# National Ambient Air Quality Standards for Ozone: Proposed Decision

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URL: https://www.frixlaw.com/law-library/documents/fr%3A96-30903

## Record

- **Collection:** Federal Register
- **Document type:** Proposed Rule
- **Published:** December 13, 1996
- **Citation:** 61 FR 65716

## Text

SUMMARY: In accordance with sections 108 and 109 of the Clean Air Act
(Act), EPA has reviewed the air quality criteria and national ambient
air quality standards (NAAQS) for ozone (O3) and particulate
matter (PM). Based on these reviews, the EPA proposes to change the
standards for both classes of pollutants.
This document describes EPA's proposed changes with respect to the
NAAQS for O3. The EPA's proposed actions with respect to PM are
being proposed elsewhere in today's Federal Register. Nonetheless, EPA
has concluded that the effects and control of each are in many
instances linked and will be affected by the other. For this reason,
EPA intends to review and, as appropriate, modify both standards on a
similar schedule, with promulgation of revised O3 standards in
June of 1997, concurrent with promulgation of revised standards for PM.
Doing so will permit States, localities and industry to address the
control of these and related pollutants on a more consistent basis.
Ozone and related pollutants have long been recognized, in both
clinical and epidemiological research, to affect public health. The
proposed revised standard would provide protection for children and
other at-risk populations against a wide range of O3-induced
health effects, including decreased lung function (primarily in
children active outdoors), increased respiratory symptoms (particularly
in highly sensitive individuals), hospital admissions and emergency
room visits for respiratory causes (among children and adults with pre-
existing respiratory disease such as asthma), inflammation of the lung,
and possible long-term damage to the lungs.
With respect to O3, EPA proposes to change the current primary
standard (last modified in 1979) in several respects:
1. Since longer exposure periods are of greater concern at lower
O3 concentrations, attainment of the standard would no longer be
based upon 1-hour averages, but instead on 8-hour averages. This
improvement was unanimously recommended by EPA's Clean Air Scientific
Advisory Committee (CASAC).
2. As a result of this change in averaging time, the level of the
standard would be lowered from the present 0.12 parts per million
(ppm). The EPA solicits comment on alternative levels of 0.09 ppm,
which generally represents the continuation of the present level of
protection, and 0.08 ppm, an increased level of protection. Based upon
its review, EPA is proposing the 0.08 ppm standard to provide increased
protection for children and asthmatics. The EPA also solicits comment
on retaining the current primary standard and on an alternative 8-hour
standard at a level of 0.07 ppm.
3. In addition, EPA proposes to change the test for attainment
(i.e., the form) of the new standard. Currently, the test of attainment
is whether a site exceeds the 1-hour standard on an average of no more
than once per year, averaged over three years. Given the natural
variation in hourly O3 levels, this ``one expected exceedance''
test can result in relatively unstable attainment/nonattainment
designations. The CASAC recommended a change to a more stable form;
consistent with this recommendation, EPA proposes a form based on a 3-
year average of 8-hour O3 concentrations. The EPA solicits comment
on a range of such concentration-based forms.
The EPA proposes to replace the current secondary standard with one
of two alternative standards: one set identical to the proposed new
primary standard or, alternatively, a new seasonal standard expressed
as a sum of hourly O3 concentrations greater than or equal to 0.06
ppm, cumulated over 12 hours per day during the consecutive 3-month
period of maximum concentrations during the O3 monitoring season,
set at a level of 25 ppm-hour. Either of the proposed alternative
secondary standards would provide increased protection against O3-
induced effects, such as agricultural crop loss, damage to forests and
ecosystems, and visible foliar injury to sensitive species.

DATES: Written comments on this proposed rule must be received by
February 18, 1997.

ADDRESSES: Submit comments (in duplicate if possible) on the proposed
rule to: Office of Air and Radiation Docket and Information Center
(6102) Attn: Docket No. A-95-58, Environmental Protection Agency, 401 M
St., SW., Washington, DC 20460.
Public Hearing: The EPA will announce in a separate Federal
Register document the date, time, and address of the public hearing on
this proposed rule.

FOR FURTHER INFORMATION CONTACT: Dr. David McKee, MD-15, Air Quality
Standards and Strategies Division, Office of Air Quality Planning and
Standards, U.S. Environmental Protection Agency, Research Triangle
Park, NC 27711, Telephone: (919) 541-5288.

SUPPLEMENTARY INFORMATION:

Docket

Docket No. A-95-58 incorporates by reference Docket No. A-92-17,
and the docket established for the air quality criteria document
(Docket No. ECAO-CD-92-0786). The docket may be inspected between 8:00
a.m. and 5:30 p.m. on weekdays, and a reasonable fee may be charged for
copying.

Availability of Related Information

Certain documents are available from the U.S. Department of
Commerce, National Technical Information Service, 5285 Port Royal Road,
Springfield, VA 22161. Available documents include: Air Quality
Criteria for O3 and Other Photochemical Oxidants (``Criteria
Document'') (three volumes, EPA/600/P-93-004aF through EPA/600/P-93-
004cF, July 1996, NTIS # PB-96-185574, $169.50 paper copy, $58.00
microfiche); and the Review of the National Ambient Air Quality
Standards for O3: Assessment of Scientific and Technical
Information (``Staff Paper'')(EPA-452/R-96-007, June 1996, NTIS #PB-96-
203435, $67.00 paper copy and $21.50 microfiche). (Add a $3.00 handling
charge per order.) A limited number of copies of other documents
generated in connection with this standard review, such as documents
pertaining to human exposure and health risk assessments, and
vegetation exposure, risk, and benefits analyses can be obtained from:
U.S. Environmental Protection Agency Library (MD-35), Research Triangle
Park, NC 27711, telephone (919) 541-2777. These and other related
documents are also available for inspection and copying in the EPA
docket identified above.
The Staff Paper and human exposure and health risk assessment
support documents are now available on the Agency's Office of Air
Quality Planning and Standards (OAQPS) Technology Transfer Network
(TTN) Bulletin Board System (BBS) in the Clean Air Act Amendments area,
under Title I, Policy/Guidance Documents. To access the bulletin board,
a modem and communications software are necessary.

[[Page 65717]]

To dial up, set your communications software to 8 data bits, no parity
and one stop bit. Dial (919) 541-5742 and follow the on-screen
instructions to register for access. After registering, proceed to
choice `` Gateway to TTN Technical Areas'', then choose `` CAAA
BBS''. From the main menu, choose `` Title I: Attain/Maint of
NAAQS'', then `` Policy Guidance Documents''. To access these
documents through the World Wide Web, click on ``TTN BBSWeb'', then
proceed to the Gateway to TTN Technical areas, as above. If assistance
is needed in accessing the system, call the help desk at (919) 541-5384
in Research Triangle Park, NC.

Implementation Activities

When the proposed revisions to the primary and secondary standards
are implemented by the States, utility, automobile, petroleum, and
chemical industries are likely to be affected, as well as other
manufacturing concerns that emit volatile organic compounds or nitrogen
oxides. The extent of such effects will depend on implementation
policies and control strategies adopted by States to assure attainment
and maintenance of the proposed standards.
The EPA is developing appropriate policies and control strategies
to assist States in the implementation of the proposed revisions to
both the primary and secondary O3 NAAQS. The resulting
implementation strategies will then be published for public comment in
the future.

Table of Contents

The following topics are discussed in today's preamble:

I. Background
A. Legislative Requirements
B. Related Control Requirements
C. Review of Air Quality Criteria and Standards for O3
II. Rationale for Proposed Decision on the Primary Standard
A. Health Effects Information
1. Effects of Short-term and Prolonged O3 Exposures
2. Potential Effects of Long-term O3 Exposures
3. Adversity of Effects for Individuals
B. Human Exposure and Risk Assessments
C. Conclusions on the Elements of the Primary Standard
1. Averaging Time
2. Level
3. Form
D. Proposed Decision on the Primary Standard
III. Communication of Public Health Information
IV. Rationale for Proposed Decision on the Secondary Standard
A. Effects on Vegetation
B. Biologically Relevant Exposure Indices
C. Vegetation Exposure and Risk Analyses
D. Conclusions on the Elements of the Secondary Standard
1. Averaging Time
2. Form
3. Level
E. Proposed Decision on the Secondary Standard
V. Revisions to Appendix H--Interpretation of the NAAQS for Ozone
A. Data Completeness
B. Data Handling and Rounding Conventions
VI. Technical Changes to Appendices D and E
VII. Implementation Program
VIII. Regulatory and Environmental Impact Analyses References

I. Background

A. Legislative Requirements

Two sections of the Act govern the establishment, review, and
revision of NAAQS. Section 108 (42 U.S.C. 7408) directs the
Administrator to identify pollutants which ``may reasonably be
anticipated to endanger public health and welfare'' and to issue air
quality criteria for them. These air quality criteria are to
``accurately reflect the latest scientific knowledge useful in
indicating the kind and extent of all identifiable effects on public
health or welfare which may be expected from the presence of [a]
pollutant in the ambient air * * *.''
Section 109 (42 U.S.C. 7409) directs the Administrator to propose
and promulgate ``primary'' and ``secondary'' NAAQS for pollutants
identified under section 108. Section 109(b)(1) defines a primary
standard as one ``the attainment and maintenance of which, in the
judgment of the Administrator, based on the criteria and allowing an
adequate margin of safety, [are] requisite to protect the public
health.'' The margin of safety requirement was intended to address
uncertainties associated with inconclusive scientific and technical
information available at the time of standard setting, as well as to
provide a reasonable degree of protection against hazards that research
has not yet identified. Both kinds of uncertainties are components of
the risk associated with pollution at levels below those at which human
health effects can be said to occur with reasonable scientific
certainty. Thus, by selecting primary standards that provide an
adequate margin of safety, the Administrator is seeking not only to
prevent pollution levels that have been demonstrated to be harmful but
also to prevent lower pollutant levels that she finds may pose an
unacceptable risk of harm, even if the risk is not precisely identified
as to nature or degree. The Act does not require the Administrator to
establish a primary NAAQS at a zero-risk level but rather at a level
that reduces risk sufficiently so as to protect public health with an
adequate margin of safety.
A secondary standard, as defined in section 109(b)(2), must
``specify a level of air quality the attainment and maintenance of
which, in the judgment of the Administrator, based on [the] criteria,
[are] requisite to protect the public welfare from any known or
anticipated adverse effects associated with the presence of [the]
pollutant in the ambient air.'' Welfare effects as defined in section
302(h) (42 U.S.C. 7602(h)) include, but are not limited to, ``effects
on soils, water, crops, vegetation, manmade materials, animals,
wildlife, weather, visibility and climate, damage to and deterioration
of property, and hazards to transportation, as well as effects on
economic values and on personal comfort and well-being.''
Section 109(d)(1) of the Act requires periodic review and, if
appropriate, revision of existing air quality criteria and NAAQS.
Section 109(d)(2) requires appointment of an independent scientific
review committee to review criteria and standards and recommend new
standards or revisions of existing criteria and standards, as
appropriate. The committee established under section 109(d)(2) is known
as the Clean Air Scientific Advisory Committee (CASAC), a standing
committee of EPA's Science Advisory Board.

B. Related Control Requirements

States are primarily responsible for ensuring attainment and
maintenance of ambient air quality standards once EPA has established
them. Under section 110 of the Act (42 U.S.C. 7410) and related
provisions, States are to submit, for EPA approval, State
implementation plans (SIP's) that provide for the attainment and
maintenance of such standards through control programs directed to
sources of the pollutants involved. The States, in conjunction with
EPA, also administer the prevention of significant deterioration
program (42 U.S.C. 7470-7479) for these pollutants. In addition,
Federal programs provide for nationwide reductions in emissions of
these and other air pollutants through the Federal Motor Vehicle
Control Program under title II of the Act (42 U.S.C. 7521-7574), which
involves controls for automobile, truck, bus, motorcycle, and aircraft
emissions; the new source performance standards under section 111 (42
U.S.C. 7411); and the national emission standards for hazardous air
pollutants under section 112 (42 U.S.C. 7412).

