SUMMARY STATEMENT FROM THE EPA ADVISORY PANEL
ON HEALTH EFFECTS OF PHOTOCHEMICAL OXIDANTS
January, 1978
Prepared for the Environmental Protection Agency
under the supervision of the Institute for Environmental
Studies of the University of North Carolina at Chapel Hill.
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I. Composition of the Panel
The Advisory Panel on Health Effects of Photochemical Oxidants (here-
after called the "Health Panel") was convened at the request of the
Office of Air Quality Planning and Standards, U. S. Environmental
Protection Agency. The Institute for Environmental Studies, University
of North Carolina at Chapel Hill, served as advisor in the selection of
panel members and as host for the panel meeting held in Chapel Hill,
N. C. on June 7th and 8th, 1977. Panel members were:
Carl M. Shy, (Panel Chairman), Director, Institute for Environmental
Studies, University of North Carolina at Chapel Hill
Stephen M. Ayres, Chairman, Department of Internal Medicine, St.
Louis Univeristy School of Medicine
David V. Bates, Dean, Faculty of Medicine, University of British
Columbia
T. Timothy Crocker, Chairman, Department of Community and Environmental
Medicine, University of California College of Medicine, Irvine
Bernard D. Godlstein, Associate Professor, Department of Medicine
and Department of Environmental Medicine, New York University School
of Medicine
John R. Goldsmith, Environmental Epidemiology Unit, California State
Department of Public Health
Staff and scientists of the U. S. Environmental Protection Agency participated
in the discussions of the Health Panel; documents prepared by FPA staff
were distributed and, where appropriate, commented on. The conclusions and
recommended guidelines for protection of public health given in this
summary statement represent a consensus of the panel members only.
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II. Purpose and Scope of the Meeting
The purpose of the panel discussions was to interpret the current
state of knowledge on health effects of ozone and other photochemical
substances, with the objective of developing a guideline to the Environ-
mental Protection agency (tPA) for the protection ot public neaitn.
These discussions were prompted by EPA's current program for review
and re-assessment of the existing air quality standard for photochemical
oxidants.
The panel reviewed studies relating to the following categories of
health effects:
A. Human studies
1. Mechanical function of the lung (controlled human exposures)
2. Asthma and lung function in children
3. Athletic performance
4. Other effects: mortality, occupational hazards
B. Toxicological studies
1. Experimental infection of animals
2. Morphological abnormalities of the respiratory system
3. Biochemical effects
4. Mutagenic and teratogenic potential
5. Performance and behavioral effects
In its discussions, the Panel considered several issues bearing on the
overall interpretation of reported studies. Among the major issues were:
relative weights to be given to published and unpublished reports, concept
of threshold concentrations for effects, human health significance of
toxicological data, chemical specificity of the air quality standard
("ozone," "oxidants," "photo-chemical substances") margins of safety, and
the health significance of exceeding a stated concentration one or more
times.
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III. Format for Discussion of Health Effects
The EPA staff requested the Panel to consider three characteristics
of population exposure that bear upon protection of public health: the
concentration at which human health risk would be increased, the duration
of exposure which is related to this risk, and the temporal exposure
pattern that would be associated with increased risk. In its deliberations
on each category of health effects, the Panel addressed the probability
that the health effects are induced by exposure to ozone or other photo-
chemical substances, the severity of each health effect and the uncertainties
of the evidence.
IV. Concept of Threshold Concentrations
A threshold was defined as a concentration between a no-effect
level and the lowest concentration at which a health effect was demon-
strated. Identification of a threshold relevant to protection of public
health requires evidence for specific exposures that produce no effect
as well as exposures that produce effects in susceptible segments of the
population. The Panel emphasized that biological reactions to pollutants
are not characterized by sharp discontinuities in dose-response relationships,
and that demonstration of no-effect levels is dependent upon the sensi-
tivity of the measurement of effects and exposure, as well as the selection
of the most sensitive groups and reaction systems. Since "thresholds"
will depend upon who is studied and what is measured, it is unlikely that
scientific evidence for a specific effects threshold can be satisfactorily
derived from existing data. Limited studies can be performed on groups
of unusually sensitive persons. Most experimental studies of humans are
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performed on small numbers of healthy subjects who do not adequately
reflect the range of human sensitivity. Toxicological studies
usually cannot utilize appropriate models of sensitive human popu-
lations. Thus, the Panel concurred in the statement that thresholds
for sensitive persons are difficult or impossible to determine experi-
mentally, while the threshold for healthy persons or animals is not
likely to be predictive of the response of more sensitive groups.
