[Federal Register Volume 66, Number 220 (Wednesday, November 14, 2001)]
[Proposed Rules]
[Pages 57268-57292]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 01-27820]
[[Page 57267]]
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Part III
Environmental Protection Agency
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40 CFR Part 50
National Ambient Air Quality Standards for Ozone: Proposed Response To
Remand; Proposed Rule
Federal Register / Vol. 66, No. 220 / Wednesday, November 14, 2001 /
Proposed Rules
[[Page 57268]]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 50
[FRL-7099-1]
RIN 2060-ZA11
National Ambient Air Quality Standards for Ozone: Proposed
Response To Remand
AGENCY: Environmental Protection Agency (EPA).
ACTION: Proposed response to remand.
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SUMMARY: On July 18, 1997, in accordance with sections 108 and 109 of
the Clean Air Act (Act), EPA completed its review of the national
ambient air quality standards (NAAQS) for ozone (O3) by
promulgating revised primary and secondary standards (62 FR 38856;
henceforth, ``1997 final rule''). On May 14, 1999, the United States
Court of Appeals for the District of Columbia Circuit (D.C. Circuit)
remanded the O3 NAAQS to EPA to consider, among other
things, the alleged beneficial health effects of O3
pollution in shielding the public from the ``harmful effects of the
sun's ultraviolet rays.'' 175 F. 3d 1027 (D.C. Cir. 1999). Today's
action provides EPA's proposed response to that aspect of the court's
remand. As explained more fully below, based on its review of the air
quality criteria and NAAQS for O3 completed in 1997, and its
additional assessment of the potential beneficial effects of
tropospheric O3, EPA has provisionally determined that the
information linking changes in patterns of ground-level O3
concentrations likely to occur as a result of programs implemented to
attain the 1997 O3 NAAQS to changes in relevant exposures to
UV-B radiation of concern to public health is too uncertain at this
time to warrant any relaxation in the level of public health protection
previously determined to be requisite to protect against the
demonstrated direct adverse respiratory effects of exposure to
O3 in the ambient air. Further, the Administrator notes that
it is the Agency's view that associated changes in UV-B radiation
exposures of concern, using plausible but highly uncertain assumptions
about likely changes in patterns of ground-level ozone concentrations,
would likely be very small from a public health perspective. As a
result, the revised O3 NAAQS will remain set at a level of
0.08 parts per million (ppm), with a form based on the 3-year average
of the annual fourth-highest daily maximum 8-hour average O3
concentrations measured at each monitor within an area. The primary
standard provides increased protection to the public, especially
children and other at-risk populations, against a wide range of health
effects directly induced by breathing O3 in the ambient air,
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. The secondary standard provides
increased protection to the public welfare against effects on
vegetation, such as agricultural crop loss, damage to forests and
ecosystems, and visible foliar injury to sensitive species associated
with direct exposure to O3 in the ambient air. Today's
action constitutes EPA's proposed response to the part of the remand of
the 1997 O3 NAAQS by the D.C. Circuit related to whether
tropospheric O3 has a beneficial effect with regard to
attenuation of naturally occurring solar radiation. Other issues
related to the 1997 O3 NAAQS are now before the D.C. Circuit
for proceedings consistent with the February 27, 2001 opinion of the
United States Supreme Court in this case, Whitman v. American Trucking
Associations, 531 U.S. 457 (2001), and are not addressed by today's
action.
DATES: Comments on this proposed response must be received by January
14, 2002.
ADDRESSES: Submit written comments (in duplicate if possible) on this
proposed response to: Air and Radiation Docket and Information Center
(6102), Attn: Docket No. A-95-58, U.S. Environmental Protection Agency,
1200 Pennsylvania Ave., NW., Washington, DC 20460. Electronic comments
are encouraged and can be sent directly to EPA at: [email protected]. Comments will also be accepted on disks in WordPerfect
in 8.0/9.0 file format. All comments in electronic form must be
identified by the docket number, Docket No. A-95-58.
FOR FURTHER INFORMATION CONTACT: Susan Lyon Stone, Office of Air
Quality Planning and Standards, U.S. Environmental Protection Agency
(C539-01), Research Triangle Park, NC 27711; e-mail
[email protected]; telephone (919) 541-1146.
SUPPLEMENTARY INFORMATION:
Docket
A docket containing information relating to EPA's review of the
O3 primary and secondary standards (Docket No. A-95-58) is
available for public inspection at the EPA's Air and Radiation Docket
and Information Center, 401 M Street, SW., Washington, DC 20460 in room
M-1500, Waterside Mall (ground floor). This docket incorporates the
docket from the previous review of the O3 standards (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 a.m. and 5:30 p.m. on weekdays, excluding legal holidays. 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:
(1) The Review of the National Ambient Air Quality Standards for
Ozone: 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.)
(2) Air Quality Criteria for Ozone 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 and
$58.00 microfiche).
A limited number of copies of other documents generated in
connection with the review of the standard, such as documents
pertaining to human exposure and health risk assessments and the
relationships between ground-level O3, ultraviolet-B (UV-B)
radiation, and health effects, 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.
Electronic Availability
The Staff Paper and documents pertaining to human health risk and
exposure assessments are available on the Office of Air and Radiation,
Policy and Guidance Web site at: http://www.epa.gov/ttn/oarpg/t1sp.html. The O3 NAAQS 1996 proposal and 1997 final rule
are available at the same Web site, at: http://www.epa.gov/ttn/oarpg/t1pfpr.html.
