Field studies, which contain elements of both controlled human exposure
and epidemiologic studies, provide the most quantitatively useful human
exposure data available for ambient photochemical oxidants. Results from
field studies are consistent with pulmonary function decrements reported in
controlled O3 exposure studies. For a 1-hour exposure to mean O3 concentrations
of 0.144 ppm, small significant group mean decreases 1n FVC (-3.3%), FEV0.75
(-4.0%), FEVx (-4.2%), MMFR (-3.2%) and PEFR (-3.9%) relative to pre-exposure
levels were reported in 59 healthy continuously exercising (V^=32 L/min)
-------
VI1-7
adolescents (Avol et al., 1985 a, b). In a separate study of 50 healthy,
adult, continuously exercising (V£ = 53 L/min) bicyclists, mean O3 concentrations
of 0.153 ppm for 1 hour produced statistically significant group mean
decreases in FEVj (-5.3%) compared to pre-exposure. (Avol et al., 1984).
This study showed that similar effects result in subjects exposed to comparable
O3 levels 1n ambient and controlled O3 exposures. Small but statistically
significant decreases in FEV^ and FVC were also reported in exercising
healthy and asthmatic adults during exposure to mean O3 concentrations of
0.165 and 0.174 ppm (Linn et al., 1980, 1983b; Avol et al., 1983). Of
importance is the fact that no recovery occurred in healthy adults during a
1 hour post-exposure rest period and FEV^ remained low or deceased further
3 hours after exposure for asthmatics (Avol et al., 1983, 1985a, b; Linn et
al., 1983a). Table VII-1 provides a summary of gorup mean % changes in
FEVi for controlled exposure and field studies.
In summary, pulmonary function decrements have been reported in healthy
adult subjects (18 to 45 years old) after 1 to 3 hours of exposure as a
function of the level of exercise performed and the O3 concentration inhaled
during exposure. Group mean data pooled from numerous controlled human exposure
and field studies and summarized in the CD (CD, p. 13-78) indicate that,
on average, pulmonary function decrements occur at:
(a) j> 0.5 ppm O3 when at rest (sitting);
(b) ^0.37 ppm O3 with light exercise (slow walking);
(c) ^0.30 ppm O3 with moderate exercise (brisk walking);
(d) ^0.24 ppm O3 with heavy exercise (easy running);
(e) ^0.18 ppm O3 with very heavy exercise (competitive running).
However, data from a field study (Avol et al., 1985) indicate that group
mean pulmonary function decrements occur during heavy exercise 1n healthy adults
-------
TABLE VII-1. LUNG FUNCTION
Ozone
Concentration Measurement8»b Exposure Act1v1tyc
ppm method duration level (Vf)
0.00 UV.UV 1 hr CE (57)
0.08
0.00 UV.UV 2 hr IE (68)
0.10
0.00 CHEM.NBKI 2 hr IE (67)
0.10
0.00 CHEM.UV 2 hr IE (68)
0.12
0.00 CHEM.UV 2 hr IE (39)
0.12
0.00 UV.UV 1 hr CE (31)
0.14e
0.00 UV.UV 1 hr CE (53)
0.156
0.00 UV.UV 2 hr IE (68)
0.15
0.00 UV.UV 1 hr CE (55)
0.15 (mouthpiece)
0.00 UV.UV 1 hr CE (57)
0.16
0.00 UV.NBKI 1 hr CE (38)
0.16e
0.00 UV.NBKI 1 hr CE (42)
0.17e
AND SYMPTOMS ATTRIBUTED TO OZONE EXPOSURES
Group Mean Sypmptoms
% Change 1n FEVj Reported
(range for O3 exp.)
No., sex
and age
of subjects
Reference
+0.6
+1.7 (ns)
+1.3
+1.1 (nd)
(range:+|0 to -10)
-0.3
-2.6 (ns)
-1.1
-4.5 (p=0.016)f
(range:+7 to -17)
-0.5
-3.4 (p=0.03)
(range:+5 to -22)
-0.3
-4.2 (p<0.01)
+0.6
-5.3 (p<0.05)
+1.3
-0.7 (nd)
(range:+5 to -10)
+0.6
-4.5 (ns)
(range:+3.5to-31)
+0.6
-6.1 (p<0.05)
-0.1
-0.8 (ns)
-0.4
-3.4 (p<0.006)
None
None
None
Cough
None
None
Lower
Resplratory
Symptoms
Cough
Lower
Respiratory
Symptoms
42 male
8 female
(26.4+6.9)
Avol et al. (1984)
20 male Kulle et al. (1985)
(25.3+4.1 yr)
10 male
(18-28 yr)
Follnsbee et al,
(1978)
22 male McDonnell et al.
(22.3+3.1 yr) (1983)
23 male
(8-11 yr)
McOonnel1 et al.
(1985b)
46 male
13 female
(12-15 yr)
42 male
8 female
(26.4+6.9 yr)
Avol et al. (1985)
Avol et al. (1984)
20 male Kulle et al. (1985)
(25.3+4.1 yr)
10 female Gibbons and Adams
(22.9+2.5 yr) (1984)
42 male
8 female
(26.4+^6.9 yr)
Avol et al. (1984)
No significant 27 male L1nn et al. (1983a)
changes In 21 female Avol et al. (1983)
symptom score (28+8 yr)
No significant 45 male L1nn et al. (1983a)
changes 1n 15 female Avol et al. (1983)
symptom score (30+11 yr)
-------
TABLE VII-1. LUNG FUNCTION CHANGES AND SYMPTOMS ATTRIBUTED TO OZONE EXPOSURES (continued)
Ozone No., sex
Concentration Measurement8^ Exposure Activity0 Group Mean Sypmptoms and age
ppm method duration level (Vf) X Change 1n FEVj Reported of subjects Reference
0.00
0.17e
0.00
0.18
0.0
0.2
0.0
0.2
0.00
0.21
0.00
0.24
0.00
0.24
0.00
0.25
UV,NBKI
CHEM.UV
UV.UV
UV.UV
UV.UV
CHEM.UV
UV.UV
UV.UV
2 hr
2 hr
2 hr
2 hr
1 hr
2 hr
1 hr
2 hr
IE (2XR)
IE (65)
IE (68)
IE (30 for
male, 18
for female
subjects)
CE (80)
IE (65)
CE (60)
IE (68)
+0.6
-2.1 (p<0.05)
-1.1
-6.4 (p=0.008)
(range:t2 to -22)
+1.3
-3.3 (nd)
(range:+5 to -20)
+0.3
-3.1 (ns)
(range:+6 to -17)
+1.9
-15 (p<0.05)
-1.1
-14.4 (p<0.005)
+0.6
-19 (p<0.05)
+1.3
-6.7 (nd)
(range:+5 to -35)
Increased
14 male
symptom
20 female
scores
(29+8 yr)
Cough
20 male
(23.3+2.8
Cough
20 male
(25.3+4.1
8 male
13 female
(18-31 yr)
Subjective
6 male
symptoms which
1 female
may limit
(18-27 yr)
performance
Cough, pain
21 male
on deep
(22.9+2.9
Inspiration,
shortness of
breath
Lower
42 male
respl ratory
8 female
symptoms
(26.4+6.9
Cough, nose/
20 male
throat
(25.3+4.1
1 rritatlon
L1nn et al. (1980)
McDonnell et al.
(1983)
Kulle et al. (1985)
Gliner et al. (1983)
Foilnsbee et al,
(1984)
McDonnell et al.
Avol et al. (1984)
Kulle et al. (1985)
Measurement method: CHEM = gas phase chetnlluminescence; 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: IE = Intermittent exercise;
CE = continuous exercise.
dPre to post difference (percent) 1n the group mean; statistical significance based on difference between O3 and
filtered air (0.0 ppm O3) exposures: ns = not significant; nd = not determined.
Measured in ambient air (mobile laboratory).
f"Suggested" significance based on Bonferronl Inequality correction (p<0.006).
-------
VII-10
exposed to mean O3 levels of 0.153 ppm and may occur in very heavily exercising
adults during controlled exposures to 0.12 ppm O3 (McDonnell et al., 1983).
Group mean pulmonary function decrements have also been reported for children
exposed to controlled O3 levels of 0.12 ppm and adolescents exposed to mean
ambient O3 levels of 0.144 ppm during heavy exercise (McDonnell et al.,
1985b; Avol et al., 1985). In general the group mean changes in lung
function in the above studies are regarded as small (< 5%), but there is
considerable intersubject variability in the magnitude of individual
pulmonary response (See Section VI.C.2). Controlled exposures to 0.12 ppm
O3 during very heavy exercise have resulted in individual pulmonary function
decrements up to 17% for adults (McDonnell et al., 1983) and up to 22% for
children (McDonnell et al., 1985b). Thus, it appears that some individuals
are intrinsically more responsive, and this group which has been referred
to as "responders" may constitute as much as 5 to 20% of the healthy adults
studi ed.
Further confirmation of the relationship between acute O3 exposure and
pulmonary function decrements is provided by several epidemiological studies
of children and young adults (Kagawa and Toyana, 1975; Kagawa et al., 1976;
Lippman et al., 1983; Lebowitz et al., 1982a, 1983; Lebowitz, 1984;
Bock et al., 1985; Lioy et al., 1985). These studies report decreased
peak flow or increased airway resistance for acute exposures to ambient O3
concentrations ranging from 0.01 to 0.186 ppm over the entire study period.
Of particular importance is the finding by Hoy et al. (1985) that a per-
sistent decrement 1n lung function of children lasted as much as a week
after the end of a smog period of four days during which peak 1-hr O3 levels
were 1n the range of 0.135 to 0.186 ppm. Whether or not the underlying
causes of the persistent decrements suggested by Lioy et al. (1985) (i.e.,
-------
vil-ll
altered epithelial permeability and changes in airway secretion) are
confirmed, the decrements represent a potentially more serious response
than the more transient effects found in controlled exposure studies.
While It has been concluded in the CD (p. 12-50) that none of these
epidemiological studies provide definitive quantitative data by themselves
due to methodological problems and confounding variables, the aggregation
of studies provides reasonably good qualitative evidence of association
between ambient O3 exposure and acute pulmonary effects. The association
is strengthened by the consistency of these epidemiological results with
the findings of McDonnell et al. (1985) and Avol et al. (1985) who reported
small decrements in pulmonary function for exercising children exposed to
0.12 ppm O3 in purified air and adolescents exposed to 0.144 ppm O3 in
ambient air, respectively.
Pulmonary function effects of chronic exposures to O3 have been
Investigated 1n epidemiological and animal toxlcological studies. Studies
comparing communities have thus far been relatively unsuccessful due to the
lack of differences 1n pollutant levels, Inadequate control of covariables,
and insufficient individual exposure data (CO, p. 12-49). Chronic exposures
for periods of days to months have resulted in increased end expiratory
lung volume in adult rats at 0.25 ppm O3 (Raub et al., 1983), increased
pulmonary resistance in adult rats at 0.2 ppm O3 (Costa et al., 1983),
decreased lung compliance in adult monkeys at 0.5 ppm O3 (Eustis et al.,
1981), decreased peak inspiratory flow in neonatal rats at 0.12 ppm (Raub
et al., 1983), and substantial decreases 1n lung function of adult monkeys
at .64 ppm O3 even after a 3 month post-exposure period (Wegner, 1982).
The relationship between acute and chronic effects 1s discussed further in
Section VII.B.
-------
VI1-12
The weight of evidence clearly indicates that healthy, heavily
exercising subjects experience statistically significant pulmonary function
decrements during controlled exposures of _> 0.12 ppm O3 for 2 hours or
ambient exposures of _> 0.144 ppm O3 for 1 hour. Table VII-1 is a summary
of these data. Level of exercise and individual respons!veness play a
major role in determining the extent of pulmonary function loss. Hue to
individual variability, potentially 5 to 20% of heavily exercising,
healthy individuals may be sufficiently responsive to O3 exposure to be
considered at increased risk of pulmonary function and symptom effects at
O3 levels near the current O3 NAAQS. The reader is referred to the dis-
cussion in section VI.C.2 for further information on frequency distribution
of response to O3. Further review of controlled exposure data is underway
to estimate the fraction of subjects responding excessively at O3 concen-
trations in the range of 0.12 to 0.40 ppm.
2. Symptomatic Effects
Respiratory symptoms have been closely associated with pulmonary
function changes in adults acutely exposed in controlled exposures to O3
(CO, Chapter 11) and in ambient air containing O3 as the predominant pollutant
(CD, Chapter 12). Although symptoms are less quantifiable than pulmonary
function measurements, this association holds for both the time-course
and magnitude of effects. Some symptoms such as cough and chest pain may
interfere with maximal inspiration and expiration.
In controlled O3 exposures, some heavily exercising (flg = 65 L/min)
adult subjects have experienced cough, shortness of breath, and pain on
deep inspiration at 0.12 ppm O3, although the group mean response was
statistically significant for cough only (McDonnell et al., 1983). Above
0.12 ppm O3, respiratory and non-respiratory symptoms which have been
-------
VI1-13
reported Include throat dryness, chest tightness, substernal pain, cough,
wheeze, pain on deep inspiration, shortness of breath, dyspnea, lassitude,
malaise, headache, and nausea (DeLucia and Adams, 1977; Kagawa and Tsuru,
1979a,b,c; McDonnell et al., 1983; Adams and Schelegle, 1983; Avol et al.,
1984; Gibbons and Adams, 1984; Follnsbee et al., 1984; Kulle et al.,
1985). At 0.2 ppm O3 and higher, controlled exposure studies of exercising
subjects have reported positive "symptom scores" with elimination of
symptoms for most subjects within 24 hours post-exposure (CD, p. 13-15).
Comparisons of symptoms reported in controlled O3 exposure studies
have been made with those reported in field studies. One study, which
provided a direct comparison of symptoms 1n exercising (Vj: = 57 L/min)
adults caused by exposure to either purified air containing 0.16 ppm O3
or oxldant-polluted ambient air which contained 0.15 ppm O3, showed no
significant differences, suggesting that increased symptoms associated
with lung function impairment were caused by only O3 (Avol et al., 1984).
Several epidemiology studies have provided evidence of qualitative associations
between ambient oxidant levels > 0.10 ppm and symptoms in children and
young adults such as throat irritation, chest discomfort, cough, and
headache (Hammer et al., 1974; Maklno and Mizoguchi, 1975). Thus, it
can be concluded that most symptoms reported in individuals exposed to O3
1n purified air are similar but not identical to those found for ambient
a Ir exposures.
An exception is eye Irritation, a common symptom associate! ^'t'n exposure
to photochemical oxidants, which has not been reported for controlled
exposures to O3 alone. This appears to hold even at O3 concentrations
much higher than would be found in the ambient air. It 1s widely accepted
that other oxidants such as aldehydes and peroxyacetyl nitrate (PAN) are
-------
VI1-14
primarily responsible for eye irritation and are generally found in
atmospheres containing higher ambient O3 levels (Altshuller, 1977; National
Research Council, 1977; U.S. Environmental Protection Agency, 1978;
Okawada et al1979).
Pulmonary function decrements have been reported in studies which do not
report symptoms. Children (age 8-11) intermittently exercising (Vg = 39 L/min)
for 2.5 hours at 0.12 ppm O3 showed small, but statistically significant
decreases in FEVj which persisted for 24 hours post-exposure but showed
no changes in frequency or severity of cough compared to control (McDonnell
et al., 1985a,b). Similarly, adolescents (age 12-15) continuously exercising
(Vjr = 31-33 L/min) during exposure to 0.144 ppm mean O3 in ambient air
showed no changes in symptoms despite statistically significant decrements
in group mean FEVj (4%) which persisted at least one hour during resting
post-exposure; the adolescents showed no changes in symptoms compared to
control (Avol et al., 1985a,b). Because symptoms can be viewed as an
early warning of related lung function impairment by O3, the lack of
symptoms in children and adolescents during exposures which induce functional
decrements may be of concern. This suggests that children may he at
higher risk since with no warning, they may not exhibit avoidance behavior.
Symptoms when combined with objective measures of lung function are
considered useful adjuncts in assessing health effects caused by O3 and
photochemical oxidants. They have been shown to be closely associated with
the time-course and magnitude of pulmonary function changes associated with
O3 exposures. To the extent symptoms associated with exposure to O3 and
other photochemical oxidant exposures are associated with discomfort, interfere
with normal activity and provide subjective evidence of functional impairment,
the staff recommends that they should be considered adverse health effects.
-------
VI1-15
3. Exercise Performance
A limited data base provides suggestive evidence of decrements in
exercise performance associated with O3 exposure. A detailed discussion
of those data can be found in the CO (p. 11-59 to p. 11-61) and is
summarized in Table 11-6 (CD, p. 11-60).
Early epidemiological evidence on high school students showed that
the percentage of track team members failing to improve performance increased
with increasing oxidant concentrations the hour before a race (Wayne et al.
1967). The authors concluded that the effects may have been related to
increased Raw or to associated discomfort which may have limited motivation
to run at maximal levels. Controlled exposure studies of heavily exercising
competitive runners have demonstrated decreased max Vp at 0.3 ppm O3
(Savin and Adams, 1979) and decreased FVC, FEF, and FEF at 0.20 ppm O3 (Adams
and Schelegle, 1983). At 0.21 ppm O3, Follnsbee et al., (1984) reported
decreases in FVC, FEV, FEF, IC, and MVV at 75% max VO2 as well as symptoms
(laryngeal and tracheal irritation, soreness, and chest tghtness on
Inspiration) in 7 distance cyclists exercising heavily (Vg = 31 L/m1n).
Too limited a data base 1s available to draw any conclusive judgments
regarding effects of O3 on exercise performance. Although subjective
statements by individuals engaged in sports Indicate possible voluntary
curtailing of activities during high-oxidant episodes, increased temperature
and relative humidity may be involved in provoking the symptoms and lung
function decrements observed in the studies above. Controlled studies of
O3 exposure have, however, demonstrated lung function Impairment and subjective
symptoms which cause individuals to reduce work load and perf-j^nance.
Because O3 is implicated at least 1n part 1n reducing exercise performance
during periods of high oxidants, the staff recommends that this effect of
-------
VI1-16
O3 be viewed as a matter of public health concern and be used in supporting
the basis for the primary standard.
4. Aggravation of Existing Respiratory Disease
Some epidemiological studies suggest an association between photochemical
smog and aggravation of existing respiratory disease. No clear evidence
is available, however, from controlled exposure or field studies to
suggest that individuals with asthma, chronic bronchitis, or emphysema
have greater lung function Impairment caused by O3 or other photochemical
oxidants than healthy persons. Individuals with preexisting respiratory
disease are considered to be especially "at risk" to 03 exposure due to
their already compromised respiratory systems and concern that Increased
symptoms or pulmonary function decrements may interfere with normal
function (CD, p. 13-70).
In controlled human exposure studies, statistically significant
group mean decrements in pulmonary function were not reported for adult
asthmatics exposed for 2 hours at rest (Silverman, 1979) or with intermittent
light exercise (Linn et al., 1978) to O3 concentrations of 0.25 ppm or
lower. Similarly, no statistically significant group mean changes in
pulmonary function or symptoms were found in adolescent asthmatics exposed
to 0.12 ppm O3 for 1-hour at rest (Koenig et al., 1985). Subjects with
chronic obstructive lung disease (COLD) performing light to moderate
intermittent exercise show no statistically significant group mean decrements
in pulmonary function during 1- and 2-hour exposures to £0.30 ppm O3
(Linn et al., 1982a, 1983; Solic et al., 1982; Kehrl et al., 1983, 1985)
and small group mean decrements in FEVi for 3-hour exposure of chronic
bronchitlcs to 0.41 ppm O3 (Kulle et al., 1984). While these controlled
exposure results suggest that Individuals with pre-existing respiratory
-------
VI1-17
disease may not be more sensitive to O3 than healthy subjects, experimental
design considerations 1n these studies suggest that the Issues of sensitivity
and aggravation of pre-existing respiratory disease remain unresolved.
Epidemiological studies do not provide a clear concentration-response
relationship between O3 and aggravation of disease. For example, one
study conducted in Los Angeles reported increased daily asthma attack
rates on cool days and days with high oxidants and particulates when
median daily maximum hourly oxidant levels were £ 0.15 ppm; questionable
exposure assessment, lack of control for medication, pollen, respiratory
infections and other pollutants limits the use of this study for developing
quantitative dose-response relationships (Whlttemore and Korn, 1980).
Despite several exposure and variable control limitations, the
Houston Area Oxidants Study (HAOS) concluded that for the study period in
which the dally maximum hourly O3 concentrations were < 0.?1 ppm near the
subjects' residence, 1) there was increased incidence of nasal and respiratory
symptoms and Increased frequency of medication use for asthmatics with
increasing O3 levels; 2) FEV\ and FVC decreased with increasing O3 and
total oxidants; and 3) increased incidence of chest discomfort, eye
Irritation, and malaise occurred at high PAN concentrations (Johnson et
al., 1979; Javitz et al., 1983). In a subsequent related study, increased
probability of an asthma attack was associated with the occurrence of a
previous attack and with exposure to increased O3 concentrations and
temperature when maximum 1-hour averages for O3 were between 0.001 and
0.127 ppm; however, other pollutants such as S02 and particulates may
have been involved (Stock et al., 1983; Holguin et al., 1985; Contant et
al., 1985).
-------
VI1-18
In a series of studies conducted 1n a Tucson community, adults with
asthma, allergies, or airway obstructive disease (ADD) were observed during
an 11 month period 1n which 1-hour dally maximum 03 concentrations were
_< 0.12 ppm (Lebowitz et al., 1982a, 1983; Lebowitz, 1984). After adjusting
for covariables, O3 and TSP levels were significantly associated with
peak expiratory flow rate 1n adults with AOD, and there was a significant
interaction for O3 and temperature with alterations 1n peak flow and
symptoms 1n asthmatics. While these results suggest an effect of O3 in
individuals with preexisting respiratory disease, Interpretation 1s
difficult due to the small sample size 1n relation to the number of
covarlates and the fact that Individual exposure data were not available.
None of these epidemiology studies by themselves definitively demonstrates
a relationship between O3 and aggravation of preexisting respiratory
disease. All of the studies report effects which may be related to
inhalable particle exposure and most have inadequate characterization of
exposure. However, the group of studies as a whole support the contention
that exposures to ambient levels of O3 and other photochemical oxidants
recently reported 1n many cities (See Appendix A) may increase the rate
of asthma attacks, an effect which has been described as an adverse effect
by the American Thoracic Society (ATS, 1985). The staff concurs with the
assessment of increased asthma attack rate as an adverse effect but
recognizes the limited and uncertain data base relating this effect to
O3 exposure. Thus, 1t is recommended that data associating O3 exposure
with aggravation of existing respiratory disease be considered In the
development of a margin of safety for the primary standard unless further
analysis sufficiently quantifies the uncertainty to permit use of the
data in developing a lowest observed effects level.
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VI1-19
5. Morphological Effects
Morphological effects of O3 have been reported exclusively in
animal toxicology studies. For this reason it is important to consider
the differences in dosimetry and sensitivity between humans and laboratory
animals, which 1s discussed in Chapter 10 of the CD. The following
discussion provides an Indication of some of the structural changes which
might occur in human lungs as a result of repeated and long-term exposures
of humans to O3.
Despite the differences 1n lung structure between humans, dogs, monkeys,
mice, rats, and guinea pigs, a characteristic lesion occurs at the junction
of the conducting airways and the gaseous exchange tissues. In all
species examined the effect is typically damage to the ciliated and Type 1
cells and hyperplasia of non-ciliated bronchiolar and Type 2 cells; an
increase 1n Inflammatory cells Is also observed (CD, p. 13-57). These
effects were reported after 7 days, 8hr/day exposures to 0.2 ppm O3 in
monkeys (Dungworth et al., 1975; Castleinan et al., 1977) and in rats exposed
for 7 days, 8 and 24 hrs/day (Schwartz et al., 1976). Similar effects
with different exposures were reported 1n rats (0.26 ppm, 6 hr, endotracheal
tube, Boatman et al., 1974), mice (0.5 ppm, 35 days, Zitnik et al.,
1978), and guinea pigs (0.5 ppm, 6 months, Cavender et al., 1978).
Inadequate data limit quantitative comparisons between monkeys and rats,
but a rough equivalency of responses has been observed under similar
exposure conditions between species, Hecause all species tested show
similar morphological responses to O3 exposure, there 1s no reason to
believe that humans exposed to O3 would not respond similarly, although
such effects may not necessarily occur at the same O3 exposure concentrations
or averaging times of exposure.
-------
VI1-20
Changes in lung structure of monkeys and rats tend to decrease after
extended exposure to O3, although structural changes In the centriacinar
region have been reported after long-term exposures of rats (Boorman et
al., 1980; Moore and Schwartz, 1981; Barry et al., 1983; Crapo et al.,
1984), monkeys (Eustis et al., 1981; Fujlnaka, 1984; Fujlnaka et al.,
1985), and dogs (Freeman et al., 1973). While cell repair begins within
18 hours of exposure (Castleman et al., 1980; Evans et al., 1976 a,b,c;
Lum et al., 1978), cell damage continues throughout long-term exposures
but at a slower rate (CD, p. 13-46).
Increases In lung collagen content are Indicative of lung structure
damage. Lung collagen content Increased after short-term exposures to
< 1.0 ppm O3 (Last et al., 1979; Last et al., 1981) and continued to
increase during long-term exposures (Last and Greenberg, 1980; Last et
al., 1984b). Weanling and adult rats exposed for 6 and 13 weeks, respectively,
and young monkeys for one year to < 1.0 ppm O3 also showed increased collagen
content in the lungs (Last et al., 1984b). In the latter study, examination
of some of the exposed weanlings and controls at six weeks post-exposure
indicated a continued Increase in lung collagen content, a result deinonstrating
that damage continued to occur during the post-exposure period.
The centriacinar inflammatory process also continues during long-
term O3 exposures arid appears to be related to remodeling of the centriacinar
airways (Boorman et al., 1980; Moore and Schwartz, 1981; Fujlnaka et al.,
1985) and to Increased lung collagen which appears mainly in the centriacinar
regions (Last et al., 1979; Boorman et al., 1980; Moore and Schwartz,
1981; Last et al., 1984b). In addition there is morphometric (Fujlnaka
et al., 1985), morphologic (Freeman et al., 1973), and functional (Costa
et al., 1973; Wegner, 1982) evidence of distal airway narrowing.
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VI1-21
Implications for humans of these lung structure changes observed
in animals are unclear at present. While the distal airway narrowing
and lesions at the junction of the conducting airways and gaseous exchange
region are similar to the changes which have been found In lungs of
cigarette smokers (Niewohner et al., 1974; Cosio et al., 1980; Hale et
al., 1980; Wright et al., 1983), there is no evidence of emphysema
in the lungs of animals exposed to only O3 based on the definition fo!"
emphysema used in the CD. Many of the lung structural changes that have
been reported for long-term exposures to < 1.0 ppm O3 in several different
species are considered adverse and relevant to standard setting if
demonstrated in humans at ambient exposure concentrations of O3. Although
the lowest O3 concentrations and shortest averaging times which could
produce structural changes in human lungs is uncertain at this time, the
staff concludes that there is a need to protect the public from O3 exposures
which may induce such adverse effects. Until further analysis clarifies
the uncertainty associated with the use of animal data to estimate lung
structural changes in humans caused by O3 exposures, the staff recommends
that these data be used as support for developing a margin of safety for
the primary standard.
6. Altered Host Defense Systems
Respiratory systems of mammals are protected from bacterial and
viral infections by the closely interrelated particle removal (both mucociliary
and phagocytic) and immunological defense systems. Numerous factors such as
poor nutrition, preexisting disease, and environmental stress may influence
or alter these host defense systems of Individuals sufficiently to permit
development of respiratory infections. Animal studies have Indicated
that exposure to O3 is one of those factors.
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VI1-22
Both j_n vivo (1 1 ve animal) and j_n vitro (1solated eel 1) studies have
demonstrated that O3 can affect the ability of the clearance and immune
systems to defend against Infection. Increased susceptibility to bacterial
infection has been reported in mice at 0.08 to 0.10 ppm O3 for a single
3-hour exposure (Coffin et al., 1967; Ehrlich et al., 1977; Miller et al.,
1978a) and at 0.10 ppm O3 for subchronic exposures (Aranyi et al., 1983).
Several related alterations of the pulmonary defenses caused by short-term
and subchronic exposures to O3 Include: 1) impaired ability to inactivate
bacteria in rabbits and mice (Coffin et al., 1968; Coffin and Gardner,
1972; Goldstein et al., 1974, 1977; Ehrlich et al., 1979); 2) impaired
performance of mucociliary clearance mechanisms (Phalen et al., 1980;
Frager et al., 1979; Kenoyer et al., 1981; Abraham et al., 1980); 3)
immuno-suppression (Campbell and Hilsenroth, 1976; Aranyi et al., 1983;
Thomas et al., 1981b; Fujimakl et al., 1984); 4) significantly reduced
number of pulmonary defense cells 1n rabbits (Coffin et al., 1968; Alpert
et al., 1971); and 5) Impaired macrophage phagocytic activity, less macrophage
mobility, more fragility and membrane alterations, and reduced lysosomal
enzymatic activity (Dowell et al., 1970; Hurst et al., 1970; Hurst and
Coffin, 1971; Goldstein et al., 1971a,b; Goldstein et al., 1974, 1977;
Hadley et al., 1977; McAllen et al., 1981; Witz et al., 1983; Amoruso et
al., 1981). Some of these effects have been shown to occur 1n a variety
of species Including mice, rats, rabbits, guinea pigs, dogs, sheep, and
monkeys.
Other studies Indicate similar effects for short-term and sub-chronic
exposues of mice to O3 combined with pollutants such as SOg, NO2, H2SO4
and particles (Gardner et al., 1977; Aranyi et al., 1983; Ehrlich, 1980,
1983; Grose et al., 1980, 1982; Phalen et al., 1980; Goldstein et al.,
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VI1-2 3
1974). Similar to human pulmonary function response to O3, activity
levels of mice exposed to O3 has been shown to play a role in determining
the lowest effective concentration which alters the immune defenses
(Illing et al., 1980).
Although this large body of evidence clearly demonstrates that short-
term and subchronic exposures to O3 can impair the immune defense systems
of animals, technical and ethical considerations have limited similar
research on human subjects. Thus inferences have been drawn and models
developed to assess the relevance of animal data to humans. For example,
animal endpoints other than Increased mortality should be appropriately
compared to Increased morbidity in humans, such as the increased prevalence
of respiratoi-y Illness in the community (CD, p. 13-48).