The Panel discussed alternatives to the "threshold" concept for
arriving at recommended guidelines for protection of public health. An
acceptable alternative considered by the Panel was
(1) to state at what level health effects have been demonstrated
in population groups, in controlled human exposures, and in
experimental animals,
(2) to evaluate the relationship between the responses of subjects
or animals studied and sensitive segments of the population,
(3) to assess the severity of each category of effect,
(4) to recognize the uncertainty in this body of evidence,
(5) to propose guidelines for a margin of safety, given the
strength of the evidence, the severity of the effects, and
the magnitude of the uncertainties,
(6) to recognize that decisions on margins of safety involve
more than scientific evidence.
V. Acceptabiliy of Cited Reports
In their assessment of evidence from the various sources of information
on health effects, Panel members agreed that greater weight should be
given to peer reviewed publications than to unpublished reports or reports
published without this review. The Panel felt that the latter category
of data should be considered, but could not serve as a major contribution
to its recoronendations concerning public health protection. Overall,
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there was a sufficient body of peer reviewed publications to serve alone
as the basis for the Panel's recommendations. In the one instance where
a significant human effect was demonstrated at a low ozone exposure, the
Panel took account of the data but made its conclusion primarily on the
basis of other published evidence.
VI. Human Studies
A. Mechanical function of the Lung
The Panel focused its discussion on the more recently published
human exposure data as reported by von Nieding, et al. (1977a, 1977b),
Hackney et al. (1975a, 1975b, 1975c» 1977), Bates and Hazucha (Bates
and Hazucha 1973, Hazucha 1973, Hazucha et al. 1973, Hazucha and Bates
1975). The Panel agreed that there was convincing evidence for pro-
nounced effects on mechanical function of the lung, as variously
measured by flow rates, airway resistance and other parameters of
ventilatory function, at ozone exposures of 0.37 to 0.75 ppm for two
hours under conditions of intermittent moderate exercise. The Panel
also accepted the validity of findings showing an effect on lung
function at 0.25 ppm, but recognized that these effects were less
pronounced than at higher concentrations and that they occurred in
Montreal subjects and not in Los Angeles subjects studied under iden-
tical protocols. The difference between the dose-response relationships
for Los Angeles and Montreal subjects was felt to be explainable by one
or more of the following factors: adaptation 1n Los Angeles subjectSf
admixture of submicronlc aerosols in the Montreal chamber, and/or
selective migration away from Los Angeles of persons who could not tolerate
previous repeated ambient ozone exposures without undue reactions.
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The Panel also identified the fact that a plateau in the dose-response
relationship in Montreal subjects was not demonstrated, and therefore that
effects may be produced at even lower concentrations than those employed.
In support of this hypothesis were the data from recent publications of
von Nieding et al. (1977a, 1977b). Differences from other study protocols
in the measurement of airway resistance and of arterial partial pressure of
oxygen were recognized. The small standard error about mean values of airway
resistance was also noted. The Panel felt that these aspects of the von
Nieding studies required replication of their results by other investigators
but that the data wasflthereby invalidated. The Panel concluded that
results of the von Nieding studies served to reinforce the conclusion that
changes in mechanical function of the lung may well occur in some subjects
at ozone concentrations less than 0.25 ppm for two hours, and that there may
be some risk of inducing functional changes at levels in the range of 0.15
to 0.25 ppm.
The Panel considered the issue of repetitive experimental exposures,
and asked whether effects on mechanical function would be more severe
with repetition of exposure or would possibly occur at lower concentrations
with repetition of exposure. The Panel consensus was that the risk of
effect was related to the total dose of ozone delivered to the respiratory
tract within a day (but not over long periods), and that this dose
increased with the frequency of exposures, with the concentrations of a
single exposure, and with the intensity of exercise of exposed subjects.