Children's Environmental Health
This proposed response to the court's remand, reaffirming the 1997
8-hour O3
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NAAQS, specifically takes into account children as the group most at
risk to the direct inhalation-related effects of O3
exposure, and was based on studies of effects on children's health
(U.S. EPA, 1996a; U.S. EPA, 1996b) and assessments of children's
exposure and risk (Johnson et al., 1994; Johnson et al., 1996a,b;
Whitfield et al., 1996; Richmond, 1997). The 8-hour O3
primary standard protects children's health with an adequate margin of
safety from the direct adverse effects associated with inhalation
exposures to ground-level O3, after considering potential
indirect beneficial effects of ground-level O3 related to
its attenuation of UV-B radiation and resultant adverse health effects.
The public is invited to submit or identify peer-reviewed studies and
data, of which EPA may not be aware, that assess results of early life
exposure to the direct effects of breathing ground-level O3
or to changes in UV-B radiation, and associated health effects, that
may result from changes in ground-level O3.
Implementation Activities
When the 8-hour primary and secondary O3 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 (VOC) or nitrogen oxides
(NOX). The extent of such effects will depend on
implementation policies and control strategies adopted by States to
assure attainment and maintenance of the standards.
The EPA will develop appropriate policies and control strategies to
assist States in the implementation of the 8-hour 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. 1997 Revision of the O3 NAAQS
1. Legislative Requirements
2. Review of Air Quality Criteria and Standards for
O3
B. Ozone NAAQS Litigation and Remand
1. Litigation Summary
2. Remand on Health Benefits Issue
C. Atmospheric Distribution of O3 and UV-B Radiation
D. Related Stratospheric O3 Program
II. Rationale for Proposed Response to Remand on the Primary
O3 Standard
A. Direct Adverse Health Effects from Breathing O3 in
the Ambient Air
1. Health Effects Associated with O3 Inhalation
Exposures
2. Human Exposure and Risk Assessments
B. Potential Indirect Beneficial Health Effects Associated with
Ground-level O3
1. Health Effects Associated with UV-B Radiation Exposure
2. Relationship Between Ground-level O3 and UV-B
Radiation Exposure
3. Evaluation of UV-B Radiation-related Risk Estimates for
Ground-level O3 Changes
C. Consideration of Net Adverse Health Effects of Ground-level
O3
D. Proposed Response to Remand on the Primary O3
NAAQS
III. Rationale for Proposed Response to Remand on the Secondary
O3 Standard
A. Direct Adverse Welfare Effects
B. Potential Indirect Beneficial Welfare Effects
C. Proposed Response to Remand on the Secondary O3
NAAQS
IV. Administrative Requirements
A. Executive Order 12866: OMB Review of ``Significant Actions'
B. Executive Order 13045: Children's Health
C. Executive Order 13132: Federalism
D. Executive Order 13175: Consultation and Coordination with
Indian Tribal Governments
E. Unfunded Mandates Reform Act
F. Regulatory Flexibility Analysis/Small Business Regulatory
Enforcement Fairness Act
G. Paperwork Reduction Act
H. National Technology Transfer and Advancement Act
I. Executive Order 13211:Energy Effects
V. References
I. Background
A. 1997 Revision of the O3 NAAQS
On July 18, 1997, in accordance with sections 108 and 109 of the
Act, EPA completed its review of the NAAQS for O3 by
promulgating revised primary and secondary standards (``1997 final
rule''). These standards were based on EPA's review of the available
scientific evidence linking direct exposures to ambient O3
to adverse health and welfare effects at levels allowed by the then
current O3 standards. The revised primary and secondary
standards were each set at a level of 0.08 ppm, with an 8-hour
averaging time and a form based on the 3-year average of the annual
fourth-highest daily maximum 8-hour average O3
concentrations measured at each monitor within an area. \1\ The new
primary standard was established to provide increased protection to the
public, especially children and other at-risk populations, against a
wide range of O3-induced respiratory health effects due to
inhalation exposures, 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. The new secondary standard
was established to provide increased protection to the public welfare
against direct O3-induced effects on vegetation, such as
agricultural crop loss, damage to forests and ecosystems, and visible
foliar injury to sensitive species.
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\1\ The form of a standard refers to the air quality statistic
that is used to determine whether an area attains the standard.
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1. 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 certain pollutants which ``may reasonably be
anticipated to endanger public health or 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.'' 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.'' \2\
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\2\ 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, man-made 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.''
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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
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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.
2. Review of Air Quality Criteria and Standards for O3
An overview of the last review of the O3 air quality
criteria and standards is presented in section I.C of the preamble to
the 1997 final rule. In summary, the 1997 review was initiated in
August 1992 with the development of a revised Air Quality Criteria
Document for Ozone and Other Photochemical Oxidants (henceforth, the
``Criteria Document''). Multiple drafts of the Criteria Document were
reviewed by CASAC and the public, resulting in a final Criteria
Document (U.S. EPA, 1996a) that reflected CASAC and public comments.\3\
The EPA also prepared a staff paper, Review of National Ambient Air
Quality Standards for Ozone: Assessment of Scientific and Technical
Information (henceforth, the ``Staff Paper'').\4\ Multiple drafts of
the Staff Paper were also reviewed by CASAC and the public, resulting
in a final Staff Paper (U.S. EPA, 1996b) that reflected CASAC and
public comments.\5\
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\3\ 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 ozone and related photochemical oxidants''
(Wolff, 1995a).
\4\ The Staff Paper evaluates policy implications of the key
studies and scientific information in the Criteria Document,
identifies critical elements that EPA staff believes should be
considered, and presents staff conclusions and recommendations of
suggested options for the Administrator's consideration.
\5\ In separate letters from the CASAC chair to the
Administrator, CASAC advised that the primary standard and secondary
standard sections of the final draft Staff Paper provide ``an
adequate scientific basis for making regulatory decisions''
concerning the O3 standards (Wolff, 1995b, 1996).