Based on current understanding of physiology, metabolism, and immune
defenses, it is generally accepted that the basic mechanisms of action
associated with defense against infectious agents are similar in humans
and animals. Similarities between human and rodent antibacterial systems
have been discussed in detail (Green, 1984), but differences in lung
structure and biological response will inevitably cause differences in
dosimetry, sensitivity, and endpoints of response. In addition other
factors such as preexisting disease, nutrition, presence of other pollutants
and environmental stresses (e.g. NO2, SOj, PM, high temperature or humidity)
can Influence the effect of exposure to O3 and infectious agents. Despite
the differences in related factors which make precise estimation of human
response from animal data difficult, it 1s reasonable to hypothesize that
humans exposed to O3 could experience Impairment of host defenses (CD,
p. 13-49). However, until further analysis quantifies uncertainty associated
with the extrapolation to humans of animal data on altered immune defenses,
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vn-a4
the staff recommends that these data be used in developing a margin of
safety.
7. Extrapulmonary Effects
Extrapulmonary effects which have been demonstrated in humans
or laboratory animals following exposure to O3 include alterations in
red blood cell morphology and enzyme activity, cytogenetic effects in
circulating lymphocytes, and subjective limitations in vigilance tasks.
Additionally, animal toxicology studies provide limited evidence for
cardiovascular, reproductive, teratological, endocrine system, and liver
metabolism effects. This wide variety of extrapulmonary effects is
probably caused by oxidative reaction products of O3. Due to the high
reactivity of O3 with biological tissue, mathematical models predict that
only a small fraction of O3 actually reaches the circulatory system
(Miller et al., 1985).
Of the extrapulmonary effects reported, cytogenetic and mutational
effects are probably the most controversial. Statistically significant
increases in frequency of sister chromatid exchanges (chromosomal alterations)
have been caused by in vitro exposures to 0.25 ppm for 1 hour (Guerrero
et al., 1979), suggesting a mutagenic response. However, in vitro responses
are not extrapolatable to in vivo responses, and homeostatic mechanisms
are not represented. Therefore, isolated in vitro exposure studies
cannot be used to provide accurate estimations of risk. In vivo animal
studies have shown significant increases in the number of chromosomal and
chromatid aberrations following 4 and 5 hour exposures to 0.2 and 0.43
ppm O3, respectively (Zelac et al., 1971a,b,; Tice et al., 1978). However,
animal studies (Gooch et al., 1976) and controlled human exposures to O3
levels as high as 0.5 ppm have shown no significant cytogenetic effects
-------
VI1-2 5
attributable to O3 (Merz et al., 1975; McKenzle et al., 1977; McKenzie,
1982; Guerrero et al., 1979), and epidemiology studies provide no evidence
of chromosomal changes induced by ambient O3 (Scott and Burkart, 1978;
Magie et al., 1982). Thus, while the animal studies are suggestive of
possible cytogenetic effects from 03, human studies have not demonstrated
such effects for realistic human exposures to O3.
Limited hematological and serum chemistry effects data indicate that
O3 can interfere with biochemical mechanisms in human blood erythrocytes and
sera but the physiological significance of these studies is unclear
(CD, p. 11-91). While the behavior of rats is significantly affected
during exposure to concentrations as low as 0.12 ppm O3 for 6 hours, it
1s unknown whether lung irritation,, odor, or a direct effect on the
central nervous system (CNS) causes change in rodent behavior at lower O3
concentrations (CD, p. 10-245). Other 03-lnduced effects such as
pentobarbital-induced sleep time alterations and hormone level changes
have been reported and cause-effect hypotheses made. With regard to
other extrapulmonary effects, exact mechanisms remain to be elucidated
and physiological significance for humans remains uncertain. Nonetheless,
the body of this evidence suggests that O3 can cause effects distant from
the lungs in animals, and hence possibly in humans. It is the staff's
recommendation that these data be used only in developing a margin of
safety.
B. Related Health Effects Issues
The purpose of this section 1s to provide an overview of important
issues related to the health effects of O3 and other photochemical oxidants.
Some issues such as attenuation of effects and the acute/chronic relation-
ship involve more than one health effect, while other issues involve
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VI1-2,6
multiple pollutants. Detailed discussion of the individual studies
associated with these issues can be found in chapters 10 to 12 of the CP.
1. Attenuation of Acute Pulmonary Effects
Attenuation of acute pulmonary response to O3 after repeated daily
exposures to O3 is a well-established and well-documented phenomenon.
Until recently, descriptive terms other than attenuation had commonly
been used to describe the response, such as "adaptation" and "tolerance".
These terms imply a reduced impact of repeated exposure to O3 whereas
recent evidence suggests that lung injury continues during the process of
attenuation.
A thorough review of the large body of supporting evidence can be
found in the CD (p. 11-44 to 11-57). Table VII-2 (CD, p. 11-45) summarizes
lung function changes following repeated exposure to O3 and demonstrates
the process of FEVj attenuation. As can be seen in the table, functional
decrements are generally greater on the second exposure day; by the fourth
or fifth day of exposure, small or no decrements are observed (Farrell et
al., 1979; Horvath et al., 1981; Kulle et al., 1982b; Linn et al., 1982b).
Attenuation of functional response to a particular O3 level does not
attenuate response to higher O3 levels, nor is the attenuation process
permanent. Subjects repeatedly exposed to 0.2 ppm O3 for five days
exhibited attenuation to that level of O3 but showed no attenuation of
response to higher (0.42 or 0.50 ppm) O3 levels (Gliner et al., 1983).
Once full attenuation is achieved it does not continue for more than 3 to
7 days for most subjects (Horvath et al., 1981; Kulle et al., 1982b; Linn
et al., 1982b), however, partial attenuation has been shown to persist
for as long as 2 weeks (Horvath et al., 1981). Attenuation of symptoms
correlates with magnitude of functional response but may last for as long
-------
TABLE VI1-2CHANGES IN LUNG FUNCTION AFTER REPEATED DAILY EXPOSURE TO AMBIENT OZONE
Ozone b
Concentration Measurement ' Exposure duration No. of Percent change In FEVj.0 on
tig/a* ppa aethod and activity subjects consecutive exposure days References
First
Second
Third
Fourth
Fifth
392
0.2
CHEM, N8KI
2
hr,
IE(30)
10
+1.4
~2.7
-1.6
---
—
FolInsbee et al., 1980
392
0.2
UV, UV
2
hr,
IE(18 & 30)
21
-3.0
-4.5
-1.1
—
—
Gllner et al., 1983
392
0.2
UV, UV
2
hr,
IE(18 & 30)
9d
-8.7
-10.1
-3.2
—
---
Gliner et al., 1983
686
0.35
CHEM, NBKI
2
hr,
IE(30)
10
-5.3
-5.0
-2.2
—
...
Folinsbee et al., 1980
784
0.4
CHEM, NBKI & MAST, NBKI
3
hr,
IE(4-5 x R)
14
-10.2
-14.0
-4.7
-3.2
-2.0
Farrell et al., 1979
784
0.4
CHEM, NBKI & MAST, NBKI
3
hr,
IE(4-5 x R)
13e
-9.2
-10.8
-5.3
-0.7
-1.0
Kulle et al., 1982b
784
0.4
CHEM, NBKI & MAST, NBKI
3
hr,
IE(4-5 x R)
ue
-8.8
-12.9
-4.1
-3.0
-1.6
Kulle et al., 1982b
784
0.4
UV, NBKI
2
hr,
IE(2 x R)
7f
ttt
t
0
Dlaeo et al., 1981
804
0.41
CHEM, NBKI & UV, UV
3
hr,
IE(4—5 x R)
209
-2.8
-0.9
0
-0.6
-1.1
Kulle et al., 1984
823
0.42
UV, UV
2
hr,
IE(30)
24
-21.1
-26.4
-18.0
-6.3
-2.3
Horvath et al., 1981
921
0.47
UV, UV
2
hr.
IE(3 x R)
ll(7)h
-11.4
-22.9
-11.9
-4.3
—
Linn et al., 1982b
980
0.5
CHEM, NBKI
2
hr.
IE(30)
8
-8.7
-16.5
-3.5
...
—
Follnsbee et al., 1980
980
0.5
CHEM, NBKI
2
5 hr, IE(2 x R)
6
-2.7
-4.9
-2.4
-0.7
—
Hackney et al., 1977a
*Measureaent Methods: MAST = KI-cou1oaetr1c (Mast aeter); CHEM = gas-phase chealluminescence, UV = ultraviolet photoaetry.
^Calibration aethods: NBKI = neutral buffered potasslua Iodide; UV = UV photoaetry.
cExposure duration and Intermittent exercise (IE) Intensity were variable; ainute ventilation (Vf) given in L/aln or as a aultlple of resting
ventilation.
^Subjects especially sensitive on prior exposure to 0.42 ppa 03 as evidenced by a decrease in FEVi-0 of aore than 20%.
These nine subjects are a subset of the total group of 21 Individuals used in this study.
eBronch1al reactivity to a aethacholine challenge was also studied.
f \
Bronchial reactivity to a hlstaalne challenge (no data on FEVi-0). SR aeasured (t). Note that on third
day hlstaalne response was equivalent to that observed 1n filtered air (see text).
^Subjects were saokers with chronic bronchitis.
hSeven subjects coapleted entire experiaent.
-------
VI1-28
as 4 weeks (Linn et al., 1982b). Thus individuals living in areas with
high O3 peaks may develop attenuated response to repeated lower O3 levels
and still respond to peak exposures, but after exposure to O3 ceases the
attenuated response eventually will return to normal.
Attenuation of functional or symptomatic response does not necessarily
imply attenuation of morphological or biochemical response. "Responses to O3,
whether functional, biochemical, or morphological, have the potential for
undergoing changes during repeated or continuous exposure. There 1s
interplay between tissue inflammation, hyperresponslveness, ensuing injury
(damage), repair processes, and changes in response. The initial response
followed by its attenuation may be viewed as sequential states in a con-
tinuing process of lung injury and repair" (CO,p. 13-41). Regulatory
implications of attenuation, therefore, are that this response 1s not a
protective mechanism but may in fact result in an Increased O3 dose to
the deep lungs and potentially cause greater tissue damage by permitting
individuals to exercise outdoors 1n high O3 levels.
2. Relationship Between Acute and Chronic Effects
In order to better assess attenuation of pulmonary responsiveness to
O3 and other effects of O3 which may not be reversible, it is Important to
understand the relationship between acute and chronic effects. Although
animal research provides some evidence, little is known with certainty
regarding either long-term implications of acute O3 exposures or chronic
effects of prolonged exposure of humans to O3. Human chamber studies
Involving long-term exposures to O3 have not been conducted due to concern
for serious health effects which may develop 1n subjects.
Various pulmonary effects demonstrated in animal studies suggest that
recovery from chronic exposure to O3 is not complete even after an extended
-------
VI1-29
period. Monkeys exposed to 0.64 ppm O3 for as long as a year (8 hr/day,
7 days/wk) continued to show either statistically significant or substantial
decreases in lung function (e.g. static lung compliance) even after a 3
mo. post-exposure period (Wegner, 1982). This was interpreted as suggesting
recovery was not complete even after three months. In several studies,
increases in lung collagen content occurred after short- and long-term
exposures to 1.0 ppm O3 (Last et al., 1979; Last and Greenberg, 1980;
Last et al., 1981; Last et al., 1984b). Adult and weanling rats exposed
for 6 and 13 weeks and monkeys exposed for one year to O3 below 1.0 ppm
showed Increased lung collagen content, and even six weeks post-exposure
weanling rats continued to show increases in collagen (Last et al.,
1984b). This suggests that damage continued during the post-exposure
period.
Significant structural alterations in the centriacinar region of the
lungs have been reported for long-term exposures of rats (Boorman et al.,
1980; Moore and Schwartz, 1981; Barry et al., 1983), monkeys (Eustis et
al., 1981), and dogs (Freeman et al., 1973). "Continuation of the
centriacinar inflammatory process during long-term O3 exposures is
especially important, as it appears to be correlated with remodeling of
the centriacinar airways (Boorman et al., 1980; Moore and Schwartz,
1981; Fujinaka et al., 1985). There is morphometric (Fujinaka et al.,
1985), morphologic (Freeman et al., 1973), and functional evidence
(Costa et al., 1983; Wegner, 1982) of distal airway narrowing. Con-
tinuation of the inflammation also appears to be correlated with the
increased lung collagen content (Last et al., 1979; Boorman et al., 1980;
Moore and Schwartz, 1981; Last et al., 1984b) that morphologically appears
predominantly in centriacinar regions of the lung (CO, p. 13-47)."
-------
VI1-30
Even though the above and numerous other animal studies show structural
changes caused by repeated short-term and long-term O3 exposures, there
1s no evidence of emphysema 1n animals exposed to O3 according to the CO.
Reevaluatlon of three studies (P'an et al., 1972; Freeman et al., 1974;
Stephens et al., 1976) cited 1n the 1978 criteria document (U.S. EPA,
1978), which reported emphysema 1n animals after prolonged exposure to
<1 ppm O3, indicates no evidence for these claims using a current definition
for emphysema. ("Emphysema 1s defined in anatomical terms as enlargement
of the gas-exchang1ng part of the lung (the acinus) accompanied by destruction
of respiratory tissue (Thurlbeck, 1984).") No similar studies have confirmed
emphysematous changes 1n O3 exposed animals since 1978 (CD, p. 13-47),
however, exceedingly few similar studies have been reported.
Until the degree of uncertainty associated with using animal studies
to estimate human effects and effect levels 1s substantially reduced or
methods are devised to study humans during long-term exposures to O3,
the relationship between acute and chronic response to O3 will remain
unclear. However, further discussion with CASAC of such issues as the
current definitions of emphysema, pre-emphysematous lesions, and lung
fibrosis may help to clarify some of the uncertainty.
3. Effects of Other Photochemical Oxidants
It has been postulated that oxidants such as peroxy acetyl nitrate
(PAN) and hydrogen peroxide (H2O2) may play a role in producing health
effects associated with photochemical oxidant exposures. While relatively
few controlled human exposure or animal toxicology studies routinely
have investigated these pollutants, field and epidemiology studies evaluate
mixtures of pollutants thus making 1t difficult to judge which oxidant
caused effects.
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VI1-31
No significant effects have been reported in controlled exposures of
Intermittently exercising healthy young and middle-aged males to PAN
concentrations of 0.25 to 0.30 ppm (Drinkwater et al., 1974; Raven et
al., 1974a,b, 1976; Gliner et al., 1975). Only one study suggested a
possible simultaneous effect of PAN (.3 ppm) and O3 (.45 ppm) (Drechsler-Parks
et al., 1984), but as with the other studies, this occurred at PAN
concentrations much higher than those reported for relatively high oxidant
areas (0.037 ppm). Except for an association of PAN with eye irritation
(Okawada et al., 1979; Altshuller, 1977; Javitz et al., 1983; U.S. EPA,
1978; National Research Council, 1977) few effects of PAN have been reported.
Field and epidemiological studies also have reported few relationships
between health effects and PAN, while animal toxicology studies suggest
that only very high PAN concentrations produce effects in animals, such as
significant alterations in host pulmonary defenses (Thomas et al., 1979,
1981a). Review of the literature on effects of PAN can be found in the
CD (pp. 11-80 to 11-84).
Even fewer studies on the health effects of H2O2 are available. No
significant effects were observed 1n rats exposed for 7 days to 0.5 ppm H2O2
in the presence of ammonium sulfate; it fs generally assumed to not
penetrate into alveolar regions possibly due to the high solubility of
H2O2 (Last et al., 1982). Other studies are of little more than mechanistic
value. In conclusion, the limited evidence available suggests that at
levels found in ambient air, PAN and H2O2 are not responsible for adverse
respiratory effects of photochemical air pollution. Ozone, the most
abundant photochemical oxidant, is considered to be chiefly responsible
for the adverse health effects of oxidants largely due to the relative
abundance compared to other oxidants (CD, p. 13-64).
-------
VIII. Staff Conclusions and Recommendations
Drawing upon the evaluation of scientific information contained in the
CD, this section provides preliminary staff conclusions and recommendations
for consideration by the Administrator in selecting a pollutant indicator,
averaging time, form, and level of the primary O3 standard. It must be
emphasized that risk and exposure analyses are currently underway and will
have a bearing on staff conclusions and recommendations in a subsequent draft
of the staff paper.
A. Pollutant Indicator
When the Environmental Protection Agency promulgated in the Federal
Register (36 FR 8186) on April 30, 1971 the NAAQS for photochemical oxidants,
the scientific data base for health effects was very limited. The SchoettUn and
Landau (1961) study, which associated increased incidence of asthma attacks
with ambient photochemical oxidants, served an important role in developing
the basis for the primary photochemical oxidants standard. Subsequent health
research, however, indicated that O3 was the predominant oxidant of concern
for public health, and on February 8, 1979, the chemical designation of the
primary standard was changed from photochemical oxidants to O3 (44 FR 8202).
Since 1979, a substantial human health effects research base has established
O3 as being "...chiefly responsible for the adverse effects of photochemical
air pollutants, largely because of its relative abundance compared to other
photochemical oxidants (CD, p. 13-64)." As discussed in section VII.B.3.
of the staff paper and section 13.6 of the CD, relatively few
controlled human studies have Investigated the health significance of
peroxyacetyl nitrate (PAN) or hydrogen peroxide (H2O2). Of the controlled
human exposure studies of PAN, only one (Drechsler-Parks et al., 1984)
suggested a possible simultaneous effect of O3 and PAN. Other controlled
-------
VII1-2
studies have reported no significant effects for PAN exposures of 0.25 to
0.30 ppm, much higher than PAN levels commonly reported in high oxidant
areas (CD, p. 13-64). Because H2O2 is highly soluble in aqueous media, it
is believed that H2O2 deposits on upper airway surfaces rather than penetrating
to the alveolar region (Last et al., 1982). However, investigations of H2O2
effects in the alveolar region have not yet been reported.
Regarding interactions with other pollutants, the CD (Sec. 13.6.3)
has concluded that O3 alone is considered responsible for observed
respiratory effects reported in controlled human exposures of O3 with SO2,
NO2, CO, and H2SO4 or other particulate aerosols. Animal toxicology
studies, however, have demonstrated additive and/or possibly synergistic
effects from exposure to O3 and NO2 (e.g., increased susceptibility to bac-
terial infection, lung structure changes) and from exposure to O3 and
H2SO4 (e.g., immune defenses, lung sensitivity). With respect to field
and epidemiology studies, the CD (p. 13-67) states:
Concerns raised about the relative contribution to untoward effects
caused by pollutants other than O3 have been diminished somewhat by
direct comparative findings in exercising athletes showing no differences
in response between chamber exposures to oxidant-polluted ambient air and
purified air containing an equivalent concentration of generated O3 (Avol
et al., 1984). Nevertheless, there is still concern that combinations of
oxidant pollutants, including precursors of oxidants, contribute to the
decreased function and exacerbation of symptoms reported in asthmatics
(Whittemore and Korn, 1980; Linn et al., 1980, 1983a; Lebowitz et al.,
1982, 1983; Lebowitz, 1984; Holquin et al., 1985) and in children and
young adults (Kagawa and Toyama, 1975; Kagawa et al., 1976; Lippmann et
al., 1983; Lebowitz et al., 1982, 1983; Bock et al., 1985; Lioy et al.,
1985). Possible interactions between 63 and total suspended particulate
matter have been reported with decreased expiratory flow in children
(Lebowitz et al., 1982, 1983; Lebowitz, 1984) and adults with symptoms of
airway obstructive disease (Lebowitz et al., 1982, 1983).
Despite the apparent interactions of O3 with other pollutants as
reported in toxicology and epidemiology studies, controlled human exposure
and field studies have not consistently demonstrated that respiratory
-------
VI11-3
effects observed in combined exposure studies of O3 and other pollutants
are caused by any pollutant(s) other than O3. This divergence in the data
base does not reject the hypothesis that some portion of the human respiratory
effects associated with exposure to photochemical oxidants may be attributed
to pollutants other than O3. However, until further human research is
performed to support or refute this hypothesis, the staff believe the
case for controlling O3 as a surrogate for protecting public health from
human exposure to O3 and other photochemical oxidants remains valid.
The question of whether O3 can serve as an abatement surrogate for
controlling other photochemical oxidants has been addressed 1n the CO
(p. 13-14) with a quote from Altshuller (1983) who concluded that "the
ambient air measurements indicate that O3 may serve directionally but cannot
be expected to serve quantitatively as a surrogate for the other products."
This conclusion appears to apply to the subset of photochemical products
of concern - O3, PAN, PPN, and H2O2 - identified 1n the CD, even though
Altshuller (1983) examined the use of O3 as an abatement surrogate for
all photochemical products (CD, p. 13-14). Lack of a quantitative,
monotonic relationship between O3 and other photochemical oxidants 1s
discussed 1n Chapter 5 and demonstrated in Table 13-2 of the CD in which
average PAN/O3 ratios for different sites and years vary from 9 to 3.
In addition, it is emphasized 1n the CD (p. 13-15) that no single measurement
methodology can quantitatively and reliably measure photochemical oxidants,
either individually or in ambient air mixtures.
In spite of the above limitations, it 1s generally recognized that control
of ambient O3 levels currently provides the best means of controlling
photochemical oxidants of potential health concern (O3, PAN, PPN, and H2O2).
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VI11-4
This recognition along with a controlled-exposure, human health data base,
which Implicates only O3 among the photochemical oxidants at levels
reported In ambient air, supports the recommendation that O3 be retained
as the pollutant Indicator for controlling ambient concentrations of
photochemical oxidants. Unless significant additional evidence which
demonstrates human health effects from exposure to ambient levels of non-
03 oxidants becomes available, It Is the staff's recommendation that
O3 remain as the surrogate for protection of public health from exposure
to all photochemical oxidants.
B. Form of the Standard
The current primary O3 NAAQS 1s expressed as an hourly average which
1s the concentration not to be exceeded on more than 1 day per year on average.
During the last standard review the decision was made to change from the
deterministic to the statistical form of the standard. The deterministic
form, which permitted only a single hourly exceedance of the standard level
1n any given year, did not adequately deal with the variations 1n O3
concentrations which are largely due to the random nature of meteorological
factors affecting formation and dispersion of O3 1n the atmosphere. In
addition, EPA further modified the standard so that one expected exceedance
would be given a dally Interpretation; that 1s, a day with two hourly
values over the standard level counts as one exceedance of the standard
level rather than two. It 1s recommended that the statistical form
(I.e., a number of 1 expected exceedances allowed per year) be retained for
the primary standard.
The Administrator may choose to establish a longer-term (e.g., monthly,
seasonal or annual) standard, as discussed 1n the following section on
averaging times. The relationships among various longer-term O3 ambient
-------
VIII-5
concentrations and existing one-hour concentrations is discussed in Appendix
A as well as in the following section.
C. Averaging Times
Exposure durations for studies reporting effects at or near ambient O3
levels fall Into two general categor1es--short-term (1 to 3 hours) and
longer-term exposures (days to months). Controlled chamber and field
studies of acute pulmonary effects of O3 have reported statistically
significant impairment of group mean lung function at O3 concentrations
_< 0.25 ppm for exposure durations of 1 to 2 hours (McDonnell et. al., 1983,
1985a,b,c; Kulle et al., 1985; Folinsbee et. al., 1984; Avol et al., 1983,
1984, 1985a,b). Subchronic and chronic exposure studies have reported a variety
of pulmonary and extrapulmonary effects for O3 exposure durations ranging
from days to years, but for ethical reasons these studies have been performed
using only animal subjects.
As was the case during the 1978 review of the ambient O3 standards, acute
effects of O3 documented in controlled human studies continue to provide
the most quantitative and strongest support for primary O3 standards
(Table VII-1, staff paper section VII.A.). Although O3 exposures continue in
these studies for 1 to 2 hours, periods of intermittent exercise during
exposure at 15 to 30 minute intervals have caused effects to occur at much
lower O3 levels than for resting subjects. It has been demonstrated that
maximum impairment of lung function occurred during or immediately after
the exercise period (Folinsbee et. al., 1977). Although some individuals
may exercise outdoors for extended periods most, do not exercise for 1-hour
or longer periods; therefore, the maximum impact of O3 for most individuals
probably occurs after a somewhat shorter time period. While consideration
may be given to standards with averaging times of less than one hour,
-------
viri-6
sufficient data do not exist to analyze such standards. As shown in Section
V, most of the alternative O3 standards investigated reduce the probability
of experiencing a high acute O3 exposure.
Epidemiology studies also provide evidence of respiratory impairment,
but interpretation of exposure averaging times associated with effects
remains uncertain. Associations have been reported between ambient O3
levels and asthma attacks (Whlttemore and Korn, 1980; Holguln et al.t 1985;
Contant et al., 1985), hospital admissions for respiratory effects (Rates
and S1zto, 1983), and lung function decrements (Lebowitz et al., 1983;
Lebowitz, 1984; Uppmann et al., 1983; Bock et al., 1985; Lioy et al.,
1985). In spite of the Inherent exposure and environmental uncertainties
of these studies, they provide human evidence for more serious health
effects which may be related to exposure averaging times somewhat longer
than the apparently transitory effects reported for 1 to 2 hour exposures
in most controlled exposure studies. In particular Hoy et al. (1985)
have reported that healthy, active children (age 7-13) experience "a persistent
decrement 1n function lasting for as much as a week after the end of a smog
period of about four days." While the implications of this persistent
shift in lung function are potentially very important, the staff believe
1t is premature to suggest a need for a multiple-day standard until further
evidence is available due to the lack of confirmation in controlled human
studies of repeated O3 exposures.
Much greater uncertainty exists for extrapolation to humans of effects
levels and averaging times associated with chronic or multiple exposures to
O3 observed 1n animal toxicology studies. Although the animal toxicology
data base which documents most of these chronic effects provides extensive
support for effects more serious than lung function decrements, uncertainties
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VI11-7
regarding dosimetry and species sensitivity must be addressed in any extrapolation
to an effect level in humans. Animal studies investigating continuous and
intermittent exposure to O3 lasting weeks to years have reported changes
in lung function and volume (6 weeks to 1 year), morphological alterations
(6 weeks to 18 months), biochemical changes (6 weeks to 1 year), and various
extrapulmonary effects (up to 1 year). With respect to some of these
alterations (e.g., lung function, biochemistry) the postexposure period
has been reported to be one of continued damage rather than complete recovery
(CO, pp. 13-46).
Although evidence demonstratlng effects of subchronic and chronic
exposure to O3 cannot be directly extrapolated to human effect levels
without consideration of the significant scientific uncertainties, there
remains a need to protect the public against longer-term exposures. This
protection could be provided by setting a separate 24-hour, seasonal, or
annual standard or by setting the short-term 1-hr standard at a level which
reduces the probability of experiencing an unacceptable chronic exposure
(see Appendix A).
D. Level of the Primary Standard
In selecting the level of the primary NAAQS for O3, the Administrator
is faced with consideration of a large and diverse health data base.
Judgments regarding the scientific quality and strength of that data base
already have been made 1n Chapters 10 to 13 of the CD. The preliminary
assessment of health effects attributed to O3 presented 1n Section VII of
this staff paper suggests a hierarchy of effects based on the strength of
data and discusses seriousness of effects observed. In addition to establishing
a lowest observed effects level from these health data, consideration must
be given to the uncertain evidence which supports a margin of safety which
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vrii-8
adequately protects public health. Ultimately, the Administrator must judge
which of the health effects attributed to O3 should be considered adverse
before a final judgment on the level of the O3 primary standard can be
made. Although scientific literature supports the conclusion that particular
O3 concentrations and exposure patterns may pose risks to human health, scientific
data can only identify the limits of a range within which a standard should
be set. Specific numeric standard levels, frequency of allowable exceedance, and
averaging times-are largely a public policy judgment.
This section draws conclusions regarding the scientific literature
used by staff to identify a lowest observed effects level for short-term
health effects attributed to O3. In addition, the more uncertain or less-
quantified evidence, which forms the basis for a margin of safety, is
considered for use in recommending short-term O3 standard options. Although
concern has been expressed for the very serious effects reported 1n long-term
animal exposure studies, the major uncertainties associated with dosimetry
and species sensitivity differences limit direct quantitative extrapolation
of effects in animals to human health effects at this time. A risk assessment
is being conducted and may provide further support for the need to protect
the public from health effects caused by long-term exposures to O3. Although
the focus of this staff paper 1s on short-term standard options, a subsequent
draft of the staff paper may better utilize long-term exposure data through
the use of risk assessment.
The strongest evidence of human health effects from exposure to O3
comes from controlled human exposure studies because O3 exposures are
known fairly accurately, other pollutants are not present, temperature and
humidity are monitored, and human subjects are used. Field studies also
provide strong evidence for similar reasons with the exception that other
-------
viri-9
ambient pollutants are present during exposure. This exception, however,
can provide support for effects occurring under real ambient conditions.
The ethical limitations of controlled human exposure and field studies
(e.g. restriction to short-term exposures, non-invasive techniques, and
limited use of infectious agents) have prevented investigation in humans of
the more serious acute and chronic exposure effects which have been reported
in animal toxicology studies. Although epidemiology studies provide
associations between health effects and "real world" ambient exposures to
photochemical oxidant pollution, the available studies provide less certain
exposure-response evidence than the controlled-exposure and field studies
and are relied on less in establishing a lowest observed effects level for 03.
Staff conclusions regarding health effects of O3 are presented below.
They are based upon the scientific review in chapters 10 to 13 of the CD
and upon the preliminary assessment in Section VII of this staff paper.
These conclusions are as follows:
1. Statistically significant group mean decrements in FEVi, representing
alterations in lung function, have been demonstrated following one and two
hour exposures of healthy, exercising children, adolescents and young adults to
O3 concentrations in the range of 0.12 to 0.16 ppm. As summarized in
Table VII-1, statistically significant FEVj decrements have been reported
in controlled exposure studies of intermittently, heavily exercising,
healthy children exposed for two hours to 0.12 ppm O3 and of continuously
heavily exercising, healthy adults exposed for one hour to 0.16 (McDonnell
et al., 1985b; Avol et al.t 1984). Field studies have demonstrated that
statistically significant group mean FEV^ decrements have been induced in
continuously heavily exercising, healthy adolescents at mean ambient O3
levels of 0.144 ppm and in continuously heavily exercising, healthy adults
-------
VIII-10
at mean ambient O3 levels of 0.153 and 0.165 ppm (Avol et al., 1985a,b;
Avol et al., 1984; Avol et al., 1983; Linn et al., 1983).