The Panel concluded that the evidence for a relationship between ozone
exposure and effects on mechanical properties was conclusive. In
discussing the severity of this effect, the Panel agreed that one exposure
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ay not portend risk of serious consequences in healthy individuals. How-
ever, a single exposure of a sensitive individual such as an asthmatic,
or other persons with airway disease, may induce a serious health effect,
and repeated exposures even of healthy individuals may lead to increased
risk of respiratory impairment in the form of irreversible effects or
susceptibility to chronic respiratory disease. However, the Panel
recognized that judgments concerning repetition of exposures fall in
the area of greatest uncertainty because experimental human studies have
not been conducted to evaluate repetitions of exposure. The Panel
also cited recent experimental evidence that the maximum stimulus to
histamine release in the lung occurred 24 hours after ozone exposure,
suggesting that exposed persons with sensitive airways may experience
untold delayed effects. These findings are not fully understood and
generally have not been incorporated into the assessment of ozone
induced health effects.
B. Asthma and Lung Function in Children
The Panel reviewed the air quality data available for interpreting
the findings of the Schoettlin and Landau (1961) asthma study. Although
there was some confusion in the early reviews of this study, it is now
clear that oxidant measurements for each day were made by the Los
Angeles Air Pollution Control District, that these data were obtained
by the potassium iodide method, and that there were significantly more
asthma epidodes in subjects on days when peak oxidant concentrations
exceeded 0.25 ppm, and finally that these peak concentrations were
associated with average maximum hourly oxidant concentration of about
0.20 ppm. From these data, the Panel agreed that the evidence supported
the statement that a proportion of asthmatics will be affected by maximum
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hourly oxidant concentrations of 0.20 ppm, and that the effect is likely
to occur at concentrations in the range of 0.15 to 0.25 ppm in some
asthmatics or other persons with sensitive airways.
The Panel also considered the recent reports of Kagawa and Toyama
(1975) and Kagawa et al. (1976) on the association of changes in lung
function of school children with oxidant exposure. These published
reports show a decrease in ventilatory function of school children
associated with increasing ambient ozone concentrations, from 0.1 to
0.30 ppm. The Panel noted that the authors stratified the data into
low and high temperature seasons, but could not isolate the effect of
ozone from other measured pollutants, since population exposures only
occur in the presence of pollutant combinations, not for single pollutants
in isolation. The Panel concluded that these studies further supported the
evidence for an increased health risk from ozone exposures over the range
of 0.15 to 0.25 ppm, and for the likelihood of a lesser but real health
risk at even lower concentrations.
The Panel expressed additional concern for ozone exposures of
young children, in view of the findings of Bartlett et al. (1974) which
demonstrated a reduction in lung elasticity and overdistention of the
lungs of rats exposed at 3-4 weeks of age for 30 days to 0.2 ppm ozone.
The Panel felt that these data were particularly significant since there
is continuous growth of lung capacity, in humans, both in terms of
number of alveoli and ventilatory function from birth to age 8 or 9
years, and since ozone exposures which compromise lung development at
these ages might have serious implications for risk of impairment later
in life.
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The evidence that ozone effects may be enhanced by other concurrent
pollutants (Bates and Hazacha 1973) was interpreted by the Panel as
indicating the desirability of providing a margin of safety between
these observed effects and the primary standard for ozone and other
photochemical substances.
C. Respiratory and Other Symptoms in Human Populations
Experimental exposures of humans and epidemiological observations
support the conclusion that ozone exposures in the range of 0.15 to
0.25 ppm are associated with increased risk of cough, chest discomfort,
susternal soreness, headache and eye irritation. Respiratory symptoms
are enhanced by more intense exercise. The Panel judged that the attempts
to obtain threshold estimates for these effects (Hammer et al., 1974)
violated biological evidence for nonlinear dose-response relationships,
and that in general, segmental regression analysis ("Hockay-stick"
function) is inappropriate for determining the onset of health risk.
In reviewing the several Japanese reports on acute respiratory and
other symptoms in school children during "photochemical smog" episodes,
the Panel noted the occurrence of acute effects at ozone levels of 0.15
ppm and above. The Panel attributed the high rate of reporting of
symptoms in the Japanese episode to a combination of several factors.
(1) biological reactions producing manifest symptoms, particularly
in actively exercising school children,
(2) Probable combination of ozone with other pollutants which interact
in their biological effects,
(3) sociological factors which in one culture may result in repression
of perceived symptoms and in another articulation of perceived
symptoms, and
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(4) psychological factors which may alter the individual's judgment
concerning the severity of symptoms.