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On November 27, 1996 EPA announced its proposed decision to revise
the NAAQS for O3 (61 FR 65716, December 13, 1996;
henceforth, ``1996 proposal''), as well as its proposed decision to
revise the NAAQS for particulate matter (PM). To ensure the broadest
possible public input on these proposals, EPA took extensive and
unprecedented steps to facilitate the public comment process, including
the establishment of a national toll-free telephone hotline and
provisions for electronic submission of comments. The EPA also held
several public hearings, participated in numerous meetings across the
country, and held two national satellite telecasts to provide direct
opportunities for public comment and to disseminate information to the
public about the proposed standard revisions. As a result of this
intensive effort to solicit public input, over 50,000 comments were
received on the proposed revisions to the O3 NAAQS by the
close of the public comment period on March 12, 1997.
The final rule, published on July 18, 1997, presented EPA's
rationale for its final decision, and addressed the major issues raised
in comments on the 1996 proposal. A comprehensive summary of all
significant comments, along with EPA's response to such comments (U.S.
EPA, 1997; henceforth, ``Response to Comments''), can be found in the
docket for the 1997 rulemaking (Docket No. A-95-58 \6\). The 1997 final
rule presented EPA's decision to replace the existing 1-hour primary
and secondary standards \7\ (each set at a level of 0.12 ppm, with a 1-
expected-exceedance form, averaged over 3 years \8\) with 8-hour
standards, each set at a level of 0.08 ppm, with a form based on the 3-
year average of the annual fourth-highest daily maximum 8-hour average
O3 concentrations measured at each monitor within an area
(as determined by 40 CFR part 50, appendix I).
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\6\ This docket incorporates by reference the docket from the
previous O3 NAAQS review (Docket No. A-92-17) and the
docket established for the Criteria Document (Docket No. ECAO-CD-92-
0876).
\7\ These 1-hour O3 standards were originally set in
1979 (44 FR 8202, February 8, 1979) and reaffirmed in 1993 (58 FR
13008, March 9, 1993).
\8\ The 1-hour 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 one, averaged over 3 years
(as determined by 40 CFR part 50, appendix H).
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B. Ozone NAAQS Litigation and Remand
1. Litigation Summary
Following promulgation of the revised 8-hour O3 NAAQS,
numerous petitions for review of the standards were filed in the D.C.
Circuit. American Trucking Associations v. EPA, No. 97-1441 (ATA). Oral
argument was held on December 17, 1998 and the Court of Appeals
rendered its opinion on May 14, 1999. American Trucking Associations v.
EPA, 175 F. 3d 1027 (D.C. Cir. 1999). A divided panel found that
section 109 of the Act, 42 U.S.C. 7409, as interpreted by EPA in
setting the revised O3 (and PM) NAAQS, effected an
unconstitutional delegation of legislative authority. Id. at 1033-1040.
The court remanded the O3 standards with instructions that
EPA should articulate an ``intelligible principle'' for determining the
degree of residual risk to public health permissible in setting revised
NAAQS. Id. In addition, the court also directed that, in responding to
the remand, EPA should consider the alleged beneficial health effects
of O3 pollution in shielding the public from the ``harmful
effects of the sun's ultraviolet rays.'' Id. at 1051-1053.
In 1999, EPA petitioned the Court of Appeals for rehearing en banc
on a number of aspects of the court's decision in the ATA case.
Although the petition for rehearing was granted in part and denied in
part, the court declined to review its ruling with regard to the
potential beneficial effects of O3 pollution. American
Trucking Associations v. EPA, 195 F. 3d 4, 10 (D.C. Cir. 1999). The
court did note, however, that it ``expressed[ed] no opinion, of course,
upon the effect, if any, that studies showing the beneficial effects of
tropospheric ozone * * * might have upon any ozone standards * * *''
Id. On January 27, 2000, EPA petitioned the Supreme Court for
certiorari on the constitutional issue and two other issues, but did
not request review of the Court of Appeals ruling regarding the alleged
beneficial health effects of O3. The EPA's petition for
certiorari was granted on May 22, 2000; oral argument was subsequently
held on November 7, 2000; and an opinion was issued on February 27,
2001. Whitman v. American Trucking Associations, 531 U.S.457 (2001).
The U.S. Supreme Court reversed the judgment of the D.C. Circuit on the
constitutional issue, holding that section 109 of the Act does not
delegate legislative power to the EPA in contravention of the
Constitution, and remanded the case to the D.C. Circuit for proceedings
consistent with its opinion. Since EPA did not seek Supreme Court
review of the Court of Appeals' decision relating to potential
beneficial health effects of O3, EPA is moving forward to
address that aspect of the lower court's remand independently.
2. Remand on Health Benefits Issue
The Court of Appeals' ruling concludes that ``EPA cannot ignore the
possible health benefits of ozone.'' \9\ American Trucking Associations
v. EPA, 175 F. 3d 1027, 1033 (D.C. Cir. 1999). According to the court
``[p]etitioners presented evidence that, according to them, shows the
health benefits of tropospheric ozone as a
[[Page 57271]]
shield from the harmful effects of the sun's ultraviolet rays--
including cataracts and both melanoma and non-melanoma skin cancer.''
Id. at 1051. In rejecting EPA's interpretation of the Act that it need
not consider alleged indirect beneficial effects of tropospheric
O3 in shielding the public from potentially harmful, but
naturally occurring, UV-B radiation from the sun, the court concluded
that ``legally * * * EPA must consider the positive identifiable
effects of a pollutant's presence in the ambient air in formulating air
quality criteria under section 108 and NAAQS under section 109.'' Id.
at 1052. As a result, the court directed EPA to ``determine whether * *
* tropospheric ozone has a beneficent effect and, if so, then to assess
ozone's net adverse health effect.'' Id. at 1053. Today's action sets
forth EPA's proposed response in that regard.