2. Analysis of group mean decrements in FEVi during 2-hr O3 exposures,
as compiled in Chapter 13 of the CD (pp. 13-27), suggests that exposure to
0.2 ppm 0^ will decrease FEVi by 1.6% during intermittent light exercise, by
2.4% during moderate exercise, by 2.8% during heavy exercise, and by 4.7%
during very heavy exercise. While this analysis does not include the
studies which report effects following 1-hr O3 exposures and continuous
exercise, it does provide a strong case for group mean response to O3
during 2-hr of intermittent exercise. It further suggests that an upper
bound of O3 for protecting the heavily exercising, average, healthy individual
from FEV} decrements of 5% may be as high as 0.21 ppm. However, the analysis
does not permit the decision maker to assess the impact of O3 exposure on
individuals with more responsive airways or on individuals with preexisting
di sease.
3. Cumulative frequency distribution of percent decrease in FEVi due
to O3 exposures of healthy exercising adult males indicates that some
fraction of subjects tested will have greater than 10% reductions in FEVi
when exposed to 0.12 ppm O3 (See Figure VI-1). While this distribution is
based on data from only one study (McDonnell et al., 1983), similar
distributions of response have been reported in many other studies (Kulle
et al., 1985; Avol et al., 1984; Haak et al., 1984; Silverman et al., 1976).
It is not yet known whether these "responders" are a specific population
subgroup or simply represent the upper 5 to 20% of the O3 response distribution
(CD, p. 13-85). Nevertheless it is important to establish criteria for
identifying and protecting "responders" since they appear to be at increased
risk to O3 exposures.
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VI11-11
4. Exacerbation of respiratory effects by interaction of other
pollutants with O3 has not yet been demonstrated in controlled human exposure
or field studies, however, epidemiology studies suggest that respiratory
effects reported near the O3 standard may be caused by O3 in combination
with other pollutants and animal studies suggest that combinations of O3 with
other pollutants may act additively or synergistical1y, depending on the
pollutants and endpoints chosen for study.
There is still concern that combinations of oxidant pollutants,
including precursors of oxidants, contribute to the decreased function
and exacerbation of symptoms reported in asthmatics (Whittemore and Korn,
1980; Linn et al., 1980, 1983a; Lebowitz et al., 1982; 1983; Lebowitz,
1984; Holguin et al., 1985) and in children and young adults (Kagawa and
Toyama, 1975; Kagawa et al., 1976; Lippmann et al., 1983; Lebowitz et
al., 1982, 1983; Bock et al., 1985; Lioy et al., 1985). Possible
interactions between O3 and total suspended particulate matter have been
reported with decreased expiratory flow in children (Lebowitz et al., 1982,
1983; Lebowitz 1984) and adults with symptoms of airways obstructive
disease (Lebowitz et al., 1982, 1983) CD, p. 13-67.
While the lack of individual exposure analysis may limit development of
quantitative exposure-response relationships in epidemiology studies, the
large body of evidence cited above supports the conclusion that ambient
pollutants other than O3 may interact with O3 to contribute to respiratory
effects reported in epidemiology studies conducted in areas with O3 levels
in the range of the current NAAQS for O3.
5. The relationship between acute and chronic respiratory effects of
O3 is not yet established, but preliminary results indicate that repeated
acute and chronic exposures to O3 may cause less reversible effects than the
apparently more transient lung function decrements produced by single one-
and two-hour exposures to O7. Persistence of lung function response in
children, as measured by peak expiratory flow rate (PEFR), has been reported
to last for as long as a week following a smog period of about four days
duration in which the 03 concentration peaks were in the range of 0.120 to
-------
VI11-12
0.185 ppm (Lioy et al., 1985). While the transient respiratory responses
reported appeared to be primarily caused by O3, the author suggested that
other pollutants such as acid sulfates may have contributed to the persistent
lung function effects. Animal toxicology research on monkeys exposed to
0.64 ppm O3 for one year provides morphometric evidence of the relationship
between functional changes and 03-induced narrowing of the peripheral
airways (Wegner, 1982; Fujinaka et al., 1985). Even after a 3-month post
exposure period the decrease in static lung compliance of 03-exposed monkeys
remained substantially different from control values, which was interpreted
by Wegner (1982) "... as an Indication that full recovery was not complete"
(CD, p. 13-46). Lung structure changes induced by O3 also have been reported
in monkeys and rats by Last et al. (1979, 1980, 1981, 1984b). Although it
appears to be premature to draw firm conclusions regarding persistent
respiratory effects associated with multiple day or longe1" term exposures
to ambient O3, the staff concludes that there is reason for concern about
respiratory function and possibly structural changes beyond the transient
pulmonary function decrements thus far reported in controlled-human exposure
and field studies.
6. Attenuation of acute pulmonary function response caused by repeated
daily exposures to O3 is a well-established phenomenon but does not
represent adaptation or tolerance. Functional decrements are greater on
the second exposure day with smaller decrements on each successive day
until the fourth or fifth day when small or no decrements are observed
(Farrell et al., 1979; Horvath et al., 1981; Kulle et al., 1982b; Linn et
al., 1982b). Attenuation of functional response, however, does not necessarily
imply attenuation of morphological or biochemical response to O3. "There
is an interplay between tissue inflammation, hyperresponsiveness, ensuing
-------
VI11-13
injury (damage), repair processes, and changes in response. The initial
response followed by its attenuation may be viewed as sequential states in
a continuing process of lung injury and repair" (CD, pp. 13-41). Attenuation
of pulmonary function or symptomatic effects, therefore, should be seen as
a human response of concern because it may result in an Increase in the
total O3 dose reaching the lungs by permitting individuals to exercise more
heavily outdoors when ambient O3 levels are high, thus resulting in continued,
and potentially greater; lung injury.
7. Work performance appears to be limited by exposure to O3; however,
too small a data base is available to quantify the magnitude of this impairment
at this time. Results of exposure to O3 during high exercise levels indicate
that discomfort may be an Important factor in limiting performance (Adams
and Schelegle, 1983; Folinsbee et al., 1984). As stated in the CD:
Subjective statements by individuals engaged 1n various sport
activities indicate that these individuals may voluntarily limit strenuous
exercise during high-oxidant concentrations. However, Increased ambient
temperature and relative humidity are also associated with episodes of
high-oxidant concentrations, and these environmental conditions may also
enhance subjective symptoms and physiological impairment during 03 exposure.
CD, pp. 11-61.
While it may be difficult to differentiate performance effects caused by O3
from those caused by other environmental conditions, exacerbation of effects
caused by O3, beyond those caused by other conditions, may prevent or
curtail normal activities and should be viewed as adversely affecting
individual performance.
8. Respiratory symptoms observed in adults acutely exposed to O3 in
controlled exposure and field studies show a close association with changes
in pulmonary function, which holds for both the time-course and magnitude
of effects. As discussed 1n the CD:
-------
VI11-14
Above 0.12 ppm O3, a variety of both respiratory and non-respiratory
symptoms have been reported in controlled exposures. They include throat
dryness, difficulty or pain in inspiring deeply, chest tightness, substernal
soreness or pain, cough, wheeze, lassitude, malaise, headache and nausea
(Delucia and Adams, 1977; Kagawa and Tsuru, 1979b; McDonnell et al.,
1983; Adams and Schelegle, 1983; Avol et al., 1984; Gibbons and Adams,
1984; Folinsbee et al., 1984; Kulle et al., 1985) CD, pp. 13-17.
Throat irritation, chest discomfort, cough, and headache in children and
young adults have been qualitatively associated with oxidant levels at
>0.10 ppm (CD, p. 13-16). In view of concern expressed by the American
Thoracic Society (ATS, 1985) for concurrent respirator function and symptomatic
effects, the staff recommends that any symptoms associated with exposure
to O3 and other photochemical oxidants be judged adverse to the extent
they curtail or otherwise interfere with the normal activities of individuals.
9. Although available laboratory evidence-tras not .yet demonstrated
that mild asthmatics are more responsive to 0^ than healthy individuals,
epidemiology provides qualitative evidence of exacerbation of asthma in adults
at ambient O3 concentrations (0.12 to 0.15 ppm) below those generally
associated with symptoms or functional changes in most healthy adults.
Whittemore and Korn (1980) and Holguln et al. (1985) found small
increases 1n the probability of asthma attacks associated with previous
attacks, decreased temperature, and incremental increases in oxidant and
O3 concentrations, respectively. Lebowitz et al. (1982, 1983) and Lebowitz
(1984) also showed effects in asthmatics, such as decreased peak expiratory
flow and increased rep1ratory symptoms, that were related to the Interaction
of O3 and temperature.CD, p. 13-54.
Uncertainties concerning Individual exposure and confounding environmental
variables limit developing exposure-response relationships with these
epidemiological data at this time and the staff recommends that these data
should be used only as a margin of safety consideration. However, until
sufficient clinical information which adequately characterizes effects of
O3 upon Individuals with more severe disease is available, the staff concludes
that the epidemiological findings suggest a need to protect asthmatics as a
-------
VI11-15
susceptible group in the population from O3 levels which may induce Increased
asthma attacks, an effect which is clearly defined as adverse by the ATS (1985)
and which the staff recommends be considered as adverse.
10. Lung structure damage induced by long-term exposures to O3 has
been demonstrated in several animal species, but due to uncertainties
associated with quantitative animal-to-human extrapolation these data
should be used at this time only as a margin of safety consideration.
Significant morphological alterations in the centriacinar region have been
reported after long-term O3 exposures of rats (Barry et al., 1983; Crapo et
al., 1984), monkeys (Eustls et al., 1981; Fujlnaka et al., 1985) and dogs
(Freeman et al., 1973). "There is morphometric (Fujlnaka et al., 1985),
morphologic (Freeman et al., 1973), and functional evidence (Costa et al.,
1983; Wegner, 1982) of distal airway narrowing" (CO, p. 13-47). Inflammation
of the centriacinar region thus appears to be correlated with lung structure
changes (Moore and Schwartz, 1981; Fujlnaka et al., 1985) and increased
lung collagen content (Last et al., 1979; 1984b; Boorman et al., 1980).
This latter effect 1s thought to suggest lung fibrosis. The previous
criteria document (U.S. EPA, 1978) cited three studies which reported
emphysema in animals exposed for long periods to <1 ppm O3; however, revaluation
based on the definition for emphysema used 1n the current CD (Section
VII.8.2) does not suggest any evidence for such claims (CD, p. 13-47).
However, increases 1n lung collagen content clearly indicate lung structure
damage. While further discussion by CASAC on this subject is warranted and
requested, the large animal data base attributing morphological damage to
O3 exposure suggests concern for chronic exposures to 03.
11. Alterations of the host defense systems have been reported 1n
animals acutely and subchronlcally exposed to O3 and provide suggestive
-------
VI11-16
evidence for similar effects in humans. Respiratory systems of mammals are
normally protected from bacterial and viral Infections by the closely
integrated particle removal and Immunological defense systems. Animal
toxicology studies have demonstrated that exposure to O3 can adversely
affect these defenses. As discussed in the CD:
In these studies, short-term (3 hr) exposure to O3 at concentrations
of 0.08 to 0.10 ppm can increase the incidence of mortality from bacterial
pneumonia (Coffin et al., 1967; Ehrlich et al., 1977; Miller et al.,
1978a). Subchronic exposures to 0.1 ppm caused similar effects (Aranyi
et al., 1983). CD, p. 13-48
While 1t is generally accepted that the basic mechanisms of action are
similar in animals and humans, a more meaningful endpoint 1n humans would
be Increased prevalence of acute respiratory disease in the community. It
should be noted that a number of other factors may Influence the O3 levels
at which respiratory disease becomes apparent (e.g., nutrition, stress,
preexisting disease). Despite these factors and a lack of experimental
confirmation in humans, "... one could hypothesize that humans exposed to
O3 could experience decrements in host defenses, but at the present time
one cannot predict the exact concentration at which effects occur 1n humans
or the severity of the effect" (CD, p, 13-49). However, until further
analysis quantifies uncertainty associated with use of animal data on
altered immune defenses, the staff recommends that these data be used only
as a margin of safety consideration.
12. Extrapulmonary effects of 0^ reported in animal studies include
alterations 1n red blood cell structure and enzyme activity, cytogenetic
effects, and limitations in vigilance, in addition to limited evidence for
cardiovascular, reproductive, teratological, endocrine system, and liver
metabolism effects. However, because these data are of uncertain physiological
Importance and current knowledge does not permit extrapolation to humans,
-------
VI11-17
the implications of these findings for human health are dificult to judge.
Until further analysis better establishes the physiological significance of
these effects on human health, the staff recommends that these effects data
be used only as margin of safety considerations.
13. Factors which have been demonstrated to affect susceptibility to
(h exposure are activity level and environmental stress (e.g., humidity,
high temperature). Those factors which either have not been
adequately tested and remain uncertain include age, sex, nutrition, and
smoking status.
14. Three groups have been identified as being "potentially at-risk"
from exposure to O3: (1) that subgroup of the general population characterized
as having preexisting respiratory disease. (2) responsive Individuals who
experience significantly greater decrements 1n lung function from exposure
to O3 than the average response of groups studied, and (3) those individuals
whose activities outdoors result in Increases in minute ventilation (CO, p.
13-84 to 13-86).
In conclusion, the short-term controlled exposure and field studies suggest
a lowest observed effects level for pulmonary function and symptoms for
healthy, exercising subjects in the range of 0.12 to 0.16 ppm O3 for an
averaging time of one to two hours. Uncertainty associated with assessment
of epidemiology and animal data prevents identifying a lowest observed
effects level for longer-term exposures at this time. The more serious
chronic effects which have been reported (e.g. lung structure changes,
increased susceptibility to infection) are being addressed in a risk assessment,
which should provide additional guidance 1n developing standards which
provide an adequate margin of safety.
Factors which staff believe should be considered in developing standard(s)
which provide an adequate a margin of safety are:
-------
VI11-18
(1) the possibility that Individuals with pre-existing respiratory disease
may experience effects at levels below those producing effects in healthy
subjects;
(2) exacerbation of respiratory effects by other pollutants in
combination with O3 during ambient exposures;
(3) attenuation of pulmonary function decrements may increase O3 dose
inhaled and result in more serious effects;
(4) work performance may be limited by exposure to O3;
(5) evidence of exacerbation of asthma at ambient O3 concentrations
(0.12 to 0.15 ppm);
(6) evidence indicating that repeated acute and chronic exposures to
O3 may cause lung structure damage;
(7) evidence of increased susceptibility to infection;
(8) extrapulmonary effects of O3 which are of uncertain biological
importance; and
(9) potentially "at risk" groups that have not been adequately tested.
E. Summary of Staff Recommendations
Based upon the staff conclusions drawn in Sections VlllA-D, the following
staff recommendations regarding the primary ozone standard are as follows:
1. In consideration of the large base of health information attributing
effects to O3 exposure and the lack of evidence which demonstrates human
health effects from exposure to ambient levels of non-03 photochemical
oxidants, staff recommends that O3 remain as the surrogate for controlling
ambient concentrations of photochemical oxidants.
2. Because the strongest and most quantitative health evidence being
used in support of the primary O3 standard is from controlled exposure
-------
vrrr-19
studies involving short-term (1- and 2-hr) exposures, it is recommended that
the 1-hr averaging time be retained. Although there are many epidemiology
studies which have identified health effects associated with O3 exposures
having much longer than one-hour averaging times, there remains great
uncertainty about which exposure characteristics (e.g., level, time, repeated
peaks) are most important. Among the more serious effects of concern are
persistent changes in lung function, aggravation of respiratory disease,
and increased hospital admissions associated with O3 levels near the current
NAAOS. In addition, other evidence reported in animal toxicology studies
suggest lung structure damage, increased susceptibility to respiratory
infection, and a variety of extrapulmonary effects following long-term
exposures to O3. The seriousness of these effects Indicates a need to
protect public health from ambient O3 exposures which reasonably can be expected
to induce such effects in humans. This protection could be provided by
setting a separate 24-hour, seasonal, monthly or annual standard. OAQPS
is currently analyzing whether it is possible to set the short-term standard
at a level which reduces the probability of experiencing an unacceptable
chronic exposure. As discussed in Appendix A (p. A-9), there is a marginally
statistically significant association (p<.05) between short- and long-term
O3 indices. (For example, a second-high daily maximum of 0.12 ppm hourly
average 1s associated with a daily daylight seasonaT mean of 0.039 ppm, and
there is a 68% chance of the daily daylight seasonal mean being between
0.028 and 0.052 ppm). The alternative of setting a separate standard could
involve quantlflcatlon of uncertainty associated with interpreting epidemiology
and animal toxicology data such as is currently being done 1n a risk assessment.
Otherwise further human research and development of animal extrapolation
models wiTI be required before an appropriate long-term standard can be
-------
VI11-20
recommended. With this association and the need for protection from long-term
exposures in mind, comment and guidance is sought from CASAC and the public
on the need for a separate long-term primary standard.
3. The current primary O3 NAAQS 1s attained when the expected
number of days per calendar year with maximum hourly average concentrations
above the level of the standard is equal to or less than one (44 FR 8202).
Staff recommends that these attributes of the O3 standard be retained.
4. Based on a staff assessment of the short-term controlled exposure,
field, epidemiology, and animal toxicology data, the range of 1-hour O3
levels of concern for standard-setting purposes is 0.08 ppm to 0.14 ppm.
The upper end of this range (0.14 ppm) represents the approximate O3 exposure
concentrations measured in controlled exposure and field studies 1n which
healthy, heavily exercising children, adolescents, and young adults have
experienced statistically significant, though small group mean decrements
in lung function. Larger individual decrements have been reported in these
studies with cumulative frequency distributions suggesting that some fraction
of subjects experiences FEV} decrements greater than 10%. Cough and lower
respiratory symptoms also have been reported 1n these studies near the
upper end of the range. Epidemiology studies provide suggestive evidence
of lung function impairment at similar or lower exposure levels, though
they are limited by uncertainties concerning exposure levels and presence
of other pollutants. Other epidemiology studies have provided evidence of
aggravation of asthma and airway obstructive disease, again limited by
uncertainties about individual exposure and other pollutants. Given the
uncertainties of extrapolating these findings to the U.S. population and
the fact that the effects of O3 on individuals with preexisting respiratory
disease have not yet been fully characterized, the staff believe that the
-------
VI11-21
upper end of the above range contains little or no identifiable margin of
safety. These uncertainties and the nature of potential effects are Important
margin of safety considerations. Neither the less certain evidence provided
by animal toxicology studies (e.g. Increased susceptibility to lung infection,
lung structure and biochemical changes, and extrapulmonary effects) nor
other epidemiology evidence suggesting respiratory effects In children and
susceptible groups provides scientific support for health risks of consequence
below 0.08 ppm for short-term exposures. These less certain data as well
as information contained in the exposure analysis should be considered in
evaluating the margin of safety provided by alternative standards in the
range of 0.08 to 0.14 ppm.
The importance of lung function Impalement in evaluating the lowest
observed effects level for short-term controlled exposures to O3 is apparent.
This effect 1s transient lasting from a few hours to as much as two days
after exposure to O3 ceases for most individuals. Statistically significant
group mean decrements of lung function do not occur in healthy subjects
tested in the range of 0.12 to 0.18 ppm O3 unless they are exposed during
very heavy exercise similar to competitive running. It has been argued
also that the magnitude of the lung function decrements reported for low-level
O3 exposures are similar to those experienced by individuals commonly
exposed to other stresses such as cold or hot temperatures, high humidity,
and physical stress. Clearly the most quantitative and certain evidence of
short-term O3 health effects is lung function impairment; however, if this
effect should be deemed to be not adverse for regulatory purposes, the
remaining evidence could suggest a higher range of consideration for alternative
standards. Although the ultimate determination of the adversity of this
effect is the prerogative of the Administrator, it is requested that CASAC
provide discussion and guidance on this Issue.
-------
IX. Critical Elements in the Review of the Secondary Standard for Ozone
This section reviews and assesses research on welfare effects attributed
to O3 and other photochemical oxidants as summarized in Air Quality Criteria
for Ozone and Other Photochemical Oxidants (CD). Where possible, judgments
are provided which identify adverse effects and levels of these effects for
secondary-standard setting.
Important categories with respect to welfare include agricultural
vegetation effects (e.g., yield loss), natural ecosystem effects, personal
comfort and well-being effects, and materials damage. Because the possible
indirect contributions of the photochemical oxidants to visibility degradation,
climatic changes, and acidic deposition cannot at present be quantified,
these atmospheric effects and phenomena are not addressed in this document
(CD, p. 1-1). They have been addressed, however, in other recent air quality
documents (U.S. EPA, 1982a,b). The approach taken in this staff paper is:
1) to describe each type of O3 effect, 2) to discuss what is known regarding
dose-response relationships of O3 exposure, and 3) to evaluate the factors
which should be considered in selecting the level, averaging time and form of
the secondary NAAQS for O3. Discussions of the status of the rural O3 exposure
analysis, the O3 economic analyses, and the welfare risk assessment are
included, but these analyses are as yet incomplete, requiring significant
additional development.
A. Mechanisms of Action for Vegetation
The responses of vascular plants to O3 may be viewed as the
culmination of a sequence of physical, biochemical and physiological events.
For ambient O3 to exert a phototoxic effect, it must first diffuse into the
plant. Such an effect will occur only if a sufficient amount of O3 reaches
the sensitive cellular sites within the leaf. Ozone from the ambient air
-------
IX -2
into the leaf space through the stomata, which can exert some control on O3
uptake to the active sites within the leaf. Once within the leaf, O3 qui ckly
dissolves 1n the aqueous layer on the cells lining the air spaces. Ozone or
Its decomposition products then diffuse through the cell wall and membrane
into the cell, where it may affect cellular or organellar processes. Ozone
injury will not occur if 1) the rate of O3 uptake 1s sufficiently small so
that the plant 1s able to detoxify O3 or Its metabolites or 2) the plant 1s
able to repair or compensate for the O3 Impacts (Ungey and Taylor, 1982).
The uptake and movement of O3 to the sensitive cellular sites are subject to
various, physiological and biochemical controls (CD, p. 7-20).
At any point along this pathway, O3 or its decomposition products may
react with cellular components. Altered cell structure and function may
result in changes in membrane permeability, carbon dioxide fixation, and
many secondary metabolic processes (Tlngey and Taylor, 1982). The magnitude
of the 03-lnduced effects will depend upon the physical environment and
the chemical environment of the plant (including other gaseous a1r pollutants
and a wide variety of chemicals), and biological factors (Including genetic
potential, developmental age of the plant and Interaction with plant pests).
Cellular injury manifests itself in a number of ways, including foliar injury,
premature senescence, reduced yield or growth or both, reduced plant vigor,
and sometimes death. Depending upon the intended use of a plant species (for
food, forage, fiber, shelter, or amenity), any of these effects discussed
above could constitute a "welfare" effect with potentially adverse effects on
soc1 ety.
1. Biochemical Response
When O3 passes into the liquid phase, It undergoes transformations
that yield a variety of free radicals (e.g., superoxide and hydroxy! radicals).
-------
IX-3
Whether these species result from decomposition of O3 or reactions between
O3 and biochemicals in the extracellular fluid has not been determined.
Ozone or its decomposition products, or both, will then react with cellular
components, resulting in structural and/or functional effects.
The potential for O3, directly or indirectly, to oxidize biochemicals
in vitro has been demonstrated. Ozone can oxidize several classes of
biochemicals including nucleotides, proteins, some amino acids and various
lipids. Data acquired from in vitro studies are best utilized to demonstrate
that many cellular constituents are susceptible to oxidation by O3. New
approaches are needed to assess the full range of in vivo biochemical
changes caused by O3. (See CD, Section 7.3.1.3 for further details.)
2. Physiological Responses
Physiological responses have been more useful than biochemical
changes in characterizing cell responses to oxidants (CD, p. 7-26). Many
consider membranes to be the primary site of action of O3 (Heath, 1980;
Tingey and Taylor, 1982). Whether the plasma membrane or some organelle
membrane is the primary site of O3 action is open to speculation (Tingey
and Taylor, 1982). However, the alteration in plasma membrane function is
clearly an early step in a series of 03-induced events that eventually
leads to leaf injury and subsequent yield loss.
The effect of O3 on key steps in photosynthesis has been measured for
several plant species as shown in Table IX-1 (CD, 7-28). Reductions in
photosynthesis may reflect the direct impairment of chloroplast function or
reduced CO2 uptake resulting from 03-induced stomatal closure, or both.
Regardless of the mechanism, a sustained reduction in photosynthesis will
ultimately affect growth, yield, and vigor of plants. Some examples of
03-induced reduction in apparent photosynthesis at exceeding 0.25 ppm are
-------
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4 kr dally/2 days
4 kr dally/2 days
).l or It
10/10 days
1.4 k
Cuwlatlva
dot* avtr
1.2.1 yr.
IS
1^
$
n"
«|C
10"
3
sr
Mat slg.
different
*0h
22C
30 t 10"
21 t I#
100"
40
No statistical InfaraatlaA.
Barnes, 1972a
Barnes, 1972a
Coyne and llngkaa, 1971
ItMNtl and Mill, 1974
Millar at «l., 1949
¦arms, 1972a
Vang at al., 1989
Fell and AramuM, 1971
Car Ism, 1979
Carlson, 1979
Botkln at at., 1972
Furukawa ond Kadata, 1*15
Coyne and Olnghaa, 1901
-------
IX-5
presented in Table IX-1. These data highlight the potential of O3 to
reduce primary productivity.
Several studies used (Table IX-1) exposures which are more closely
related to the ambient atmosphere. Miller et al. (1969) found that a 3-year
old ponderosa pine seedlings sustained a 25 percent reduction in apparent
photosynthesis after a 60 day exposure to an O3 concentration of 0.15 ppm
for 9 hours a day. Yang et al. (1983) exposed three clones of white pine to
O3 concentrations of 0.10, 0.20 or 0.30 ppm for 4 hours per day for 50 days
in CSTR chambers. Net photosynthesis was reduced in the foliage of sensitive
and intermediate clones by 14 to 51 percent in direct relation to O3 dose
and clonal sensitivity. Coyne and Bingham (1978) exposed field-grown snap
beans to an O3 concentration of 0.072 ppm for 4 hours a day for 18 days.
Apparent photosynthesis was reduced 18 percent in plants treated with O3.
In addition to depressing photosynthesis in the foliage of many plant
species, O3 inhibits the allocation and translocation of photosynthate
(e.g., sucrose) from the shoots to other organs (Tingey, 1974; Jacobson,
1982), often referred to as partitioning. Tingey et al. (1971a) found
that when radish plants were exposed to O3 (0.05 ppm for 8 hrs a day, 5
days per week for 5 weeks), hypocotyl (stem) growth was inhibited 50 percent
while foliage growth was inhibited only 10 percent. Ponderosa pine exposed
to 0.10 ppm O3 for 6 hours per day for 20 weeks stored significantly less
sugar and starch in their roots than did control plants (Tingey, 1976a).
Several other studies have measured this partitioning effect of O3 on
photosynthate in carrot, parsley, sweet corn, cotton and pepper (Oshima,
1973; Bennett and Oshima, 1976; Oshima et al. 1978; Oshima et al., 1979;
Bennett et al., 1979). Plants were exposed to O3 concentrations of 0.12 to
0.25 ppm for 3 to 6 hours for 0.2 percent to 7 percent of the total growth
-------
IX-6
period of all the plants. In all species but pepper, root dry weight was
depressed much more than leaf dry weight. The reduction in photosynthate
translocation to roots and the resulting decrease in root size indicate
that the plant had fewer stored reserves, possibly rendering it more sensitive
to injury from cold, heat, or water stress. When less carbohydrate is
present in roots, less energy will be available for root-related functions.
An ozone-induced suppression of nitrogen fixation by root nodules could
affect total biomass and agricultural yield, especially in areas where soil
nitrogen is low.
Reproductive capacity (flowering and seed set) is reduced by O3 in
ornamental plants, soybean, corn, wheat and some other plants (Adedipe et
al., 1972a; Feder and Campbell, 1968; Heagle et al., 1972, 1974; Shannon
and Mulchl, 1974). These data suggest that O3 impairs the ferti 1 izaf.ion
process in plants. This suggestion has been confirmed in tobacco and corn
studies using low concentrations (0.05 to 0.06 ppm) of O3 (Fede^, 1968,
Mumford, 1972). In addition to these physiological effects which are
directly related to productivity, there are many secondary metabolic responses
in a plant exposed to O3, such as increase in stress ethylene, which may
contribute to the manifestation of foliar injury (CD, p. 7-31).
B. Factors Affecting Plant Response
The magnitude of plant response to O3 exposure can be affected by
biological, physical, and chemical variables. Each plant exposed to a
given concentration of O3 will respond to a different extent depending on
such biological factors as genetics, stage of development, and presence
of pests or disease as well as such physical factors as temperature, humidity,
light intensity, and soil moisture. Chemical factors in the environment
of plants can also modify plant response by either magnifying effects, as
-------
IX-7
with multiple pollutants, or by reducing effects, as with antioxidant
sprays. All of these determinants of response can overlap, thus potentially
creating a complex myriad of causes for the effects observed.
1. Biological Factors
a. Plant Genetics
Differential susceptibility of individual plants to O3 exposure
is determined by genetic composition. Genetic variance in response to O3 is
seen among species, cultivars, and Individuals within a population. Although
foliar injury has been used as the most common measure of comparative O3
sensitivity, other measures such as yield and physiological effects substantiate
differential results based on genetic differences. In fact the relative O3
sensitivity of cultivars within a species can vary with dose and nature of
response measured (Tlngey et al:, 1972; Heagle, 1979b). Differences in
relative sensitivity of cultivars have been reported between controlled O3
exposures and ambient air field studies (Taylor, 1974; Meiners and Heggested,
1979; Hucl and Beyersdorf, 1982; DeVos et al., 1983). The nature of inherited
O3 sensitivity may help to explain this disparity. Changes 1n gene expression
during plant development and due to environmental variations may explain in
part the potential variability in plant response.
b. Developmental Factors
The stage of plant development plays a role in determining sensitivity
to O3. Just prior to or at maximum leaf expansion, plant foliage appears
to be most sensitive because stomata are functional, Intercellular spaces
are expanded, and barriers to gas exchange are minimal (CD, p. 7-34). Stages
of plant development also can be affected by O3 exposure. Premature aging
and leaf drop have been demonstrated in numerous field and controlled studies
(Menser and Street, 1962; Heggestad, 1973; Hofstra et al., 1978; Pell et al.,
-------
IX-8
1980; Reich, 1983; Mooi , 1980). The premature leaf drop and senescence
decrease the amount of photosynthate that a leaf can contribute to plant
growth. It can be concluded that the effects of O3 on the senescence process,
whenever initiated, may be responsible for many of the documented reductions
in yield (CO, p. 7-34).
c. Pathogen and Pest Interactions with Ozone
Disease has been defined as the result of a complex interaction
between host plant, environment, and pathogen; problems caused by both
pathogens and insects have been termed disease (CD, p. 7-35). Ozone can
affect the development of disease in plant populations. Laboratory evidence
suggests that O3 (at ambient concentrations or greater for 4 or more hours)
inhibits infection by pathogens and subsequent disease development (Laurence,
1981; Heagle 1982). Increases, however, in diseases from "stress pathogens"
have been noted. For example, plants exposed to O3 were more readily injured
by Botrytis than plants not exposed to O3 (Manning et al., 1970a,b; Wukasch
and Hofstra, 1977a,b; Bisessar, 1982). Both field and laboratory studies
have confirmed that the roots and cut stumps of 03-injured ponderosa and
Jeffrey pines are more readily colonized by a root rot (Heterobasidion annosus).