[[Page 65718]]

C. Review of Air Quality Criteria and Standards for O3

The last review of O3 air quality criteria and standards was
completed in March 1993 with notice of a final decision not to revise
the existing primary and secondary standards (58 FR 13008). The
existing primary and secondary standards are each set at a level of
0.12 ppm, with a 1-hour averaging time and a 1-expected-exceedance
form, such that the standards are 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 1, averaged over 3 years (as
determined by 40 CFR Part 50, Appendix H).1
---------------------------------------------------------------------------

\1\ A more complete history of the O3 NAAQS is presented in
section II.B of the Office of Air Quality Planning and Standards
Staff Paper, Review of National Ambient Air Quality Standards for
O3: Assessment of Scientific and Technical Information (U.S.
EPA, 1996b).
---------------------------------------------------------------------------

The EPA initiated this current review in August 1992 with the
development of a revised Air Quality Criteria Document for O3 and
Other Photochemical Oxidants (henceforth the ``Criteria Document'').
Several workshops were held by EPA's National Center for Environmental
Assessment (NCEA) to discuss health and welfare effects information
during the summer and fall of 1993. An external review draft of the
Criteria Document made available to the public and to the CASAC in the
spring of 1994 was reviewed at a public CASAC meeting held on July 30-
31, 1994. Based on comments made at the meeting, NCEA staff prepared a
second external review draft, which was reviewed at a public CASAC
meeting on March 20-21, 1995. At the same meeting, the CASAC also
reviewed draft portions of a staff paper prepared by the Office of Air
Quality Planning and Standards (OAQPS), Review of National Ambient Air
Quality Standards for Ozone: Assessment of Scientific and Technical
Information (henceforth, the ``Staff Paper''), focusing on health
effects and the primary NAAQS. Taking into account CASAC and public
comments, staff revised both documents and made new drafts available
for public and CASAC review during the summer of 1995. The OAQPS staff
also prepared and made available draft portions of the Staff Paper
focusing on welfare effects and the secondary standard.
A public CASAC meeting was held on September 19-20, 1995, at which
time CASAC came to closure in its review of the draft Criteria Document
and the primary standard sections of the draft Staff Paper. In a
November 28, 1995 letter from the CASAC chair to the Administrator,
CASAC advised that the final draft Criteria Document ``provides an
adequate review of the available scientific data and relevant studies
of O3 and related photochemical oxidants'' (Wolff, 1995a).
Further, in a November 30, 1995 letter, CASAC advised the Administrator
that the primary standard portion of the draft Staff Paper ``provides
an adequate scientific basis for making regulatory decisions concerning
a primary O3 standard'' (Wolff, 1995b). The final Criteria
Document (U.S. EPA, 1996a) reflects CASAC and public comments received
at and subsequent to the September 1995 CASAC meeting.
Based on comments on the Staff Paper from the September 1995 CASAC
meeting, revisions were made to the secondary standard sections of the
Staff Paper, which were reviewed at a public CASAC meeting held on
March 21, 1996. At that meeting and in a subsequent letter to the
Administrator, CASAC concluded that the secondary standard sections of
the draft Staff Paper ``provide an appropriate scientific basis for
making regulatory decisions concerning a secondary O3 standard''
(Wolff, 1996).
The focus of this current review of the air quality criteria and
standards for O3 and related photochemical oxidants is on public
health and welfare effects associated with exposure to ambient levels
of tropospheric O3. Tropospheric O3 is chemically identical
to stratospheric O3, which is produced miles above the earth's
surface and provides a protective shield from excess ultraviolet
radiation. In contrast, tropospheric O3 at sufficient
concentrations has been associated with harmful effects due to its
oxidative properties and its presence in the air that people and plants
take up during respiratory processes. Ozone is not emitted directly
from mobile or stationary sources but, like other photochemical
oxidants, commonly exists in the ambient air as an atmospheric
transformation product. Ozone formation is the result of chemical
reactions of volatile organic compounds (VOC), nitrogen oxides
(NOX), and oxygen in the presence of sunlight and generally at
elevated temperatures. A detailed discussion of atmospheric formation,
ambient concentrations, and health and welfare effects associated with
exposure to O3 can be found in the final Criteria Document (U.S.
EPA, 1996a) and in the final Staff Paper (U.S. EPA, 1996b).
This review of the scientific criteria for O3 has occurred
simultaneously with the review of the criteria for particulate matter
(PM). These criteria reviews, as well as related implementation
strategy activities to date, have brought out important linkages
between PM and O3. A number of community epidemiological studies
have found similar health effects to be associated with exposure to PM
and O3, including, for example, aggravation of respiratory disease
(e.g., asthma), increased respiratory symptoms, and increased hospital
admissions and emergency room visits for respiratory causes. Laboratory
studies have suggested potential interactions between O3 and
various constituents of PM. Other key similarities relating to exposure
patterns and implementation strategies exist between PM, specifically
fine particles, and O3. These similarities include: (1)
Atmospheric residence times of several days, leading to large urban and
regional-scale transport of the pollutants; (2) similar gaseous
precursors, including NOX and VOC, which contribute to the
formation of both O3 and fine particles in the atmosphere; (3)
similar combustion-related source categories, such as coal and oil-
fired power generation and industrial boilers and mobile sources, which
emit particles directly as well as gaseous precursors of particles
(e.g., sulfur oxides (SOX), NOX, VOC) and O3 (e.g.,
NOX, VOC); and (4) similar atmospheric chemistry driven by the
same chemical reactions and intermediate chemical species that form
both high fine particle and O3 levels. High fine particle levels
are also associated with significant impairment of visibility on a
regional scale.
These similarities provide opportunities for optimizing technical
analysis tools (i.e., monitoring networks, emission inventories, air
quality models) and integrated emission reduction strategies to yield
important co-benefits across various air quality management programs.
These co-benefits could result in a net reduction of the regulatory
burden on some source category sectors that would otherwise be impacted
by separate O3, PM, and visibility protection control strategies.
In recognition of the multiple linkages and similarities in effects
and the potential benefits of integrating the Agency's approaches to
providing for appropriate protection of public health and welfare from
exposure to PM and O3, EPA is conducting the reviews of the NAAQS
for both pollutants on the same schedule. Accordingly, today's Federal
Register contains a separate notice announcing proposed revisions to
the PM NAAQS. Linking the PM and O3 review schedules provides an
important

[[Page 65719]]

opportunity for more effective and efficient air quality management--
both in terms of communicating a more complete description of the
health and welfare effects associated with the major components of
urban and regional air pollution, and by helping the States and local
areas to plan jointly to address both PM and O3 air pollution at
the same time with one process, and to work jointly with industry to
address common sources of air pollution. The EPA believes this
integrated approach will lead to more effective and efficient
protection of public health and the environment.

II. Rationale for Proposed Decision on the Primary Standard

This notice presents the Administrator's proposed decision to
replace the existing 1-hour O3 primary NAAQS with a new 8-hour
standard, based on a thorough review, in the Criteria Document, of the
latest scientific information on human health effects associated with
exposure to ambient levels of O3, including evaluation of key
studies published through 1995. This decision also takes into account
and is consistent with: (1) Staff assessments of the most policy-
relevant information in the Criteria Document and staff analyses of
human exposure and risk, presented in the Staff Paper, upon which staff
recommendations for a new O3 primary standard are based; (2) CASAC
advice and recommendations, as reflected in discussion of drafts of the
Criteria Document and Staff Paper at public meetings, in separate
written comments, and in CASAC's letters to the Administrator; and (3)
public comments received during the development of these documents,
either in connection with CASAC meetings or separately.
The rationale for the proposed revisions of the O3 primary
NAAQS includes consideration of: (1) Health effects information to
inform judgments as to the likelihood that exposures to ambient O3
result in adverse health effects for exposed individuals; (2) insights
gained from human exposure and risk assessments to provide a broader
perspective for judgments about protecting public health from the risks
associated with O3 exposure; (3) specific conclusions with regard
to the elements of a standard (i.e., averaging time, level, and form)
that, taken together, would be appropriate to protect public health
with an adequate margin of safety; and (4) alternative views of the
significance of the effects and factors to be considered in policy
judgments about the appropriate level of the standard.

A. Health Effects Information

The following summary of human health effects associated with
exposure to ambient levels of O3 is based on integrative
information from human clinical, epidemiological, and animal
toxicological studies, as presented in the Criteria Document and Staff
Paper. Based on this information, an array of health effects has been
attributed to short-term (1 to 3 hours), prolonged (6 to 8 hours), and
long-term (months to years) exposures to O3. Acute health effects
2 induced by short-term exposures to O3, generally while
individuals were engaged in heavy exertion, include transient pulmonary
function responses, transient respiratory symptoms, and effects on
exercise performance. The current O3 primary NAAQS is generally
based on these acute effects associated with heavy exercise and short-
term exposures. Other health effects associated with short-term or
prolonged O3 exposures include increased airway responsiveness,
susceptibility to respiratory infection, increased hospital admissions
and emergency room visits, and transient pulmonary inflammation.
---------------------------------------------------------------------------

\2\ ``Acute health'' effects of O3 are defined as those
effects induced by short-term and prolonged exposures to O3.
Examples of these effects are functional, symptomatic, biochemical,
and physiologic changes.
---------------------------------------------------------------------------

Since the last review of the air quality criteria for O3 was
completed, available information has increased substantially on effects
associated with prolonged and long-term exposures. Based on this new
information, similar acute health effects have been observed following
prolonged exposures at concentrations of O3 as low as 0.08 ppm and
at moderate levels of exertion.\2\ Although chronic effects 3 such
as structural damage to pulmonary tissue and carcinogenicity have been
investigated in a substantial number of laboratory animal studies,
these effects have not been adequately established in human studies to
draw any conclusions at this time.
---------------------------------------------------------------------------

\3\ ``Chronic health'' effects of O3 are defined as those
effects induced by long-term exposures to O3. Examples of these
effects are structural damage to lung tissue and accelerated decline
in baseline lung function.
---------------------------------------------------------------------------

This array of effects is briefly summarized below for short-term
and prolonged O3 exposures, and for long-term O3 exposures.
Further, judgments are presented with respect to when these
physiological effects become so significant that they should be
regarded as adverse to the health of individuals experiencing the
effects.
1. Effects of Short-term and Prolonged O3 Exposures

a. Pulmonary Function Responses

Transient reductions in pulmonary function have been observed in
healthy individuals and those with impaired respiratory symptoms (e.g.,
asthmatic individuals) as a result of both short-term and prolonged
exposures to O3. The strongest and most quantifiable exposure-
response information on such pulmonary function responses to O3
has come from controlled human exposure studies. The evidence from such
studies clearly shows that reductions in lung function are enhanced by
increased levels of activity involving exertion, typically reported as
``exercise'' in clinical studies, and by increased O3
concentrations. Pulmonary function decrements generally tend to return
to baseline levels shortly after short-term exposure, and effects are
typically attenuated upon repeated short-term exposures over several
days.
As discussed in section V.C.1 of the Staff Paper, numerous
experimental studies of exercising adults have demonstrated decrements
in lung function both for exposures of 1-3 hours at 0.12 ppm
O3 and for exposures of 6.6 hours at 0.08 ppm O3.
These studies provide conclusive evidence that O3 levels commonly
monitored in the ambient air induce lung function decrements in
exercising adults. The extent of lung function decrements varies
considerably among individuals. Further, numerous summer camp studies
provide an extensive and reliable database on lung function responses
to ambient O3 and other pollutants in children and adolescents
living in the Northeastern U.S., southern California, and Southern
Canada. Lung function changes reported at ambient O3
concentrations in these studies are comparable to those reported in
children and adults exposed under controlled experimental conditions,
although direct comparisons are difficult to make because of
differences in experimental design and analytical approach.

b. Respiratory Symptoms and Effects on Exercise Performance

As discussed in section V.C.2 of the Staff Paper, various transient
human respiratory symptoms, including cough, throat irritation, chest
pain on deep inspiration, nausea, and shortness of breath, have been
induced by O3 exposures of both healthy individuals and those with
impaired respiratory systems. Increasing O3 exposure durations and
levels have been shown to elicit increasingly more severe