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\9\ For the reasons discussed in the Response to Comments (U.S.
EPA, 1997, pp. 128-135), EPA did not consider in the 1997 review
adverse health effects caused by the potential increase in UV-B
radiation that could result from reductions in ground-level
O3 brought about by control programs implemented to
attain a revised O3 NAAQS.
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C. Atmospheric Distribution of O3 and UV-B Radiation
The focus of the 1997 review of the air quality criteria and
standards for O3 and related photochemical oxidants was on
public health and welfare effects associated with direct exposure to
ambient levels of O3 in the lower troposphere, essentially
at ground level. People are directly exposed to ground-level
O3 simply by breathing ambient air; similarly, plants are
directly exposed through their respiratory processes. Ground-level
O3 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. Ground-level
O3 formation is the result of chemical reactions of VOC,
NOX, and oxygen in the presence of sunlight and generally at
elevated temperatures. As a principal ingredient in photochemical smog,
elevated episodic concentrations of ground-level O3
typically occur in the summertime. High concentrations may be found in
and downwind of major urban centers as well as across broad regions of
elevated precursor emissions. A detailed discussion of atmospheric
formation, ambient concentrations, and health and welfare effects
associated with direct exposure to O3 can be found in the
Criteria Document and Staff Paper.
Naturally occurring O3 is found in two sections of the
earth's atmosphere, the stratosphere and the troposphere. The
demarcation between these two layers varies between about 8 and 18
kilometers (km) above the earth's surface. As illustrated in Figure 1,
depicting the vertical profile of O3, most naturally
occurring O3 (> 90 percent) resides in the stratosphere,
with the remaining O3 ( 10 percent) in the troposphere. The
band of O3 between about 15 and 30 km is commonly known as
the ``ozone layer.''
Man-made air pollution has significantly perturbed the natural
distribution of O3 in both layers. It is now widely accepted
that emissions of long-lived chlorofluorocarbons (CFCs) and other
compounds can deplete the natural O3 layer in the
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[GRAPHIC] [TIFF OMITTED] TP14NO01.001
stratosphere. And, as summarized above, much shorter lived emissions of
VOC and NOX can markedly increase ``smog'' O3 in
the lowest portion of the troposphere, which is termed the planetary
boundary layer. This fluctuating planetary boundary or ``mixing'' layer
of the troposphere can extend as high as 1 to 3 km above the ground.
Assuming a fairly high summertime O3 pollution reservoir of
65 parts per billion (ppb) in a typical 1 km mixing layer, Cupitt
(1994) estimated that pollution would add less than 1 percent to the
expected total vertical profile of tropospheric and stratospheric
O3 (i.e., ``total column'' O3) that would occur
in the natural environment.
Ozone at ground level and throughout the troposphere is chemically
identical to stratospheric O3. Stratospheric O3
occurs far too high to present any threat of direct respiratory-related
adverse effects to people or plants from ambient ground-level
exposures, but is known to provide a natural protective shield from
excess radiation from the sun by absorbing UV-B radiation \10\ before
it penetrates to ground level. Recognizing that exposure to UV-B
radiation has been associated with adverse health and welfare effects,
EPA and international scientific, regulatory, and legislative
organizations have for some time focused on understanding the effects
of UV-B radiation and on controlling the man-made pollution that is
causing the depletion of the O3 layer in the stratosphere,
as discussed in section I.D below.\11\
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\10\ UV-B radiation refers to the region of the solar spectrum
within the range of wavelengths generally from 280-290 nanometers
(nm) at the lower end, to 315-320 nm at the upper end.
\11\ For example, in 1977 and again in 1990, Congress added
provisions to the Act to address stratospheric O3
depletion and the resultant increase in exposure to UV-B radiation.
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During the 1997 review, EPA recognized that tropospheric
O3 also absorbs UV-B radiation (U.S. EPA, 1996a, p. 5-79),
such that ground-level O3 formed by man-made pollution has
the potential to provide some degree of additional shielding beyond the
natural levels that would otherwise occur in the absence of man-made
pollution. The relationship between ground-level O3 and UV-B
radiation, as well as the health effects associated with exposure to
UV-B radiation and consideration of the UV-B radiation-related health
risks associated with changes in ground-level O3 are
discussed in section II.B below. In response to the remand on the
health benefits issue, EPA's assessment of the net adverse health
effects of ground-level O3 is discussed in section II.C
below, as a basis for today's proposed decision on the primary
O3 NAAQS, summarized in section II.D below.
D. Related Stratospheric O3 Program
In the 1970s, scientists first grew concerned that certain
chemicals could
[[Page 57273]]
damage the earth's protective stratospheric O3 layer, and
these concerns were validated by the discovery of thinning of the
O3 layer over Antarctica in the southern hemisphere. Because
of the risks posed by stratospheric O3 depletion and the
global nature of the problem, leaders from many countries decided to
work together to craft a workable solution. Since 1987, over 175
nations have signed a landmark environmental treaty, the Montreal
Protocol on Substances that Deplete the Ozone Layer. The Protocol's
chief aim is to reduce and eventually eliminate the production and use
of man-made O3 depleting substances, such as CFCs. By
agreeing to the terms of the Montreal Protocol, signatory nations
ratifying the Protocol--including the United States--commit to take
actions to protect the stratospheric O3 layer and to reverse
the damage due to the use of O3 depleting substances.