The degree of infection was correlated with the foliar injury (James et al.,
1980; Miller et al., 1982). Studies in the San Bernardino National Forest
showed that 03-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). At any stage of the disease cycle O3 may alter the success of
invading organism by direct effects on them or by modifying the ability of
the host plants to defend against attack.
2. Physical Factors
Environmental conditions before and during plant exposure are influential
in determining plant response. The influence of environmental factors has
-------
IX-9
been studied primarily under controlled conditions, but field observations
have substantiated the results. Factors which can potentially influence
response of plants to O3 include light intensity, temperature, relative
humidity, soil moisture, and soil fertility. Variations in one or more of
these parameters can cause plants to be more or less sensitive to O3 exposures.
The CD has identified the following generalizations concernlng the influence
of these factors on plant response (CD, p. 7-242).
a. Light conditions conducive to stomatal opening appear to enhance
O3 injury due to increased O3 absorption.
b. No consistent relationship between temperature and response to
O3 has been reported; however, plants do not appear to be as sensitive
at extremely high or low temperatures.
c. Plant injury tends to increase with increasing relative humidity
as a result of the effect of humidity on stomatal opening. McLaughlin
and Taylor (1980) demonstrated that plant absorb significantly more
O3 at high humidity than at low humidity.
d. Decreasing soil moisture increases plant water stress, and causing
a reduction in plant sensitivity to O3. The reduced O3 sensitivity
is apparently related to stomatal closure, which reduces O3 uptake
(U.S. EPA, 1978, Olszyk and Tibbitts, 1981, Tingey et al., 1982).
Water stress, however, does not provide a permanent tolerance
to O3 (Tingey et al., 1982).
3. Chemical Factors
The chemical environment of plants can include air pollutants,
herbicides, fungicides, insecticides, nematocides, antioxidants, and chemical
protectants. These factors, which may influence plant response to O3, can be
grouped into two areas: multiple pollutants and chemical sprays.
-------
IX-10
a. Multiple Pollutants
Studies indicate that the joint action of O3 and sulfur dioxide (SO2)
may cause more visible injury to plants than expected from exposure to the
individual gases (Schertz et al., 1980a,b; Beckerson and Hofstra, 1979; Olszyk
and Tibbitts, 1981). This synergism (injury enhancement) is most common at
low concentrations of each gas and when foliar injury induced by each gas,
individually, is small. At higher concentrations or when extensive injury
occurs the effects tend to be antagonistic (less than additive) (CO, p. 7-243).
Field studies have investigated the influence of SO2 on plant response
to O3. at ambient and higher concentrations for several plant species - soybean
(Heagle, et al., 1983c; Reich and Amundson, 1984), beans (Oshima, 1978;
Heggestad and Bennett, 1981), and potatoes (Foster et al., 1983b). O3 altered
plant yield, but SO2 had no significant effect and did not interact with O3
to reduce plant yield unless the SO2 exposures were much greater than typically
found in the ambient air in the U.S.
The applicability of the yield results from pollutant combination studies
to ambient conditions is not known. An analysis of ambient air monitoring
data (SAROAD, 1981; EPRI-SURE) indicate that at sites where the two pollutants
were co-monitored, ten 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 averaged concentrations of 0.05 ppm or
greater for both pollutants. At this time, it appears that most of the
studies of the effects on pollutant combinations (O3 and SOg) on plant yield
have used a longer exposure duration and a higher frequency of pollutant co-
occurrence than occur in the ambient air (CD, p. 1-66).
-------
IX-11
Only a few studies have Investigated the effects of O3 when combined
with other pollutants, and no clear trend is available. Preliminary studies
using three pollutant mixtures (O3, SO2, NO2) showed that the additions of
SO2 and NO2 (at low concentrations) caused a greater growth reduction than
O3 alone (Sanders and Reinert, 1982; Relnert and Gray, 1981).
b. Chemical Sprays
Chemical sprays long have been used to protect agricultural crops from
pests and diseases. Fungicides, herbicides, insecticides, and nematocides
control damage caused by fungus, weeds, insects, and nematodes, respectively.
They also have been shown to alter sensitivity of plants to air pollutants.
Studies of the effects of pesticides on O3 sensitivity have shown differing
results, with some chemicals (e.g., nematoxides, phenamiphos, etc) increasing
sensitivity and others (e.g., benomyl, carboxin) reducing sensitivity of
plants to O3 (Miller et al., 1976; Sung and Moore, 1979).
Antioxidants, which are commonly used to reduce rubber cracking and
food spoilage, have been reported to reduce vegetation injury caused by O3
{Kendrick et al., 1962). Addition of antioxidants to insecticides, herbicides
and fungicides have been shown to increase their effectiveness (Rubin et al.,
1980; Koiwai et al., 1977; Gilbert et al., 1977). Ethylenediurea (EDU), a
widely used antioxidant, prevented visible injury in bean plants exposed
for 150 minutes to 0.8 ppm O3 (Carnahan et al., 1978). Reduced bronzing,
delayed leaf drop, and increased yield have also been attributed to EDU (Hofst
et al., 1978; Weidensaul, 1980). Extensive testing of EDU indicates that
treatment of flowers, herbs, and woody vegetation with EDU can reduce O3
injury (Cathey and Heggestad, 1982; McClenahan, 1979). In conclusion,
many chemicals can apparently protect against ozone injury but none
appears to be sufficiently cost-effective to be used solely for this
purpose (CD, p. 7-72).
-------
X-l
X. PRELIMINARY ASSESSMENT OF WELFARE EFFECTS CONSIDERED IN SELECTING
SECONDARY STANDARD(S) FOR OZONE
Of the phytotoxic compounds commonly found in the ambient air O3
is the most prevalent, impairing crop production and injuring native
vegetation, and ecosystems more than any other air pollutant (Heck et al.,
1980). Ozone has also been shown to damage elastomers, textile fibers and
dyes and certain types of paints. Other photochemical oxidants of importance
to vegetation ecosystems and materials effects are nitrogen dioxide (NO2) and
peroxyacetyl nitrates. Air Quality Criteria for Oxides of Nitrogen (U.S.
EPA, 1982) and Review of the NAAQS for NO?: Assessment of Scientific and
Technical Information (U.S. EPA, 1984) previously assessed the phytoxicity of
NO2, and thus NOg will not be discussed in this staff paper. In addition,
while at a given dose the peroxyacetyl nitrates are more phytotoxic than
O3 (p. X-22), they generally occur at significantly lower ambient concen-
trations. Because phytotoxic concentrations of peroxyacetyl nitrates are
less widely distributed than those of O3 (CD, p. 7-1), the focus of this
staff paper will be on the effects of O3.
The objective of this section of the staff paper is to assess the current
basis for the O3 secondary NAAQS as contained in Chapters 7, 8 and 9 of the
CD to determine whether new effects information suggests any change in existing
secondary NAAQS for O3. In a future draft, the staff paper will also include
the evaluations and judgments provided by a risk assessment, which is currently
being developed. Effects on vegetation and ecosystems include physiological
and biochemical changes, foliar injury, reduction in growth and yield, and
reduction in diversity of species and primary productivity of natural ecosystems.
-------
X-2
A. Vegetation Effects
1. Types of Effects
Plant response to O3 exposure may be expressed as biochemical,
physiological, visible injury, growth, yield, reproductive and ecosystem
effects. Biochemical and physiological alterations are the basis of all
subsequent effects as described in section IX A.l. of this paper. Visible
foliar injury provides one of the earliest manifestations of short-term
effects of O3; however, measurement of visible foliar injury is not always
well correlated with reduction in growth and yield (CO, p. 7-224).
Effects on plants and plant communities are usually classified as either
injury or damage. Injury includes all plant reactions, such as reversible
changes in plant metabolism (e.g., altered photosynthesis), leaf necrosis,
altered plant quality, or reduced growth, which do not impair yield or intended
use of a plant (Guderian, 1977). Damage or yield loss involves any effect
which reduces the quantity, use, or value (e.g., aesthetic) of a plant or any
impairment in the intended use of a plant.
This section will attempt to assess the data with regard to foliar
injury effects and reductions in growth and yield. For purposes of this
staff paper, greater emphasis will be placed on damage or yield loss than
on injury. Growth and yield losses provide an important measure of the
effects of O3 because such losses impair the intended use of the plant
and generally constitute damage, where as foliar injury may or may not
be considered damage. These growth and yield loss effects have thus become
the focus of most of the exposure response models and assessments to be
discussed later.
a. Visible Foliar Injury Effects
The first documented observation of O3 injury to vegeta-
tion in the field was by Richards et al. (1958) who described O3 stipple on
-------
X-3
grape vine leaves. Other studies soon after confirmed that foliar injury was
being caused by O3 from nearby cities (Heggestad and Middleton, 1959; Daines
et al., 1960). Numerous subsequent studies have reported vegetation injury
at rural sites caused by O3 transported long distances from urban centers
(Heck et al., 1969; Kelleher and Feder, 1978; Skelly, 1980; Edinger et al.,
1982).
The symptoms caused by exposure to O3 differ on dicotytedonous (broad-
leaved) and monocotyledonous (narrow leaved) plants. Dicotyledonous plants
exposed to a high concentration of O3 for a short period of time (acute
injury) develop dark water soaked areas within a few hours due to injury of
the palisade cell membranes (CD, p. 7-79). Leaves may show partial recovery,
or these areas may form characteristic flecks or stipple when the water soaked
area dries. Flecks are small tan lesions formed when groups of palisade
and/or mesophyll cells die and the associated epidernal cells collapse (CD,
p.7-81). Individual lesions may be small, but groups of them can extend and
affect a considerable portion of the leaf. "Stipples" are small groups of
red, purple, or black palisade cells that have accumulated dark pigments
coincidentally with cell death.
Foliar injury in monocotylendenous plants generally appears as chlorotic
spots or white flecks between veins, potentially extending to form long white
or yellow steaks between parallel veins of sensitive plants. Two classic
symptoms of O3 injury in conferous plants are tipburn and chlorotic mottle.
Tipburn is characterzed as a dieback of the ends of newly elongating needles,
turning the needle tip reddish brown, and later, gray. Chlorotic mottle
results when small patches of needle tissue are injured and turn yellow,
giving the needle a mottled appearance.
-------
X-4
Of the many approaches taken to estimate the O3 levels and exposure
times required to induce these foliar injury effects, most have involved
short-term exposures (less than one day) and have measured visible injury as
the response variable. Various plant species were exposed to a range of 03
levels and exposure durations by Heck and Tingey (1971), who evaluated the
resulting data by regression analysis. Data for several species were
summarized 1n Table X-l (CD, p. 7-225) to illustrate the range of O3 levels
and exposure times required to induce 5 and 20% foliar injury on sensitive,
intermediate, and less sensitive species.
TABLE X-l. OZONE CONCENTRATIONS FOR SHORT-TERM EXPOSURE THAT PRODUCE
5 OR 20 PERCENT INJURY TO VEGETATION GROWTH UNDER SENSITIVE CONDITIONS3
Ozone Concentrations that may Produce 5% (20%) Injury:
Exposure
time, hr
Sensitive plants
Intermediate plants
Less
sensitive plants
0.5
0.35 to 0.50
(0.45 to 0.60)
0.55 to 0.70
(0.65 to 0.85)
> 0.70 (0.85)
1.0
0.15 to 0.25
(0.20 to 0.35)
0.25 to 0.40
(0.35 to 0.55)
> 0.40 (0.55)
2.0
0.09 to 0.15
(0.12 to 0.25)
0.15 to 0.25
(0.25 to 0.35)
> 0.30 (0.40)
4.0
0.04 to 0.09
(0.10 tO 0.15)
0.10 to 0.15
(0.15 to 0.30)
>_ 0.25 (0.35)
8.0
0.02 to 0.04
0.07 to 0.12
_> 0.20 (0.30)
3The concentrations 1n parenthesis are for the 20% injury level. Table
from U.S. Environmental Protection Agency (1985, p. 7-225).
-------
X-5
Limiting value analysis fs an alternative approach to estimating
O3 levels and exposure durations which induce foliar injury. Such an analysis
was performed on more than 100 studies of cultu^al crops and 18 studies
of tree species and yielded the following range of concentration and exposure
durations that were likely to induce visible injury (Jacobson, 1977):
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
Foliar Injury in sensitive plants provide a good understanding of the
occurrence of elevated O3 concentrations in a given area. Among the plants
that have been identified as indicators of pollutants are milkweed (Duchelle
and Skelly, 1981), eastern white pine (Benoit et al., 1982), ponderosa and
Jeffrey pine (Miller, 1973) Bel W-3 tobacco (Postiiumus, 1976) and lichens
(Sigal and Nash, 1983). Although the presence of visible foliar symptoms on
vegetation cannot, be directly related to 3 ri .j^owth or yield, they do
indicate that elevated levels of O3 have occurred. The detection of visible
symptoms is an indication that additional studies should be undertaken to
determine if effects on growth and yield are occurring (CO, pp. 7-88).
Despite the Importance of visible symptoms, It must be "ecognized that
long-term exposure to low pollutant concentrations may adversely affect plant
health without producing visible symptoms. Chronic Injury from this type of
exposure may be represented by reductions in growth, and/or yield, or premature
-------
X-6
senescence resulting from changes in photosynthesis, respiration, chlorophyll
content or other processes (Dochinger et al., 1970; Feder, 1978; Heck, 1966;
Posthumus, 1976).
Because plant growth and production depend on photosynthetically
functional leaves, various studies have been conducted to assess the relation-
ship 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 (Tingey et al., 1971a; Tingey and Reinart,
1975; Kress and Skelly, 1982; Adedipe et al., 1972) while others have reported
significant foliar injury without yield loss (Heagle et al., 1974; Oshirna et
al., 1975). Relative sensitivities of two potato cultivars were reversed when
judged by foliar injury versus yield reductions (Pell et al., 1980). Foliar
injury in field corn was reported at lower O3 concentrations than yield loss,
but at higher O3 levels yield loss was increased to a greater extent than
foliar injury; similarly it was reported that foliar injury was not a good
predictor of yield loss for wheat (Heagle et al., 1979a,b). Therefore,
no precise relationship exists between foliar injury and yield loss for
species of plants for which foliage is not part of the yield (CD, p. 7-143).
b. Growth and Yield Effects
As mentioned previously, growth and yield effects provide
an important measure of the effects of O3 on vegetation. For purposes of
assessing exposure-response relationships derived from the existing studies,
yield loss is defined as an impairment of or decrease in the value of the
intended use of the plant. This concept includes reduction in aesthetic
values, changes in crop quality, and occurrence of foliar injury when foliage
is the marketable part of the plant. The actual amount of yield loss due to
decreased aesthetic value or appearance may be more difficult to quantify
-------
X-7
than yield loss in weight or bulk but is extremely important for crops
such as tobacco, spinach, and ornamentals. Such effects occur at concen-
trations as low as 0.041 ppm for several weeks or 0.10 ppm for 2 hours, and
can constitute a yield loss when marketability of the plant is decreased
(Menser and Hodges, 1972).
Most of the recent studies of O3 induced yield loss have measured effects
on the weight of the marketable plant organ. These effects will be the
primary focus of this section. Studies conducted to estimate the impact of
O3 on the yield of various crop species have been grouped into two types,
depending on the experimental design and statistical methods used to analyze
the data: (1) studies that developed predictive equations relating O3 exposure
to plant response, and (2) studies comparing discrete treatment levels to a
control using analyses of variance. The advantage of the regression approach
is that it permits the estimation of the O3 impact on plant yield over the
range of concentrations, not just at the treatment means as is the case with
the analysis of variance methods.
1. Open Top Chamber Studies
Data from a series of studies conducted hy the National Crop
Loss Assessment Network (NCLAN) have been analyzed to develop predictive
equations relating 7-hour seasonal mean O3 exposures to crop yield loss.
Examples of the relationship between O3 concentration and plant yield a<-e
shown in Figure X-l (CD, p. 230) and X-2 (CD, p. 231). These cultivars/spec!es
were selected because they illustrate the kinds of exposure response that
occurs and the type of year to year variation in plant response to O3 that
may occur. The derived regression equations can be used to determine the
concentrations that would be predicted to cause a specific yield loss or to
estimate the predicted yield loss that would result from a specific O3
-------
X-8
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-------
X-9
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X-10
concentration. Both of the approaches cited above have been used to summarize
the data on crop response to O3 using the Weibull (Rawlings and Cure, 1985)
function.
As an example of response, the O3 concentrations that would be predicted
to cause a 10 to 30 percent yield loss have been estimated (Table X-2 (CO,
p. 7-232). A brief review of these data 1n the table suggest that: (1) a
10% mean yield loss 1s predicted for several species when the 7-hour seasonal
mean concentration of O3 exceeds 0.04-0.05 ppm; (2) grain crops were generally
less sensitive to O3 than other crops; (3) sensitivity differences within a
species may be as large as differences between species. In addition to
differences in sensitivity among species and cultlvars, the data in Figure X-l
and X-2 illustrate year to year variations in plant response to O3.
Although linear regression equations have been used to estimate yield
loss, there appear to be systematic deviations from the data for some species
and cultlvars even though the equations had moderate to high coefficients of
determination (R^), The use of plateau-linear, polynomial equations and the
recently developed Weibull model (Heck et al., 1983) appeared to fit the data
better. Based on available data, it 1s recommended that curve linear exposure
response functions be used to describe and analyze plant response to O3
(CD, p. 7-106).
Although NCLAN provides valuable dose-response information on a variety
of crops, the program has limitations that must also be considered. The
potential artificiality of the O3 exposure treatments may complicate the
application of results. The use of the 7-hour seasonal mean concentration,
a relatively new summary exposure statistic, makes comparisons with pre-
viously published studies difficult. It also does not accurately represent
the temporal exposure dynamics of ambient air. Although, the lack of validation
-------
X-ll
TABLE X-2. COMPILATION OF 03 CDNTRATIONS PREDICTED TO CAUSE
1QX ANO 3OS YIELD LOSSES AS WELL AS YIELD LOSSES PREDICTED TO OCCUR AT
7-HR SEASONAL MEAN 0, CONCENTRATIONS OF 0.04 ANO 0.06 PPN
Oa concentrations ppa, Percent yield losses predicted
predicted to causes to occur it 7-hr seasonal
Species yield lotsas of: aean 0, concentration of:
30* 0.04 ppa 0.06 ppa
Leauaa croos
Soybean, Corsoy
0.048
0.082
6.4
16.6
Soybean, Davis (31)
0.038
0.071
11.5
24.1
Soybean, Oavls (CA-82)
0.048
0.081
6.4
16.5
Soybean, Davis (PA-82)
0.059
0.081
2.0
10.4
Soybean, Essex
0.048
0.099
7.2
14.3
Soybean, Forrest
0.076
0.118
1.7
5.3
Soybean, WIlHaas.
0.039
0.093
10.4
18.1
Soybean, Hodgson
0.032
0.066
15.4
18.4
Bean, Kidney
0.033
0.063
14.9
28
Peanut, NC-6
0.046
0.073
6.4
19.4
Grain croos
Wheat,, Aba
0.059
0.095
3.3
10.4
Wheat,' Arthur 71
0.056
0.094
4.1
11.7
Wheat, Roland
0.039
0.067
10.3
24.5
Wheat, Vona
0.028
0.041
28.8
51.2
Wheat* Blueboy II
0.088
0.127
0.5
2.8
Wheat, Coker 47-27
0.064
0.107
2.2
8.4
Wheat, Holly
0.099
0.127
0.0
0.9
Wheat, Oasis
0.093
0.135
0.4
2.4
Corn, PAG 397
0.095
0.126
0.3
1.5
Corn, Pioneer 3780
0.075
0.111
1.4
5.1
Corn, Coker 16
0.133
0.175
0.0
0.3
Sorghua, OeKalb-28
0.108
0.186
0.0
2.7
Barley, Poco
0.121
0.161
0.0
0.5
Fiber croos
Cotton, Acala SJ-2 (81)
0.044
0.096
8.3
16.2
Cotton, Acala SJ-2 (82)
0.032
0.055
16.1
35.1
Cotton, Stonevllle
0.047
0.075
4.6
16.2
Horticultural croos
Tomato, Murrleta (81)
0.079
0.108
0.8
3.7
Toaato, Murrleta (82)
0.040
0.059
10.3
31.2
Lettuce, Eaplre
0.053
0.075
0.0
16.8
Spinach, Aaerica
0.046
0.082
6.8
17.2
Spinach, Hybrid
0.043
0.082
2.6
9.2
Spinach, Vlroflay
0.048
0.080
6.0
16.7
Spinach, Winter Blooa
0.049
0.080
5.8
16.5
Turnip, Just Right
0.043
0.064
7.7
24.9
Turnip, Pur Top W. 6.
0.040
0.064
10.1
26.5
Turnip, Shogoln
0.036
0.060
13.0
29.7
Turnip, Tokyo Cross
0.053
0.072
3.3
15.6
*The yield losses ere derived froa Welbull equations and are based on the control
yields 1n charcoal-filtered air.
Source: Oerlved froa Heck et al. (1984b).
-------
X-12
of the model is unsettling, that is a common deficiency among all models.
While the limitations mentioned above create uncertainties that should be
considered in any application of the results, the staff concludes that
with appropriate caveats, the NCLAN data provides useful information on
crop loss due to O3 exposure.
2. Greenhouse and Controlled Environment Studies
The effects of O3 on plant yield may be affected by a host
of genetic and environmental factors. In addition to the use of
regression approaches in the studies previously discussed, various other
approaches have been used to investigate the effects of O3 on crop yield
under more controlled (to various degrees) conditions as shown in Tables 7-22
and 7-23 of the CD (CD, p. 7-130 to 7-138). These studies were designed to
test whether specific O3 treatments were different from the control using
analysis of variance. To summarize the data, the lowest O3 concentra-
tions that significantly reduced yield was taken from each study (Table
X-3; CD, p. 7-234) and this concentration was frequently the lowest con-
centration used in the study. Although it is difficult to estimate a
no-effect exposure concentration, the data generally seem to indicate that O3
concentrations of 0.10 ppm (frequently the lowest concentrations used in the
study) for a few hours a day for several days to several weeks Induced yield
losses of 10-55 percent.
It is difficult to extrapolate data from studies conducted under more
controlled conditions (greenhouse, growth chamber) to field conditions.
The more controlled chamber data, however, does serve to strengthen the
demonstration of O3 effects in the field. Concentrations of 0.10 ppm and
above appear to consistently cause yield reductions, although exceptions
can be found. In studies which used concentrations below 0.10 pm, the
-------
TABLE X-3. OZONE CONCENTRATIONS AT WHICH SIGNIFICANT YIELD LOSSES HAVE BEEN NOTED FOR
A VARIETY OF PLANT SPECIES EXPOSED UNDER VARIOUS EXPERIMENTAL CONOITIONS
Yield reduction,
0a concentration,
Plant species
Exposure duration
t of control
ppa
Reference
Alfalfa
7 hr/day, 70 days
51, top dry wt
0.10
Neely et al., 1977
Alfalfa
2 hr/day, 21 day
16, top dry wt
0.10
Hoffaan et al.. 1975
Pasture grass
4 hr/day, 5 days/wk, 5 wk
20, top dry wt
0.09
Horsaan et al., 1980
Iadfno clover
6 hr/day, 5 days
20, shoot dry wt
0.10
Blua et al., 1982
Soybean
6 hr/day, 133 day*
55, seed wt/plant
0.10
Heagle et a1.t 1974
Sweet corn
6 hr/day, 64 days
45, seed wt/plant
0.10
Heagle et al. ( 1972
Sweet corn
3 hr/day, 3 days/wk, 8 wk
13, ear fresh wt
0.20
Oshlaa, 1973
Wheat
4 hr/day, 7 day
30, seed yield
0.20
Shannon and Hulchl, 1974
Radfsh
3 hr
33, root dry wt
0.25
Adedlpe and Orarod, 1974
Beet
2 hr/day, 38 days
40, storage root dry wt
0.20
Ogata and Haas, 1973
Potato
3 hr/day, every 2 wk.
25, tuber wt
0.20
Pell et al., 1980
120 days
Pepper
3 hr/day, 3 days/wk, 11 wk
19, fruit dry wt
0.12
Bennett et al., 1979
Cotton
6 hr/day, 2 days/wk, 13 wk
62, fiber dry wt
0.25
Oshlaa et al., 1979
Carnation
24 hr/day, 12 days
74, no. of flower buds
0.05-0.09
Feder and Caapbell, 1968
Coleus
2 hr
20, flower no.
0.20
Adedlpe et al., 1972
Begonia
4 hr/day, once every 6 days
55, flower wt
0.25
Relnert and Nelson, 1979
for a total of 4 tlaes
Ponderosa pine
6 hr/day, 126 days
21, stea dry wt
0.10
Wllhour and Neely, 1977
Western whit*
r\ 4 nA
6 hr/days, 126 days
9, stea dry wt
0.10
Wllhour and Neely, 1977
pine
Loblolly pine
6 hr/day, 28 days
18, height growth
0.05
Wllhour and Neely, 1977
Pitch pine
6 hr/day, 28 days
13, height growth
0.10
Wllhour and Neely, 1977
Poplar
12 hr/day, 5 ao
*1333, leaf abscission
0.041
Wllhour and Neely, 1977
Hybrid poplar
12 hr/day, 102 days
58, height growth
0.15
Patton, 1981
Hybrid poplar
8 hr/day, 5 day/wk, 6 wk
50, shoot dry wt
0.15
Patton, 1981
Red aaple
8 hr/day, 6 wk
37, height growth
0.25
Dochlnger and Townsend, 1979
American
6 hr/day, 28 days
9, height growth
0.05
Kress and Skelly, 1982
sycaaore
6 hr/day, 28 days
Sweetgua
29, height growth
0.10
Kress and Skelly, 1982
White ash
6 hr/day, 2B days
17, total dry weight
0.15
Kress and Skelly, 1982
Green ash
6 hr/day, 28 days
24, height growth
0.10
Kress and Skelly, 1982
Willow oak
6 hr/day, 28 days
19, height growth
0.15
Kress and Skelly, 1982
Sugar aaple
6 hr/day, 28 days
12, height growth
0.15
Kress and Skelly, 1982
-------
X-14
response varied among species (Table 7-22; CD, p. 7-130). Concentrations
of 0.05 ppm in extended or repeated exposures have been shown to cause yield
reductions in some species or cultivars, no effects in others, and increased
yield in others (Table 7-23; CD p. 7-135). Although these studies seem to sug-
gest that a higher O3 concentration was required to cause an effect that was
estimated from the regression studies, it should be noted that the concentra-
tions derived from the regression studies were based on a 10% yield loss,
while the studies using analysis of variance indicate that 0.10 ppm frequently
induced substantial losses (10 to 55 percent).
3. Ambient Air Exposure studies
Ambient air exposure studies conducted to date demonstrate
that O3 in many areas of the country can reduce plant yield. Although the
most severe effects appear to Occur in areas with high O3 concentrations
such as the South Coast Air Basin and the San Bernadino Mountains in
California, other agricultural areas in the country can be impacted as well.
Recently, open top chamber studies evaluating the yield of plants grown
in the presence of O3 (ambient air) versus charcoal-fi ltered air have
demonstrated losses in tomato (33 percent), bean (2fi percent), soybean
(20 percent), snapbean (0 to 22 percent), sweet corn (9 percent), several
tree species (12 to 67 percent), and forbes, grasses and sedges (9 to 33
percent) (Table X-4; CD, p. 7- 237). Field studies in the San Rernadino
Forest during the last 30 years indicate that ambient O3 reduced the height
growth of ponderosa pine by 25 percent, annual radial growth by 37 percent
and the total volume of wood produced by 84 percent (Miller et al., 1982).
Oxidant-induced changes in forest ecosystems will be discussed in more
detail in Section B.
-------
TABLE X-4. EFFECTS OF AMBIENT OXIDANTS ON YIELD OF SELECTEO CROPS
Mant species
Oa
concentration,
PP"
Exposure duration
Percent yield
reduction
froa control
Location
of study
Reference
Tom to
(Fireball 861 VR)
0.035
(0.017-0.072)
99 day average (0600-2100)
33, fruit fresh
weight
New York
Maclean and
Schneider, 1976
Bean
(lendergreen)
0.041
(0.017-0.090)
43 day average (0600-2100)
26, pod fresh wt
Snap bean-(3 cult1vers:
Astro, BBL 274, BBL
290)
0.042
3 ao average (0900-2000)
1, pod weight
Maryland
Heggestad and
Bennett, 1981
Soybean (4 cultlvars:
Cutler, York. Clark,
Oare)
>0.05
31X of hr between
(0800-2200) froa late
June to aild-Septeaber
over three suaaers, SX
of the tlae the concen-
tration was above 0.08 ppai
20, seed wt
Maryland
Howell et al.,
1979; Howell and
Rose, 1980
Forbs, grasses, sedges
0.052
0.051
0.035
1979, 8 hr/day average
(1000-1800), Aprll-
Septeaber
1980, 8 hr/day average
(1000-1800), Aprll-
Septeaber
1981, 8 hr/day average
(1000-1800), April-
Septeaber
32, total above
ground bloaas
20, total above
ground bloaass
21, total above
ground bloaass
Virginia
Virginia
Duchelle et al.,
1983
Sweet corn
(Bonania)
>0.08
SEX of hr (0600-2100)
between 1 July and
6 Septeaber
9, ear fresh wt
California
Thoapson et al.,
1976a
(Monarch Advance)
>0.08
28, ear fresh wt
-------
X-16
Antioxidant chemical protectants appear to provide another objective
method of estimating the Impact of ambient O3 on crop production (Toivonen
al., 1982). Some limitations, however, must be kept in mind. The chemical
itself may alter plant growth and therefore results must be Interpreted
carefully. Also, the chemical may not be effective against all concentra-
tions of all pollutants and result in an underestimation of yield loss
(Manning et al., 1974).