One or more of these factors may account for the apparently high
incidence of chest discomfort and eye irritation in affected
juvenile groups and for the associated extrapulmonary mani-
festations such as numbness, fainting and necessity for
hospitalization. Thus the Panel concluded that the Japanese
reports of symptoms at 0.15 ppm should be given due weight
in arriving at a guideline for public health protection.
The repetition of these episodes with associated symptoms
adds to their- significance.
D. Athletic Performance
The Panel's previous comments concerning the inappropriateness of
segmental regression analysis was stated to apply to Wayne et al.'s (1967)
study of athletic performance. The data as presented irt the original
study do not suggest a plateau in the dose-response function. Never-
theless, some members of the Panel were unconvinced of an association
between impaired performance and oxidant concentrations less than 0.15
ppm. However, these members stated that their judgment was based on a
visual truncation of data points rather than on quantitative statistical
analysis. The Panel noted that a recent paper (Folinsbee et al. 1977)
has documented a decline in maximal oxygen uptake in healthy young
subjects exercising under controlled experimental exposure to 0.75 ppm
ozone, thus suggesting a mechanism for the effect on athletic performance.
E. Other Effects: Mortality, Occupational Hazards
Review of existing studies fails to show any evidence for increased
risk of mortality in association with daily oxidant concentrations
measured in the Los Angeles basin. The Panel stated that there was no
new evidence to alter this conclusion.
The Panel expressed concern with the absence of studies of different
groups occupationally exposed to ozone. These groups include airline
pilots and crews, workers exposed to coronal discharges in the electric
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utility industry, and other persons working in the vicinity of ultraviolet
lights, e.g., in cold storage rooms. The Panel was quite convinced that
some adverse reactions would be produced in these occupational settings,
and expressed concern that the absence of systematic studies will lead to
continued exposures without identification of the induced health risks.
F. Conclusions from Human Studies
The Panel reached consensus on the conclusion that short term exposures
to ozone in the range of 0.15 ppm to 0.25 ppm may impair mechanical function
of the lung, and may induce respiratory and related symptoms in sensitive
segments of the population. These symptoms and effects will be more
readily induced in exercising subjects, particularly in a complex urban
atmospheric environment in which ozone can interact with other pollutants.
Short term exposures only 3 or 4 times this level, that is, exposures
to 0.75 ppm for two hours, can induce severe symptoms in exercising sub-
jects. Such experiments are ethically unacceptable.
The Panel judged that the occurrence of respiratory symptoms and
alteration of mechanical function of the lung have important public health
implications, particularly for the developing lungs of young children.
Although such effects appear to be reversible in exposed young adults, they
represent a potentially serious risk for asthmatics and other individuals
with airway disease. In the population of individuals with varying states
of biological adaptability, exposures which produce the above described
effects may at times overwhelm the biological defense of some persons. Thus
reversibility of effects in experimentally exposed healthy subjects should not
be generalized to the entire population.
The Panel related many of the experimental human effects to a two-hour
averaging time. However, the Panel noted that more intense exercise was
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likely to bring about respiratory symptoms and ventilatory function effects
within a period of one hour. Panel members concurred that it was not
possible to perform a fine tuning on the averaging time associated with
this category of effects, and agreed that a one-hour averaging time represented
a satisfactory estimate of the exposure duration which should be considered
in a primary air quality standard aimed at protection of public health.
To some extent, a one-hour averaging time may provide a desirable addition
to the margin of safety, in that it may better protect actively exercising
persons.
VIII. Animal Toxicology Studies
A. Experimental Infection of Animals
Increased susceptibility to bacterial infection following ozone exposure
at 0.1 ppm is described by several investigators (Coffin et al. 1968, Ehrlich
et al. 1976, Gardner et al. 1974) in reports that do not fulfill the desi-
deratum of peer reviewed publications. These reports are, however, con-
sistent with a larger body of published evidence (Coffin and Gardner 1972,
Goldstein et al. 1971a, 1971b, Goldstein and Hoeprich 1972, Goldstein et al.