In 1990, Congress amended the Act by adding title VI (sections 601-
618) to address the issue of stratospheric O3 depletion.\12\
Most importantly, the amended Act required the gradual end to the
production of certain chemicals that deplete the O3
layer.\13\ In addition, the Act requires EPA to develop and implement
regulations for the responsible management of O3 depleting
substances in the United States. The EPA has developed several
regulatory programs under these authorities that include: ending the
production and import of O3 depleting substances (57 FR
33754, July 30, 1992) and identifying safe and effective alternatives
(59 FR 13044, March 18, 1994), ensuring that refrigerants and halon
fire extinguishing agents are recycled properly (58 FR 28660, May 14,
1993), banning the release of O3 depleting refrigerants
during the service, maintenance, and disposal of air conditioners and
other refrigeration equipment (60 FR 40420, August 8, 1995), and
requiring that manufacturers label products either containing or made
with the most harmful O3 depleting substances (58 FR 8136,
February 11, 1993). Because of their relatively high O3
depletion potential, several man-made compounds, including CFCs, carbon
tetrachloride, methyl chloroform, and halons were targeted first for
phaseout. The EPA continues to develop additional regulations for the
protection of public health and the environment from effects associated
with the depletion of the stratospheric O3 layer.
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\12\ Title VI replaced the provisions regarding stratospheric
O3 depletion enacted in 1977. 42 U.S.C. 7671.
\13\ Both the Act and the Montreal Protocol, however, provide
for limited ``essential use exemptions'' for the continued
production and import of very small quantities of CFCs and other
O3 depleting substances needed for certain essential
uses, for example, for metered dose inhalers used by people with
asthma and other respiratory diseases.
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Besides implementing and enforcing stratospheric O3
protection regulations in the U.S., EPA continues to work with other
U.S. government agencies and international governments to pursue
ongoing changes to the Montreal Protocol and other treaties. These
refinements to the Protocol and other treaties are based on ongoing
scientific assessments of O3 depletion that are coordinated
by the United Nations Environment Programme (UNEP) and the World
Meteorological Organization (WMO), with cooperation from EPA and other
agencies around the globe (UNEP, 1998; and WMO, 1998).
In addition to these regulatory and scientific activities, EPA
maintains several education and outreach projects to help protect the
American public from the health effects of overexposure to ultraviolet
(UV) radiation. Chief among these projects is the UV Index, a tool that
provides a daily forecast of the next day's likely UV levels across the
United States. \14\ The UV Index, which EPA launched in partnership
with the National Weather Service, serves as the cornerstone of EPA's
SunWise School Program, the goal of which is to educate young children
and their caregivers about the health effects of overexposure to the
sun, as well as simple steps that people can take to avoid
overexposure. \15\
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\14\ Information about the UV Index is available from the EPA
Stratospheric Ozone Hotline at (800) 296-1996 or at http://www.epa.gov/sunwise/uvindex.html.
\15\ Information about EPA's SunWise School Program is available
at http://www.epa.gov/sunwise/.
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II. Rationale for Proposed Response To Remand on the Primary
O3 Standard
Today's action presents the Administrator's proposed response to
the remand, reaffirming the 8-hour O3 primary standard
promulgated in 1997, based on: (1) Information from the 1997 criteria
and standards review that served as the basis for the 1997 primary
O3 standard, including the scientific information on health
effects associated with direct inhalation exposures to O3 in
the ambient air, consideration of the adversity of such effects for
individuals, and human exposure and risk assessments (section II.A
below); (2) a review of the scientific information in the record of the
1997 review (but not considered as part of the basis for the 1997
standard) on the health effects associated with changes in UV-B
radiation, the association between changes in ground-level
O3 and changes in UV-B radiation, and predictions of changes
in ground-level O3 levels likely to result from attainment
of alternative O3 standards \16\ (section II.B below); and
(3) consideration of the net adverse effects of ground-level
O3, taking into account both direct adverse inhalation-
related health effects and the potential for indirect beneficial health
effects associated with the shielding of UV-B radiation by ground-level
O3 (section II.C below).
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\16\ In complying with the direction of the Court of Appeals in
its remand on the health benefit issue, we have considered the large
amount of relevant information in the record of the 1997 review, and
in doing so, have based this proposed response on all the
information available to the court in reaching its decision.
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A. Direct Adverse Health Effects From Breathing O3 in the
Ambient Air
This section briefly summarizes information on the direct adverse
health effects from breathing O3 in the ambient air,
information as to when those effects become adverse to individuals, and
insights gained from human exposure and risk assessments intended to
provide a broader perspective for judgments about protecting public
health from the risks associated with direct O3 inhalation
exposures.\17\
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\17\ See the 1996 proposal and 1997 final rule for more complete
summaries and the Criteria Document and Staff Paper for more
detailed discussion.
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1. Health Effects Associated With O3 Inhalation Exposures
Based on information from human clinical, epidemiological, and
animal toxicological studies, 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. Long-
established acute health effects \18\ 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.\19\ The 1997
review included substantial new information on similar effects
associated with prolonged exposures at concentrations as low as 0.08
ppm and at moderate levels of exertion. Other health effects associated
with short-term or prolonged
[[Page 57274]]
O3 exposures include increased airway responsiveness,
susceptibility to respiratory infection, increased hospital admissions
and emergency room visits, and transient pulmonary inflammation. The
1997 review also included new information on chronic health effects
\20\ associated with long-term exposures. This array of effects is
briefly summarized below, followed by considerations as to when these
physiological effects could become medically significant such that they
should be regarded as adverse to the health of individuals experiencing
them.
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\18\ ``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.