Ethylenediurea (EDU), developed as a chemical protectant to prevent
oxidative effects of O3, has been used extensively to reduce visible O3
injury 1n greenhouse and field studies and to estimate ozone-induced
yield loss. Several studies have reported estimates of the impact of
O3 on yield by comparing yield data from plots with and without EDU
treatment (Table X-5; CO, p. 235). For a seven-week study in which
ambient O3 exceeded 0.15 and 0.08 ppm on five separate days at each
concentration, EDU treatment reduced foliar injury of onions and in-
creased yield by 37.8% (Wakasch and Hofstra, 1977). During a June to
August study in which ambient O3 exceeded 0.08 ppm on 15 days with a
maximum of 0.14 ppm, EDU treatment increased yield of the Tiny Tim
tomato by 30% but had no effect on the New Yorker cultivar (Legassicke
and Ormrod, 1981). Other studies with beans (Toivonen et al., 1982),
tobacco (Bissessar and Palmer, 1984), and potatoes (Bissessar, 1982)
provided evidence of EDU increasing yield by 35%, 18%, and 35.5% re-
spectively. These and other studies demonstrate the effectiveness of
antioxidants to improve crop yield and to estimate ozone-induced crop
loss for several crop species. The data clearly show that O3 concentra-
tions occurring durlng these studies reduced crop yields between 10 and
40% although O3 levels only occasionally exceeded 0.08 ppm.
-------
X-17
TABLE X-5 . THE EFFECTS OF 03 ON CROP YIELD
AS DETERMINED BY THE USE OF CHEMICAL PROTECTANTS
Yield reduction 03 exposure,
Species * of control ppa Reference
Beans (green)
41
>0.08 for total
of 27 hr over
3.5 months
Manning et al., 1374
Onion
38
>0.08 on 5 days out
of 48
Wukasch and Wofstra, 1377
Tomato
30
>0.08 on 15 days
over 3 months
Legasslcke and Ormod, 1381
Bean (dry)
24
>0.08 on 11 days
(total of 34 hr)
over 3 months
Temple and Blsessar, 1373
Tobacco
18
>0.08 on 14 days
during the summer
Blsessar and Palmer, 1384
Potato
36
>0.08 ppa on 18 days
(total of 68 hr)
over 3 months
Blsessar, 1382
Potato
25
_c
Clarke et al., 1383
*A11 the species were treated with the antioxidant EDU except the bean study by
Manning et al. (1374) which used the systemic fungicide benomyl.
^Y1e1d reduction was determined by comparing the yields of plants treated with
chemical protectants (control) to those that were not treated.
cTh1s study was run over 2 years when the 03 doses were 65 and 110 ppurhr,
respectively, but the yield loss was similar both years.
-------
X-18
A comparison of the values reported in the ambient air studies (Tables
X-4 and X-5) with actual ambient air quality data reveal that the hourly and
dally maximum exposures over 0.08 ppm seen in the studies generally are
within those seen in ambient data. For instance, the bean study undertaken
by Manning saw 27 hours above 0.08 ppm of O3 exposure over a 3.5 month time
period. Air quality data from Johnson et al. (1985) can be compared with
this exposure, when "normalized" for a 3.5 month period. That data would
Indicate that the mean expected number of hours over 0.08 ppm for 69 agri-
cultural areas is 52 for a 3.5 month period. (The range would be 0 - 206
hours.) This mean is almost twice the 27 hours used by Manning et al.
The total of 68 hours > 0.08 ppm seen by Blsessar (1982) over a
three-month period is generally higher than the typical agricultural
area, however. In fact, only 18% of the 69 areas investigated in
Johnson et al. (1985) would see that many or more hours > 0.08 ppm
in a normalized season (of 242 days).
Turning to the daily maximum values > 0.08 ppm presented in Table X-5,
they must be made relative to a standard time 1n order to compare them to
ambient data. The normalization 1s to a six-month season, using the same
percentage of days seen 1n Table X-5. These percentages are shown below
for the studies.
Reference
% of Days > 0.08 ppm Dalily Maximum for a
Normalized Six-Month Season
1. Wakasch and Kofstra, 1977
10.4
2. MacLean and Schneider
11.0
3. Temple and Blsessar, 1979
4. Bisessar and Palmer, 1984
12.2
15.6
5. Legassicke and Ormod, 1981
16.7
6. Bissessar, 1982
20.0
-------
X-19
EPA air quality Indicates (McCurdy, 1986) that the mean percentage of
days > 0.08 ppm for a sample of 65 non-SMSA areas is 10.2%. Thus, all of the
above studies have more days over 0.08 ppm than the mean of the sample,
although the first two have values quite close to it. The Bisessar (1982)
study's value of 20% would be expected in only 10% of the areas, and the
Legassicke and Ormod (1981) estimate of 16.7% would be expected in 17% of all
areas.
The data from Howell et al. (1979) and Thompson et al. (1976a) are
difficult to deal with because of the long daily time period used for
analysis: 14 and 15 hours, respectively. However, the values of % hours
over 0.08 ppm presented in the Howell study are low compared to
most agricultural areas, probably in the lowest 25% or so. The hours
_> 0.10 ppm and 0.12 ppm are generally higher than seen in the typical
rural area. The very high relative number of days over 0.08 ppm and
0.12 ppm reported in the Thompson et al. (1976a) study, on the other hand,
are unique to California areas and are not seen in other areas.
2. Related Vegetation Issues
a. Empirical Models
Empirical response models for effects of O3 on plants a^e mathematical
functions that describe a relationship between O3 exposure and a biological
response. These models quantitatively define the entire relationship between
the range of exposures and have been used both for crop production forecasting
and to interface biological systems with economic models.
Categories of empirical exposure response models include physiological
injury, growth and yield-loss models. Physiological response models are
used as research tools to summarize relationships or allow comparisons among
species while injury models generally estimate the magnitude of foliar
-------
x-zo
Injury Incurred from pollutant exposures. Growth models quantify pollutant-
induced changes in biomass accumulation. Yield loss models are most difficult
to develop but are needed to estimate production and economic losses since
they provide direct relationships between yield and pollutant exposure.
The three types of yield loss models which describe plant response 1n the
absence of a known functional relationship between O3 levels and yield a^e
linear, plateau-linear, and Weibull functions. Non-l1near models, which have
been used in describing situations for which response to O3 appears to have a
threshold, are the plateau-linear model and Weibull model. The plateau-linear
model incorporates a threshold value but does not allow curvature of any
increase in yield followed by a decrease. The Weibull model, however, can
take on plateau shape followed by curved gradual decreases.
National Crop Loss Assessment Network (NCLAN) yield losses have been
modeled by Heck et al. (1983, 1984) who used a three parameter Weibull
function. The Weibull function chosen has a flexible form which covers
the range of observed biological responses, is biologically realistic,
has parameters with clear interpretations, and offers a method of sum-
marizing species responses by developing a common proportional model
(Rawlings and Cure, 1985). The Weibull model subsequently has been used
with NCLAN data previously modeled with other functional forms (CD, p. 7-170),
b. Statistics Used to Characterize Ozone Exposures
Important factors needed to adequately characterize O3 exposures
in vegetation exposure studies Include time, concentration, and dynamic
nature (I.e., constant or variable). Which of the components of exposure
actually causes plant response, however, remains unclear. Although many
studies tend to report exposures as mean O3 concentrations, the averaging
times can be peak hourly, daily, weekly, monthly, or seasonal means; numbei"
-------
X-21
of hours above selected concentration; or number of hours above selected
concentration Intervals. None of these statistics has adequately characterized
the relationship among concentration, exposure duration, Interval between
exposures and plant responses. The lack of correlation between exposure
statistics and ambient air measurements have posed a major problem for
those trying to assess the effects of O3 exposure.
The implication inherent in the use of mean O3 concentrations is
that all O3 concentrations are equally effective in causing plant responses.
Use of the mean statistic minimizes the importance of peak concentrations
by treating low-level long-term exposures the same as high concentration
short-term exposures. Studies with beans and tobacco, however, have shown
that a given dose (concentration x time) distributed over a short period
induced more injury than did the same dose distributed over a longer period
(Heck et al., 1966). Concentration was shown to approximately twice as
effective as time of exposure at causing foliar Injury 1n tobacco plants
(Tonneijck, 1984). Results of several other studies also have supported
the greater importance of concentration than time in determining plant
response (Bennett, 1979: Heck and Tingey, 1971; Henderson and Reinert,
1979; Reinert and Nelson, 1979, Amiro et al. (1984)). Thus, a judgment must
be made as to whether greater protection of plants from O3 exposure is
provided by limiting short-term peak exposures than by limiting long-term
average exposures.
Not only are concentration and time important but the dynamic nature of
the O3 exposure is also important; i.e., whether the exposure 1s at a
constant or variable concentration. Musselman et al. (1983) recently
demonstrated that although constant concentrations cause the same type of
plant response as variable concentrations at equivalent doses, the constant
-------
X—22
concentrations had less effect on plant growth responses. This finding has
been confirmed by other studies. Ashmore found significant yield reductions
in radishes exposed to ambient O3 when the maximum O3 concentration exceeded
0.06 ppm at least 101& of the days when the crop was growing. Initial
studies have compared the response of alfalfa to daily peak and episodic O3
exposure profiles which had the equivalent total O3 dose over the growing
season (Hogsett et al., 1985) alfalfa yield was reduced to a greater extent
in the episodic that the daily peak exposure. The plants that displayed
the greater growth reduction (1n the episodic exposure) have a significantly
lower 7-hour seasonal mean concentration thus raising the possibility that
the 7-hour seasonal mean may not properly consider peak concentrations.
Studies with SO2 also showed that plants exposed to variable concentrations
exhibited a greater plant response than those exposed to a constant concentration
(McLaughlin et al., 1979).
c. Exposure and Response to PAN
Response to peroxyacetyl nitrate (PAN) exposure has been assessed
using the Iim1t1ng-value method to estimate the lowest PAN concentration
and exposure duration required to produce visible injury on plants (Jacob-
son, 1977). The range of PAN levels and exposure durations which this
analysis suggests will produce foliar injury are: 1) 0.20 ppm for 0.5 hr;
2) 0.10 ppm for 1.0 hr; and 3) 0.035 ppm for 4.0 hr. (CD, p. 7-256). To
reduce the likelihood of foliar injury to some plants, more recent studies
have been suggested that PAN exposures may need to be 30 to 40% lower than
the values cited above (Tonneijck, 1984).
Few studies are available which report the effects of PAN on growth
and yield. A study of the effects on non-vascular plants indicates that
growth, photosynthesis, and respiration of algae can be adversely affected
-------
X-2 3
by exposure to PAN (Gross and Dagger, 1969). Fumigation of lichens with
0.05 ppm and 0.10 ppm PAN for several days inhibited photosynthesis (Sigal
and Taylor, 1979). Vascular plants which have been studied to determine
the effects of PAN on growth and yield include radishes, oats, tomatoes,
pinto beans, beets, and barley. These plants were exposed in greenhouse
studies to PAN concentrations up to 0.04 ppm for 4 hours per day, twice
per week from germination to maturity with no significant effects (Taylor
et al., 1983). In the same study, similar exposures of lettuce and
Swiss chard produced yield losses of 13% and 23t, respectively, without
visible foliar injury. Although it is possible for severe PAN exposure to
make some crops unmarketable, it is unlikely that PAN concentrations suf-
ficient to cause v1si bile injury or reduced yield will occur in the
United States except perhaps 1n some areas of California and a few other
localized areas.
B. Natural Ecosystem Effects
The previous section discussed the responses of individual species of
agricultural plants, trees and other native vegetation to O3. The
responses are well documented and include: (1) injury to foliage, (2)
reductions in growth, (3) losses in yield, (4) alterations in reproductive
capacity, and (5) increased susceptibility to pests and pathogens. This
section discusses the effects of O3 stress on simple and complex plant
communities to illustrate that such effects, because of the interconnections
and relationships among ecosystem components, can produce perturbations in
ecosystems. Stresses placed on plant communities and the ecosystems of
which they are a part can produce changes that are long lasting and that
may be Irreversible. No attempts have been made to examine the effects
of PAN on ecosystems since there 1s little data and trees and other woody
plants appear to be resistant to PAN (CD, p. 8-1).
-------
X-24
Evidence indicates that any impact of ozone on ecosystems will depend
on the responses to O3 of the producer community. Producer species (trees
and other green plants) are of particular importance in maintaining the
integrity of an ecosystem since producers provide, through the process of
photosynthesis, all of the new organic matter (food, energy) added to an
ecosystem. Ozone induced changes in photosynthesis influences energy
flow and mineral nutrient cycling. Alteration of these processes in
ecosystems can set the stage for changes in community structure by influencing
the nature and direction of successional changes (Woodwell, 1970; Bormann,
1985), with possibly irreversible consequences (see e.g., Odum, 1985,
Bormann, 1985). The sequence of responses outlined by Bormann is given
in Table X-5 to assist in understanding ecosystem effects (CD, p. 8-4).
1. Forest Ecosystems
Temperate forest ecosystems within the United States are currently
experiencing 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. Air
pollution is among the chronic stresses to which trees are exposed.
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
trees in these forests in 1962 (Miller et al., 1963). Late^, Jeffrey
pine was also found to be injured by O3 exposure. Oxidant injury of
eastern white pine has been observed for many years 1n 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
-------
X-25
TABLE x"6- CONTINUUM OF CHARACTERISTIC ECOSYSTEM
RESPONSES TO POLLUTANT STRESS
Phase Response characteristics
0 No response occurs. Manmade pollutants are absent or
constitute insignificant stress. Plant growth occurs
under natural conditions.
1 Ecosystems serve as sinks for pollutants. Species
and/or ecosystem functions are relatively unaffected.
Self-repair occurs.
II Sensitive species or individuals are subtly and
adversely affected. A reduction in photosynthesis-,
a change fn reproductive capacity, or a change in ~
predisposition to insect or fungus attack may occur.
Ill Decline occurs in the populations with sensitive
species; some individuals will be last. Their ef-
fectiveness as functional members of the ecosystem
diminishes. Ultimately, species could be lost from
the system.
IV Large plants, trees, and shrubs of all species die.
The basic structure of the forest ecosystem is changed.
Biotic regulation is affected as forest layers are
peeled off: first trees, tall shrubs, and, under
the most severe conditions, short shrubs and herbs.
The ecosystem is dominated by weedy species not
previously present and by small scattered shrubs
and herbs.
V The ecosystem collapses. The loss of species and
changes in ecosystem structure, nutrients, and soil
so damage the system that self-repair is impossible.
Source: Adapted from Bormann (1985).
-------
X-26
(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 Benoit et al. (1982) and on the Cumberland
Plateau of east Tennessee by Mann et al. (1980) and McLaughlin et al. (1982).
In addition, ozone injury in natural plant communities has been reported by
Treshow and Stewart (1973) and by Duchelle et al. (1983).
a. Effects on Plant Processes
A discussion of individual tree response is the first step in
explaining ecosystem response. In forest ecosystems, tree populations are
the controller organisms. They determine the structure, energy flow
and nutrient cycling (Ehrlich and Mooney, 1983). Though trees are woody
perennial plants, they respond to O3 exposure in the same manner as
agricultural crops. The same plant processes of photosynthesis, nutrient
uptake, biosynthesis, respiration, and translocation are affected. The
alteration of these physiological processes is the fundamental cause of
all other effects ranging from the molecular to the ecosystem level
(CD, p. 8-5).
Inhibition or reduction in the rate of photosynthesis is possibly
the most significant effect of O3 entry into the leaves of sensitive
plants. Ozone inhibits photosynthesis, decreases formation of organic
compounds needed for plant growth, and can alter the transport and
allocation of the decreased products of photosynthesis so that sugar storage
and root growth are reduced. Trees in which O3 has been shown to reduce
photosynthesis are loblolly pine and slash pine (Barnes, 1972), ponderosa
pine (Miller et al., 1969; Coyne and Bingham, 1981), eastern white pine,
(Barnes, 1972, Yang et al., 1983; Botkin et al., 1972) black oak, sugarmaple
(Carlson, 1979), and a poplar hybrid (Furukawa and Kadota, 1975)
(Table IX-1, p. 4).
-------
X - 27
Miller et al. (1969), Coyne and Bingham (1981), and Yang et al. (1983)
relate visible injury symptoms and reduced tree growth to the effect of
O3 on photosynthesis. Miller et al. (1969) found that exposure of 3-year
old ponderosa pine seedlings under controlled conditions to concentrations
of 0.15, 0.30, and 0.40 ppm 9 hr/day for 30 days reduced photosynthesis
by 10, 70 and 85 percent, respectively. In addition, it was noted that a
reduction in photosynthesis was accompanied by a decrease in the sugar
content of injured needles. Tingey et al. (1976) observed that the
amounts of soluble sugars, starch, and phenols tended to increase in the
tops and decrease In the plant roots of ponderosa pine seedlings exposed
to 0.10 ppm O3 for 6 hours per day for 20 weeks. The sugars and starches
stored in the tree roots were significantly less when compared with the
controls (CD, p. 8-12).
Coyne and Bingham (1981) measured photosynthesis and stomatal
conductance of attached ponderosa pine needles in relation to cummulative
O3 dose. The decline in photosynthesis and stomatal function normally
associated with aging was accelerated as O3 injury symptoms increased.
Premature senescence and abscission of needles occurred soon after
photosynthesis reached its lowest level. In a study of white pine, Yang
et al. (1983) also observed that decrease in rates of photosynthesis due
to O3 exposure was closely associated with visible needle injury, premature
senescence and reduction in biomass (CD, p. 8-11).
b. Effects on Growth
Studies made along the Blue Ridge Parkway support the view
that exposure to O3 reduces growth in sensitive trees (Benoit et al.,
1982). Eastern white pine located in experimental plots situated along
-------
X - 28
the Blue Ridge Parkway were studied to determine the radial growth increment
during the 1955 to 1978 period. Growth of trees classified as sensitive
was 25 percent less than in tolerant trees; growth was 15 percent less in
trees classified as intermediate in sensitivity. Mean radial increments
for all trees during the last 10 years of the study were smaller than for
the previous 24 years. During the period of the study, concentrations of
0.05 to 0.07 ppm of O3 were recorded on a recurring basis, with episodic
peaks of 0.12 ppm or higher occurring (Benoit et al., 1982) {CD, p. 8-7).
Hayes and Skelly (1977) monitored total oxidants and recorded oxidant
related injury on eastern white pine in three rural Virginia sites between
April 1975 and March 1976. Injury was associated with total oxidant peaks
of 0.08 ppm for 1-hr or higher. Peak 1-hr ozone concentrations of 0.17
have been measured in the Blue Ridge Mountains (Skelly, 1980). Monthly
8-hr average O3 concentrations ranged from 0.035 to 0.065 ppm during the
oxidant season (April - October) and peak hourly concentrations ranged
from 0.0Q to 0.13 ppm (Skelly et al., 1984). Increased injury symptoms
were observed on pine trees previously classified as sensitive or Intermediately
sensitive after an O3 episode. Hayes and Skelly (1977) suggested that
continued exposure of white pine to acute and chronic oxidant concentrations
could influence their vigor and reproductive ability, ultimately resulting
in replacement by tolerant species.
A steady decline in annual ring increments was also noted on the
Cumberland Plateau of east Tennessee 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 1n sensitive
white pine when compared to both tolerant trees and trees of intermediate
sensitivity. Annual occurrences of O3 at hourly concentrations of 0.08
-------
X-29
ppm or greater were associated with the growth reductions. The reduction
in growth on the Blue Ridge Parkway and on the Cumberland Plateau, as in
the case of the San Bernadino 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;
(2) reduced storage capacity of carbohydrates in the fall and resupply
capacity in the spring to support new needle growth; (3) shorter new
needles, resulting in lower gross photosynthetic productivity; (4) reduced
availability of photosynthate for external usage (including repair of
chronically stressed tissues of older needles); and 5) premature casting
of older needles (McLaughlin et al., 1982). Degeneration of feeder roots
and mycorrhizae usually precedes the onset of above ground symptoms
(Manion, 1981). Decreases 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, to defoliation by insects, and
to attack by the pine beetle. Growth reductions in trees (Table X-7)
grown under controlled conditions have also been observed (Mooi, 1980;
Kress et al., 1982; Kress and Skelly, 1982; Jensen, 1979; McClenahen, 1979;
Jensen and Dochinger, 1974; Jensen and Masters, 1975) (CD, p. 8-9).
Injury by O3 to native herbaceous vegetation growing in the Virginia
mountains was also observed (Duchelle et al., 1983). Ambient O3
concentrations were shown to reduce growth and productivity of graminoid
and forb vegetation. For each year of the study, biomass production was
greatest for vegetation grown in filtered-air chambers. Common milkweed
and common blackberry were the only two native species to develop foliar
injury. Ozone episodes occurred several times during the period of the
study. Peak hourly concentrations ranged from 0.08 to 0.12 ppm; however,
-------
TABU X- 7. Iff (CIS Of 01 ONE MOEO 10 FILICtft All ON IK YIUO Of SUECTfO I iff MOPS
Plant tpKltl
0»
concentration
i*posure duration
Percent yield reduction
Iron control
Monitoring^ C*1lkritlMC fuilutloa'
•ctkod mIM facility Reference
Poplar .
(Dortjw)
(Iiilud)
AacrlcM Sycanore
(16*SVC-19)
(lt-SYC-23)
taerlcaa Sycafcer*
(1HK-U)
(H-SYCIJ)
Sweetgua
Amr lean Sycanore
Hlitl Hit
Greea ask
0.041
0.041
O.OS
O.OS
O.OS
O.OS
O.OS
0.10
0.1S
O.OS
0.10
0.1S
O.OS
0.10
0.1S
O.OS
0.10
0.1S
12 kr/day, S no
12 kr/day, S ma
§ itr/day. 20 days
ft kr/day, 20 day
ft kr/day, 20 day»
i kr/day, 20 day
i kr/day, 21 days
ft kr/day, 28 days
0 kr/day, 28 days
0 kr/day, 20 days
*14*. stea length; 12 ilea dry Ml;
no. of dropped leaves; i,
total dry wt
2, stea length; 4, stca dry wt;
~492, no. of dropped leaves: 0,
total dry wt
9*, kelgkt growtk
2, kelgkt growtk
II, kelgkt growtk
0*. kelghi growtk
•1. kelgkt growlk; 10, total dry wt
29", kelgkt growth; H. total dry Ml
45", kelglit growtk; 42*. total dry wt
~4, kelgkt growtk; 2), total dry wt
2!*, kelglit growtk; 61*. total dry wt
21*. kelgkt growtk; 6)*, total dry wt
*12, kelgkt growtk; *Hm, total dry wt
9, kelglit growtk; I. total dry wt
It, kelgkt growtk; 17", total dry wt
2. kelgkt growtk; 14, total dry wt
24", height growtk, 20, total dry wt
30", height growtk; 3). total dry wt
Ckea.
Ckea.
Ckea.
Ckea.
Chea.
Ckea.
Ckea.
Chea.
N0K1
NOKI
IX N0KI
IX NOKI
Constant
source,
NOKI, UV
Constant
source,
NBKI, IN
Constant
source,
NBKI, UV
Constant
source,
NOKI, W
6N-CN
CH-CM
CM
(SIR
CSIR
CSIR
CSIR
CSIR
Hoot, 1900
Noel, 1900
Rrosa at
nl., 1902b
Kress et
•l.a 1902b
Kress and
Shelly.
1902
Kress and
Skell*.
1902
Kress and
Skelly,
1982
-------
1ABIE X-7. fFftCIS OF OIONE MMKO 10 f IlIEREB AIR ON VIEIB OF SEIECIEB 1REI CROfS (continued)
Plant species
°» .
concentration
Ixposure duration
Fercent yield reduction
I ram contraI
Monitoring
Method
Calibration* Fialoatlon*
facility Reference
Willow Mk
Sugar upli
Yellow poplar
Vollow poplar
CottMMOOd
Mi It* »k
lAlte ash
¦lack cherry
Hybrid poplar
(MS 207 ~ HE 211)
o.as
0.10
0.05
0.10
0.1S
0.05
0.10
0.1S
0.10
0.10
0.10
0.10
0.20
0.10
0.40
0.10
0.20
0.10
0.40
0.1S
ft hr/
-------
1ABIE X"7- IfFECIS OF OJONE AOMD 10 f IIIEMO All ON VIELO Of 5EIECIED 1REE CROTS (continued)
riant tpccUt
0S
concentration
Ixpeiur* duration
Percent yield reduction
froa control
Kooltorlng
•ethod
Calibration* Fuotgatlon'
aathod
Facility lefarcnc*
Hybrid mlir
(201) ^
Vallew birch
tfilte birth
Olgtooth upti
latter* coltonwoid
led aaple (ltl NE)
(167 M)
(111 OH}
table)ly pine
(4-S a S23)
(14-5 x S17)
labial ly pine
fitch plna
0.20
0.20
0.25
0.2)
0.25
0.25
0.25
a. 05
0.05
0.05
0.10
0.15
0.05
0.10
0. IS
1.5 hr/day, S day/wfc, 5, height
0, height
f Mil
0 hr/day, 5 day/wfc.
0 hr/day, i wfc
0 hr/day, 20 days
I hr/day, 20 dayi
6 hr/day, 28 days
9, height
IS wk
34, height
~7, height
10, height
12, height
17*. height
0, height grewth
10*, height grewth; II. Ulil dry wt
it*, height growth; 22*, total dry wt
41*. height grewth; 20*. total dry wt
4 height grewth; 0, total dry wt
II*. height grewth; 19 total dry wt
26*, height growth; 24*. total dry wt
(not given)
NASI
NASI
Chen.
Chea.
(not given)
N0KI
IX NOKI
U MM
CM
CH-CH
CN
CM
Canstant CSTI
source,
NOKI, IN
Jtnten,
1979
Jenien and
Hosiers,
19)5
Oochlnger
and lown-
lend, 1979
Krata at
al., 1902a
I
Kract and
ttelly, •
1902
-------
TABLE X- 7. irricis OF OIOMC AMMO 10 fllllMD All ON YIEIO Of SElfCIED l*€E CIOTS (continued)
Hant specie*
Oj
CMCMlrillM
pp«
fxposure duration
Percent yield reduction
Iram control
Monitoring^
aethod
Calibration*
¦ethod
funlgatlon^
facility
Reference
Virginia pin*
60S
0.10
0.15
6 kr/day. 20 days
i.
helylit growth; «2, total dry wt
height grMlli; 3, total dry wt
height grow III; |J, total dry wt
Utile ipruci
0.25
1 hr/day. 5 day/wk.
IS wk
5.
height
Hast
M0KI
GH-CM
Jensen and
Matters,
19IS
Japanese larch
0.21
height
Mast
NBR1
GN-Ctt
'~ * m Increase ibm 11m central
*Chea. • clie*tluBlM»c«*c*; Hiit • Matt neter (coutoMtrlc); W ¦ ylimldtt spectro»etry
CMBKI * neutral patutlui Iodide
^GM » greenhouse; CS1I * CMtliMaut illrrad tank reKlw; CM * NaufMlurtd cluabcr ether than CS1I or GC; CH-CN * CH t* |rH
-------
X-34
monthly hourly average concentrations ranged from 0.03 to 0.06 ppm.
Treshow and Stewart (1973) conducted one of the few studies
investigating the impact of air pollution on natural plant communities.
Grassland, oak, aspen, and conifer communities in Salt Lake Valley, Utah
were studied. Two dominant species, cheatgrass and aspen considered key
to community integrity were found to be sensitive. In both cases single
2-hr exposures to 0.15 ppm O3 caused severe injury. Removal of the
dominant species from plant communities could result in a shift to another
species. In a companion study conducted in portable plastic chambers,
O3 exposures of 0.15 to 0.3 ppm for 3 hr per day 5 days/week throughout the
growing season reduced root and top growth and fewer seeds were produced
(Harwood and Treshow, 1975).
c. Ecosystem Responses: The San Bernadino Study
One of the most thoroughly studied ecosystems in the United
States is the mixed coniferous forest ecosystem in the San 8ernadino
Mountains of Southern California. The San Bernadino Forest is located at
the eastern end of the 80 mile long South Coast Air Basin, where a severe
pollution problem has been created by the previous three decades of extensl
urban and industrial development (Miller and Elderman, 1977). Sensitive
plant species in the National Forest, such as ponderosa pine, began
showing unmistakable injury in the early 1950's (Miller and Elderman, 1977)
but the source of the injury was not identified as O3 until 1962 (Miller
et al., 1963). Extensive visible injury and concern about the possible
adverse effects of chronic O3 exposure on an important forest ecosystem
led to an interdisciplinary study conducted by the University of California
Riverside, from 1973 to 1978. This interdisciplinary study of the pine
-------
X - 35
and mixed conifer forests is the most comprehensive and best documented
report on the effects of oxidants on an ecosystem (Miller et a!., 1982)
(CD, p. 8-30).
All of the major ecosystem processes were shown by the study to be
affected directly or indirectly. Ozone associated stress on trees
decreased photosynthesis, affected directly or indirectly translocation
of carbon (energy), mineral nutrients, and water, and reduced trunk
diameter, tree height and seed production in ponderosa and Jeffrey pine
(Miller et al., 1982). FoUar injury of O3 sensitive ponderosa and Jeffrey
pines was observed when 24-hr O3 concentrations ranged from 0.05 to 0.06 ppm.
During the period of the study, average 24-hr O3 concentrations during
the months of May through September ranged from a background of 0.03 ppm
to a maximum of 0.10 to 0.12 ppm. A comparison of radial growth of
ponderosa pine during years (1910 to 1940) of low pollution (< .03 ppm)
with years (1941 to 1971) of high pollution (0.03 to 0.12 ppm) indicated
that O3 exposure reduced the average annual radial growth by approximately
40 percent, height by 25 percent, and wood volume by 84 percent in trees
less than 40 years of age. The marketable volume of trees 30 years of
age was reduced by 83 percent in the areas with the highest O3 concentrations
(Miller and Elderman, 1977). In addition, stressed pines also became
more susceptible to root rot and pine bettle as result of weakening by
photochemical oxidants (Stark and Cobb, 1969).
O3 incited stress on sensitive ponderosa and Jeffrey pine and to a
lesser extent on sensitive white fir, black oak, increase cedar and sugar
pine, accompanied by fire, brought about the removal of the pine forest
overstory. A shift in dominance to self-perpetuating fire adapted, O3-
tolerant shrub and oak species resulted. These mixtures provide fewer
-------
X-36
commodity and amenity values than the former pine forest (Miller et al.,
1982).