[[Page 65720]]

symptoms that persist for longer periods in increasingly larger numbers
of individuals. Symptomatic and pulmonary function responses follow a
similar time course during an acute exposure and the subsequent
recovery, as well as over the course of several days during repeated
exposures. As with pulmonary function responses, the severity of
symptomatic responses varies considerably among subjects. For some
outdoor workers or active people who are highly responsive to ambient
O3, respiratory symptoms may cause reduced productivity or may
curb the ability or desire to engage in normal activities. Furthermore,
O3-induced interference with exercise performance, either by
reducing maximal sustainable levels of activity or reducing the
duration of activity that can be tolerated at a particular work level,
is likely related to such symptomatic responses.

c. Increased Airway Responsiveness

Increased airway responsiveness is an indication that the airways
are predisposed to bronchoconstriction which can be induced by a wide
variety of external stimuli (e.g., pollens, dust, cold air, sulfur
dioxide (SO2), etc.). A high level of bronchial responsiveness is
characteristic of asthma. Ozone exposure causes increased
responsiveness of the pulmonary airways to subsequent challenge with
bronchoconstrictor drugs such as histamine or methacholine. Changes in
airway responsiveness tend to resolve somewhat more slowly than
pulmonary function changes, typically disappearing after 24 hours, and
appear to be less likely to attenuate with repeated exposure.
As a result of increased airway responsiveness induced by O3
exposure, human airways may be more susceptible to a variety of
stimuli, including antigens, chemicals, and particles. For example, as
cited in section V.C.3 of the Staff Paper, healthy subjects after being
exposed to O3 concentrations as low as 0.20 ppm for 1 hour and
0.08 ppm for 6.6 hours have experienced small increases in nonspecific
bronchial responsiveness, which usually resolve within 24 hours.
Asthmatic subjects typically have increased airway responsiveness at
baseline. Whereas the differences in baseline nonspecific bronchial
responsiveness between healthy individuals and sensitive asthmatics may
be as much as 100-fold, changes induced by O3 exposure are usually
only 2- to 4-fold. With regard to O3-induced increases in airway
responsiveness (e.g., to specific inhaled antigens, cold air, and
SO2) ongoing studies will need to be completed and evaluated
before conclusions can be drawn. Because enhanced response to antigens
in asthmatics could lead to increased morbidity (i.e., medical
treatment, emergency room visits, hospital admissions) or to more
persistent alterations in airway responsiveness, these health endpoints
raise concern for public health, particularly for individuals with
impaired respiratory systems.

d. Increased Susceptibility to Respiratory Infection

When functioning normally, the human respiratory tract, like that
of other mammals, has numerous closely integrated defense mechanisms
that provide protection from the adverse effects of a wide variety of
inhaled particles and microbes. To the extent that these defense
mechanisms can be broken down or impaired by the inhalation of O3,
as discussed in section V.C.4 of the Staff Paper, O3 exposures can
result in increased susceptibility to respiratory infection and related
respiratory dysfunction. Evidence of such effects has come primarily
from a very large number of laboratory animal studies with generally
consistent results. One of the few studies of moderately exercising
human subjects exposed to 0.08 ppm O3 for 6.6 hours reported
decrements in alveolar macrophage function, the first line of defense
against inhaled microorganisms and particles in the lower airways and
air sacs.
No single experimental human study or group of animal studies
conclusively demonstrates that human susceptibility to respiratory
infection is increased by exposure to O3. However, taken as a
whole, the data suggest that acute O3 exposures can impair the
host defense capability of both humans and animals, possibly by
depressing alveolar macrophage function and perhaps also by decreasing
mucociliary clearance of inhaled particles and microorganisms. This
suggests that humans exposed to O3 may be predisposed to bacterial
infections in the lower respiratory tract. The seriousness of such
infections may depend on how quickly bacteria develop virulence factors
and how rapidly mechanisms are mobilized to compensate for depressed
alveolar macrophage function.

e. Hospital Admissions and Emergency Room Visits

Increased summertime hospital admissions and emergency room visits
for respiratory causes have been associated with ambient exposures to
O3 and other environmental factors. As cited in section V.C.5 of
the Staff Paper, numerous studies conducted in various locations in the
Eastern United States (U.S.) and Canada consistently have shown a
relationship between ambient O3 levels and increased incidence of
emergency room visits and hospital admissions for respiratory causes,
even after controlling for modifying factors, as well as when
considering only concentrations 3. Such associations
between elevated ambient O3 during summer months and increased
hospital admissions have a plausible biological basis in the human and
animal evidence of functional, symptomatic, and physiologic effects
discussed above and in the increased susceptibility to respiratory
infections observed in laboratory animals.
Individuals with preexisting respiratory disease (e.g., asthma,
chronic obstructive pulmonary disease) may generally be at increased
risk of such effects, and some individuals with respiratory disease may
have an inherently greater sensitivity to O3. On the other hand,
individuals with more severe respiratory disease are less likely to
engage in the level of exertion associated with provoking responses to
O3 exposures in healthy humans. On balance, it is reasonable to
conclude that evidence of O3-induced increased airway resistance,
nonspecific bronchial responsiveness, susceptibility to respiratory
infection, increased airway permeability, airway inflammation, and
incidence of asthma attacks suggests that ambient O3 exposure
could be a cause of increased hospital admissions, particularly for
asthmatics.

f. Pulmonary Inflammation

Respiratory inflammation can be considered to be a host response to
injury and indicators of inflammation as evidence that respiratory cell
damage has occurred. Inflammation induced by exposure of humans to
O3 may have several potential outcomes: (1) Inflammation induced
by a single exposure (or even several exposures over the course of a
season) could resolve entirely; (2) repeated acute inflammation could
develop into a chronic inflammatory state; (3) continued inflammation
could alter the structure and function of other pulmonary tissue,
leading to disease processes such as fibrosis; (4) inflammation could
interfere with the body's host defense response to particles and
inhaled microorganisms, particularly in potentially vulnerable
populations such as children and older individuals; and (5)
inflammation could amplify the lung's response to other agents such as
allergens or toxins. For humans, only the first of these potential

[[Page 65721]]

outcomes has been demonstrated in the laboratory. However, this is
expected because regulations concerning human experimental studies
require that long-term damage be avoided. Hence, study protocols only
involved brief exposures.
Exposures of laboratory animals to O3 for periods 8
hours have been shown to result in cell damage, inflammation, and
increased leakage of proteins from blood into the air spaces of the
respiratory tract. In general, higher O3 concentrations are
required to elicit a response equivalent to that of humans. This may
partly result from study design differences, in which humans were
exposed while exercising, whereas most animal studies were done at
rest, resulting in differences in effective ventilation rates.
Laboratory animals studies done at night, during the animals' active
period, or in which ventilation rates were increased with coexposure to
carbon dioxide (CO2) tend to support this view. The extent and
course of inflammation and its constitutive elements has been evaluated
by using bronchoalveolar lavage (BAL) to sample cells and fluid from
the lung and lower airways of humans exposed to O3. Several such
studies cited in section V.C.7 of the Staff Paper have shown that
exercising humans exposed (1 to 4 hours) to 0.2 to 0.6 ppm O3 had
O3-induced markers of inflammation and cell damage. The lowest
concentration of prolonged O3 exposure tested in humans, 0.08 ppm
for 6.6 hours with moderate exercise, also induced small but
statistically significant increases in these endpoints.
Thus, it is reasonable to conclude that repeated acute inflammatory
response and cellular damage discussed above is potentially a matter of
public health concern; however, it is also recognized that most, if not
all, of these effects begin to resolve in most individuals within 24
hours if the exposure to O3 is not repeated. Of possibly greater
public health concern is the potential for chronic respiratory damage
which could be the result of repeated O3 exposures occurring over
a season or a lifetime. Evidence for these chronic effects is discussed
below.
2. Potential Effects of Long-term O3 Exposures
Epidemiologic studies that have investigated potential associations
between long-term O3 exposures and chronic respiratory effects in
humans thus far have provided only suggestive evidence of such a
relationship. Most studies investigating this association have been
cross-sectional in design and have been compromised by incomplete
control of confounding variables and inadequate exposure information.
Other studies have attempted to follow variably exposed groups
prospectively. As cited in Section V.C.8 of the Staff Paper, studies
conducted in southern California and Canada have compared lung function
changes over several years between populations living in communities
with high and low ambient O3 levels. The findings suggest small,
but consistent, decrements in lung function among inhabitants of the
more highly polluted communities; however, associations between O3
and other copollutants and problems with study population loss have
reduced the level of confidence in these conclusions.
In a large number of animal toxicology studies, ``lesions'' 4
in the centriacinar regions of the lung (i.e., the portion of the lung
where the region that conducts air and the region that exchanges gas
are joined) are well established as one of the hallmarks of O3
toxicity. Studies have been conducted using rats, mice, and primates.
In one study in which rats were exposed to an urban pattern of O3
exposure, changes indicative of cell and tissue damage were reported,
although post-exposure damage was mainly reversible. A similar study of
identically exposed groups of rats found: (1) Increases in expiratory
resistance suggesting central airway narrowing after 78 weeks of
exposure, (2) reduced tidal volumes at all evaluation times during the
exposure, and (3) generally reduced breathing frequency, although no
single evaluation time was statistically significant. Another related
study with a similar protocol reported reduced lung volume, which is
consistent with a ``stiffer'' lung (i.e., restrictive lung disease). A
recent multicenter chronic study illustrates some of the complex
interrelationships among the structural, functional, and biochemical
effects. The three types of health endpoints mentioned above were
evaluated in a collaborative project using rats exposed for 20 months.
Lung biochemistry and structure were affected at 0.5 ppm and 1.00 ppm
O3, but not at 0.12 ppm O3, although no effects on pulmonary
function were observed at any exposure level.
---------------------------------------------------------------------------

\4\ Differing views have been expressed by CASAC panel members
regarding the use of the term ``lesion'' to describe the O3-
induced morphological (i.e., structural) abnormalities observed in
toxicological studies. Section V.C.8 of the Staff Paper describes
and discusses these degenerative changes in more detail.
---------------------------------------------------------------------------

In summary, the collective data on long-term exposure to O3
garnered in studies of laboratory animals and human populations have
many ambiguities. It is clear from toxicology data that the
distribution of O3 ``lesions'' is roughly similar across species
(including monkeys, rats, mice) with responses that are concentration
dependent (and perhaps time or exposure-pattern dependent). Under
certain conditions, some of these structural changes may become
irreversible. It is unclear, however, whether ambient exposure
scenarios encountered by humans result in similar ``lesions'' or
whether there are resultant functional or impaired health outcomes in
humans chronically exposed to O3. The epidemiologic lung function
studies generally parallel those of the animal studies, but these
studies lack good information on individual O3 exposure history
and are frequently confounded by personal or copollutant variables.
Thus, the Administrator recognizes that there is a lack of a clear
understanding of the significance of repeated, long-term inflammatory
responses, and that there is a need for continued research in this
important area. Nevertheless, the currently available information
provides at least a biologically plausible basis for considering the
possibility that repeated inflammation associated with exposure to
O3 over a lifetime may result in sufficient damage to respiratory
tissue such that individuals later in life may experience a reduced
quality of life, although such relationships remain highly uncertain.
Studies of laboratory animals exposed to O3 have been
relatively inconclusive with regard to genotoxicity and
carcinogenicity, particularly at lower O3 concentrations. Only
long-term exposure of laboratory animals to a high concentration of
O3 (1.0 ppm) has been shown to evoke a limited degree of
carcinogenic activity in one strain of female mice, whereas rats were
unaffected. Furthermore, there was no concentration response
relationship established, perhaps due to the limited scope of the
studies, and there is inadequate information from other research to
provide mechanistic support for the finding in mice. (For further
discussion, see section V.C.9 in the Staff Paper.)
Several epidemiologic studies cited in Section V.C.6 of the Staff
Paper have attempted to find associations between daily mortality and
O3 concentrations in various cities around the U.S. Although an
association between ambient O3 exposure in areas with very high
O3 levels and daily mortality has been suggested by these studies,
the data are limited.
3. Adversity of Effects for Individuals
Some population groups have been identified as being sensitive to
effects