\19\ The 1-hour O3 primary NAAQS set in 1979 was
generally based on these acute effects associated with heavy
exercise and short-term exposures.
\20\ ``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.
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a. Effects of Short-Term and Prolonged O3 Exposures
(i) Pulmonary function responses. Transient reductions in pulmonary
function have been observed in healthy individuals and those with
impaired respiratory systems (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
responses has come from controlled human exposure studies, which
clearly show that reductions in lung function are enhanced by increased
levels of activity involving exertion and by increased O3
concentrations. Numerous such 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, providing conclusive
evidence that O3 levels commonly monitored in the ambient
air induce lung function decrements in exercising adults. Further,
numerous summer camp studies provide an extensive and reliable data
base on comparable lung function responses to ambient O3 and
other pollutants in children and adolescents. The extent of pulmonary
function decrements varies considerably among individuals, pulmonary
function generally tends to return to baseline levels shortly after
short-term exposure, and effects are typically attenuated upon repeated
short-term exposures over several days.
(ii) Respiratory symptoms and effects on exercise performance.
Various transient respiratory symptoms, including cough, throat
irritation, chest pain on deep inspiration, 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 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, may curb the ability or desire to engage in
normal activities, and may interfere with maximal exercise performance.
(iii) Increased airway responsiveness. Increased airway
responsiveness is an indication that the airways are predisposed to
bronchoconstriction, with a high level of bronchial responsiveness
being characteristic of asthma. 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, 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. 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.
(iv) 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. Evidence that inhalation of
O3 may break down or impair these defense mechanisms comes
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. While no single experimental human study or
group of animal studies conclusively demonstrates that human
susceptibility to respiratory infection is increased by exposure to
O3, taken as a whole, the data suggest that acute
O3 exposures can impair the host defense capability of both
humans and animals, potentially resulting in a predisposition to
bacterial infections in the lower respiratory tract.
(v) 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. Numerous studies
consistently have shown such a relationship, even after controlling for
modifying factors, as well as when considering only O3
concentrations 0.12 ppm. 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.
(vi) 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. Exposures of
laboratory animals to O3
[[Page 57275]]
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 humans, the extent and
course of inflammation and its constitutive elements have been
evaluated by using bronchoalveolar lavage (BAL) to sample cells and
fluid from the lung and lower airways. Several such studies 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, with the lowest concentration of prolonged O3
exposure tested in humans, 0.08 ppm for 6.6 hours with moderate
exercise, inducing small but statistically significant increases in
these endpoints. Thus, it is reasonable to conclude that repeated acute
inflammatory response and cellular damage 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 that could be the result of repeated O3 exposures
occurring over a season or a lifetime.
b. 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. The findings from such studies conducted in southern
California and Canada 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. Other epidemiologic studies have
attempted to find associations between daily mortality and
O3 concentrations in various cities around the United
States. 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.
In a large number of animal toxicology studies, ``lesions'' \21\ 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. Under certain conditions, some of the
structural changes seen in these studies 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.
---------------------------------------------------------------------------
\21\ 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.
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The epidemiologic lung function studies generally parallel those of
the animal studies, but 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. In summary, the
collective data on long-term exposure to O3 garnered in
studies of laboratory animals and human populations have many
ambiguities. Nevertheless, the currently available information provides
at least a biologically plausible basis for considering 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.
c. Adversity of Effects for Individuals
Some population groups have been identified as being sensitive to
effects associated with exposures to ambient O3 levels, such
that individuals within these groups are at increased risk of
experiencing such effects. Population groups at increased risk include:
(1) Active children and outdoor workers who regularly engage in outdoor
activities; \22\ (2) individuals with preexisting respiratory disease
(e.g., asthma or chronic obstructive lung disease); \23\ and (3) some
individuals, referred to as ``hyperresponders,'' who 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.
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\22\ 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.
\23\ While not necessarily more responsive than healthy
individuals in terms of the magnitude of pulmonary function
decrements or symptomatic responses, these individuals may be at
increased risk since 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.
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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. Based on these guidelines, with CASAC
concurrence, 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) were defined, together with judgments as to the potential
impact on individuals experiencing varying degrees of severity of these
responses.\24\
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\24\ These gradations and impacts are summarized in the 1996
proposal and discussed in the Criteria Document (Chapter 9) and
Staff Paper (section V.F, Tables V-4 and V-5).
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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 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, EPA has concluded 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.
2. 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.
\25\ This broader context
[[Page 57276]]
includes consideration, to the extent possible, of the particular
population groups at risk for various health effects, the number of
people in at-risk groups likely to be exposed to O3
concentrations shown to cause health effects, the number of people
likely to experience certain adverse health effects under varying air
quality scenarios, and the kind and degree of uncertainties inherent in
these assessments. These quantitative assessments add to our
understanding of the overall body of evidence linking O3
inhalation exposures to adverse health effects. The EPA believes, and
CASAC concurred, that the models used in these assessments were
appropriate and that the methods used represent the state of the art.
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\25\ See the 1996 proposal (61 FR 65723-6) and 1997 final rule
(62 FR 38860-1) for a more complete summary of these assessments. A
detailed description of the exposure and risk models and their
application at the time of the 1996 proposal are presented in the
Staff Paper and associated technical support documents (Johnson et
al., 1994; Johnson et al., 1996 a,b; McCurdy, 1994a; Whitfield et
al., 1996). Following proposal, supplemental exposure and risk
analyses were done to analyze the specific standard proposed and
alternative standards on which comment was solicited, as well as to
refine the procedures used to simulate O3 concentrations
upon attainment of alternative standards (Richmond, 1997).