The foregoing studies indicate that the impact of O3 changes the
composition and successlonal of patterns of plant communities. It 1s
apparent that 1n some natural communities exposed to O3, the disturbance
may be large enough to 1n time reduce the potential of the site to support
life (Woodwell, 1974). The entire array of plants 1s changed by disturbance
from one 1n 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 Bernadino National Forest,
where the mixed conifer forest is being replaced by low growing shrubs
and annual herbs. It 1s also occurring in the eastern United States
where the degradation of the Appalachian forest from North Carolina to
Maine 1s currently taking place as the red spruce and other large long
lived species are being removed by at present unknown forces (Johnson and
Slccama, 1983).
2. Interrelated Ecosystems
a. Aquatic Ecosystems
It is extremely Important to consider that an adverse impact
on a forest or agricultural ecosystem may in turn adversely affect 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.
-------
X-37
Finer sediments can reduce water quality, affecting public and industrial
water supplies and recreational areas. Turbidity 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,
sedimentation, and eutrophication of adjacent or nearby aquatic systems.
Interfacing areas, such as wetlands and bogs, may be especially vulnerable
to impact (CD, p. 8-44).
b. 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 usually highly
manipulated monocultures of similar genetic and age composition and are
unable to maintain themselves without the addition of nutrients, energy,
and human effort; opportunistic 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 O3, its market value can be destroyed. When this occurs, efforts are made
to find a resistant cultivar, as with tobacco, or to grow a crop less
-------
X - 38
sensitive to O3 stress. Cost alone would prevent replacement of the
variety of species in a natural ecosystem.
C. Materials Damage
Research over a period of more than two decades has shown that
ozone has the ability to react with both manmade and natural materials.
While some research has been done on the effects of total oxidants, the
only components of total oxidants studied individually are ozone and NO2.
In spite of the research focus on O3, however, the amount of damage from
O3 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 paint. Ideally,
the nature and amount of O3 damage to the materials can be approximated
by physical damage functions in combination with ambient air concentrations.
The economic impact of O3 related damage can then be estimated by using
accelerated repair and replacement costs. Because little recent work has
been reported on the effects on nonbiological materials, it is necessary
to rely on older studies which, in many cases, do not provide sufficient
information to assess the amount and costs of oxidant related damage.
1. Elastomers
The effects of O3 on elastomers are the best documented natural
rubber and synthetic polymers/copolymers of butadiene, isoprene, and
styrene account for the bulk of elastomer production for products such as
automobile tires and protective electrical coverings. The mechanism of
O3 damage on elastomers shares similarities and differences with simple
oxidation from atmospheric oxygen. Ozone damage, usually in the form of
cracking, tends to be more of a surface phenomenon than simple oxidation.
It Is greatly accelerated by mechanical stress, which produces fresh
surface areas at crack boundaries. Simple oxidation, on the other hand,
-------
X-39
is slower; it occurs more In the bulk of a material, and it is less
affected by the degree of stress (Mueller and Stickney). At pollutant
concentrations and stress levels normally encountered outdoors (and in
many indoor environments), the elastomer hardens or becomes brittle and
cracked, losing its physical integrity. High humidity and mechanical
stress greatly affect the formation, depth of cracking, and, in automotive
tires, the adhesion piles (Davies, 1979; Wenghoefer, 1974) (CD, p. 9-3).
O3 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 O3 dose was
demonstrated by Bradley and Haagen-Smit (1951), who used a specially
formulated ozone sensitive natural rubber (NR). Samples exposed to 20,000
ppm cracked almost instantaneously, and those exposed to lower concentrations
took a proportionately longer time to crack. Cracking occurred at a ''ate
of 0.02 to 0.03 ppm-hr over the entire range of concentrations.
Haynfe et al. (1976) exposed samples of a tire sidewall to O3 at
concentrations of 0.08 and 0.5 ppm for 250 to 1000 hr under 10-20 percent
strain. From these and other data, they estimated that at the O3 standard
of the time (0.08 ppm, 1 hr average), and at the annual N0X standard of
0.05 ppm, it would take 2-5 years for a crack to penetrate cord depth.
In addition to stress, factors affecting the cracking rate include
atmospheric pressure, humidity, sunlight, and other atmospheric pollutants.
Veith and Evans (1980) found a 16-percent difference in cracking rates
reported from laboratories located at various geographic locations (CD, p. 9-49).
O3 has been found to affect the adhesion of piles (rubber-layered
strips) in tire manufacturing. Exposures to ozone concentrations of
-------
X-40
0.05 to 0.15 for a few hours significantly decreased adhesion in an
NR/SBR blend, causing a 30 percent reduction at the highest O3 level.
This adhesion problem worsened at higher relative humidities. 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 NO2 did, with or without high relative humidity (CD, p. 9-49).
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 NO2. Subsequent work by Schmitt
(1960, 1962) confirmed the fading action by ozone and the importance of
relative humidity 1n the absorption and reaction of vulnerable dyes.
Later Beloin (1972, 1973) noted the acceleration in fading of certain
dyes at an O3 concentration of 0.05 ppm and a relative humidity of 90
percent (CD, p. 9-50).
Both the type of dye and the material in which it is incorporated
are important factors 1n the resistance a fabric has to O3. Haylock and
Rush (1976, 1978) showed that anthraquinone dyes on nylon fibers were
sensitive to fading from O3 at a concentration of 0.2 ppm for 16 hrs,
while Haynie et al. (1976) and Upham et al. (1976) found no effects from
O3 concentrations of 0.1 to 0.5 on royal blue acetate, red rayon-acetate,
or plum cottom. Field studies by Nipe (1981) and laboratory work by
Kamath et al. 1982 showed a positive association between O3 levels and
dye fading of nylon materials at an O3 concentration of 0.2 ppm and at
various relative. In summary, dye fading is a complex function of ozone
concentration, relative humidity, and the presence of other gaseous
-------
X-41
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 O3 damage (CO, p. 9-50).
The degradation of fibers from exposure to ozone is poorly characterized.
In general, most synthetic fibers such as modacrylic and polyester are
relatively resistant; and cotton, nylon, and acrylic fibers show variable
sensitivities to the gas. Ozone reduces the breaking strength of these
fibers, and the degree of reduction depends on the amount of moisture
present. Under laboratory conditions, Bogaty et al. (1952) found a 20
percent loss in breaking strength in cotton textiles under high-moisture
conditions after exposure to a 0.06 ppm concentration of ozone for 50
days. They equated these conditions to a 500- to 600-day exposure under
natural conditions. Kerr et al. (1969) found a net loss of 9 percent in
breaking strength of moist cotton fibers exposed to ozone at a concentration
of 1.0 ppm for 60 days. The limited research in this area indicates that
ozone in ambient air may have a minimal effect on textile fibers, but
additional research is needed to verify this conclusion (CD, p. 9-51).
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.
-------
X -42
Pigments in artists' paints have also been tested under controlled
conditions for 3 months at an average exposure level of 0.4 ppm of ozone.
While fading occurred in anthraqulnone-based pigments, no quantitative
information on dose-response relationships is available.
Among the various materials studied, research has narrowed the type
of materials most likely to affect the economy from increased O3 exposure.
These Include elastomers and textile fibers and dyes. Among these, natural
rubber, used for tires is probably the most economically important.
While the limitations of McCarthy et al. (1983) preclude the reliable
estimation of damage costs, the figures indicate the magnitude of potential
damage from exposures to O3 1n ambient air (CD, p. 9-52).
0. Effects on Personal Comfort and Well-Being
The Clean Air Act requires that secondary NAAQS for a pollutant specify
a level of air quality which is adequate to protect public welfare from
any known or anticipated adverse effects. Section 302(h) Includes personal
comfort and well-being in referring to effects on welfare. Those effects of
a pollutant in humans which are not identified as being adverse health effects
but do affect personal comfort and well-being are covered by this provision.
Symptoms are defined generally as subjective evidence of disease o-* physical
disturbance but are not necessarily adverse health effects.
Symptomatic effects associated with human exposure to O3 and other
photochemical oxidants may contribute to a reduction 1n personal comfort
and well-being. Similar but not Identical symptoms have been reported
for clinical O3 and community photochemical oxidant exposures. Eye
irritation, for example, commonly is associated with ambient photochemical
oxidant levels of about 0.10 ppm but does not occur during controlled O3
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X-43
exposures at much higher levels than found in ambient air. Symptoms such
as eye, nose, and throat irritation, chest discomfort, cough and headache
have been reported at > 0.10 ppm in children and adults (Hammer et al.,
1974; Makino and Mizoguchi, 1975; Okawda et al., 1979). Impairment of
athletic performance in high school students may have been caused by
irritative symptoms associated with 0.12 ppm oxidants (Wayne et. al.,
1967; Herman, 1972). Other symptoms commonly reported in clinical O3
studies are throat dryness, difficulty or pain during deep inspiration,
chest tightness, substernal soreness or pain, wheezing, lassitude, malaise,
and nausea. All of the above symptoms potentially can contribute to
personal discomfort and should be considered in setting primary and/or
secondary ambient standards.
-------
XI. Staff Conclusions and Recommendations Regarding the Secondary Standard
Drawing upon the evaluation of scientific information contained in
the CD, this section provides preliminary staff conclusions that should
be considered by the Administrator in selecting the pollutant indicator,
form, averaging time and level of the O3 secondary standard. The primary
focus of this discussion will be vegetation and ecosystem effects, as this
data base provides the best support for the secondary standard for ozone.
Materials damage and effects on personal comfort and well-being will be
covered in the final section. Risk and benefit analyses covering vegetation
effects are currently underway and will have a bearing on staff conclusions
and recommendations in a subsequent draft of the staff paper.
A. Pollutant Indicator
On February 8, 1979, the chemical designation of the O3 primary
and secondary standards was changed from photochemical oxidants to O3
(44 FR 8202). EPA changed the designation of the standard to O3 since
the Federal Reference Method (FRM) for determining compliance specifically
measured O3 as a surrogate for total oxidants, and because a substantial
vegetation effects research base has established O3 as being "chiefly
responsible for the adverse effects of photochemical air pollutants,
largely because of its relative abundance compared to other photochemical
oxidants (CO, p. 13-64)."
Peroxyacetyl nitrate (PAN) is an extremely phytotoxic air pollutant
that is produced by photochemical reactions similar to those that produce
O3. Controlled exposures of plants to PAN have indicated that PAN
can cause foliar injury and yield losses in sensitive cultivars of leafy
vegetable crops (p. X-22). However, a comparison of PAN concentrations
likely to cause either visible injury or reduced yield with measured
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XI-2
ambient concentrations (CO, Chapter 5) indicates that it is unlikely
that PAN related effects occur in plants in the U.S. except in some areas
of California and possibly in a few other localized areas. Because
phytotoxic concentrations of PAN generally occur at significantly lower
ambient concentrations and are less widely distributed than O3 (CD, p. 7-1),
the focus of this standard review will be the effects of O3.
The question of whether O3 can serve as an abatement surrogate for
controlling other photochemical oxidants is addressed in the CD (p. 1-44)
with a quote from Altshuller (1983) who concluded that "the ambient air
measurements indicate that O3 may serve directionally but cannot be
expected to serve quantitatively as a surrogate for the other products."
This conclusion appears to apply to the subset of photochemical products
of concern - O3, PAN, PPN, and H2O2 - identified in the CD, even though
Altshuller (1983) examined the use of O3 as an abatement surrogate for
all photochemical products. Lack of a quantitative, monotonic relationship
between O3 and other photochemical oxidants is discussed in Chapter 5
of the CD in which average PAN/O3 ratios for different sites and years
vary from 9 to 3. In addition, it is emphasized in the CD (p. 1-44) that
no single measurement methodology can quantitatively and reliably measure
O3 and other photochemical oxidants, either individually or in ambient
air mixtures.
In spite of the above limitations, it is generally recognized that
control of ambient O3 levels currently provides the best means of controlling
photochemical oxidants of potential welfare concern (O3, PAN, PPN, and
H2O2). This recognition along with a controlled-exposure, welfare data
base which implicates only O3 among the photochemical oxidants at levels
reported in ambient air, supports the recommendation that O3 be retained
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XI -3
as the pollutant indicator for controlling ambient concentrations of
photochemical oxidants. Unless significant additional evidence which
demonstrates welfare effects from exposure to ambient levels of non-
03 oxidants becomes available, it is the staff's recommendation that
O3 remain as the surrogate for protection of public health from exposure
to photochemical oxidants.
B. Form of the Standard
The current secondary O3 NAAQS is expressed as an hourly average which
is the concentration not to be exceeded on more than 1 day per year on average.
During the last standard review the decision was made to change from the
deterministic to the statistical form of the standard. The deterministic
form, which permitted only a single hourly exceedance of the standard level
in any given year, did not adequately deal with the variations in O3
concentrations which are largely due to the random nature of meteorological
factors affecting formation and dispersion of O3 in the atmosphere. In
addition, EPA further modified the standard so that one expected exceedance
would be given a daily interpretation; that is, a day with two hourly
values over the standard level counts as one exceedance of the standard
level rather than two. It is recommended that the statistical form
(i.e., a number of expected exceedances allowed per year) be retained for
the secondary standard.
The Administrator may choose to establish a longer-term (e.g., seasonal)
standard, as discussed in the following section on averaging times.
The relationships among various longer-term O3 ambient concentrations and
existing one-hour concentrations is discussed in Appendix A as well as in
the following section.
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XI-4
C. Averaging Times
In selecting the most appropriate averaging time to protect vegetation
and ecosystems from exposure to 03, questions immediately arise concerning
which components of an exposure are most important in causing vegetation
responses. The studies conducted thus far offer some useful information
in assessing the answer to this question, but to date research has not
yet clearly defined which components of exposure are the most critical in
eliciting plant responses (CD, p. 7-7). In light of these uncertainties,
the selection of an averaging time which correlates well with the effects
of concern is a difficult task. Not only is there little consensus in
the scientific community as to the most appropriate summary statistic,
researchers are currently using many different exposure statistics in
their studies, thus making comparisons between studies extremely difficult.
This section assesses the Information available on which to base a judgment
regarding the averaging time for the secondary standard.
The current ozone standard level is specified as a one-hour average.
Rather than specify different standard levels for different averaging
times, it was deemed prudent during the last standard review to retain
the concept of a standard specified for a single averaging time. As this
issue is revisited in this review, it is worth noting the data EPA used
to support the 1979 decision (44 FR 8202). Because of the extremely
limited data base relating short term, low level O3 concentrations and
yield reduction, it was necessary to rely on the more extensive data
available on foliar injury responses. A judgment was made in the proposal
that foliar injury rates in the range of 5 to 10 percent were undesirable
because of the potential for detectable reductions 1n growth and yield.
This approach was criticized by many scientists because of the uncertainty
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X1-5
associated with correlating yield reduction and foliar injury. Consequently,
EPA decided to base its decision on the few yield loss studies available,
which indicated that growth and yield responses are related to the long-term
(growing season) mean of the daily maximum 6 to 8 hour average concentrations.
EPA concluded that the 2-month mean concentrations expected to occur when
the primary standard of 0.12 ppm was attained would not cause significant
growth and yield reductions.
When reviewing the current data base for vegetation effects, it is
apparent that the bulk of the scientific research that has been completed
since the last standard review focuses on reduction in growth and yield
from various long-term (days, months) exposures. The majority of short-term
(few hours) exposures focus on foliar injury or physiological changes as
the response measure, both of which are important but have somewhat
uncertain implications for growth or yield loss (p. X-6). While short-term
exposures to high concentrations can have rapid and dramatic effects, such
as visible leaf injury, reduced photosynthetic rate, and cell death,
these effects cannot be readily extrapolated to evaluate their significance
in relation to long-term exposures (CD, p. 7-9).
There are several studies in which short-term exposures have resulted
in growth and yield reduction: exposure of cherry belle radish to 0.25
ppm O3 for three hours resulted in a 38 percent ("eduction in root dry
weight; exposure to 0.10 ppm O3 for two hours resulted in a 9 percent
reduction in the average of three growth responses of capri petunia
(Adedipe, 1972); a 16 percent reduction in leaflet area growth rate was
reported in pinto bean exposed to 0.05 ppm O3 for 12 hours (Evans, 1973).
In addition, some cultivars of crops such as spinach and tobacco expedience
yield losses due to extensive foliar injury at 0.10 ppm for 2-hours
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XI-6
(Menser and Hodges, 1972). Thus, although a few studies relate short-term
exposures and yield loss, there is very little yield loss data which
employs exposures that are easy to relate to the 1-hr average of the
current secondary standard. While consideration may be given to retaining
the 1-hr averaging time, the justification for such an averaging time
would be based on the protection it affords against long-term concentrations
which have been related to yield loss.
As stated previously, the bulk of the evidence since the last standard
review has focused on reduction in growth and yield from various long-term
exposures. The data base has been summarized previously (Sec. X.A.I.)
and consists of open top chamber studies, greenhouse and other controlled
experiments, and various ambient air exposures. Most of these studies have
characterized the exposure-response relationship in terms of the seasonal
daily daylight mean O3 concentration, although various averaging times
have been used. Several concerns have been raised about the use of means
1n summarizing distributions of concentrations over a growing season,
which is the temporal unit of interest (Sec. X.A.2).
The most notable use of a particular mean statistic is the 7-hr
seasonal mean used by NCLAN. The NCLAN experimental procedures and hence
the estimated exposure-response functions rely on O3 levels or exposures
which correspond to a seasonal 7-hr average (0900-1600 hr per day, averaged
over the growing season). According to Heck et al., (1982), the 7-hr
daily daylight period was chosen because it corresponds to the period of
greatest plant sensitivity to pollution. In addition, the relatively
regular diurnal fluctuation of O3 concentrations allows some abbreviation
in the way dose can be reported; the concentration during the middle
seven hours of the day 1s assumed to Include the highest concentrations
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XI —7
of the day (Heagle and Heck, 1980). Therefore, the 7-hr seasonal mean is
thought to reflect the variable concentration that occurs during the day
rather than a constant concentration (Heck, 1986). It has been suggested,
however, that the use of the seasonal mean as well as other mean statistics
1n characterlzlng exposure Implies that all concentrations are equally
effective 1n eliciting a plant response and minimizes the contribution of
peak concentrations. According to the CD (p. 7-10), the mean treats low
level long-term exposures the same as high concentration short-term ones.
Several authors have reported the greater Importance of concentration
compared to exposure duration in causing injury (e.g., Heck et al., 1966;
Bennett, 1979, Heck and Tingey, 1971, Relnert and Nelson, 1979).
Not only are concentration and time important but the dynamics of
exposure are also1important; that 1s, whether the exposure 1s at a fixed
or variable concentration. Fixed concentrations have been shown to have
less effect on plant growth responses than variable or episodic exposures
at equivalent doses (Musselman et al., 1983; Hogsett et al., 1985).
Generally, assessment of human physiological responses as well as vegetation
responses to O3 have stressed the importance of episodic exposures (high
concentrations over short periods of time) in eliciting a biological
response (Rogers, 1985).
Although episodic exposures are clearly important and can result in
significant damage, a special word is warranted about the unique problems
of forest trees, and therefore ecosystems, in coping with O3 on a long-term
basis (Benoit, et al., 1982; Mann, et al., 1980). Forest responses to O3
depend not only on the concentration and the duration of the 03 exposure
but on the seasonality of elevated pollutant levels in relation to annual
growth processes (Taylor, 1985). Although trees respond to (13 in the
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XI-8
same manner as agricultural crops (CD, p. 8-5), trees are perennial
crops; therefore effects can accumulate over time, or may be mitigated
through short- or long-term recovery. Physiological injury, not visible
or obvious to the unaided eye may be taking place, which could result in a
growth reduction at some future point in time. For example, using shoot
elongation as an indicator of tree performance, O3 induced growth effects
in one season for many species will be delayed to the following year.
McLaughlin et al. (1982) found that patterns in annual growth in white
pine along the Cumberland Plateau reflected a loss in capacity for short-term
recovery and eventual loss of tree vigor. The primary cause of the
decline observed was chronic exposure to elevated concentrations of O3,
possibly accompanied by low levels of SO2 and other pollutants. The
importance of the chronic stress experienced by forest ecosystems is
referred to by several authors (e.g., Smith, 1985; McLaughlin, 1985).
Assessment of the evidence above suggests the importance of short-
term episodic exposures as well as seasonal or other long-term exposures
for plants and ecosystems to O3. The question that remains is whether
better protection from O3 exposure is provided by limiting short-term
peak exposures or by limiting long-term average exposures, or both. Given
that no exposure statistic developed to date adequately captures frequency
of occurrence, duration, and developmental stage of the plant, we must
evaluate the available alternatives in light of whether they are reasonable
biologically and practical from a standard setting point of view. In
setting a short-term standard, the staff concludes that attention should
be given to identifying those dose surrogates that are correlated with
repeated peak exposure. One option would be to set a multiple exceedance
standard that would protect plants against repeated peaks above a given
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XI-9
level. The ambient air exposure studies offer some guidance as to the
appropriate level of concern (see following section). Alternatively, the
present 1-hour averaging time could be retained as a reasonable surrogate
for repeated peak exposures. Johnson et al. (1986) found that indicators
of repeated peaks above 0.08 ppm, 0.10 ppm, and 0.12 ppm are fairly well
correlated (0.6 < < 0.8) with the characteristic largest daily maximum,
a robust estimator of the second largest daily maximum. Therefore, the
staff concludes that the 1-hour standard set at an appropriate level can
provide reasonable protection from the repeated peaks of concern.
In addition, it may be possible to set a 1-hour standard at a level
which reduces the probability of experiencing a high chronic exposure.
A number of analyses examine the relationship between peak and mean
exposure statistics (McCurdy, 1985; Johnson, et al., 1986; Lefohn, 1984;
Heck et al., 1984a, 1984b). For the most part, these analyses conclude
that a fairly good relationship exists between some pairs of air quality
indicators but not others. Stronger relationships exist for the longer-term
averaging periods (months or longer). The relationship between the second
high value or peak values and the seasonal averages are generally not
stable or predictable with any degree of confidence (McCurdy, 1985; Heck,
1984, 1984b; Lefohn, 1984; Johnson et al., 1986). Thus, McCurdy concludes
"if the highest monthly average O3 concentration level in a non-SMSA
area is reduced there is reasonable assurance that the seasonal
average will be reduced also. The same can be said for the reverse
relationship. Such assurance, however, cannot be given for a situation
where the highest daily maximum is reduced. This action may be
associated with a large reduction in seasonal mean or it may not be"
(Appendix A).
Riven the uncertainty in the relationship between a 1-hour averaging
time and the seasonal concentrations to which plants might be exposed, we
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XI-10
suggest that serious consideration be given to setting both a 1-hour
(level to be discussed in next section) and a longer term secondary
standard. The longer term average could be expressed as the 7-hour daily
daylight average over a month, the O3 season, or the growing season. We
suggest a 3-month rolling average based on the maximum 3-month consecutive
daily daylight average not exceeding a given level (to be discussed in
next section). A 3-month average seems most relevant biologically because
it represents the average growing season for most crops in the U.S. Comment
and guidance is sought from CASAC regarding the need for a separate long-term
secondary standard and the most appropriate averaging time for such a standard.
D. Level of the Standard
As mentioned previously growth and yield effects provide the most
easily assessed and most quantitative measure of the effects of O3 on
vegetation. Although foliar injury is not always well correlated with
reduction in growth and yield, in the previous standard review it was
necessary to utilize this imperfect parameter to evaluate the effect of
ozone on plant growth and yield. A judgment was made in the proposal
that foliar injury rates in the range of 5 to 10 percent were undesirable
because of the potential for detectable reductions in growth and yield
associated with this level of injury. The bulk of the data available
since the last standard review uses growth and yield loss as the response
measure. Therefore, we could utilize this parameter to evaluate different
levels of the secondary standard. Alternatively, a broader range of
effects could be considered adverse, including: foliar injury, premature
senescence, reduced photosynthesis, altered translocation of nutrients
from shoots to other plant organs, and reduced plant vigor. Whether a plant
recovers from these effects or experiences damage at some later point in
time depends on a variety of biological and physical factors. Although
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XI-11
there is no precise relationship between foliar injury (and other physiological
effects) and growth and yield reductions (p. X-6), these more subtle effects
are often early warning signals of potentially harmful effects on plant
vigor (CD, 7-143). CASAC guidance and comment is sought on the range of
effects which should be considered adverse for purposes of standard setting.
If growth and yield loss is the effect of concern, a question which
immediately arises is the degree of growth and yield loss which is to be
considered adverse. Studies tend to report observed yield reductions of
10 percent or greater as this is the level that can be detected with some
degree of confidence. In addition, for major agronomic crops such as soybean,
a 10 percent yield loss would generally be considered significant. If
yield loss is determined to be the effect of concern, the staff proposes
that losses in the range of 10 percent be considered adverse and that the
basis for the secondary standard for ozone be to protect against exposures
that may reasonably be expected to produce yield losses in this range for
commercially important crops and important indigenous vegetation. Clearly
this is a judgment that merits discussion; there may be reason to consider
yield losses other than 10 percent or effects other than yield loss
adverse for some crops. As stated earlier, staff seeks guidance on the
range of effects to be considered. It is difficult to discuss the level
of a standard without also specifying the averaging time under consideration.
Therefore, this section will review the data used to support a judgment
about the appropriate level for three alternative averaging times discussed
in the previous section: a 1-hour average, a number of occurrences above
a given level (multiple exceedance); and a 3-month rolling average.
As discussed in the previous section on averaging times there is
relatively little data relating short-term (few hours) exposures and
yield loss, the effect of concern (p. XI-5). The CD indicates that the
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XI -12
lower limit for effects on growth and yield is a mean O3 concentration of
0.05 for exposure durations greater than 16 days and increasing to 0.10
at 10 days ( CD, p. 7-77). In the case of some cultivars of crops such
as spinach and tobacco, yield loss due to extensive foliar injury occurs
at concentrations as low as 0.10 ppm for 2 hours (Menser and Hodges, 1972).
Since these effects constitute a yield loss and affect the marketability
of the plant, the staff concludes they should be protected against.
One of the criteria for a short-term standard is protection from
exposure to repeated peaks. A repeated peak standard could be set to
protect plants against a number of peaks above a given level. Because of
the way in which most exposures are reported, there is limited data
available for judging the number of peaks above some level that should be
considered adverse. The ambient air exposure studies, particularly those
employing the chemical protectant ethylenediurea (EDU), offer some
insight into this question because exposures were reported in terms of
percent of hours > 0.08 ppm. A comparison of the values reported in the
ambient air exposure studies (p. X-16 to X-19) with actual air quality data
reveal that the hourly and daily maximum exposures over 0.08 ppm seen in
the studies are generally within the range of concentrations seen in ambient
air. The yield losses reported in these studies range from 10-40 percent.
The significance of peaks over 0.08 ppm is also reported for white pine
by Hayes and Skelly (1977) and Mann et al. (1980), who found that oxidant
injury on white pine in rural Virginia and on the Cumberland Plateau was
associated with total oxidant concentrations of 0.08 ppm or higher.
Based on the evidence cited above, the staff concludes that protection
from repeated peaks over 0.08 ppm is desirable.
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XI -13
An alternative way to achieve this protection is to set a 1-hr standard
as a surrogate for repeated peaks exposures. For discussion purposes, the
range of 0.08 - 0.12 ppm has been evaluated. An analysis of data from 82
monitors located in rural or remote areas indicates that at 0.12 ppm,
there is a 10% chance that 32% or more of days in a 3-month growing
season will exceed a daily daylight (9 am - 4 pm) 1-hour maximum of 0.08
ppm; at 0.10 ppm, there is a 10% chance that 22% or more of days will
exceed 0.08 ppm, and at 0.08 ppm there is a 10% chance that 14% or more
of days will exceed 0.08 ppm (Johnson et al., 1986). A comparison of
these values to those seen in the ambient air exposure studies (p. X-18)
indicates that considerable yield loss could result from the repeated
peak exposures > 0.08 ppm when a 0.12 ppm standard 1s attained. Thus,
there is some question as to whether a 1-hour standard of 0.12 ppm is
adequate for protecting crops from repeated peaks > 0.08 ppm. Comment
and guidance is sought from CASAC regarding the appropriate range for a
1-hour secondary standard.
In addition to offering some protection from repeated peak exposures,
the 1-hour standard must also be evaluated in terms of the protection it
affords against long-term averages of concern. An assessment of the
available data from open top chambers suggest that 10 percent yield
losses can occur for several major crops when concentrations exceed
0.04-0.05 ppm for a 7-hour seasonal mean (Sec. X.A). Table X-2 (p. X-ll)
gives the percent yield loss predicted to occur at a 7-hour seasonal mean
concentrations of 0.04 and 0.06 ppm. At 0.04 ppm, losses of 10% or more
occur in one or two cultivars of soybean, wheat, cotton, tomato and
turnip. Other crops such as peanut, corn, sorgum, barley and spinach did
not report yield losses exceeding 10 percent. At 0.06 ppm most cultivars,
with the exception of the more tolerant grain crops, had yield losses
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XI-14
ranging from 10-51 percent. Data from greenhouse and other controlled
chambers indicate significant yield reductions were noted for various tree
and crop species exposed to 0.05 to 0.10 ppm of O3 for one to several weeks
(Tables X-3, X-7 ). While the controlled environment studies cannot be
extrapolated to field conditions, they do serve to strengthen the demonstration
of effects found in the field. Thus the staff concludes that the range of
concern for long-term exposure of crops as well as trees and other native
vegetation is 0.04-0.06 ppm.
As mentioned previously, a number of analyses have demonstrated a rather
uncertain relationship between peak indicators (1-hr standard) and long-
term means. Johnson et al., (1986) reported 3-month daily daylight mean
statistics for agricultural and remote areas and found that the correlations
between the mean statistics and the characteristic largest daily maximum, an
estimator of the second largest daily maximum, are significant at p < 0.05;
however, the correlations are modest (R^'s in the range of 0.3-0.4). Based
on the fitted regression line, the 7-hour 3-month mean 1s predicted to be
0.052 ppm when the characteristic largest dally maximum is 0.12 ppm.
This analysis indicates there is a 10% probability that the 7-hour 3-month
mean will exceed 0.063 ppm when the characteristic largest daily maximum is
0.12 ppm. When the characteristic largest daily maximum 1s 0.10 ppm, the
7-hour 3-month mean 1s predicted to be 0.048 ppm and there is a 10% probability
that the 7-hour 3-month mean will exceed 0.058. Thus, if the long-term level
of concern is 0.04 - 0.06 ppm, there is some question as to whether a 1-hour
standard of 0.12 ppm 1s adequate. In addition, the rather weak relationship
between peak indicators and long-term Indicators calls for the consideration
of a separate long-term standard (p. XI-9).