[[Page 65722]]

associated with exposures to ambient O3 levels, such that
individuals within these groups are at increased risk of experiencing
the above effects. Such groups at increased risk include active
children and outdoor workers who regularly engage in outdoor activities
that involve heavy levels of exertion during short-term periods of
elevated ambient O3 levels or moderate levels of exertion during
prolonged periods of elevated ambient O3 levels. Exertion
increases the amount of O3 entering the airways and can cause
O3 to penetrate to peripheral regions of the lung where lung
tissue is more likely to be damaged. Secondly, individuals
characterized as having preexisting respiratory disease (e.g., asthma
or chronic obstructive lung disease), while not necessarily more
responsive than healthy individuals in terms of the magnitude of
pulmonary function decrements or symptomatic responses, may be at
increased risk. That is, the impact of O3-induced responses on
already-compromised respiratory systems may more noticeably impair an
individual's ability to engage in normal activity or may be more likely
to result in increased self-medication or medical treatment. It is
recognized that limitations on using such individuals in experimental
studies have prevented a more complete assessment of the full range of
potential responses to O3 or their health significance in such
individuals. Finally, some individuals are unusually responsive to
O3 relative to other individuals with similar levels of activity
or with a similar health status and may experience much greater
functional and symptomatic effects from exposure to O3 than the
average individual response. The mechanisms and characteristics
responsible for increased sensitivity to O3 exposure have not been
defined; thus, it is not clear whether these ``hyperresponders''
constitute a population subgroup with a specific risk factor or simply
represent the upper end of the O3 response distributions within
the general and at-risk populations.
In making judgments as to when the effects discussed above become
significant enough that they should be regarded as adverse to the
health of individuals in these sensitive populations, the Administrator
has looked to guidelines published by the American Thoracic Society
(ATS) and the advice of CASAC. While recognizing that perceptions of
``medical significance'' and ``normal activity'' may differ among
physicians, lung physiologists, and experimental subjects, the ATS
(1985) defined adverse respiratory health effects as ``medically
significant physiologic or pathologic changes generally evidenced by
one or more of the following: (1) Interference with the normal activity
of the affected person or persons, (2) episodic respiratory illness,
(3) incapacitating illness, (4) permanent respiratory injury, and/or
(5) progressive respiratory dysfunction.'' Human health effects for
which clear, causal relationships with exposure to O3 have been
demonstrated (e.g., functional and symptomatic responses) fall into the
first category listed in the ATS definition. Human health effects for
which statistically significant associations have been reported in
epidemiology studies fall into the second and third categories. These
more serious effects include respiratory illness that may require
medication (e.g., asthma), but not necessarily hospitalization, as well
as emergency room visits and hospital admissions for acute occurrences
of respiratory morbidity. Human health effects for which associations
have been suggested but not conclusively demonstrated fall primarily
into the last two categories. Evidence of these most serious health
endpoints for O3 comes from studies of effects in laboratory
animals, which can be extrapolated to humans only with a significant
degree of uncertainty, and from human epidemiological studies.
Application of these guidelines, in particular to the least serious
category of effects related to ambient O3 exposures, involves
judgments about which medical experts on the CASAC panel and public
commenters have expressed a diversity of views. To help frame such
judgments, the EPA staff defined gradations of individual functional
responses (e.g., decrements in forced expiratory volume (FEV1),
increased airway responsiveness) and symptomatic responses (e.g.,
cough, chest pain, wheeze), together with judgments as to the potential
impact on individuals experiencing varying degrees of severity of these
responses. These gradations and impacts, summarized below, are
discussed in the Criteria Document (Chapter 9) and Staff Paper (section
V.F, Table V-4a, 4b, 4c for individuals with impaired respiratory
systems and Table V-5a, 5b, 5c for healthy individuals) and incorporate
significant input from the CASAC panel of medical experts. The CASAC
panel expressed a consensus view that these ``criteria for the
determination of an adverse physiological response was reasonable''
(Wolff, 1995b).
For individuals with impaired respiratory systems, small functional
responses (e.g., FEV1 decrements of 3% to 10%,
increased nonspecific bronchial responsiveness 1 decrements 10% but 300%, lasting up to 24 hours) and/
or moderate symptomatic responses (frequent spontaneous cough, marked
discomfort on exercise or deep breath, wheeze accompanied by shortness
of breath, lasting up to 24 hours) would likely interfere with normal
activity for many such individuals and would likely result in
additional or more frequent use of medication. Large functional
responses (e.g., FEV1 decrements 20%, increased
nonspecific bronchial responsiveness >300%, lasting longer than 24
hours) and/or severe symptomatic responses (e.g., persistent
uncontrollable cough, severe discomfort on exercise or deep breath,
persistent wheeze accompanied by shortness of breath, lasting longer
than 24 hours) would likely interfere with normal activity for most
such individuals and would likely increase the likelihood of seeking
medical treatment or visiting an emergency room.
For active healthy individuals, it is judged that moderate levels
of functional responses (e.g., FEV1 decrements >10% but 1
decrements >20% lasting longer than 24 hours) and/or severe symptomatic
responses (e.g., persistent uncontrollable cough, severe discomfort on
exercise or deep breath, lasting longer than 24 hours) would likely
interfere with normal activity for many sensitive individuals.
In judging the extent to which such impacts represent effects that
should be regarded as adverse to the health status of individuals, an
additional factor that

[[Page 65723]]

the Administrator has considered is whether such effects are
experienced repeatedly by an individual during the course of a year or
only on a single occasion. While some experts would judge single
occurrences of moderate responses to be a ``nuisance,'' especially for
healthy individuals, a more general consensus view of the adversity of
such moderate responses emerges as the frequency of occurrence
increases. Thus, the Administrator agrees with the judgments presented
in the Staff Paper that repeated occurrences of moderate responses,
even in otherwise healthy individuals, may be considered to be adverse
since they could well set the stage for more serious illness.

B. Human Exposure and Risk Assessments

To put judgments about health effects that are adverse for
individuals into a broader public health context, the Administrator has
taken into account the results of human exposure and risk assessments.
This broader context includes consideration, to the extent possible, of
the size of particular population groups at risk for various effects,
the likelihood that exposures of concern will occur for individuals in
such groups under varying air quality scenarios, and the kind and
degree of uncertainties inherent in assessing the risks involved. Such
considerations provide a basis for judgments about the various levels
of risk and the adequacy of public health protection afforded by the
current NAAQS and alternative standards.
1. Exposure Analyses
The EPA conducted exposure analyses to estimate O3 exposures
for the general population and two at-risk populations, ``outdoor
children'' and ``outdoor workers,'' living in nine representative U.S.
urban areas. The areas include a significant fraction of the U.S. urban
population, 41.7 million people, the largest areas with major O3
nonattainment problems, and areas that are in attainment with the
current NAAQS. Exposure estimates were developed for a recent year, as
well as for modeled air quality that simulated conditions associated
with attainment of the current NAAQS and various alternative standards.
The exposure analyses provide estimates of the size of at-risk
populations exposed to various concentrations under different
regulatory scenarios, as presented in section V.G of the Staff Paper
and summarized below. These estimates are an important input to the
risk assessment summarized in the next section.
The probabilistic NAAQS exposure model for O3 (pNEM/O3)
used in these analyses builds on earlier deterministic versions of NEM
by modeling random processes within the exposure simulation. The pNEM/
O3 model takes into account the most significant factors
contributing to total human O3 exposure, including the temporal
and spatial distribution of people and O3 concentrations
throughout an urban area, the variation of O3 levels within each
microenvironment, and the effects of exertion (which is represented by
ventilation rate) on O3 uptake in exposed individuals. A more
detailed description of pNEM/O3 and its application is presented
in section V.G of the Staff Paper and associated technical support
documents (Johnson et al., 1994; Johnson et al., 1996 a,b; McCurdy,
1994a).
The regulatory scenarios examined in the exposure analyses include
1-hour O3 standards of 0.12 ppm (the current NAAQS) and 0.10 ppm,
and 8-hour standards of 0.07, 0.08, and 0.09 ppm, the range of
alternative 8-hour standards recommended in the Staff Paper and
supported by CASAC as the appropriate range for consideration in this
review. These analyses used 1- and 5-expected-exceedance forms of the
standards and are based on use of a single year of data. These
estimates were also used to roughly bound exposure estimates for other
concentration-based forms of the standard under consideration (e.g.,
the second- and fifth-highest daily maximum 8-hour average O3
concentration, averaged over a 3-year period) by using air quality
analyses that compare alternative forms of the standard, as presented
in Section IV and Appendix A of the Staff Paper. The estimated
exposures reflect what would be expected in a typical or average year
in an area just attaining a given standard over a 3-year compliance
period. Additional air quality and exposure analyses were done to
estimate the exposures that would be expected in the worst year of a 3-
year compliance period.
The exposure estimates were done in terms of both ``people
exposed'' (i.e., the number of people who experience a given level of
air pollution, or higher, at least one time during the time period of
analysis) and ``occurrences of exposure'' (i.e., the number of times a
given level of pollution is experienced by the population of interest).
Individual exposures were estimated in terms of dose, where dose is
defined as the product of O3 concentration and ventilation rate
over a defined period. Distributions of exposure estimates over the
entire range of actual or simulated ambient O3 concentrations were
developed as important input to the risk analysis, although results
also were developed in terms of the frequency of exposures to ambient
O3 concentrations above the lowest O3 concentrations at which
health effects have been clearly associated with exposure to O3 in
controlled human exposure studies (i.e., 0.12 ppm, 1-hour average, and
0.08 ppm, 8-hour average, respectively).
Key observations important in comparing estimated exposures
associated with attainment of the current NAAQS and alternative
standards under consideration include:
(1) Children who are active outdoors (representing approximately 7%
of the population in the study areas) appear to be the at-risk
population group examined with the highest percentage and number of
individuals exposed to O3 concentrations at and above which there
is evidence of health effects, particularly for 8-hour average
exposures at moderate exertion to O3 concentrations
0.08 ppm.
(2) On both an absolute number and a percentage basis, exposure
estimates are higher for the 8-hour average effects level of 0.08 ppm
at moderate exertion than for the 1-hour average effects level of 0.12
ppm at heavy exertion.
(3) Estimated exposures above these effects cutpoints, even on a
percentage basis, vary significantly across the urban areas examined in
this analysis. However, general patterns of exposure can be seen in
comparing the current NAAQS and alternative standards, particularly in
looking at the seven current nonattainment areas examined. For example,
for estimates of the mean percent of outdoor children exposed to 8-hour
average O3 concentrations 0.08 ppm while at moderate
exertion, the following patterns are seen: the range of estimates
associated with the current 1-hour NAAQS is approximately 1-21%,
dropping to approximately 3 NAAQS and under a recent year of air
quality (``as is'' air quality). The O3 health risk assessment
considers the same alternative air quality scenarios and the same nine
urban areas that were examined in the human exposure analyses described
above.
The objective of the risk assessment was to estimate the magnitude
of risks to population groups believed by EPA and CASAC to be at
greatest risk either due to increased exposures (i.e., outdoor children
and outdoor workers) or increased susceptibility (e.g., asthmatics)
while characterizing, as explicitly as possible, the range and
implications of uncertainties in the existing scientific database.
While the risk estimates are subject to uncertainties as discussed
below and should not be viewed as demonstrated health impacts, EPA
believes they do represent reasonable estimates as to the possible
extent of risk for these effects given the available information.
Although it does not cover all health effects caused by O3, the
risk assessment was intended as a tool, together with other information
presented in the Staff Paper and in the revised Criteria Document, to
aid the Administrator in judging which alternative O3 NAAQS would
reduce risks sufficiently to protect public health with an adequate
margin of safety.
The health risk assessment builds upon the earlier O3 NAAQS
health risk assessment work developed during the previous review of the
standard. The health risk model takes into account (1) concentration-
response or exposure-response relationships used to characterize
various respiratory effects of O3 exposure, (2) distributions of
O3 1-hour and 8-hour daily maximum concentrations upon attainment
of alternative NAAQS obtained from the pNEM/O3 analyses described
above, and (3) distributions of population exposure, in terms of both
the number of individuals in the general population, outdoor workers,
and outdoor children exposed and the number of occurrences of exposure,
upon attainment of alternative O3 NAAQS, obtained from the O3
exposure analyses. A more detailed description of the risk assessment
methodology and its application is presented in Section V.H of the
Staff Paper and associated technical support document (Whitfield et
al., 1996).