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a. Exposure Analyses
The EPA conducted exposure analyses to estimate O3
exposures for the general population and two at-risk populations,
active children who regularly engage in outdoor activity (i.e.,
``outdoor children'') and ``outdoor workers,'' living in nine
representative U.S. urban areas.\26\ Exposure estimates were developed
for a baseline year (e.g., 1993, 1994), using monitored O3
air quality data (i.e., the ``as is'' scenario), as well as for
simulated air quality conditions reflecting attainment of the 1-hour
NAAQS and various alternative standards. The exposure analyses provide:
(1) Estimates of the number of people exposed in each of these
population groups to various O3 concentrations, and the
number of occurrences of such exposures, under different regulatory
scenarios,\27\ which are an important input to the risk assessment
conducted for certain adverse health effects (summarized in the next
section); and (2) estimates of the frequency of occurrences of
O3 ``exposures of concern,'' \28\ which help to put into
broader perspective other O3-related health effects that
could not be included in the risk assessment (summarized below).
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\26\ The areas include a significant fraction of the U.S. urban
population, 41.7 million people, the largest urban areas with major
O3 nonattainment problems, and two large urban areas that
are in attainment with the 1-hour NAAQS.
\27\ Estimates of ``people exposed'' reflect the number of
people who experience exposures to a given concentration of
O3, or higher, at least one time during the period of
analysis, and estimates of ``occurrences of exposure'' reflect the
number of times a given O3 concentration is experienced
by the population of interest.
\28\ ``Exposures of concern'' refer throughout to O3
exposures at and above 0.08 ppm, 8-hour average, at moderate
exertion. Such exposures are particularly relevant to a
consideration of a number of health effects, discussed in section
I.A.1 above, that have been observed in controlled human studies
under these exposure conditions, but for which data were too limited
to allow for quantitative risk assessment. Exposures at and above
0.12 ppm, 1-hour average, at heavy exertion, are also of concern;
however, the focus here is on 8-hour average exposures since
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.
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The computer model used in these analyses, the probabilistic NAAQS
exposure model for O3 (pNEM/O3), combines
information on O3 air quality with information on patterns
of human activity to produce estimates of O3 inhalation
exposures. This model has been developed to take into account the most
significant factors contributing to total O3 inhalation
exposure including: the temporal and spatial patterns of ground-level
O3 concentrations throughout an urban area; the variations
of O3 levels within a comprehensive set of
``microenvironments''; \29\ the temporal and spatial patterns of the
movement of people throughout an urban area; and the effects of
variable exertion levels (represented by ventilation rates), associated
with a range of activities that people regularly engage in, on
O3 uptake in exposed individuals. The analysis of these key
factors incorporated extensive data bases, including, for example, data
from ground-level O3 monitoring networks in these areas,
data from numerous research studies that characterized the activity
patterns of the general population and at-risk groups 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),\30\ and census data on relevant factors such as age, work
status, home location and type of air conditioning system present, and
work place location.
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\29\ The five indoor and two outdoor microenvironments included
in this exposure model account for the highly localized variations
in O3 concentrations to which people are exposed that are
not directly reflected in the concentrations measured at ambient
ground-level O3 monitoring sites.
\30\ See, for example, Tables V-8 and V-9 in the Staff Paper,
pp. 83-84.
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The regulatory scenarios examined in the exposure analyses include
both 1-hour O3 standards, at levels of 0.12 ppm (the 1979
NAAQS) and 0.10 ppm, and 8-hour standards, at levels of 0.07, 0.08, and
0.09 ppm, with 1- and 5-expected exceedance forms, i.e., 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 estimates were also used to roughly bound exposure
estimates for concentration-based forms of the standards under
consideration (e.g., the second- and fifth-highest daily maximum 8-hour
average O3 concentration, averaged over a 3-year
period).\31\ The estimated exposures are based on a single year of air
quality data and 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 analyses were done to estimate exposures
that would be expected in the worst year of a 3-year compliance period.
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\31\ As discussed in section IV and appendix A of the Staff
Paper.
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Based on the results of the exposure analyses, children who are
active outdoors (representing approximately 7 percent of the population
in the study areas) appear to be the at-risk population group examined
with the highest percentage and number of individuals likely to
experience exposures of concern. Estimated exposures of concern varied
significantly across the urban areas examined in this analysis, with
far greater variability associated with the 1-hour NAAQS in contrast to
the more consistent results associated with alternative 8-hour
standards.\32\ Despite this variability across areas, general patterns
can be seen in comparing alternative standards. For example, for
aggregate estimates of the mean percent of outdoor children likely to
experience exposures of concern within the seven nonattainment areas:
the range of estimates associated with the 1-hour NAAQS is
approximately 0.3-24 percent, whereas for alternative 8-hour standards
(of the same 1-expected-exceedance form as the 1-hour NAAQS), the
ranges are approximately 3-7 percent for a 0.09 ppm standard, 0-1
percent for a 0.08 ppm standard, and essentially zero for a 0.07 ppm
standard. Within any given urban area, these
[[Page 57277]]
differences in estimated exposures of concern between alternative
standards are statistically significant.
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\32\ The observed area-to-area variability reflects differences
in the shape of air quality distributions and differences in the
relationships between 1-hour and 8-hour peak concentrations across
urban areas, as well as differences in the percentage of homes with
air conditioning (which impacts exposure estimates when individuals
are indoors) and the frequency of warm versus cool days (which
impacts exposure estimates because different sets of human activity
patterns are used for warm versus cool days in the exposure model)
across the nine urban areas (Richmond, 1997).