1974 and others) that establishes indices of infection or of mortaility
from bacterial infection as sensitive measures of the effect of ozone in
rodent lung. Additional stress such as heat, exercise or a combination with
other pollutants, according to some reports, may enhance the effect of
ozone on susceptibility to infection, and may thereby lower the ozone
dose at which the organism will be adversely affected.
The Panel agreed that these finding have definite human health implications
although an exposure level associated with such effects in humans may be
different. These reactions in mice represent basic biological responses to
infectious agents, and there is no reason to believe that pollutant induced
alterations of basic defense mechanisms in experimental mice would not
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occur iri similarly exposed and challenged humans. However, the Panel is not
aware of epidemiological evidence that susceptibility to infection increases
in persons exposed to ozone and other photochemical materials. However,
the biochemical and cellular alterations described below for rodents suggest
that multiple epithelial and biochemical targets are perturbed by ozone
exposure. Since similar epithelial perturbations occur in humans when
viral infection precedes the onset of bacterial pneumonia, it is reasonable
to expect that chemical injury to respiratory epithelium will predispose to
infection. Ozone induced irritation of the major bronchi in man does
occur at ozone concentrations in the range of 0.25 ppm. Hence it is
possible that ozone damage at the level of respiratory bronchioles and
alveoli occurs in man as well as rodents, leading to promotion of sus-
ceptibility to bacterial infection of the lower respiratory tract. The
Panel observed that it may be particularly difficult to demonstrate these
relationships because bacterial pneumonia is a disease of low incidence,
occurring more in the winter season when oxidant concentrations are
typically low. It is possible that concentrations of ozone high enough
to injure macrophages do not reach the alveoli in man but do so in rodents
because of anatomic differences between human and rodent lungs. In this
case, the significance of the animal data on ozone-induced susceptibility
to infection lies in the demonstration that a measurable effect on a
biologically important system (defense against infection) occurs in rodents
at concentrations that also produce measurable responses in man (altered
mechanical function of the lung).
B. Morphological Abnormalities of the Respiratory System
A range of morphological effects was noted in association with experi-
mental ozone exposures of 0.2 to 1.0 ppm. These effects varied from
replacement of Type I with Type II alveolar cells, which are not known to
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have associated harmful consequences, to emphysematous changes and terminal
bronchiole and alveolar damage. These effects occurring after long-term
low concentrations, raise the level of suspicion that repeated or chronic
exposures have the potential for inducing similar effects in humans.
C. Biochemical Effects
The Panel observed that there is an impressive variety of biochemical
alterations associated with ozone exposures over the range of 0.1 to
1.0 ppm. The Panel judged that effects induced by 0.1 to 0.2 ppm exposures
are probably largely adaptive while effects caused by levels of 0.5 ppm
and greater have definite toxic potential. The Panel judged that these
biochemical changes are significant in demonstrating that there are
ozone-induced effects at cellular sites and organ systems distant from
the lung. While many of the biological reactions were in the nature of
a protective response and could possibly be prevented or reversed with
increased vitamin E levels in the lung or increased antioxidants at
other tissue sites, nevertheless they represented the organism's response
to stress. The Panel agreed that such perturbations in biological systems
may pose a health risk to the population of impaired or susceptible
individuals. One of the panel members noted that, in experimental
studies, Canadian subjects who manifested greater change in mechanical
function of the lung than in Los Angeles subjects also showed greater
hemolysis of red blood cells. These observations suggest that ozone
levels which produce lung function changes can also lead to biochemical
changes and other reactions of definite concern to health, and vice versa.
Overall, the Panel felt that there is not a sharp dividing line between
protective responses and potential for pathological consequences.
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D. Genetic and Teratogenic Potential
The Panel focused its attention on the reports of chromosom.il abnor-
malities in peripheral leukocytes first observed upon exposure of intact
hamsters to 0.2 ppm ozone for five hours (Zelac, 1971). One experimental
study of humans (Merz et al. 1975) found similar abnormalities in individuals
exposed to 0.5 ppm ozone. The significance of chromosomal aberrations in
peripheral blood cells has not been determined. Furthermore these studies
have not,been replicated, and the Panel agreed that there was insufficient
evidence to evaluate the long term implications of these reports. Although
confirmation of the results may suggest another category of ozone-induced
effects, the preliminary evidence does not suggest these effects occur at
drastically lower levels of exposure. It was further noted that genetic
consequences of population exposures to human mutagens are very difficult
to identify, even for such well recognized mutagens as ionizing radiation.