a. Adverse Lung Function and Respiratory Symptom Responses

Risk estimates have been developed for several of the respiratory
effects observed in controlled human exposure studies to be associated
with O3 exposure. These include lung function decrements (measured
as changes in FEV1) and moderate or severe pain on deep
inspiration (PDI). Each of the effects is associated with a particular
averaging time and, for most of the acute (1- to 8-hour) responses,
effects also are estimated separately for specific ventilation ranges
[measured as equivalent ventilation rate (EVR)] that correspond to the
EVR ranges observed in the health studies used to derive exposure-
response relationships.
An effect, or endpoint, can be defined in terms of a measure of
biological response and the amount of change in that measure thought to
be of concern. For lung function decrements, estimates are provided for
the lower end, midpoint, and upper end of the range of response that
might be considered an adverse health effect (i.e., 10, 15,
or 20% FEV1 decrements) as discussed in II.A.3 above. For acute
symptomatic effects, estimates are provided for responses that EPA
considers to be of most concern (e.g., moderate and severe PDI). Due to
limitations in the available data, the risk assessment provides
estimates only for each individual health endpoint rather than various
combinations of functional and symptomatic responses.
The acute exposure-response relationships developed were based on
the clinical studies and were applied to ``outdoor children,''
``outdoor workers,'' and the general population. While these specific
clinical studies only included adults aged 18-35, findings from other
clinical studies and summer camp field studies in at least six
different locations in the northeast United States, Canada, and
Southern California indicate changes in lung function in healthy
children similar to those observed in healthy adults exposed to O3
under controlled chamber conditions.
While different risk measures are provided by the O3 health
risk assessment, EPA has focused on ``headcount risk'' estimates.
Headcount risk provides estimates of both the number of people affected
and the number of incidences of a given health effect, considering
individuals' personal exposures as they go about their daily activities
(e.g., from indoors to outdoors, moving from place to place, and
engaging in activities at different exertion levels).

[[Page 65725]]

A major input to the headcount risk model is the series of
population exposure distributions for the alternative NAAQS analyzed.
Using available exposure estimates, risk estimates were calculated for
the nine urban areas examined in the exposure analysis. For 8-hour
exposures under moderate exertion, outdoor children represent the
population group experiencing the greatest exposure, and, therefore,
this population also has the highest risk estimates in terms of the
percent of the population estimated to respond. Therefore, this summary
of results focuses on the risk estimates for outdoor children.
Whitfield et al. (1996) presents results of the headcount risk
estimates for each of the nine urban areas for outdoor children and
outdoor workers.
Table 1 presents a summary of risk estimates for 8-hour and 1-hour
health endpoints for outdoor children upon attainment of alternative 8-
hour, 1- and 5-expected exceedance standards and the current 0.12 ppm,
1-hour standard. The risk estimates in Table 1 are for effects
associated with exposure under moderate exertion. These risk estimates
represent an aggregate estimate for the nine urban areas examined; an
aggregate estimate is presented since there is significant variability
in this risk measure across the areas. The uncertainty in these risk
estimates associated with sample size considerations is characterized
by the 90 percentile credible intervals shown.

Table 1.--Percent of Outdoor Children Estimated to Experience Various Health Effects 1 or More Times per Year
Associated With 8- and 1-Hour Ozone Exposures Upon Attaining Alternative Standards*
----------------------------------------------------------------------------------------------------------------
Alternative standards Pulmonary function Pulmonary function Moderate or severe
----------------------------------------------------- decrements, FEV1 decrements, FEV1 pain on deep
15% 20% inspiration
Level Averaging time and form associated with 8- associated with 8- associated with 1-
hour exposures hour exposures hour exposures
----------------------------------------------------------------------------------------------------------------
0.07 ppm................ 8-hour, 1 expected 3.0 0.4 (0.1-1.8) 0.3 (0.01-1.9)
exceedance. **(1.0-6.6)
0.08 ppm................ 8-hour, 1 expected 5.1 (2.2-9.6) 1.4 (0.5-3.7) 0.6 (0.05-2.7)
exceedance.
8-hour, 5 expected 6.7 (3.3-11.9) 2.3 (0.8-5.3) 0.8 (0.1-3.2)
exceedances.
0.09 ppm................ 8-hour, 1 expected 7.7 (3.3-13.3) 2.7 (1.0-6.1) 0.9 (0.1-3.5)
exceedance.
8-hour, 5 expected 9.5 (5.1-15.9) 3.8 (1.5-7.9) 1.3 (0.2-4.2)
exceedances.
0.12 ppm................ 1-hour, 1 expected 8.3 (8.2-14.2) 3.0 (1.1-6.6) 1.0 (0.1-3.6)
exceedance.
----------------------------------------------------------------------------------------------------------------
* Estimates represent aggregate results for 9 urban areas examined. The total number of outdoor children
residing in the 9 urban areas was 3.1 million.
** 90% credible interval.

Key observations important in comparing estimated health risks
associated with attainment of the current NAAQS and alternative
standards under consideration include:
(1) On both an absolute number and a percentage basis, risk
estimates are higher for effects associated with 8-hour exposures under
moderate exertion than for effects associated with 1-hour exposures
under heavy exertion.
(2) Reflecting a continuum of risk, there is a decreasing trend in
the median estimates of the population estimated to experience the lung
function and symptomatic responses as one moves along the range of
alternative 8-hour average, 1-expected exceedance standards under
consideration. For example, based on the aggregate risk estimates
summarized in Table 1, the median percent of outdoor children estimated
to experience FEV1 decrements greater than 15% is reduced from
about 7.7% for a 0.09 ppm, 8-hour standard to about 5.1% for a 0.08
ppm, 8-hour standard. Attaining a 0.07 ppm, 8-hour standard results in
a further reduction to about 3.0% of outdoor children estimated to
experience this effect.
(3) In general, the differences in risk estimates for outdoor
children associated with 1- and 5-expected exceedance standards set at
the same standard level are relatively modest within the continuum of
risk. For example, the risk estimates for lung function decrements
15% associated with a 5-expected exceedance standard set at
0.08 ppm fall between the risk estimates for the 0.08 and 0.09 ppm, 1-
expected exceedance, 8-hour standards. Similarly, the risk estimates
for a 5-expected exceedance standard set at 0.09 ppm fall between the
risk estimates for the 0.09 and 0.10 ppm, 1-expected exceedance, 8-hour
standards. The risk estimates for the current 0.12 ppm, 1-hour standard
fall between the risk estimates for the 0.09 ppm, 1- and 5-expected
exceedance standards.
(4) Multiple occurrences of lung function decrements 15%
and 20% associated with 8-hour exposures under moderate
exertion are estimated to occur for outdoor children upon attainment of
any of the alternative 1- or 8-hour standards analyzed. The average
seasonal numbers of occurrences per responder across the urban areas
included in the analysis range from four to about nine for lung
function decrements 15% and from two to about five for lung
function decrements >20%, such that some individuals will experience
more frequent occurrences of effects during the O3 season, whereas
others will experience fewer occurrences than the average in any given
area.
(5) Based on comparisons of air quality distributions, risk
estimates are generally comparable between 8-hour standards with 5-
expected exceedances or fifth-highest daily maximum concentration
forms. As noted in the previous discussion of the exposure estimates,
for either form the worst year of a 3-year compliance period would be
higher than for the average or typical year. For example, about 95% of
current nonattainment areas meeting either form of an 8-hour, 0.08 ppm
standard would have 10 or fewer exceedances in the worst year, compared
to an average of less than five exceedances in a typical year. Risk
estimates for a year in which there were 10 exceedances of 0.08 ppm, 8-
hour average vary from urban area to urban area but fall between the
risk estimates for a 5-expected exceedance standard of 0.08 ppm and a
5-expected exceedance standard set at 0.09 ppm.
The EPA believes, and CASAC concurred, that the models selected to
estimate exposure and risk are appropriate and that the methods used to
conduct the health risk assessment represent the state of the art.
Nevertheless, the Administrator and CASAC recognize that there are many
uncertainties inherent in such analyses. The resulting ranges of
quantitative risk

[[Page 65726]]

estimates do not reflect all of the uncertainties associated with the
numerous assumptions inherent in such analyses (Wolff, 1995b). Some of
the most important caveats and limitations concerning the health risk
assessment for lung function and respiratory symptom endpoints include:
(1) The uncertainties and limitations associated with the exposure
analyses discussed above, (2) the extrapolation of exposure-response
functions below the lowest-observed-effects levels to an estimated
background level of 0.04 ppm, and (3) the inability to account for some
factors which are known to affect the exposure-response relationships
(e.g., assigning children the same symptomatic response rates as
observed for adults and not adjusting response rates to reflect the
increase and attenuation of responses that have been observed in
studies of lung function and symptoms upon repeated exposures). A more
complete discussion of assumptions and uncertainties is contained in
the Staff Paper and in the technical support document (Whitfield et
al., 1996).

b. Excess Respiratory-Related Hospital Admissions

As discussed earlier in this notice, several epidemiology studies,
mainly conducted in the northeastern portion of the U.S. and
southeastern Canada, have reported excess daily respiratory-related
hospital admissions associated with elevated O3 levels during the
O3 season. To gain insight into the possible impact of just
attaining alternative 1- and 8-hour O3 standards, EPA has
developed a risk model for this endpoint. The model is based on the
regression coefficient (and the corresponding standard error) developed
by Thurston et al. (1992) for New York City and estimated daily maximum
hourly average O3 levels over an entire season at various monitors
in New York City upon attainment of alternative standards (as developed
for the pNEM/O3 analysis). The regression coefficient (11.7
admissions/ppm O3/106 people) and its standard error (4.7
admissions/ppm O3/106 people) were used to define a
probabilistic concentration-response relationship. The model is
described in more detail in Whitfield et al. (1996). One-hour daily
maximum O3 concentrations for one O3 season under various
alternative air quality standards were used to estimate the number of
excess respiratory-related admissions of asthmatics (i.e., those
attributable to O3 concentrations higher than background). The
O3 concentration-response relationship developed by Thurston et
al. (1992) was based on air quality data from the Queens monitor.
Therefore, the risk estimates based on the Queens County monitor most
closely represent the air quality index used in the original study and
are summarized below. In each analysis, the air quality was adjusted to
just attaining a particular standard at the monitor with the highest
O3 levels for the New York area, and the O3 levels were
adjusted at the other monitors using the procedures described in
Johnson et al. (1996a).
Based on Table V-20 in the Staff Paper, the hospital admissions
model results in a median estimate of excess respiratory-related
admissions for asthmatic individuals attributable to O3 exposure
of approximately 390 (with a 90% credible interval of approximately
130-640) per year for the New York City area based on ``as is'' air
quality using 1991 data. Just attaining the current 0.12 ppm, 1-hour
standard is estimated to reduce excess hospital admissions to about 210
(with a 90% credible interval of 70-340), which is approximately a 50%
decrease in O3-induced admissions due to concentrations in excess
of the estimated 0.04 ppm estimated background level. Upon attaining
the 0.08 ppm, 8-hour, 1 expected exceedance standard, for example, the
median estimate for excess respiratory-related hospital admissions
attributable to O3 exposure is further reduced to approximately
115 (with a 90% credible interval of approximately of 40-190). This
represents a 70% decrease in O3-induced hospital admissions from
the ``as is'' scenario and about a 45% decrease from the current 1-hour
standard.
It should be recognized that the O3-induced excess hospital
admissions represent a relatively small fraction of the overall
respiratory-related hospital admissions for asthmatics over the seven
month O3 season. Based on an estimated 15,000 admissions per year
during the O3 season, the reduction in hospital admissions for
asthmatics for any respiratory-related reason in going from ``as is''
air quality to attaining a 0.08 ppm, 8-hour, 1-expected exceedance
standard is about 2%. Similarly, the reduction from attaining the
current 1-hour standard to attaining a 0.08 ppm, 8-hour, 1-expected
exceedance standard represents about a 0.6% decrease in total
respiratory admissions for asthmatics due to all causes.
Key observations important in comparing hospital admission risk
estimates associated with attainment of the current NAAQS and
alternative standards under consideration include:
(1) Risk estimates for excess hospital admissions for asthmatics
attributable to O3 exposures in excess of an estimated background
level of 0.04 ppm are projected to be significantly reduced (about 45%)
under a 0.08 ppm, 8-hour, 1-expected exceedance standard compared to
the current 1-hour NAAQS.
(2) The excess hospital admissions risk estimates associated with
1- and 5-expected exceedance standards set at 0.08 ppm are very
similar.
(3) When viewed from the perspective of respiratory-related
admissions for asthmatics due to all causes, the excess hospital
admissions attributable to O3 exposures in excess of an estimated
background concentration of 0.04 ppm constitute a relatively small
portion of total admissions. For example, comparing the risk estimates
associated with the current 1-hour NAAQS and a 0.08 ppm, 8-hour, 1-
expected exceedance standard results in only about a 0.6% reduction in
respiratory hospital admissions for asthmatics due to all causes.
In taking these observations into account, the Administrator
recognizes the uncertainties and limitations associated with the
hospital admission risk assessment. These include: (1) The inability at
this time to quantitatively extrapolate the risk estimates for the New
York City area to other urban areas, (2) uncertainty associated with
the underlying epidemiological study that served as the basis for
developing the concentration-response relationship used in the
analysis, and (3) uncertainties associated with the air quality
adjustment procedure used to simulate attainment of alternative
standards for the New York City area. A more complete discussion of
these uncertainties and limitations is presented in the Staff Paper and
technical support document (Whitfield et al., 1996).