Although it has been suggested that woody perrenials are somewhat
less sensitive to ozone than other vegetation for short-term exposures
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XI — 15
(Harkov and Brennan, 1979; Taylor, 1985; CD, p. 7-73), there is relatively
little information on which to assess the impact of cummulative effects
over multiple years on forest trees. Based on the information currently
available, staff suggests that the averaging times and levels of concern
discussed here are adequate to protect forest trees and native vegetation
as well as crops. Of the ecosystems affected by ozone, forest ecosystems
are the largest and economically most important. Although air pollution
is thought to be one of the stresses contributing to observed forest
declines in the U.S., there is still no clear evidence of a single causal
agent. The data assessed in this staff paper regarding O3 effects on
trees in chambers and In the field (Sec. X.B.), document a variety of
effects Including injury to foliage, reductions in growth and yield,
alterations in reproductive capacity and Increased susceptibility to pest
and pathogens. Although there is relatively little Information available
on which to evaluate the consequences of regional air pollution on forest
ecosystems, reduction in diversity of forest composition has been established
as a typical response to air pollution stress (McLaughlin, 1985). This
simplification of community composition has occurred in the heavily
industrialized Ohio River Valley and in the San Bernadino Mountains, and
is thought to be taking place in the high elevation spruce stands of the
Northeast (McLaughlin 1985). The staff concludes that given the preventive
nature of the act, such potential ecosystem effects provide strong supportive
evidence for the levels and averaging times previously discussed for
vegetation.
E. Summary of Staff Recommendations
Based upon the conclusions drawn in Section XIA-D, the staff recom-
mendations regarding the secondary standard are as follows:
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XI-16
1. In consideration of the large base of welfare information attributing
effects to O3 exposure and the lack of evidence which demonstrates welfare
effects from exposure to ambient levels of non-03 photochemical oxidants, it is
recommended that O3 remain as the surrogate for controlling ambient concen-
trations of photochemical oxidants.
2. The current secondary standard is attained when the expected number
of days per calendar year with maximum hourly average concentrations above
0.12 ppm is equal to or less than one (44 FR 8202). Staff recommends that
the statistical form of the O3 standard be retained.
3. Because the bulk of the data available since the last standard
review uses growth and yield loss as the response measure, this parameter
could be utilized to evaluate different levels of the secondary standard.
Alternatively a broader range of effects could be considered adverse
including: foliar Injury, premature senescence, reduced photosynthesis,
altered carbon allocation and reduced plant vigor. Although there 1s no
precise relationship between these effects and growth and yield reduction,
these more subtle effects are often early warning signals of potentially
harmful effects on plant vigor. CASAC guidance and comment is sought on
the range of effects which should be considered adverse for purposes of
standard setting.
4. Effects of O3 on vegetation and ecosystems have been demonstrated
to occur from both short-term and long-term exposures. Although there are
a limited number of studies in which short-term (1-2 hrs) exposures have
resulted 1n growth and yield reduction, there Is a growing body of evidence
that repeated peaks above a given level are important 1n eliciting plant
response. Because analyses to date Indicate a fairly strong relationship
between the second highest dally maximum value and repeated peaks of concern,
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XI-17
staff recommends setting a 1-hr standard as a surrogate for repeated peak
exposures.
The bulk of the evidence since the last standard review focuses on
reductions in growth and yield from various long-term exposures. Exposure-
response relationships were typically characterized in terms of the daily
daylight mean concentration, although various averaging times have been
used. In addition, forest ecosystems are thought to be affected by
chronic exposure to O3. The staff concludes that serious consideration should
be given to setting a long-term standard to protect crops as well as
trees and other native vegetation from long-term exposures to O3.
5. Because most exposures are reported in terms of a mean, there is
limited data available which easily relates to the present 1-hr averaging
time. EPA analyzed the range of 0.08 - 0.12 ppm for the short-term
standard on the basis of whether these levels provide adequate protection
from a) repeated peaks over 0.08 ppm and b) long-term average concentrations
in the range of 0.04 - 0.06 ppm. An analysis of air quality data from
rural and remote areas indicates that considerable yield loss could
result from repeated peaks exceeding 0.08 ppm when a 0.12 ppm standard
is attained. In terms of protection from the long-term concentrations of
concern (0.04 - 0.06 ppm), there is a 10% probability of the 3-month mean
being 0.063 ppm or greater when a 0.12 standard is attained. Thus, there
is some question as to whether a 1-hr standard of 0.12 ppm is adequate for
protecting crops from repeated peaks > 0.08 ppm or from long-term exposures
of concern.
Based on available open top chamber, greenhouse and other controlled
chamber data, the staff concludes that the range of concern for long-term
exposure of crops as well as trees and other native vegetation is 0.04-0.06 ppm.
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XI—18
CASAC guidance and comment 1s sought on the range for the short-
and long-term secondary standards.
6. There appears to be no threshold level below which materials
damage will not occur; exposure of sensitive materials to any non-zero
concentration of ozone (including natural background levels) can produce
effects if the exposure duration is sufficiently long. However, the
slight acceleration of aging processes of materials which occurs at the
level of the proposed NAAQS is not judged to be significant or adverse.
Consequently, it is proposed that the level of the secondary standard be
based on protection of vegetation and ecosystems.
7. Effects on personal comfort and well-being, as defined by human
symptomatic effects, have been associated with ambient photochemical
oxidant levels of >0.10 ppm in children and adults. These effects include
eye, nose, and throat irritation, chest discomfort, cough, and headache.
In addition, cough, chest pain on deep inspiration, chest tightness,
wheezing, lassitude, malaise, and nausea have been reported 1n controlled
O3 exposure studies. If these effects should be determined to not
constitute adverse health effects In setting the primary standard, then
it 1s the staff's recommendation that they be considered to be effects on
personal comfort and well-being and be used 1n developing a basis for
secondary ambient standards for O3.
-------
APPENDIX A: AIR QUALITY
This Appendix briefly characterizes existing ambient air quality in
urban and non-urban areas of the country. Emphasis is placed upon two
indices of air quality: (1) the expected number of exceedances of the
current 0.12 ppm O3 NAAQS, and (2) characteristic highest concentrations
actually monitored. The material presented here expands and updates the
information presented in Chapter 5 of the CD. The data generally come from
1981-1984 information contained in EPA's SAROAD (Storage and Retrieval of
Aerometrlc Data) data base system, but data are presented for other time
periods also.
The focus on expected number of exceedances 1s due to the definition
of the O3 NAAQS:
The standard is attained when the expected number of days per calendar
year with maximum hourly concentrations above 0.12 part per million
(235 pg/m^) 1s equal to or less than 1. (40 CFR 50.9, 1984)
The expected number of exceedances is determined by a mathematical formula
explained in Appendix H of 40 CFR 50 (1984). The formula 1s more fully
described in an EPA guidance document (Curran, 1979).* A characteristic
highest concentration (CHC) 1s that air quality value that is expected to
be exceeded no more than one time per year on average. There are a
number of ways to choose the CHC, ranging from using statistical
distribution fits to the data to a tabular "look-up" approach (Curran,
*The formula, rearranged to remove a term, 1n words 1s:
Estimated Number Number of Measured Number of Number of Days
of Exceedances in Dally Values Above * Days 1n the - Assumed to be
a Year (Ozone 0.12 ppm Ozone Season <0.12 ppm
Season) 3 Number of Valid Daily Maxima
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A-2
1979). A modified version of the look-up approach is used here because
it is the simplest method and is used by most states in analyzing ozone
air quality (AMTB, 1981). The CHC under this approach is the n+1 highest
observed daily maximum value where n equals the number of years of valid
data.* Thus, if there are three years of data, the CHC is the 4th-highest
value in the ranked order data set. If there is one year of data, it is
the second-highest value.
A. Ambient Ozone Air Quality in Urban Areas
There are 331 Metropolitan Statistical Areas (MSAs) in the 50 states.
Of the 331 areas, and using 1982-1984 air quality data, 223 (67.4%) have
sufficient expected exceedance data and valid characteristic highest
concentrations. The distribution of expected exceedances for MSAs appear
in Table A-l.
1. Expected Exceedances of the Existing Ozone NAAQS
The data indicate that 113 MSAs (50.7%) have more than one
expected exceedance in a year. Thus, a significant proportion of U.S. urban
areas exceeded the existing O3 standard concentration level in at least one
year during the 1982-1984 time period.
Approximately 110 million people live in these non-attaining MSAs.
That is slightly over one-half of the total U.S. population (1980 Census
estimates). Over 20 million people live in MSAs that have 25 or more
estimated expected exceedances in at least one year between 1982 and
1984. Over 9 million people live in the two MSAs that have almost 150
*A valid year of data is one that contains a valid daily maximum one-hour
average for 75% of all the days in the state-defined "ozone season." A
valid day has data for 75% of the hours between 9 am and 9 pm (9 hours).
An O3 season is a fixed period of months that Is expected to contain
most, if not all, high O3 days in the year for each state; it varies from
4 months (June through September) in northern-tier states to 12 months in
some southern states.
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A-3
TABLE A-l
DISTRIBUTION OF EXPECTED NUMBER OF
EXCEEDANCES OF THE 0.12 PPM 03 STANDARD
FOR METROPOLITAN STATISTICAL AREAS
(1982-1984 Data Base)
Expected Number of % of Cumulative
Exceedances MSAs Total % Total
<1.0
110
49.3
49.3
1.1-2.0
33
14.8
64.1
2.1-3.0
16
7.2
71.3
3.1-4.0
10
4.5
75.8
4.1-5.0
8
3.6
79.4
5.1-6.0
4
1.8
81.2
6.1-7.0
3
1.3
82.5
7.1-8.0
4
1.8
84.3
8.1-9.0
5
2.2
86.5
>9.0
30
13.5
100.0
TOTALS 223 100.0
Note: There are 331 MSAs in the 50 states. Thus, adequate O3 data are
available for 67.4% of all MSAs. Of these areas, 50.7% (113) do
not attain the current O3 standard.
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A-4
expected exceedances of the O3 NAAQS in one year during the 1982-1984
time period. This does not necessarily mean that everyone living in these
MSAs experience high O3 concentrations. See Section V.
2. Characteristic Highest Concentrations
As mentioned, 223 MSAs of all sizes have valid characteristic
highest concentration (CHC) data. The distribution of these values are
shown in Table A-2. The data indicate that 109 (48.9% of all MSAs
have a CHC of 0.120 ppm or larger. These values are roughly comparable
to the number of MSAs that have more than one expected exceedance of
the existing O3 NAAQS.
The highest CHC for all SMSAs is 0.36 ppm for the Los Angeles -
Long Beach, CA MSA. This is closely followed by the 0.34 ppm value for
the Riverside-San Bernardino, CA MSA. (These two MSAs are in the same
air basin in Southern California.) Other MSAs having a CHC of 0.250 ppm
or higher are Anaheim-Santa Ana, CA and Las Vegas, NV.
3. Trends in Ozone Air quality
EPA publishes a "Trends Report" every spring; the most recent
version contains 1975-1983 data (Hunt, 1985). The report presents data
for both expected exceedances and characteristics highest concentrations--
in this case the second-highest daily maximum one-hour value at certain
"indicator" monitoring sites used for trends analyses purposes.
On average, expected exceedances showed a general downward trend in
the 1975 to 1981 time period, although a change in calibration methods in
the late 1970s raises questions about the magnitude of the trend (CD, p. 5-5).
Expected exceedances leveled off in 1982 but increased significantly in
1983 (Hunt, 1985 p. 3-37). The trend in CHCs roughly followed the same
pattern (Hunt, 1985 p. 3-36). The report attributes the increase in 1983
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A-5
TABLE A-2
DISTRIBUTION OF 03 DESIGN VALUES
FOR METROPOLITAN STATISTICAL AREAS
(1982-1984 Data Base)
Design
Value
(ppm)
Number of
MSAs
% of
Total
Cumulati ve
% Total
£.080
6
2.7
2.7
.081-.100
36
16.1
18.8
.101-.120
72
33.3
52.1
.121-.140
44
19.7
71.8
.141-.160
31
13.9
85.7
.161-.180
16
7.2
92.9
.181-.200
7
3.1
96.0
>.200
11
4.0
100.0
TOTALS
223
100.0
-
Note: 109 MSAs have a design value
MSAs with data.
> .12 ppm. They are
48.9 of the total
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A-6
O3 indicators to increasing emissions of volatile organic chemicals
(precursors of ambient O3 and other oxidants) and to meteorological
conditions in 1983 that favored oxidant formation.
The averaged data presented in the Trends Report can mask changes in
individual urban areas due to the "canceling-out" effect of using data
from many sites in a combined index. When trends in individual urban
areas that exceed the 0.12 ppm standard are investigated, the following
conclusions can be drawn (McCurdy, 1984a):
a. 1983 was a bad year for ozone CHCs compared to 1982 for most
urban areas; 83% of the areas had a higher CHC in 1983 than in
1982. Only 6% of the areas had a lower value.
b. There is no clear-cut trend in O3 air quality. No urban area
has a monotonically increasing or decreasing trend in its CHC
during the 1979-1983 time period.
c. Approximately 67% of non-attaining urban areas had a CHC in 1983
higher than its corresponding value in 1979 (or 1980 if the 1979
value was missing).
4. Longer-Term Ozone Averages
Usually only indices of short-term O3 air quality are of interest,
since the existing O3 NAAQS in essence is a peak daily maximum standard.
More emphasis, however, is being placed on longer-term averages in order
to ascertain if chronic O3 exposures could perhaps be a problem.
A few analyses on longer-term O3 averages in urban areas have been
undertaken. Results of two such analyses are included in Table A-3.
The daily daylight period used in the analyses is 8:00 am - 4:00 pm (8 hours).+
Two long-term periodic aggregation times are used: the 3rd quarter (July,
August, September) and the "season," which is the 2nd and 3rd quarters
(Apri1-September).*
+For the most part, this is local standard time (LST) but a few states
report their data to EPA in local daylight savings time (LDST).
*Th1s season is not to be confused with the "ozone season" discussed
earlier as the time period for which O3 data are available from the States.
The term season hereafter specifically refers to the 6 month, April-to-
September time period.
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A-7
As can be seen, there is not much difference between the 3rd quarter
and seasonal averages for either data set. The difference is not
statistically significant at p<.05, but the statistical test is marred by
a lack of independence between the two data sets since 3rd quarter values
are included in the seasonal average data set. However, the difference
between seasonal means for the two data sets is marked, which raises
concern about stability of long-term air quality indices of O3, since
different samples result in greatly different statistics.
A number of analyses were undertaken on the relationship between
short-term peaks and long-term averages of O3 (McCurdy 1984b, 1985).
While the specific indices used vary,* a number of conclusions can be
drawn concerning the relationship in general:
a. there is a statistically significant association (at p < .05)
between short- and long-term O3 indices.
b. the ratio of peak-to-mean indices, 1n this case between the
second-highest daily maximum value and the daily daylight seasonal
average, follows a narrow distribution (McCurdy, 1984b). The
distribution is shown in Figure A-l. Approximately two-thirds
of the ratios will fall between 2.3 and 4.3. However, the ratio
can get as high as 9.4 in some urban areas with a relatively low
mean O3 average and a very high peak concentration. (This is
the case in some California urban areas.) Using the median ratio,
a second-high daily maximum of 0.12 ppm is associated with a
daily daylight season mean of 0.039 ppm, and there is a 68%
chance of it being between 0.028 and 0.052 ppm.
c. A statistically significant, but marginal, functional relationship
exists between the seasonal average and short-term peak (p<05,
r2 3 0.38). The relationship is reciprocal: the peak value can
be predicted from the mean with some degree of confidence and vice
versa. Using it to predict seasonal means from second-high
daily maximums (which are more widely known than the averages)
gives the following regression equation:
*Two peak Indicators used were the CHC, as defined above, and the second-
highest daily maximum value in a year; some long-term averages used were
monthly averages, separate 2nd- and 3rd quarter averages, and the six
months seasonal averages.
-------
A-8
TABLE A-3
DESCRIPTIVE STATISTICS ASSOCIATED WITH LONG-TERM OZONE
DAILY DAYLIGHT AIR QUALITY INDICATORS IN MSAs
(1981-1983 AIR QUALITY)
Analysis la Analysis 2&
Statistic
3rd Quarter
Average
(ppm)
Seasonal
Average
(ppm)
3rd Quarter
Average
(ppm)
Seasonal
Average
(ppm)
Mean
.050
.047
.043
.043
Std. Deviation
.011
.008
.014
.012
Range
.042
.034
.130
.108
Mi nimum
.028
.029
.011
.013
Maximum
.070
.064
.141
.121
Sample Size
65
65
274
283
Notes: aAnalysis 1 is reported in McCurdy (1985). It consists of MSAs paired
with non-SMSAs to determine if simple functional relationships could be
developed among short- and long-term air quality indicators.
bAnalysis 2 is reported in McCurdy (1984b). It consists of data from
counties contained in 194 MSAs around the country.
-------
A-9
Daily Daylight Seasonal Mean = 0.0217 +
[0.1539 * Second-High
Oaily Maximum]
Using the equation to predict the mean from short-term peak
values gives the following results:
2nd High Daily Daylight
Daily Maximum Seasonal Mean
(PP"0 (ppm)
.08 .034
.12 .040
.16 .046
.20 .052
.24 .059
d. Statistically significant functional relationships (p < .05)
exist between the seasonal average and the expected number of
days above various short-term daily maximum peak concentration
levels. Six concentration levels were investigated: every
0.02 ppm over the range of 0.10 to 0.20 ppm. The following
regression equation of the form y^ = a + bx can be used to
predict the number of expected days, y, in an ozone season
with a daily maximum concentration equal to or greater than
the threshold t, as a function of the daily daylight seasonal
mean, x. The (a) term is a constant; the (R^) statistic is a
measure of "predictability" of the equation shown. (It actually
indicates how much of the variance in the dependent variable
is "explained" by the independent variable x.)
Dally Maximum
Value (t) Regression Regression Coefficient
Constant Coefficient of Determination
(ppm) (a) (b) (R2)
.10 -43.3 1,379.7 0.60
.12 -34.3 968.2 0.50
.14 -27.6 728.8 0.44
.16 -22.2 569.8 0.40
.18 -18.6 469.6 0.38
.20 -14.6 363.9 0.36
For a daily daylight seasonal mean of 0.043 ppm, the second
equation would predict that 7 days would be at or above 0.12
ppm; the fourth equation predicts that 2 days would be at or
above .16 ppm.
Taken together, the analyses indicate that reasonable relationships
among short- and long-term O3 air quality Indicators 1n urban areas can
-------
100
90
80
70
60
50
40
30
20
10
A-10
Figure A-l
IMULATIVE FREQUENCY DISTRIBUTION OF THE RATIO OF
PEAK-TO-MEAN OZONE INDICES IN MSA COUNTIES
Median*3.09
i
¦Mean»3.29
j I i L
8
10
n»283
S0-0.996
Ratio of Peak-to-Mean Ozone Indices
-------
A-11
be developed. They can then be used, for instance, to estimate the impact
that controlling emissions to meet a short-term O3 standard might have on
a longer-term average concentration.* Other relationships can be developed
and used to estimate how many expected exceedances of the short-term
standard might be expected from various long-term standards. More analyses
of the type described above will be undertaken during the O3 NAAQS review
process as possible alternative long-term standards are specifically
identified.
B. Ambient Ozone Air Quality in Non-MSA Areas
Data representing O3 air quality in non-MSA areas are presented in
this part of the Appendix. They are not necessarily "rural" areas or
"remote" areas, which are labels used by some authors to designate monitoring
sites used in their analyses. The monitoring sites used here come from
sites outside of a MSA; they are located in agricultural and forested
areas. However, no distinction 1s made here among these areas except
when information from non-EPA researchers is used. In those cases, the
author's own designation is used. Some of the non-MSA areas are located
downwind of, and near to, MSAs; thus, some of the sample areas used are
affected by transported ozone from urban areas. The data used here come
primarily from Johnson et al., (1985) and McCurdy (1985).
1. Short-Term Air Quality
Data from over 65 non-MSAs were analyzed. Descriptive statistics
for short-term indices of air quality are contained in Table A-4; the
indices are:
~Assuming that emission reductions do not alter the basic air quality
distribution Itself.
-------
A-12
a. second-highest daily maximum 1-hour average (a variant of the
CHC; see above).
b. second-highest daily daylight (8 a.m. - 4 p.m.) 1-hour average.
c. expected number of exceedances of the 0.12 ppm O3 standard.
Cumulative frequency distribution of the first two indices, using data
from McCurdy (1985), appears as Figure A-2.
The two 2nd-high indices are correlated (r = 0.74) and are significantly
different (at p < .05).* This indicates that the highest daily values seen
in non-SMSA areas occur later than 4 pm (or, less likely, earlier than
8 am). (This finding is corroborated by other evidence presented in
McCurdy (1985)). The explanation for the difference probably is transported
O3 coming into the non-SMSA area from urban areas in the early evening.
Johnson et al. (1985) reported separate information for agricultural and
"remote" (generally forested) areas. Certain descriptive statistics for these
areas appear in Table A-5. It is obvious that the means of the three
statistics computed are larger for rural agricultural sites than for the
remote sites. This indicates that ozone levels are generally higher in
rural areas than in remote, forested areas, as might be expected.
The 2nd-high daily maxima values for remote areas are similar to
1-hour maxima for forest sites monitored under the National Air Pollution
Background Network (mean = 0.098, range = 0.07-0.145; CD, p. 5-28). The
2nd-high daily maxima values for agricultural areas shown in Table A-5 are
similar to the 95th percentile all-hours values reported in Lefohn (1984)
for rural areas.
*However, the independence assumption of the difference-in-means test
is violated due to both data sets containing the same hourly values.
This makes the finding of a large difference between the CHC and
daily daylight value even more remarkable.
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A-13
TABLE A-4
DESCRIPTIVE STATISTICS ASSOCIATED WITH SHORT-TERM OZONE
AIR QUALITY INDICATORS IN NON-MSA AREAS
Number of Expected
Exceedances of 0.12 ppm
2nd High 2nd-High
Dally Maximum Daily Daylight Daily All
Statistic
(ppm)
(ppm)
Maximum
Hours
Mean
.109 .110
.080
1.4
4.3
Std. Deviation
.021 .025
.013
3.2
11.6
Range
.126 .136
.074
21.7
73.6
Minimum
.044 .060
.034
0.0
0.0
Maximum
.170 .196
.108
21.7
73.6
Sample Size
65a 82b
65a
65a
82b
Sources: aData for the sample size of 65 areas are from McCurdy (1985), using
1981-1983 aerometrlc data.
bThe 82-areas data are from Johnson et al. (1985), using 1982-1984
information.
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A-14
Figure A-2
CUMULATIVE FREQUENCY DISTRIBUTION OF
SHORT-TERM OZONE AIR QUALITY INDICATORS
IN NON- MSA AREAS
2nd-High
Daily
Oaylight
Values
2rid-High
Daily
Maximum
Values
n=65
.02
.04
.06
.08
10
,12
,14
.16
.18
Ozone Concentration (ppm)
-------
A-15
2. Repeated Peak Indices
There is some interest in air quality indices for O3 focused on the
number or percent of hourly or daily O3 peaks occurring over an extended period
(e.g., season, year). These indices generally are for the number of days
having a daily maximum one-hour peak concentration over some specified
value, or "cutpoint," or for the number of hours in a year over the outpoint.
Two hourly repeated peak indices appear in Table A-5. Summary statistics
for four repeated dally peak indices appear in Table A-6.
From Table A-5, it is seen that 5 hours per year can be expected to
exceed the 0.12 ppm NAAQS standard level 1n agricultural areas, on average.
This number drops to less than 1 per year in remote areas. For a lower
cutoff, 0.08 ppm, almost 119 hours per year can be expected to exceed it on
average in agricultural areas. This statistic again drops for remote areas:
down to about 37 hours per year, on average.
Turning to the daily maxima repeated peaks data depicted in Table A-6,
daily maximum values of 0.06 pm are exceeded about 31% of all days, on
average. The corresponding value for daily daylight maxima is about 13%
of all days. (This difference is another indicator that long-range
transport is responsible for high O3 levels in non-SMSA areas.) Around
10% of all days in non-SMSAs, on average, see a daily maximum > 0.08
ppm, but only 1.4% of all days see a daily daylight maximum greater than
0.08 ppm, on average. Similarly, the CO provides values for four rural
sites whose percentage of time with concentrations > 0.08 ppm ranged from
0.6% to 1.8% (CO, p. 5-26). The mean for the four sites is 1.4%.
As might be expected, there are high correlations among the repeated
peak O3 indicators (r's in the 0.7-0.9 range). The repeated peak
Indicators are fairly well correlated with the 2nd-high daily daylight
-------
A-16
TABLE A-5
DESCRIPTIVE STATISTICS ASSOCIATED WITH SHORT-TERM OZONE AIR
QUALITY INDICATORS IN AGRICULTURAL AND REMOTE AREAS
(1982-1984 DATA)
Expected Exceedances of
2nd High Hourly Concentrations of:
Daily Maximum
(ppm) .08 ppm .12 ppm
Statistics
Agrlc.
Remote
Agric.
Remote
Aqric.
Remote
Mean
.113
.093
118.9
37.2
5.0
0.8
Std. Deviation
.025
.020
108.8
34.1
12.5
1.6
Range
.129
.061
474.2
91.3
73.6
5.0
Minimum
.067
.060
0.0
0.0
0.0
0.0
Maximum
.196
.121
474.2
91.3
73.6
5.0
Sample Size
69
13
69
13
69
13
Source: Johnson, et al. (1985).
-------
A—17
TABLE A-6
OESCRIPTIVE STATISTICS ASSOCIATED WITH REPEATED DAILY PEAKS
OF OZONE AIR QUALITY IN NON-MSA AREAS
(1981 - 1983 DATA)
Percentage of Days > Cutpoint Shown
Daily Maximum 1-Hour Daily Daylight 1-Hour
Statistic 0.06 ppm 0.08 ppm 0.06 ppm 0.08 ppm
Mean
31.1
10.2
12.7
1.4
Std. Deviation
16.3
8.3
10.2
1.8
Range
68.5
32.0
32.9
7.8
Mi nimum
0.0
0.0
0.0
0.0
Maximum
68.5
32.0
32.9
7.8
Sample Size
65
65
65
65
Source: McCurdy (1985).
-------
A -18
peak index and with the 3rd quarter average (see below). The r value
for these two sets of indicators is in the 0.7 - 0.9 range. The
correlations between repeated peak measures and the 2nd-high daily maximum
index are significant at p < 0.5, but they are modest (r's in the range of
0.4 - 0.6).
3. Longer-Term Averages
Summary data for four long-term O3 average air quality indices
appear in Tables A-7 and A-8. While the mean values are fairly "tight"
in Table A-7, difference-in-means tests indicate that some means are
significantly different at p < 0.5; for example, the mean daily daylight
value is statistically different than the seasonal average value. (Again,
the samples are not totally independent.) Most of the other values shown
in Table A-7 are not significantly different, however. In addition,
correlations among the long-term averages vary widely. The r value for
the daily daylight mean with the others is in the range of 0.2 - 0.3;
for the remaining indices, the r value is on the order of 0.7 - 0.9.
Daily daylight means are highly correlated with repeated peak indices.
This last finding differs to some degree from results presented in
Lefohn (1984). He found no correlation between seasonal averages of
daily daylight means and number of hours > 0.10 ppm. The 7-hour and
12-hour means presented in Lefohn (1984) for 45 rural site-years also seem
to be higher than the seasonal mean data presented in Table A-7. Dif-
ferences in site selection criteria and years of analysis used in the two
studies probably can explain the different results. Therefore, the
result reported above probably cannot be generalized.
Means for agricultural and remote areas contained in Johnson et al.
(1985) appear in Table A-8. The time period for these means is the entire
-------
A-19
TABLE A-7
DESCRIPTIVE STATISTICS ASSOCIATED WITH LONG-TERM OZONE
DAILY DAYLIGHT AVERAGES IN NON-MSA AREAS
(1981 - 1983 DATA)
Mean Daily Highest Monthly 3rd Quarter Seasonal
Daylight Value Average Average Average*
Statistic (ppm) (ppm) (ppm) (ppm)
Mean .039 .053 .045 .044
Std. Deviation .008 .009 .010 .008
Range .035 .048 .041 .037
Minimum .018 .023 .021 .021
Maximum .054 .071 .061 .058
Sample Size 65 55 65 65
Source: McCurdy (1985).
*A season is April through September. It is not to be confused with the
O3 season, which varies by State and is specified for data gathering purposes.
-------
A-20
ozone season, so the data cannot be directly compared with Table A-7
information. While the means are not much different between agricultural
and remote areas, the range between minimum and maximum ozone seasonal
means is much narrower for remote areas than for agricultural areas.
The month having the highest valid daily daylight average varies
with the non-MSA area, but generally falls in May, July, or August.
This is shown by the following data.
Number of
MSAs Having
Highest the Highest Percent of
Month Month Total
April 1 1.6
May 21 33.9
June 8 12.9
July 17 27.4
August 15 24.2
TOTAL 62 100.0
4. Relationships Among Air Quality Indicators in Non-MSA Areas
Extensive analyses of relationships among air quality indicators for
different time periods have not been undertaken fn non-MSA areas. Results
from two analyses will be discussed in this section. The first analysis
was done by Ambient Standards Branch staff. Four indicators of interest
used in their analysis are:
a. highest monthly average of daily daylight (3 am - 4 pm) hourly
values.
b. 90th percentile of daily maximum 1-hour values.
c. second-highest daily maximum 1-hour value.
d. seasonal average (April - September) of daily daylight hourly
values.
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A-21
The focus is on ratios of the first three indicators listed above with
the fourth. A plot of the cumulative frequency distributions for the three
ratios appears as Figure A-3.
A difference-in-means tests indicates that there 1s a statistically
significant (p < .001) difference among the three ratios. (Since the
denominator of the ratios is the same, this finding implies that the
air quality indicators are themselves significantly different.) The
plot indicates that the ratios for two of the averaging times -- highest
month-to-seasonal mean and 90th percentile daily maximum-to-seasonal
mean — are narrowly distributed. For instance, the middle 50% values
of the first ratio mentioned fall between 1.13 and 1.25. The middle 50%
values of the 90th percentile daily maximum-to-seasonal mean fall between
1.55 and 1.80. These are both narrow ranges.
The 2nd-highest daily maximum-to-seasonal mean ratio, however, shows
a broad distribution and a wide 50% mid-range of values. Fifty percent of
all values for this ratio are expected to fall between 2.1 and 3.0.
These findings indicate that a fairly stable relationship exists
between some pairs of air quality indicators in non-MSAs but not others.