Veninga's observation (1967) of increased neonatal deaths and congenital
abnormalities in newborn mice was cited by the Panel as grounds for raising
the index of concern over the potential teratogenic effects of ozone. The
evidence for the mutagenic effect of ozone in bacterial systems and lung
tumorigenesis was also noted. The Panel observed that, were similar
findings demonstrated for food additives or pesticides, these substances
would undoubtedly be banned from use.
E. Performance and Behavioral Effects
Few experimental studies of performance and behavioral effects of
ozone have been reported and the Panel considered this category of effects
to be a neglected area of research both in animal and human ozone studies.
The effects of ozone and other oxidant exposure on athletic performance
(Wayne et al. 1967) and on motor vehicle accidents (Ury 1968) provide
epidemiological evidence for impact on performance in humans.
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F. Implications of Animal Toxicology Data
The Panel observed that the ozone dose which caused chronic tissue
damage in the lungs of experimental animals was much closer to ambient
concentrations than are the doses of carcinogens employed to produce tumors
in laboratory animals. The chronic respiratory diseases related to similar
tissue changes in humans were felt to be at least as important, from a
public health perspective, as respiratory cancer. Thus, it was noted
that the margin of difference between ozone concentrations that produce
serious toxicological effects in animals (as well as symptomatic and lung
function changes in humans) and ambient levels of ozone is much smaller
than for any other atmospheric pollutant. The Panel also emphasized that
there was a remarkable clustering and convergence of various toxicological
experimental human, and epidemiologically observed effects within a narrow
ozone concentration range, that is 0.2 to 0.6 ppm. These findings further
reinforce the judgment that there is not a sharp cut-off for ozone dose-
response relationship. The Panel hypothesized that exposures above maximum
observed background levels of 0.05-0.06 ppm may well be associated with
some increased health risk; this perception is based on the convergence
of various effects at concentrations minimally above background (less than
one order of magnitude).
The Panel pointed out that chronic disease effects of long term
ozone exposure in man cannot be quantitatively related to specific ozone
concentrations of short (hourly or daily) averaging times due to the long
period of disease induction and the varied exposures of individuals during
the period of induction. Epidemiological studies may establish relation-
ships between long-term ozone exposure and human chronic disease risk,
but we must rely on toxicological studies to guide us in quantifying the
ozone level that may induce chronic effects.
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VIII. "Ozone" vs. "Oxidant" Standard
The question was raised by the EPA staff whether the Health Panel felt
that an ozone standard or a standard for ozone and other photochemical
substances was required for protection of public health. The Panel agreed
that two characteristics of ozone exposure should be cited with reference
to public health protection: (1) ozone itself is a primary cause of most
of the health effects reported in toxicological and experimental human
studies and the evidence for attributing many health effects to this
substance alone is very compelling, and (2) ozone measurements should
be considered as an index for the complex of atmospheric photochemical
substances some of which are known to produce health effects which either
are not attributable to pure ozone, e.g., eye irritation, or which may
possibly augment the effects of pure ozone. The Panel judged that it was
not appropriate at this time to consider a primary air quality standard
for specific photochemical compounds other than ozone.
The Panel agreed that when ozone is measured specifically, in contrast
to measurements of total oxidants, it should be considered both as a
causal agent of adverse health effects in its own right and as an index
for the photochemical mixture which is associated with a broader range
of health consequences. Beyond this, the Panel did not reach consensus
as to whether the primary air quality standard should be expressed solely
as an ozone standard or as a standard for ozone and other photochemical substances.
Some Panel members were concerned that a standard for ozone alone would lead
some to dismiss epidemiological evidence relating health effects to "oxidant"
concentrations and further to discount the occurrence of symptoms and
effects not attributable to pure ozone. Other Panel members believed that
citing ozone as an index as well as primary agent in its own right would
obviate these problems.