c. Conclusions on the Elements of the Primary Standard

In selecting a primary standard for O3, the Administrator must
specify: (1) Averaging time, (2) O3 concentration (i.e., level),
and (3) form (i.e., the air quality statistic to be used as a basis for
determining compliance with the standard).5 All three of these
elements are necessary to define a standard. Based on the assessment of
relevant scientific and technical information in the Criteria Document,
section VI of the Staff Paper outlines a number of key factors to be
considered in specifying each of these elements, as well as
recommendations to focus consideration on a discrete range of options
for each

[[Page 65727]]

element. The factors reflect an integration of information on acute and
chronic health effects associated with exposure to ambient O3;
expert judgments on the adversity of such effects for individuals; and
policy judgments, informed by air quality analyses and quantitative
risk assessment when possible, as to the point at which risks would be
reduced sufficiently to achieve protection of public health with an
adequate margin of safety.
---------------------------------------------------------------------------

\5\ This review focused only on a standard for O3, as the
most appropriate surrogate for photochemical oxidants.
---------------------------------------------------------------------------

This approach to selecting a proposed primary standard was endorsed
by members of CASAC (Wolff, 1995b), particularly through their advice
to the Administrator that ``EPA's risk assessments must play a central
role in identifying an appropriate level'' and their recognition that
the selection of a specific concentration and form ``is a policy
judgment.'' Further, it was the consensus view of CASAC that the ranges
of levels (0.07 to 0.09 ppm) and forms (1 to 5 exceedances) recommended
in the Staff Paper were appropriate.
Thus, the Administrator has focused her consideration on the
recommended options and key factors outlined in the Staff Paper. The
considerations that were most influential in the Administrator's
selection of each specific element of the proposed standard are
outlined below.
1. Averaging Time
The Administrator concurs with the unanimous recommendation of
CASAC (Wolff, 1995b) ``that the present 1-hr standard be eliminated and
replaced with an 8-hr standard,'' and that more research is needed to
resolve uncertainties about potential chronic effects before
appropriate consideration can be given to establishing a long-term
(e.g., seasonal or annual) standard. These judgments are supported by
the following key observations and conclusions:
(1) The 1-hour averaging time specified in the current NAAQS was
originally selected primarily on the basis of health effects associated
with short-term (i.e., 1- to 3-hour) exposures, with qualitative
consideration given to preliminary information on potential
associations with longer exposure periods.
(2) Substantial new health effects information available for
consideration in this review demonstrates associations between a wide
range of health effects and prolonged (i.e., 6- to 8-hours) exposures
below the level of the current 1-hour NAAQS.
(3) Results from the quantitative risk analyses show that attaining
a standard with a 1-hour averaging time reduces the risk of
experiencing health effects associated with both 1-hour and 8-hour
exposures. Likewise, attaining an 8-hour standard reduces the risk of
experiencing health effects associated with both 8-hour and 1-hour
exposures. Thus, reductions in risks from both short-term and prolonged
exposures can be achieved through a primary standard with an averaging
time of either 1 or 8 hours. As a result, establishment of both 1-hour
and 8-hour standards would not be necessary to reduce risks associated
with the full range of observed acute health effects.
(4) The 8-hour averaging time is more directly associated with
health effects of concern at lower O3 concentrations than is the
1-hour averaging time. It was thus the consensus of CASAC ``that an 8-
hr standard was more appropriate for a human health-based standard than
a 1-hr standard.'' (Wolff, 1995b)
(5) While there is a large animal toxicology database providing
clear evidence of associations between long-term (e.g., from several
months to years) exposures and lung tissue damage, with additional
evidence of reduced lung elasticity and accelerated loss of lung
function, there is not corresponding evidence for humans. Moreover, the
state of the science has not progressed sufficiently to permit
quantitative extrapolation of the animal-study findings to humans.
Thus, the Administrator concludes that consideration of a separate
long-term O3 standard is not appropriate at this time. As
discussed below, however, the Administrator has considered the
possibility of long-term effects in selecting the level of the
standard, which will provide protection against such effects to the
extent they may occur in humans, by lowering overall air quality
distributions and, thus, reducing cumulative long-term exposures.
2. Level
The Administrator's consideration of an appropriate level for an 8-
hour standard to protect public health with an adequate margin of
safety necessarily reflects a recognition, as emphasized by CASAC, that
it is likely that ``O3 may elicit a continuum of biological
responses down to background concentrations'' (Wolff, 1995b). Thus, in
the absence of any discernible threshold, it is not possible to select
a level below which absolutely no effects are likely to occur. Nor does
it seem possible, in the Administrator's judgment, to identify a level
at which it can be concluded with confidence that no ``adverse''
effects are likely to occur. In such a case, as CASAC has advised, the
traditional paradigm for standard-setting cannot be applied in the
usual way, and assessments of risk ``must play a central role in
identifying an appropriate level'' (Wolff, 1995b). Thus, the
Administrator's task becomes one of attempting to select a standard
level that will reduce risks sufficiently to protect public health with
an adequate margin of safety, since a zero-risk standard is neither
possible nor required by the Act. Consequently, as CASAC recognized,
``the selection of a specific level * * * is a policy judgment''
(Wolff, 1995b). The Administrator's policy judgment on the level of the
proposed standard is framed by the above considerations and informed by
the following key observations and conclusions:
(1) During the last review of the O3 criteria and standards,
the CASAC concluded that the existing 1-hour standard set at 0.12 ppm
O3 provided ``little, if any, margin of safety,'' and the upper
end of the range of consideration for a 1-hour standard should be 0.12
ppm (McClellan, 1989). In addition, several members of the CASAC panel
recommended that consideration should be given to a lower 1-hour level
of 0.10 ppm to offer some protection against effects for which there
was preliminary information at that time of associations with 8-hour
exposures to O3.
Regarding currently available evidence of O3-related effects:
(2) Based on a significant body of information available since the
last review, there is now clear evidence from human clinical studies
that O3 effects of concern are associated with the 8-hour
exposures tested. Studies were done at 8-hour exposure levels of 0.12,
0.10, and 0.08 ppm). This includes evidence of the following
statistically significant responses at 6- to 8-hour exposures to the
lowest concentration evaluated, 0.08 ppm O3, at moderate exertion:
lung function decrements, respiratory symptoms (e.g., cough, pain on
deep inspiration), nonspecific bronchial responsiveness, and
biochemical indicators of pulmonary inflammation. Field studies provide
evidence of similar functional and symptomatic effects at ambient
O3 exposures that are consistent with the clinical findings.
Laboratory animal studies provide supporting evidence of O3-
induced biochemical indicators of inflammation and functional changes.
(3) Numerous epidemiological studies have reported excess hospital
admissions and emergency department visits for respiratory causes (for
asthmatic individuals and the general population) attributed primarily
to ambient O3 exposures, including O3

[[Page 65728]]

concentrations below the level of the current standard, with no
discernible threshold at or below this level. The biological
plausibility of attributing such effects to ambient O3 exposures
is supported by human studies showing increased nonspecific bronchial
responsiveness, laboratory animal studies showing pulmonary changes
that decrease the effectiveness of the lung's defenses against
bacterial respiratory infections, and the reasonable anticipation that
O3 exposures also increase the risk of respiratory infections in
humans, based on the many similarities between animal and human defense
mechanisms.
(4) Long-term laboratory animal studies suggest that changes in
lung biochemistry and structure may, under certain circumstances,
become irreversible, although it is unclear whether long-term exposures
to ambient O3 levels result in similar chronic health effects in
humans.
Regarding the types and severity of O3-induced physiological
effects that are considered to be adverse to the health status of
individuals experiencing such effects:
(5) With regard to lung function decrements and respiratory
symptoms, the Administrator recognizes that these O3-induced
effects are transient and reversible, and concludes that the extent to
which such effects are adverse to the health status of an individual
depends upon the severity, duration, and frequency with which an
individual experiences such effects throughout the O3 season.
While group mean responses in clinical studies at the lowest exposure
level tested of 0.08 ppm are typically small or mild in nature,
responses of some extremely sensitive individuals are sufficiently
severe and extended in duration to be considered adverse. This would
especially be true to the extent that those individuals likely to
experience such effects would, on average, experience them several
times a year.
(6) With regard to increased hospital admissions and emergency room
visits, the Administrator judges that such effects are clearly adverse
to individuals.
(7) With regard to pulmonary inflammation, the Administrator
recognizes that singular occurrences of inflammation are likely
reversible and potentially of little health significance. On the other
hand, repeated inflammatory responses associated with exposure to
O3 over a lifetime have the potential to result in damage to
respiratory tissue such that individuals later in life may experience a
reduced quality of life. Furthermore, there is the possibility that
repeated pulmonary inflammatory responses could adversely affect
asthmatic individuals by resulting in increased medication use, medical
treatment, and/or emergency room visits and hospital admission.
Accordingly, the Administrator judges that repeated exposures to
O3 levels that produce inflammation of the lungs are adverse to
individuals likely to experience such exposures over long periods of
time.
The Administrator has considered the results of the exposure and
risk analyses and the following key observations and conclusions from
these analyses in putting effects considered to be adverse to
individuals into a broader public health perspective and making
judgments about the level of a standard that would reduce risk
sufficiently to protect public health with an adequate margin of
safety:
(8) The median risk estimates for functional and symptomatic
effects, as well as for excess hospital admissions and emergency room
visits due to respiratory causes, are approximately the same or only
marginally smaller for some of the 0.09 ppm 8-hour standard options
evaluated (including those with forms ranging from 1- to 3-expected-
exceedances 6) as compared to the current 0.12 ppm 1-hour NAAQS
(risk estimates are somewhat larger for a 0.09 ppm 8-hour 5-expected-
exceedance form as compared to the current NAAQS).
---------------------------------------------------------------------------

\6\ Based on air quality comparisons, since risk estimates are
only currently available for the 1- and 5-expected-exceedance forms
of a 0.09 ppm standard.
---------------------------------------------------------------------------

(9) Within any given urban area, statistically significant
reductions in exposure and risk associated with functional and
symptomatic effects result from alternative 8-hour standards as the
level changes from 0.09 ppm to 0.08 ppm to 0.07 ppm. These reductions
represent differences of hundreds of thousands of times that children
would likely experience such effects under the range of alternative
standards considered relative to the current standard.7 There are
significant uncertainties in such quantitative estimates, however, and
there is no break point or bright line that differentiates between
acceptable and unacceptable risks within this range.
---------------------------------------------------------------------------