The better relationships are obtained for the longer-term averaging
periods (months or longer) or non-extreme "cutpoints" (i.e., 90 percentile)
in air quality distributions. The second-high/long-term relationship, on
the other hand, is not stable or predictable, with any reasonable degree
of confidence. In practice, then, if the highest monthly average O3
level In a non-MSA area is reduced, there 1s reasonable assurance that
the seasonal average will be reduced also. The same can be said for the
reverse relationship. Such assurance, however, cannot be given for a
-------
A-22
Figure A-3
CUMULATIVE FREQUENCY DISTRIBUTION OF THE
RATIOS OF SHORT-TO-LONG TERM OZONE INDICES
TO THE SEASONAL AVERAGE OF DAILY DAYLIGHT VALUES
100
u
3
n=28
Ratio
A. Highest Month by Average of Daily Daylight Values
B. 90th Percentile Daily Maximum
C. 2nd-High Daily Maximum
-------
A-23
situation where the highest daily maximum is reduced. This action may
be associated with a large reduction in seasonal mean or it may not be.*
The second analysis was undertaken by Johnson et al (1985). One of
their aims was to develop prediction models to relate peak air quality
indicators to longer-term averages. These models are reproduced here for
various dependent variables for rural agricultural sites.
9am-4pm
O3 seasonal = 0.0262 + [0.149 * Second-Highest Daily Maximum]
mean
R2 - 0.24 (p < 0.05)
9am-9pm
O3 seasonal 3 0.0269 + [0.130 * Second-Highest Daily Maximum]
mean
R2 = 0.23 (p < 0.05)
Expected Hours
Per Year = -295 + [3,640 * Second-Highest Daily Maximum]
> 0.08 ppm
R2 ¦ 0.70 (p < 0.05)
Expected Hours
Per Year 3 -41 + [400 * Second-Highest Daily Maximum]
> 0.12 ppm
R2 » 0.65 (p < 0.05)
Using these equations, a second-highest daily maximum of 0.12 ppm results
in the following predictions (best estimate and 95% confidence interval
(C.I .)):
*As an example, if the "peak" (second-highest daily maximum) is reduced
by 0.06 ppm, the best estimate of change in the seasonal mean would be
a reduction of 0.026 ppm. However, there is a ten percent chance that
the reduction could be as low as 0.017 ppm or as high as .030 ppm.
-------
A-24
Variable
Unit
Lower
Bound
C.I.
Best
Estimate
Upper
Bound
C.I.
9am-4pm O3 Seasonal Mean ppm
9am-9pm O3 Seasonal Mean ppm
Expected Hours > 0.08 ppm hours
Expected Hours > 0.12 ppm hours
0.041
0.041
119
4
0.044
0.043
142
7
0.047
0.045
165
10
As discussed above, a large reduction in a short-term peak indicator
would result in only a small change in longer-term average indicator.
For instance, reducing the second-highest daily maximum to 0.08 ppm from
0.12 ppm (a 33% reduction) reduces the 9am-4pm O3 seasonal mean from a
predicted 0.044 ppm to a 0.038 ppm predicted mean (a 14% reduction).
-------
A-25
REFERENCES
Air Management Technology Branch (AMTB). Guideline for Use of City-
Specific EKMA in Preparing Ozone SIPs. Research Triangle Park,
N.C.: U.S. Environmental Protection Agency, 1981. (EPA-450/4-
80-027).
Code of Federal Regulations (CFR); various titles and sections.
Curran, Thomas C. Guideline for the Interpretation of Ozone Air Quality
Standards. Research Triangle Park, N.C.: U.S. Environmental
Protection Agency, 1979. (EPA 450/4-79-003).
Hunt, W.F. (ed). National Air Quality and Emissions Trends Report, 1983.
Research Triangle Park, N.C.: U.S. Environmental Protection Agency,
1985. (EPA 450/4-84-029.
Johnson, Ted; Ferdo, Alicia; and Capel, Jim (1985). Relationships Between
Selected Air Quality Indicators Used to Predict Ozone Damage to C-ops
and Woodlands. Durham, N.C.: PEI Associates, Inc., 1985.
Lefohn, Allen S. "Exposure Considerations Associated with Characterizing
Ozone Ambient Air Quality Monitoring Data." Paper presented at the
APCA Specialty Conference; Houston, November 1984.
McCurdy, Thomas (1984a). Memorandum: Preliminary Analyses of Trends in
Ozone Values in Urban Areas, 1979-1983. Ambient Standards 8ranch,
U.S. Environmental Protection Agency; October 22, 1984.
McCurdy, Thomas (1984b). Miscellaneous Analyses of Alternative O3 NAAQS
Formulations and Their Impact on O3 Non-Attainment and Cost Analyses
Procedures. Research Triangle Park, N.C.: U.S. Environmental Protection
Agercy, 1984.
McCurdy, Thomas (1985). An Analysis to Develop Simple Functional Relationships
Tnat Relate Short-Term Ozone Air Quality Concentrations to Rural Area
Air Quality Indicators. Research Triangle Park, N.C.: U.S. Envi"onmental
Protection Agency, 1985.
-------
APPENDIX B: HEALTH RISK ASSESSMENT
As part of its ongoing review of the national ambient air quality
standards (NAAQS) for ozone, the Office of A1r Quality Planning and
Standards (OAQPS) of the U.S. Environmental Protection Agency (EPA) has
contracted with Systems Applications, Inc. (SAI) to conduct an ozone
NAAQS health risk assessment. That assessment will estimate the public
health risk associated with just attaining alternative ozone standards.
Together with the results of an ozone exposure analysis being conducted
for the EPA, the results of the risk assessment will aid EPA decision
making regarding the adequacy of the margin of safety for alternative
primary ozone NAAQS under consideration. This Appendix briefly describes
the health risk assessment project. A more detailed discussion of the
ozone health risk assessment project is contained 1n Hayes et a 1. (1986).
The relationship between the exposure analysis and health risk
assessment projects is indicated in Figure 1. The risk assessment is
intended to characterize, as explicitly as possible, the range and
implications of uncertainties in the existing scientific data base, making
full use of current scientific knowledge (as reflected in the ozone
criteria document) and scientific expertise (as reflected 1n the scientific
judgments of recognized experts). The ozone risk assessment is not
intended as a substitute for scientific research nor to produce new
scientific knowledge.
Structure of the Ozone Risk Assessment
The ozone exposure and health risk assessment projects have 6 major
components, as depicted in Figure 1. The first 3 components focus on
estimating ozone exposures for the sensitive population and are described
-------
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-------
B-3
on pp. V-l - V-7 of this staff paper. The fourth component concerns
assessment of exposure-response relationships and the fifth component
integrates the outputs from the expos'ure and exposure-response components
to generate headcount risk estimates. The sixth component integrates
estimated cumulative probability distributions of the highest ozone
concentrations occurring upon attainment of alternative ozone standards
with the probabilistic exposure-response relationships to generate
benchmark risk estimates. A more detailed description of component
models 4,5, and 6 follows.
Component model 4 involves the development of probabilistic exposure-
response relationships for the health effect indicators of interest.
The goal of the ozone risk assessment is to determine probabilities
of occurrence of specified adverse consequences in light of the currently
available scientific information about the variables and relationships of
interest. If extensive data was available from carefully controlled
experiments on the sensitive populations at ozone levels of interest, then
probabilistic exposure-response relationships could be developed directly.
Since the available data base is more limited for most, if not all, ozone
health endpoints, an important aspect of the risk assessment will involve
the use of probability encoding to represent judgments from health experts
concerning the exposure-response relationships of interest.
Probability encoding involves interviewing health experts to assess
their estimated probabilities of the proportions of the sensitive population
that would suffer a particular adverse health effect, at given exposure
levels. Care is taken to ensure that the experts carefully review rele-
vant data and that they understand the exact definitions of the sensitive
groups, the health effects, and the exposure levels. The encoding proto-
-------
B-4
col is developed to structure the encoding process in a manner consistent
with the nature of the experts' information and with the way the experts
find it most convenient to think about the problem. Therefore, encoding
protocols will differ for different health endpoints, and flexibility is
necessary on an expert-by-expert basis. The final result, however, is a
representation of an expert's judgment about the exposure-response
relationship.
With any experimental data, statistical methods may be used to
characterize the uncertainty associated with random variability as well as
with measurement and sampling error. In situations where experimental data
are sparse and may be only indirecty relevant (e.g., because the experimental
population is different from the sensitive population of interest), this
experimental variability may represent only a small portion of the
scientific uncertainty about the exposure-response relationship. The
probability encoding process is designed to capture not just this sta-
tistically-based uncertainty, but uncertainty about how the results
generalize to a different situation, about the exact nature of the process
linking ozone exposure to physiological effects, and about other factors
pertaining to the exposure-response relationship. It is convenient to
think about two general sources of uncertainty: that which represents
variation in the way people respond to a pollutant, and that which repre-
sents the absence of perfect knowledge about all of the mechanisms in-
volved. The probability encoding process is designed to capture both
types of uncertainty. While precisely expressed mathematically, the
probabilistic exposure-response relationship is not necessarily a measure
of truth, but of the state of the encoded expert's informed opinion.
Such a probabilistic relationship characterizes the certainty, or lack
-------
B-5
thereof, of a single expert's views; the collection of relationships
obtained from several experts represents the consensus, or lack thereof,
among different experts.
The use of probability encoding in the NAAQS context began with the
initial development of a risk assessment methodology under the auspices of
OAQPS in the late 1970s. General approaches to risk assessment for NAAQS
were developed and presented by several teams. Two of these approaches,
both of which used probability encoding, were applied to carbon monoxide,
and at the same time some experimentation with probability encoding of
dose-response relationships was conducted. Probability encoding has sub-
sequently been used to obtain judgments about dose-response relationships
for adverse health effects associated with exposure to lead. The encoding
procedures planned for ozone are similar in general nature to those used
in the lead study (Wallsten and Whitfield, 1986).
The primary steps in the ozone risk assessment are as follows:
(1) Encode selected experts. For each EPA-specified health endpoint,,
the protocols whereby expert opinion will be encoded will be developed
and tested. After obtaining EPA and CASAC concurrence on those
protocols, selected experts will be encoded. Encodings will be
performed in a manner similar to that of Wallsten and Whitfield
(1986). Currently, the encoding of four health endpoints is planned,
with 4 experts to be encoded per endpoint. Each expert will be
visited twice, for a total of 32 encoding sessions.
(2) Determine probabilistic exposure-response relationships. The
process by which probabilistic exposure-response relationships are
obtained from the encoding data is illustrated in Figure 2. The
results of an encoding session produce the data points plotted in
-------
B-6
1.00
0.95
0)
I— o
•r- C
.O
> <*-
Q
fO »—
f— 01
3 >
E
-------
B-7
Figure 2a. Through the interviewing process, several sets of points
are elicited, each set representing, for a different exposure protocol
(e.g., a certain ozone concentration, at a certain exercise level,
and for a certain time period), the expert's judgments about the
probability that a given fraction of the sensitive population group
will experience the specified health endpoint at that concentration,
for that exposure protocol. The encoding data points are then fit
analytically using appropriate mathematical functions (e.g., equal-
variance, normal-on-log-odds, or other suitable distributions). The
mathematical functions Fz (Z,C) shown in Figure 2a can be inverted
to yield the exposure-response relationship Z (C,F2) in Figure 2b.
The inversion is illustrated in the figure as follows: For several
probabilities (e.g., 5, 50, and 95 percent), affected population
fractions are determined for each encoded concentration level. The
fractions are then plotted as in Figure 2b. For reference, the
numbered points in Figure 2a correspond to those in Figure 2b.
(3) Obtain exposure estimates. As stated earlier, an ozone exposure
analysis is being conducted separately using the NEM population
exposure model. Exposure estimates will be made for conditions of
exact NAAQS attainment fn 10 to 12 different urban areas for alternative
ozone 1-hour standards in the range 0.08 to 0.14 ppm, as well as,
for current ozone levels in these urban areas. Exposure distributions,
which will be developed for each urban area-standard combination and
for the nationwide urban population, will be obtained and used in
the health risk assessment.
(4) Perform risk modeling. Component Model 5 involves using the
exposure distributions obtained from component models 2 and 3
-------
B-8
and the probabilistic exposure-response relationships developed in
component model 4, to generate headcount risk estimates by exercising
appropriate risk models. Component model 6 involves integrating
estimated air quality distributions with probabilistic exposure-response
estimates to generate benchmark risk estimates. A discussion of head-
count and benchmark risk measures follows.
Two different kinds of NAAQS risk may be distinguished: headcount
and benchmark (Feagans and Biller, 1981). In distinguishing between
the two, 1t is useful to consider the difference between a "hazard"
and a "population risk." A hazard is a source of potential danger
(e.g., a cliff). Harm to any particular individual is experienced
only when that hazard is encountered and adverse consequences actually
befall the individual (e.g., when a moutain climber on the cliff
slips and falls). In the NAAQS context, the hazard is the potential
risk posed by the existence of ambient pollutant concentrations at a
certain level, whether or not any sensitive individual actually
encounters them. The population risk, by contrast, is the risk that
adverse health effects will occur considering both the probability
that sensitive individuals will be exposed to certain pollutant
concentrations and the probabilities that such levels will cause the
specified health effect.
Benchmark risk is a measure of the hazard and may be defined as the
probability, upon NAAQS attainment, that concentrations will exceed
the level that would adversely affect a specified percentage of the
sensitive population if all were actually exposed under the same
exposure conditions. A model of benchmark risk (see Feagans and
Biller, 1981) may be expressed as follows:
-------
B-9
R(Z;C ) » / F (Z.C) dP (C;C )
s 0 2
(1)
where R is the benchmark risk, Z is the fraction of the sensitive
population that would experience the health effect to at least the
given degree if exposed under common exposure conditions, Fz is the
cumulative probability distribution for the Zth-fraction benchmark
concentration (that is, the analytic fit to the encoding data--see
Figure 2a), Pc is the cumulative distribution of the highest
concentrations occurring during a given time period, under conditions
qf NAAQS attainment, and Cs is the concentration level of the standard.
Headcount risk, by contrast, expresses the probability that a
specified number of adverse health effects incidents will occur, as
sensitive groups move about, from indoors to outdoors, from one
different indoor microenvironment to another. A headcount risk
model (after Feagans and Biller, 1981) may be formulated as follows:
where H is the number of health endpoint occurrences, N is the
number of possible exposures per person in the modeled time period
(e.g., 8,760 hours per year), P is the number of persons in the
sensitive group, Fz is the probability that Z fraction of the
sensitive population would experience the health endpoint if exposed
under common exposure conditions (see Figure 2b for an illustration
of the calculation of Z), E is the NEM-generated exposure distribution
for just attaining the NAAQS, which is set at a concentration
level of Cs. Currently, the ozone risk assessment plans to generate
both headcount and benchmark risk estimates (for each alternative
standard, for each health endpoint).
(2)
-------
B-10
(5) Aggregate results. Risk calcualtions must be made for each
health endpoint, for each expert's probabilistic exposure-response
relationship, for each alternative standard, and for each of 10 to 12
urban areas. The substantial number of calculations must be aggregated
into nationally representative numbers for effective presentation to
decision makers. The aggregation procedure is currently under development.
Health Endpoint Categories
The risk assessment seeks to estimate the probability that certain
"events" will occur under conditions of NAAQS attainment. Events are
defined as the occurrence of certain precisely defined health "endpoints
An endpoint is defined in terms of a specific category of health response
(e.g., impairment in pulmonary function), an indicator to be used as the
measure of that health response (e.g., forced expiratory volume in the
first 1 second of a maximal expiration, FEVi), and a level of that
indicator considered to be potentially adverse (10 percent decrement,
say). An example of a health endpoint might be the following: the
occurrence of an adverse effect on pulmonary function as evidenced by a
greater than 10 percent decrement in FEV^.
OAQPS has retained the responsibility for specifying the health
endpoints to be included in the risk assessment. After consultation with
various agency staff members, health experts, and the risk assessment
team, OAQPS has selected the following endpoint categories to be included in
the health risk assessment:
(1) Pulmonary function impairment and increased symptoms
(2) Aggravation of asthma
(3) Increased susceptibility to respiratory infection
(4) Development of bronchiolitis or fibrosis.
-------
B-ll
The first three endpoint categories pertain to the acute, short-term
effects of ozone exposure; the fourth category is related to both short-
term and longer-term (or subchronic) exposures.
-------
B-12
REFERENCES
Feagans, T.B. and W.F. Biller, 1981, "Risk assessment; describing the
protection provided by ambient air quality standards." The Environmental
Professional 3: 235.
Hayes, S.R.; Wallsten, T.; Winkler, R. (1986) Design document for a
study to develop health risk estimates for alternative ozone NAAQS.
San Rafael, CA: Systems Applications, Inc.
Wallsten, T.S. and R.G. Whitfield (1985) "Elliciting the probabilistic
judgments of experts about lead-induced health effects: A methodology
and application. Annual Meeting of the Society for Risk Analysis,
Alexandria, VA.
Wallsten, T.S. and R.G. Whitfield (1986) Estimating the risks of
lead-induced health effects. Argonne, IL: Argonne National Laboratory
(Draft).
-------
APPENDIX C: GLOSSARY OF PULMONARY TERMS AND SYMBOLS**
Acetylcholine (ACh): A naturally occurring substance 1n the body having
Important parasympathetic effects; often used as a bronchoconstrlctor.
Aerosol: Solid particles or liquid droplets that are dispersed or suspended
In a gas, ranging 1n size from 10-* to 102 micrometers (um).
A1r spaces: All alveolar ducts, alveolar sacs, and alveoli. To be contrasted
with AIRWAYS.
Airway conductance (Gaw): Reciprocal of airway resistance. Gaw = (1/Raw).
A1rway resistance (Raw): The (frictional) resistance to airflow afforded by
the airways between the airway opening at the mouth and the alveoli.
Airways: All passageways of the respiratory tract from mouth or nares down to
and including respiratory bronchioles. To be contrasted with AIR SPACES.
Allergen: A material that, as a result of coming into contact with appropriate
tissues of an animal body, induces a state of allergy or hypersensitivity;
generally associated with idiosyncratic hypersensitivities.
Alveolar-capillary membrane: A fine membrane (0.2 to 0.4 |jm) separating
alveolus from capillary; composed of epithelial cells lining the alveolus,
a thin layer of connective tissue, and a layer of capillary endothelial
cells.
Alveolus: Hexagonal or spherical air cells of the lungs. The majority of
alveoli arise from the alveolar ducts which are lined with the alveoli.
An alveolus is an ultimate respiratory unit where the gas exchange takes
place.
Asthma: A disease characterized by an increased responsiveness of the airways
to various stimuli and manifested by slowing of forced expiration which
changes in severity either spontaneously or as a result of therapy. The
term asthma may be modified by words or phrases indicating its etiology,
factors provoking attacks, or its duration.
~References: Bartels, H.; Dejours, P.; Kellogg, R. H.; Mead, J. (1973) Glossary
on respiration and gas exchange. J. Appl. Physiol. 34: 549-558.
American College of Chest Physicians - American Thoracic Society
(1975) Pulmonary terms and symbols: a report of the ACCP-ATS
Joint Committee on pulmonary nomenclature. Chest 67: 583-593.
"•"Adapted from Appendix A, Volume V of the CD.
C-l
-------
Breathing pattern: A general term designating the characteristics of the
ventilatory activity, e.g., tidal volume, frequency of breathing, and
shape of the volume time curve.
Bronchiole: One of the finer subdivisions of the airways, less than 1 mm in
diameter, and having no cartilage in its wall.
Bronchiolitis: Inflammation of the bronchioles which may be acute or chronic.
If the etiology 1s known, 1t should be stated. If permanent occlusion of
the lumens is present, the term bronchiolitis obliterans may be used.
Bronchitis: A non-neoplastic disorder of structure or function of the bronchi
resulting from Infectious or noninfectious irritation. The term bronchitis
should be modified by appropriate words or phrases to indicate its etiol-
ogy, its chroniclty, the presence of associated airways dysfunction, or
type of anatomic change. The term chronic bronchitis, when unqualified,
refers to a condition associated with prolonged exposure to nonspecific
bronchial Irritants and accompanied by mucous hypersecretion and certain
structural alterations in the bronchi. Anatomic changes may include
hypertrophy of the mucous-secreting apparatus and epithelial metaplasia,
as well as more classic evidences of inflammation. In epidemiologic
studies, the presence of cough or sputum production on most days for at
least three months of the year has sometimes been accepted as a criterion
for the diagnosis.
Bronchoconstrictor: An agent that causes a reduction in the caliber (diame-
ter) of airways.
Bronchodilator: An agent that causes an increase in the caliber (diameter) of
ai rways.
Bronchus: One of the subdivisions of the trachea serving to convey air to and
from the lungs. The trachea divides into right and left main bronchi
which in turn form lobar, segmental, and subsegmental bronchi.
Carbon monoxide (CO): An odorless, colorless, toxic gas formed by incomplete
combustion, with a strong affinity for hemoglobin and cytochrome; it
reduces oxygen absorption capacity, transport, and utilization.
Carboxyhemoglobin (COHb): Hemoglobin in which the iron is associated with
carbon monoxide. The affinity of hemoglobin for CO is about 300 times
greater than for Og.
Chronic obstructive lung disease (COLO): This term refers to diseases of
uncertain etiology characterized by persistent slowing of airflow during
forced expiration. It is recommended that a more specific term, such as
chronic obstructive bronchitis or chronic obstructive emphysema, be used
whenever possible. Synonymous with chronic obstructive pulmonary disease
(C0P0).
Closing capacity (CC): Closing volume plus residual volume, often expressed
as a ratio of TLC, I.e. (CC/TLCX).
C-2
-------
Closing volume (CV): The volume exhaled after the expired gas concentration
is inflected from an alveolar plateau during a controlled breathing
maneuver. Since the value obtained is dependent on the specific test
technique, the method used must be designated in the text, and when
necessary, specified by a qualifying symbol. Closing volume is often
expressed as a ratio of the VC, i.e. (CV/VCX).
Conductance (G): The reciprocal of RESISTANCE. See AIRWAY CONDUCTANCE.
FEV^/FVC: A ratio of timed (t * 0.5, 1, 2, 3 s) forced expiratory volume
(FEVt) to forced vital capacity (FVC). The ratio is often expressed in
percent 100 x FEV^/FVC. It is an index of airway obstruction.
Forced expiratory flow (FEFx): Related to some portion of the FVC curve.
Modifiers refer to the amount of the FVC already exhaled when the measure-
ment is made. For example:
FEF75% * instantaneous forced expiratory flow after 75%
of the FVC has been exhaled.
200-1200 a mean forced expiratory flow between 200 ml
and 1200 ml of the FVC (formerly called the
maximum expiratory flow rate (MEFR).
FEF25-75% * mean forced expiratory flow during the middle
half of the FVC [formerly called the maximum
mid-expiratory flow rate (MMFR)].
FEFmax * the maximal forced expiratory flow achieved during
an FVC.
Forced expiratory volume (FEV): Denotes the volume of gas which is exhaled in
a given time interval during the execution of a forced vital capacity.
Conventionally, the times used are 0.5, 0.75, or 1 sec, symbolized FEVq.5,
FEVq.75, FEVi#o. These values are often expressed as a percent of the
forced vital capacity, e.g. (FEV^g/VC) X 100. Forced inspiratory
Forced vital capacity (FVC): Vital capacity performed with a maximally forced
expiratory effort.
Functional residual capacity (FRC): The sum of RV and ERV (the volume of air
remaining in the lungs at the end-expiratory position). The method of
measurement should be indicated as with RV.
Gas exchange: Movement of oxygen from the alveoli into the pulmonary capillary
blood as carbon dioxide enters the alveoli from the blood. In broader
terms, the exchange of gases between alveoli and lung capillaries.
Gas trapping: Trapping of gas behind small airways that were opened during
inspiration but closed during forceful expiration. It is a volume differ-
ence between FVC and VC.
C-3
-------
Hemoglobin (Hb): A hemoprotein naturally occurring in most vertebrate blood,
consisting of four polypeptide chains (the globulin) to each of which
there is attached a heme group. The heme is made of four pyrrole rings
and a divalent iron (Fe2+-protoporphyrin) which combines reversibly with
molecular oxygen.
Histamine: A depressor amine derived from the amino acid histidine and found
in all body tissues, with the highest concentration in the lung; a powerful
stimulant of gastric secretion, a constrictor of bronchial smooth muscle,
and a vasodilator that causes a fall in blood pressure.
Hypoxia: Any state in which the oxygen in the lung, blood, and/or tissues is
abnormally low compared with that of normal resting man breathing air at
sea level. If the Pq2 is low in the environment, whether because of
decreased barometric pressure or decreased fractional concentration of
O2, the condition is termed environmental hypoxia. Hypoxia when referring
to the blood is termed hypoxemia. Tissues are said to be hypoxic when
their Pq2 is low, even if there is no arterial hypoxemia, as in "stagnant
hypoxia" which occurs when the local circulation is low compared to the
local metabolism.
Inspiratory capacity (IC): The sum of IRV and TV.
Lung volume (V[_): Actual volume of the lung, including the volume of the
conducting airways.
(I
Maximal aerobic capacity (max V O2): The rate of oxygen uptake by the body
during repetitive maximal respiratory effort. Synonymous with maximal
oxygen consumption.
Maximum expiratory flow rate (MEFR): Synonymous with FEF200-1200*
Maximum mid-expiratory flow rate (MMFR or MMEF): Synonymous with FEF25_75%.
Maximum ventilation (max Vg): The volume of air breathed in one minute during
repetitive maximal respiratory effort. Synonymous with maximum ventilatory
minute volume.
Minute ventilation (V^): Volume of air breathed in one minute. It is a
product of tidal volume (V-j-) and breathing frequency (fp). See VENTILA-
TION.
Mucociliary transport: The process by which mucus is transported, by ciliary
action, from the lungs.
Mucus: The clear, viscid secretion of mucous membranes, consisting of mucin,
epithelial cells, leukocytes, and various inorganic salts suspended in
water.
Nasopharyngeal: Relating to the nose or the nasal cavity and the pharynx
(throat).
C-4
-------
Nitrogen oxides: Compounds of N and 0 in ambient air; i.e., nitric oxide (NO)
and others with a higher oxidation state of N, of which NO2 is the most
important toxicologically.
Oxidant: A chemical compound that has the ability to remove, accept, or share
electrons from another chemical species, thereby oxidizing it.
Particulates: Fine solid particles such as dust, smoke, fumes, or smog, found
in the air or 1n emissions.
Pathogen: Any virus, microorganism, or etiologic agent causing disease.
Peak expiratory flow (PEF): The highest forced expiratory flow measured with
a peak flow meter.
Peroxyacetyl nitrate (PAN): Pollutant created by action of UV component of
sunlight on hydrocarbons and N0X in the air; an ingredient of photochem-
ical smog.
Pulmonary edema: An accumulation of excessive amounts of fluid in the lung
extravascular tissue and air spaces.
Pulmonary emphysema: An abnormal, permanent enlargement of the air spaces
distal to the terminal nonrespiratory bronchiole, accompanied by destructive
changes of the alveolar walls and without obvious fibrosis. The term
emphysema may be modified by words or phrases to Indicate its etiology,
fts anatomic subtype, or any assocfated airways dysfunction.
Residual volume (RV): That volume of air remaining in the lungs after maximal
exhalation. The method of measurement should be indicated in the text
or, when necessary, by appropriate qualifying symbols.
Resistance flow (R): The ratio of the flow-resistive components of pressure
to simultaneous flow, in cm l^O/liter per sec. Flow-resistive components
of pressure are obtained by subtracting any elastic or inertial components,
proportional respectively to volume and volume acceleration. Most flow
resistances in the respiratory system are nonlinear, varying with the
magnitude and direction of flow, with lung volume and lung volume history,
and possibly with volume acceleration. Accordingly, careful specification
of the conditions of measurement is necessary; see AIRWAY RESISTANCE,
TISSUE RESISTANCE, TOTAL PULMONARY RESISTANCE, COLLATERAL RESISTANCE.
Respiratory frequency (fR): The number of breathing cycles per unit of time.
Synonymous with breathing frequency (f|j).
Specific airway conductance (SGaw): Airway conductance divided by the lung
volume at which it was measured, i.e., normalized airway conductance.
SGaw * Gaw/TGV.
Specific airway resistance {SRaw}: Airway resistance multiplied by the volume at
which it was measured. SRaw ¦ Raw x TGV.
Sulfur dioxide (SO2): Colorless gas with pungent odor, released primarily
from burning of fossil fuels, such as coal, containing sulfur.
C-5
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STPD conditions (STPD): Standard temperature and pressure, dry. These
are the conditions of a volume of gas at 0°C, at 760 torr, without
water vapor. A STPD volume of a given gas contains a known number
of moles of that gas.
Synergism: A relationship in which the combined action or effect of two or
more components is greater than the sum of effects when the components
act separately.
Tidal volume (TV): That volume of air inhaled or exhaled with each breath
during quiet breathing, used only to indicate a subdivision of lung
volume. When tidal volume is used in gas exchange formulations, the
symbol Vj should be used.
Total lung capacity (TLC): The sum of all volume compartments or the volume
of air in the lungs after maximal inspiration. The method of measurement
should be indicated, as with RV.
Total pulmonary resistance (Rl): Resistance measured by '•elating flow-dependent
trans pulmonary pressure to airflow at the mouth. Represents the total
(frictional) resistance of the lung tissue (Rfj) and the airways (Raw).
s Raw + ^ti•
Trachea: Commonly known as the windpipe; a cartilagfnous air tube extending
from the larynx (voice box) into the thorax (chest) where it divides into
left and right branches.
Ventilation: Physiological process by which gas is renewed in the lungs. The
word ventilation sometimes designates ventilatory flow rate (or ventila-
tory minute volume) which is the product of the tidal volume by the
ventilatory frequency. Conditions are usually indicated as modifiers;
i .e.,
Vf s Expired volume per minute (BTPS),
and
Vf ¦ Inspired volume per minute (BTPS).
Ventilation is often referred to as "total ventilation" to distinguish it
from "alveolar ventilation" (see VENTILATION, ALVEOLAR).
Ventilation, alveolar (VA): Physiological process by which alveolar gas is
completely removed and replaced with fresh gas. Alveolar ventilation is
less than total ventilation because when a tidal volume of gas leaves the
alveolar spaces, the last part does not get expelled from the body but
occupies the dead space, to be reinspired with the next inspiration.
Thus the volume of alveolar gas actually expelled completely is equal to
the tidal volume minus the volume of the dead space. This truly complete
expiration volume times the ventilatory frequency constitutes the alveolar
ventilation.
Vital capacity (VC): The maximum volume of air exhaled from the point of
maximum inspiration.
C-6
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