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IX. Recommended Guidelines for the Protection of Public Health
In considering the margin of safety between concentrations that
represent a public health risk and the recommended standard, the Health
Panel called attention to several conslusions that were previously
stated:
1. There appears to be a finite probability of health risk
associated with population exposure to ozone concentrations
above observed maximum background levels, i.e., 0.05 to 0.06
ppm. Specifically, there is evidence from studies of ozone
and other photochemical oxidants for alterations of
mechanical function of lung in humans, for exacerbation of
asthma in humans, for alteration of ventilatory function in
school children, for induction of acute respiratory symptoms
in exercising children and young adults, for impaired athletic
performance in young adults. The Panel judged, as discussed
in the previous sections, that these effects may be induced
by short term exposures to ozone in the range of 0.15 to 0.25 ppm.
An unreplicated study of airway resistance in humans and
repeated studies of susceptibility to experimental respiratory
infection in animals further suggest the possibility of adverse
effects in some persons at short term ozone exposure of 0.10 ppm.
2. In contrast to most other atmospheric pollutants, there is a
convergence of experimental animal, experimental human, and
epidemiological studies demonstrating effects at relatively
low ozone concentrations, 0.15 to 0.35 ppm. These concentrations
represent a relatively small margin of difference between
observed minimum background levels and concentrations causing
increased health risks.
3. The implications of these demonstrated health risks are
significant to the overall health of human populations.
4. There is new evidence for biological reactions to combinations
of ozone with other commonly occurring atmospheric pollutants.
In reviewing the body of evidence on health effects, the Health
Panel concluded that there is no compelling reason to suggest a change
from the concentration defined by the existing primary air quality
standard, namely, 0.08 ppm. This conclusion was based upon the previously
cited Panel consensus that a variety of adverse effects are likely to
occur in some segments of the population from short-term ozone exposures
of ">.15 to 0.25 ppm, and upon other evidence that suggests, though less
conclusively, the possibility of effects at concentrations as low as 0.10
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ppm. The Panel recognized that this standard provides very little margin
of safety, for the reasons cited immediately above.
In considering the appropriate averaging time to be associated with
this recommended concentration limit, the Panel judged that a one-hour
exposure limit would provide some slight margin of safety for exercising
individuals, whereas two or three hour exposures at the same level would
tend to increase the delivered dose and thus raise the level of risk.
Thus the Panel concluded that a primary standard of 0.08 ppm for one
hour represents a level of exposure which would be consistent with pro-
tection of public health.
The issue of how many times the 0.08 ppm one-hour level could be
exceeded without increased health risk was addressed. The Panel agreed
that the level of health risk increased (1) in proportion to the hourly
concentration above 0.08 ppm, (2) in proportion to the number of hours
in one day above 0.08 ppm, and (3) in proportion to the frequency of
days in which hourly averages exceed 0.08 ppm, though the latter
conclusion was recognized to be quite judgmental and generally lacking
in confirmatory studies. Nevertheless, the Panel could cite no medical
reason to suggest that any exceedances of the standard were without
health risk.
In offering its recommendation of a 0.08 ppm one-hour exposure limit
as a guideline for the protection of public health, the Panel proposed
that this guideline be considered as a public health objective for
developing control strategies, rather than a signal for injunctive legal
actions. Excursions above the 0.08 ppm hourly limit should call for
evaluation of implementation strategies and not for crisis reactions
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that are disruptive of normal activities. As previously stated, the
level of health risk is judged to be proportional to the concentration,
duration and frequency of exposures above the standard. The Panel is
not suggesting that small health risks are acceptable, but that occasional
excursions should be evaluated in the context of long term goals and
the difficulty of reducing the primary emissions necessary to achieve
the standards. Overall, however, the Panel judges that there is now
more experimental and epidemiological evidence to be concerned with
ozone exposures above the standard than when the standard was originally
established, and that this concern should reinforce the determination
to implement the control strategies required to achieve the primary
standard.
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Senate Committee on Public Works Print Serial Mo. 93-15. Washington,
D. C.: U. S. Government Printing Office, pp. 507-540.
Folinsbee, L. J., F. Silverman, and R. J. Shephard (1977). Decrease
of maximum work performance following ozone exposure. J. Appl. Physiol.
42:531-536.
Coffin, D. L. and D. E. Gardner (1972). Interaction of biological
agents and chemical air pollutants. Ann. Occup. Hyg. 15:219-234.
Coffin, D. L., E. J. Blomer, D. E. Gardner, and R. Holzman (1968).
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