\7\ With regard to these risk analyses, CASAC concluded ``that
there is no `bright line' which distinguishes any of the proposed
standards (either the level or the number of allowable exceedances)
as being significantly more protective of public health,'' and noted
that the differences in percent of outdoor children responding
between the present standard and the most stringent standard ``are
small and their ranges overlap for all health endpoints.'' (Wolff,
1995b) To address any apparent differences between EPA's and CASAC's
conclusions, it is important to note that EPA's risk analysis report
(Whitfield et al., 1996) makes clear that there are statistically
significant differences in estimated risk for alternative standard
levels; whether one judges the differences to be significant or
small can depend on whether one focuses on percentages, as CASAC's
letter did, or on total numbers of times that children or other at-
risk individuals experience such effects. The overlap in the ranges
of risk referred to in the CASAC letter reflect differences among
cities used in EPA's risk analysis (e.g., air quality, esposure
patterns, environmental factors), not random uncertainties in risk
estimates within any given city. Thus, the fact that the ranges
overlap does not mean that there are no real or statistically
significant differences in protection among alternative standards.
---------------------------------------------------------------------------

(10) Similarly, reductions in hospital admissions and emergency
room visits for asthmatic individuals are estimated to occur with each
change in the level of the standard from 0.09 ppm to 0.08 ppm to 0.07
ppm. However, hospital admissions for asthmatic individuals associated
with ambient O3 exposures within the range of standard levels
under consideration represent a relatively small fraction of the total
respiratory-related hospital admissions for asthmatics over the O3
season.
(11) Estimated exposures to O3 concentrations 0.08
ppm (at which increased nonspecific bronchial responsiveness, decreased
pulmonary defense mechanisms, and indicators of pulmonary inflammation
have been observed in humans) are essentially zero at the 0.07 ppm
standard level for most areas evaluated in the exposure analyses for
the at-risk population of outdoor children. Such exposures of outdoor
children increase to approximately 0 to 1.3% at the 0.08 ppm level,
while the estimated range at the 0.09 ppm level rises to 3-7% for the
areas evaluated.
(12) While recognizing that extremely sensitive individuals may
experience adverse but transient effects with a standard set at 0.08
ppm, no CASAC panel member supported selection of 0.07 ppm as the level
of a primary standard. Of the members who expressed their personal
views, three indicated a preference for a level of 0.08 ppm, one for a
range of 0.08 to 0.09 ppm, three for a level of 0.09 ppm (with one of
the three expressing a preference for selecting a form that would
result in equivalent protection to the current standard), and one for a
range of 0.09 to 0.10 ppm, associated with public advisories for
O3 levels at and above 0.07 ppm. Other CASAC panel members also
expressed support for such public notices or advisories reflecting
potential effects for extremely sensitive individuals associated with
O3 levels as low as 0.07 ppm.

[[Page 65729]]

After carefully assessing the key observations and conclusions
drawn from the available scientific evidence and analyses, and taking
into account the advice of CASAC and comments from the public, the
Administrator focused her consideration on two policy options for the
level of the primary O3 standard: 0.08 ppm and 0.09 ppm. A
standard set at a level of 0.09 ppm (within the middle of the range of
forms discussed below) would result in approximately equivalent public
health protection as that afforded by the current standard; a 0.08 ppm
level would provide greater protection. In her judgment, the selection
of either level could properly take into account the available
scientific and technical information and would be consistent with the
views expressed by her scientific advisors, since none of the CASAC
panel members expressed the view that the standard level should be set
below 0.08 ppm. On the other hand, the Administrator is aware of
alternative views that place great weight on margin of safety
considerations, leading to support by some commentors for a standard
level option of 0.07 ppm, as discussed further below.
In deciding between the 0.08 ppm and 0.09 ppm alternatives, the
Administrator took into account several factors including: (1)
Estimates of risk, in terms of the percentage of children likely to
experience respiratory symptoms and decreases in lung function of
concern; (2) estimates of exposures to the lowest concentration at
which other, more uncertain effects have been observed; and (3) the
body of health effects evidence as a whole.
In considering risk estimates, she noted that there is a continuum
of increasing risk reduction in going from the upper end of the range
of consideration (0.09 ppm, with a 5-expected-exceedance form) down to
the lower end of this range (0.08 ppm, with a 1-expected-exceedance
form) and below, and that the current 1-hour standard provides a level
of protection within but near the top of this range. These quantitative
risk estimates are summarized in Table 1 above, showing the varying
percentages of children estimated to experience these symptomatic and
functional effects of concern for the alternative 0.08 and 0.09 ppm 8-
hour standards. Quantitative risks could be estimated for these effects
because studies are available that allow for a determination of how the
percentages of individuals likely to experience such effects vary as a
function of the O3 concentrations to which they are exposed.
With respect to exposure estimates, she noted that these
alternative standards provide differing degrees of protection from
exposures to O3 concentrations that have been associated with
other potentially adverse, but more uncertain effects, including
nonspecific bronchial responsiveness (related, for example to
aggravation of asthma) and inflammation of the lungs (related to
potential chronic aggravation of bronchitis or long-term damage to the
lungs). For these effects, the evidence is not sufficient to conduct a
quantitative risk assessment, but the relative protection of the
alternative standards can be considered in terms of the percentages of
outdoor children who would be exposed one or more times to the lowest
concentration at which evidence of these effects has been observed
(i.e., 0.08 ppm). As noted above, in summarizing key observations from
the exposure assessment, the percentages of outdoor children likely to
be exposed to the level are approximately 3 to 7% for a 0.09 ppm
standard (with a 1-expected-exceedance form) and approximately 0 to
1.3% for a 0.08 ppm standard with the same form. For comparison, these
exposures range from approximately 1 to 21% for the current 1-hour
standard of 0.12 ppm,8 dropping to essentially 0% for a 0.07 ppm
8-hour standard. While the public health risks associated with these
effects are uncertain and cannot be assessed definitively, the
Administrator finds these different exposures to be an important factor
in making this policy choice.
---------------------------------------------------------------------------

\8\ The wide range of exposures for this 1-hour standard
(compared to the narrower ranges for the 8-hour standards) reflects
much greater variability across cities in the extent to which a 1-
hour standard limits 8-hour exposures.
---------------------------------------------------------------------------

Both the quantitative risk estimates for respiratory symptoms and
decreased lung function and the exposure estimates associated with
bronchial responsiveness and inflammation of the lung provide an
important perspective in assessing the public health implications of
effects observed in individuals exposed to various O3
concentrations. Nonetheless, the Administrator believes that these
estimates alone do not provide a clear basis for making a policy choice
between the 0.09 and 0.08 ppm levels for an 8-hour standard.
Finally, the Administrator noted that in a number of clinical
studies examining all of the effects discussed above in human subjects,
various researchers have consistently reported statistically
significant effects at an exposure level of 0.08 ppm. This exposure
level reflects the lowest level that researchers have chosen to conduct
the relevant studies, and it does provide a strong point of consistency
in the currently available scientific evidence. Effects at this level
observed in clinical studies are also consistent with the results of
epidemiological and summer camp studies reporting similar symptomatic
and functional effects associated with exposures to ambient levels of
O3 that broadly span this clinical lowest-observed-effects level.
The Administrator has weighed the importance of increased
protection for those extremely sensitive individuals who may experience
symptomatic and functional effects at lower O3 concentrations than
the population as a whole, the uncertainties in considering the
potentially more serious but as yet uncertain chronic effects. For all
these reasons, the Administrator is proposing to set the level of an 8-
hour O3 standard at 0.08 ppm.
However, as noted above, in making this judgment, the Administrator
is mindful that a range of views has been expressed as to the
appropriate policy choice between 0.08 ppm and 0.09 ppm for an 8-hour
standard level. For example, while some CASAC members supported the
choice of the proposed 0.08 ppm, fully half or more of the CASAC panel
members expressing views on a specific level supported a specific level
or range of levels that include 0.09 ppm.
Those that favored a 0.09 ppm standard did so on the basis of
several kinds of judgments. As the CASAC noted, it is unclear whether
there is a threshold level for the various health effects discussed
above. For this reason, some CASAC members and others have suggested
that it is difficult to determine if a margin of safety exists for any
particular level and therefore, in their opinion the differences in
health protection may not be significant enough to justify a change
from the current standard.
Others may support a 0.09 ppm standard on the basis of
uncertainties about: (1) The medical significance of the reported
effects of O3 exposure at these levels for individuals
experiencing such effects; (2) the public health significance of the
degree of exposure and risk reduction likely to be achieved by moving
from 0.09 ppm O3 to 0.08 ppm O3; (3) the appropriate weight
to be given to the health endpoints that could not be addressed in the
quantitative risk assessment; and 4) how to address the various
uncertainties in the scientific evidence on health effects and in the
exposure and risk estimates in making a policy decision on a standard
level

[[Page 65730]]

that will protect public health with an adequate margin of safety.
A policy decision to set a 0.09 ppm 8-hour standard would place
more weight on the transient and reversible nature of reported
decrements in lung function, increased respiratory symptoms, and lung
inflammation, and would call into question the medical significance of
moderate levels of such effects, particularly for healthy individuals.
This view would also emphasize the relatively small fraction of the
overall respiratory-related hospital admissions for asthmatics that are
estimated to be linked to O3 exposures over the O3 season.
Thus, it could be reasonable to judge that any incremental reduction in
such risk achieved by levels below 0.09 ppm O3 would be of little
consequence when viewed from a broader public health perspective.
Further, this view would note the lack of evidence linking O3-
induced markers of inflammation and cell damage with chronic
respiratory damage in humans. In this view, while the potential for
O3-induced chronic respiratory damage would be a matter of public
health concern, additional research would be needed before such
concerns should be reflected in margin of safety considerations. These
interpretations of the evidence and judgments as to the nature and
significance of the reported O3-induced health effects, could
justify a judgement that an 8-hour standard set at 0.09 ppm O3
protects public health with an adequate margin of safety. Thus, the
Administrator solicits public comment on this alternative of a 0.09 ppm
level for an 8-hour standard.
In sharp contrast, the Administrator also notes that others would
make a different set of judgments as to the significance of O3-
induced health effects and the appropriate public health policy
response. To reflect these views, the Administrator is also requesting
comment on the alternative of establishing the level of an 8-hour
standard at 0.07 ppm. A standard set at this level, within a range of
forms (as discussed in the next section), would be highly precautionary
in nature. A policy decision to select such a standard would reflect an
emphasis on (1) The many studies that have reported observed effects in
humans at moderate levels of exercise at an exposure level of 0.08 ppm;
(2) judgments that the reported decrements in lung function, increased
respiratory symptoms, and indicators of inflammation, even when
transient and reversible at moderate levels, are adverse effects; and
(3) judgments that even the most sensitive responders should be
afforded protection against the occurrence of such effects through
national ambient air quality standards. This view would judge that even
a relatively small number of O3-induced excess hospital admissions
do pose a significant public health problem, especially considering
that for every hospital admission, there are likely many more patients
visiting physicians and an increasing use of medication. Further, even
though no clear linkage has been established between the O3-
induced markers of inflammation, cell damage, and chronic respiratory
damage shown in animal toxicological studies and similar effects in
humans, this view would hold that the possibility of such a link
suggests the need for a wide margin of safety.
Based on these judgments as to the nature and significance of the
reported O3-induced health effects, some commentors would reach
the policy judgment that an 8-hour standard should be set at 0.07 ppm
to protect public health with an adequate margin of safety. In
recognition of this view, the Administrator also solicits public
comment on an 0.07 ppm level for an 8-hour standard.
Based on the comments received and the accompanying rationale, the
Administrator may choose at the time of final promulgation to adopt a
standard from within the range of alternatives on which she is
requesting comment, with further specification of the form of such a
standard (as discussed in the next section), in lieu of the 0.08 ppm
level of the 8-hour O3 standard she is proposing today.
3. Form
The current primary NAAQS is expressed in a ``1-expected-
exceedance'' form. That is, the standard is formulated on the basis of
the expected number of days per year, on average, on which the level of
the standard will be exceeded. More specifically, the test for
determining attainment of the standard specifies that the expected
number of days per year on which the level is exceeded is to be less
than or equal to 1.0 (values equal to or greater than 1.05 round up),
averaged over a three year period, and that specific adjustments are to
be made for missing data. The current NAAQS is applied on a site-by-
site basis; data from multiple air quality monitoring sites are not
combined.
Since promulgation of the current NAAQS in 1979, a number of
concerns have been raised about the 1-expected-exceedance form. These
include, in particular, the year-to-year stability of the number of
exceedances, the stability of attainment status of an area, the data
handling conventions, including the procedures for adjusting for
missing data, and the evaluation of air quality on a site-by-site basis
rather than some form of averaging across monitoring sites. These
issues are discussed in some detail in section V.I of the Staff Paper,
and alternative forms that would address such issues are recommended
for consideration.
In evaluating alternative forms for the primary standard, the
adequacy of the public health protection provided is of foremost
consideration. However, consistent with the advice of CASAC, the
Administrator is also interested in considering alternative forms that
provide increased stability and thereby reduce the likelihood of areas
``flip-flopping'' in and out of attainment simply as a result of
natural variability in meteorological conditions that are conducive to
O3 formation. Such instability can have the effect of reducing
public health protection by disrupting ongoing implementation plans and
associated control programs.
Based on information presented in sections IV and V.I of the Staff
Paper and the advice of CASAC, the Administrator has focused her
consideration on the following alternatives:
(1) Revising the current 1-expected-exceedance form of the standard
to allow for multiple (up to five) expected exceedances per year,
averaged over three years. A multiple-exceedance form would be based on
a less extreme air quality statistic and, thus, would increase the
stability of the expected-exceedance form.
(2) Adopting a concentration-based statistic, such as the three-
year average of the nth-highest daily maximum 8-hour average O3
concentration, as an alternative to an expected exceedance statistic.
Air quality analyses presented in the Staff Paper indicate that, for
example, the 3-year average of the annual third highest daily maximum
8-hour concentration provides approximately the same health protection
as the 3-expected-exceedance form averaged over the same period.
Similarly, the 3-year average of the annual fifth-highest daily maximum
8-hour average concentration approximately corresponds to an expected-
exceedance form that allows five expected exceedances averaged over
three years.
The CASAC acknowledged that selecting from this range of
alternative forms is a policy judgment, especially given the nature of
the health effects and the absence of a ``bright line'' that clearly
differentiates between acceptable and unacceptable risks within this
range. However, CASAC did

[[Page 65731]]

recommend that a more robust, concentration-based form (one that would
allow for multiple exceedances) be adopted to provide additional
stability in control programs, and thus in public health protection, by
insulating an area from the impacts of extreme meteorological events
(Wolff, 1995b).
In reaching her proposed decision on the form of the standard, the
Administrator first assessed the degree of health protection that would
be provided by alternative expected-exceedance forms of the standard.
Having decided to propose a level of 0.08 ppm for an 8-hour primary
standard, as discussed above, the Administrator focused on the degree
of risk reduction that would be achieved by a 1-expected-exceedance
form as compared to a 5-expected-exceedance form. Examination of the
quantitative risk assessment results discussed above revealed that,
within the range of one to five expected exceedances, the dominant
factor in determining the degree of risk reduction achieved is the
level of the standard, with the number of expected exceedances being
associated with smaller differences in risk estimates within a
continuum of risk.
In considering possible forms within the range of one to five
expected exceedances, the Administrator took into account as the
foremost consideration the adequacy of public health protection
provided. This includes consideration of (1) aggregate risk for those
health effects for which quantitative risk analyses have been done; (2)
consideration of exposures associated with those effects for which no
quantitative risk estimates could be developed; and (3) the magnitude
of peak measurements of 8-hour average O3 concentrations, and the
number of days on which the level of the standard would likely be
exceeded, based on an analysis of historical air quality data (Freas,
1996). Based on these considerations, the Administrator judges that the
middle of the range, three expected exceedances, would represent a
reasonable policy choice. Relative to a standard set at the upper end
of the range (i.e., a 5-expected-exceedance standard), a 3-expected-
exceedance standard would serve to better limit the number of days in
which the level of the standard would be exceeded in areas that just
attain the standard 9, as well as limiting the magnitude of peak
measurements of 8-hour average O3 concentrations that would occur
in such areas.10 A 3-expected-exceedance standard would also
provide significantly increased stability relative to a standard set at
the lower end of the range (i.e., the current 1-expected-exceedance
form 11). The Administrator believes that such a policy choice
would appropriately reflect the advice of CASAC.
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\9\ Areas that ``just attain the standard'' are defined as those
whose design value falls between 0.075 and 0.084 ppm. Based on 1993-
1995 air quality data, 95% of monitoring sites that just attain a
0.08 ppm standard with a 3-expected-exceedance form would have 6 or
fewer days on which the standard would be exceeded, in the worst of
the three years, as compared to 10 days or fewer days with a 5-
expected-exceedance form (Freas, 1996).
\10\ Based on 1993-1995 air quality data, 4% of monitoring sites
that just attain a 0.08 ppm standard with a 3-expected-exceedance
form would have 8-hour peak O3 concentrations (in terms of the
4th highest daily maximum concentration in three years) above a
benchmark level of 0.09 ppm, as compared to 22% of such sites with a
5-expected exceedance form (Freas, 1996).
\11\ In comparing alternative 8-hour standards to the current
standard (0.12 ppm, 1-hour average) with a 1-expected-exceedance
form, 77% of monitoring sites that just attain the current standard
would have 8-hour peak O3 concentrations (in terms of the 4th
highest daily maximum concentration in three years) above a
benchmark level of 0.09 ppm.
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The Administrator also considered whether the form should be
expressed in terms of expected exceedances or generally equivalent
concentration-based statistics. As discussed in the Staff Paper, a
concentration-based statistic has certain advantages over the expected-
exceedance form. The principal advantage is that a concentration-based
form is more directly related to the ambient O3 concentrations
that are associated with health effects. That is, given that there is a
continuum of effects associated with exposures to varying levels of
O3, the extent to which public health is affected by exposure to
ambient O3 is related to the actual magnitude of the O3
concentration, not just whether the concentration is above a specified
level. With an exceedance-based form, days on which the ambient O3
concentration is well above the level of the standard are given equal
weight to those days on which the O3 concentration is just above
the standard (i.e., each day is counted as 1 exceedance), even though
the public health impact on the two days is significantly different.
With a concentration-based form, days on which higher O3
concentrations occur would weigh proportionally more than days with
lower O3 concentrations, since the actual concentrations are used
directly in determining whether the standard is attained. Further,
based on analyses of historical air quality data (Freas, 1996),
concentration-based forms control peak measures of O3
concentrations somewhat better than the corresponding exceedance-based
forms 12, although exceedance-based forms tend to limit the
numbers of days on which the level of the standard is exceeded somewhat
better than concentration-based forms 13. A concentration-based
form also has greater temporal stability than the expected-exceedance
form and, thus, would facilitate the development of more stable
implementation programs by the States.
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\12\ For example, whereas 4% of monitoring sites that just
attain a 0.08 ppm standard with a 3-expected-exceedance form would
have 8-hour peak O3 concentrations above the benchmark of 0.09
ppm, only 1% of such sites with a 3rd (or 2nd) highest daily maximum
concentration form would do so. Similarly, whereas 22% of just-
attain sites with a 5-expected-exceedance form would have peak
concentrations above the 0.09 ppm benchmark, 17% of such sites with
a 5th highest daily maximum concentration form would do so.
\13\ For example, whereas 95% of monitoring sites that just
attain a 0.08 ppm standard with a 3-expected-exceedance form would
have 6 or fewer days on which the standard would be exceeded, in the
worst of the three years, with a 3rd highest concentration form 95%
of such sites would have 7 or fewer such days. Similarly, with a 5-
expected-exceedance form, 95% of such sites would have 10 or fewer
such days, as compared to 11 or fewer days with a 5th highest
concentration forms (Freas, 1996).
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Taking the factors discussed above into account, as well as the
advice of CASAC and the observations and conclusions discussed in the
Staff Paper, the Administrator believes that the primary standard
should be expressed in terms of concentrations rather than expected
exceedances. As indicated above, the 3-year average of the annual
third-highest daily maximum 8-hour average O3 concentration would
provide approximately the same degree of health protection as the 3-
expected-exceedance form averaged over the same period. Accordingly,
the Administrator proposes to express an 8-hour primary standard of
0.08 ppm as the 3-year average of the annual third-highest maximum 8-
hour average O3 concentration, so as to reduce risk sufficiently
to protect at-risk populations, including outdoor children, outdoor
workers, and persons with preexisting respiratory disease, against
adverse health effects with an adequate margin of safety. Such a
standard would also provide a more stable basis upon which the States
can design and implement their O3 control programs. Given the
range of views discussed in the above section on level of the standard,
however, the Administrator also solicits comment on other
concentration-based forms within the range of the second- to the fifth-
highest daily maximum 8-hour average O3 concentrations.

[[Page 65732]]

The Administrator has also considered whether the above conclusions
on the form of a standard would be affected if she selected one of the
alternative levels of a standard discussed in the previous section.
During the last review of the O3 criteria and standards the CASAC
concluded that the existing 1-hour standard of 0.12 ppm O3
provides little, if any, margin of safety, and during this review the
new evidence focuses on effects below the level of the current NAAQS.
In general, the risks projected (based on air quality analyses) for a
3-expected-exceedance form of a 0.09 ppm standard are only marginally
below those estimated to occur upon attainment of the current NAAQS.
Taking these factors into account, the Administrator judges that
consideration of a form for an alternative 0.09 ppm 8-hour standard
should be limited to the third-highest daily maximum 8-hour average
O3 concentration, averaged over 3 years, so as not to relax the
level of protection afforded by the current standard. With regard to
the alternative of a possible 0.07 ppm 8-hour standard, the
Administrator judges that the conclusions discussed above with respect
to the 0.08 ppm level are applicable, such that consideration of the 3-
year average of the annual third-highest daily maximum 8-hour average
O3 concentration is appropriate, with comment solicited on forms
within the range of the second to the fifth highest.
The Administrator recognizes that none of the levels and forms
under consideration would provide a risk-free standard, due to the
continuum of risk likely posed by exposures to ambient O3
potentially down to background levels. Accordingly, the Administrator
believes, consistent with the advice of CASAC, that it would be
appropriate to provide additional information to the public about the
nature of risks associated with exposures to ambient O3. Such
information could be particularly useful to extremely sensitive
individuals in making personal decisions about avoiding exposures with
the potential to cause transient adverse effects on days when 8-hour
average O3 concentrations are predicted to be at or near the level
of the proposed standard. As discussed in Section III below, one way to
provide such information might be in conjunction with the Pollutant
Standards Index already in use in many metropolitan areas.
A number of commentors have raised the issue of whether data from
multiple monitoring sites, rather than data from the highest monitor
might be used to determine when the primary standards for O3 are
attained.14 These commentors have suggested that some form of
averaging across monitors might be appropriate in order to increase the
degree to which monitoring data used in determining attainment of the
standard reflects population exposure and aggregate population health
risk. Averaging data from multiple monitors in an area would produce a
more stable measure of air quality, and could take into account broader
population exposure patterns across an area than would the current
approach of considering data from each monitor independently. When
considering averaging approaches for O3, it should be recognized
that the bulk of the human health effects evidence supporting the
decision on an appropriate O3 standard is based on controlled
human exposure studies that relate known O3 exposures directly to
responses in individuals.15 Moreover, as discussed previously in
this notice, the O3 exposure analysis and the lung function and
respiratory symptoms components of the health risk assessments, which
were considered in developing this proposal, reflect the movement of
people through time and space within an urban area and incorporate air
quality data from the various monitors within each urban area in
estimating population exposure and health risk for various population
groups. For these reasons, it would be considerably more difficult to
determine an appropriate level for a spatially averaged primary
standard.
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\14\ Spatial averaging of monitoring data is also discussed in
the notice of a proposed decision on the PM NAAQS published today,
specifically with regard to an annual PM2.5 standard. Different
considerations apply in the two cases principally because of
differences between (1) the nature of the health effects evidence
for O3 and PM2.5; (2) a single proposed O3 standard,
in cont

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Source: Frix Law Library, https://www.frixlaw.com/law-library/documents/fr%3A96-30903. Public record. Not legal advice.