---------------------------------------------------------------------------
In looking more specifically at a comparison between 8-hour
standards at the 0.09 ppm and 0.08 ppm levels, aggregate estimates of
the mean percentage of outdoor children likely to experience exposures
of concern are estimated to be approximately 3 percent at the 0.08 ppm
level (ranging from 2-10 percent in the nine areas), increasing to
approximately 11 percent at the 0.09 ppm level (ranging from 7-29
percent in the nine areas).\33\ Thus, based on these analyses, a
standard set at 0.09 ppm would allow more than three times as many
children to experience exposures of concern as would a 0.08 ppm
standard, with the number of children likely to experience such
exposures increasing from approximately 100,000 to more than 300,000 in
these nine areas alone. These exposures of concern are judged by EPA to
be an important indicator of the public health impacts of those
O3-related effects for which information is too limited to
develop quantitative estimates of risk, but which have been observed in
humans at a level of 0.08 ppm for 6- to 8-hour exposures. Such effects
include increased nonspecific bronchial responsiveness (related, for
example, to aggravation of asthma), decreased pulmonary defense
mechanisms (suggestive of increased susceptibility to respiratory
infection), and indicators of pulmonary inflammation (related to
potential aggravation of chronic bronchitis or long-term damage to the
lungs).
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\33\ Based on the supplemental analyses that used the third-
highest concentration-based form of the standards (Richmond, 1997).
---------------------------------------------------------------------------
In taking these observations into account, the Administrator and
CASAC recognize the uncertainties and limitations associated with such
analyses, including the considerable, but unquantifiable, degree of
uncertainty associated with a number of important inputs to the
exposure model. A key uncertainty in model inputs results from
limitations in the human activity data base that may not adequately
account for day-to-day repetition of activities common to children,
such that the number of people who experience multiple occurrences of
high exposure levels may be underestimated. Small sample size also
limits the extent to which ventilation rates associated with various
activities may be representative of the population group to which they
are applied in the model. In addition, the air quality adjustment
procedure used to simulate air quality distributions associated with
attaining alternative standards, while based on generalized models
intended to reflect patterns of air quality changes that have
historically been observed, contains significant uncertainty,
especially when applied to areas requiring very large reductions in air
quality to attain alternative standards or to areas that are now in
attainment with the 1-hour NAAQS.\34\
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\34\ A more complete discussion of uncertainties and limitations
is presented in the Staff Paper and technical support documents
(Johnson et al., 1996a,b; Richmond, 1997).
---------------------------------------------------------------------------
b. Risk Assessments
The EPA conducted an assessment of health risks for several
categories of respiratory effects considering the same population
groups, alternative air quality scenarios, and urban areas that were
examined in the human exposure analyses described above. The objective
of the risk assessment was to estimate to the extent possible 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
uncertainties inherent in the assessment. While different risk measures
are provided by the assessment, EPA has focused on ``headcount risk''
estimates which include: (1) Estimates of the number of people likely
to experience a given health effect and (2) estimates of the number of
incidences of a given health effect likely to be experienced by the
population group of interest (n.b., some individuals likely experience
that given health effect more than once in a year). While the estimates
of numbers of people and incidences of effects are subject to
uncertainties and should not be viewed as demonstrated health impacts,
EPA believes they do represent reasonable estimates of the likely
extent of these effects on public health given the available
information.
This risk assessment builds upon earlier O3 risk
assessment approaches developed during the previous O3 NAAQS
review. The risk models produce estimates of risk by taking into
account: (1) Exposure-response or concentration-response relationships
used to characterize various respiratory effects of O3
exposure; (2) distributions of population exposures upon attainment of
alternative standards resulting from the exposure analyses described
above; and (3) distributions of 1-hour and 8-hour daily maximum
O3 concentrations upon attainment of alternative standards,
developed as part of the exposure analyses. The assessment addresses a
number of adverse lung function and respiratory symptom effects as well
as increased hospital admissions, as discussed below.
(i) Adverse lung function and respiratory symptom effects. Risk
estimates have been developed for several of the respiratory effects
observed in controlled human exposure studies to be associated with
O3 exposure for which sufficient quantitative dose-response
information was available. These effects include lung function
decrements (measured as changes in FEV1) and pain on deep
inspiration (PDI).\35\ More specifically, these effects, or health
endpoints, are defined not only in terms of physiological responses,
but also the amount of change in that response judged to be of medical
significance (as discussed in section II.A.3 above). For decrements in
FEV1 responses, risk estimates are provided for the lower
end, midpoint, and upper end of the range of response considered to be
an adverse health effect (i.e., 10, 15, or 20 percent
FEV1 decrements), while for PDI responses, risk estimates
are provided for moderate and severe responses. Although some
individuals may experience a combination of responses, risk estimates
could only be provided for each individual health endpoint rather than
various combinations of functional and symptomatic responses.
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\35\ 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 studies used to derive
exposure-response relationships.
---------------------------------------------------------------------------
The exposure-response relationships used to characterize these
functional and symptomatic effects were based on the controlled human
exposure studies, and were applied to ``outdoor children,'' ``outdoor
workers,'' and the general population.\36\ These exposure-response
relationships were combined with the results of the exposure analyses,
which provided distributions of population exposures estimated to occur
upon attainment of alternative standards, 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.
---------------------------------------------------------------------------
\36\ While these studies only included adults aged 18-35,
findings from other clinical studies and summer camp field studies
in several locations across the U.S. and Canada indicate changes in
lung function in healthy children similar to those observed in
healthy adults exposed to O3 under controlled laboratory
conditions.
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[[Page 57278]]
Following from the results of the exposure analyses showing outdoor
children to be the population group experiencing the greatest
exposures, this population group also has the highest estimated risk in
terms of the percent of the population, and the numbers of children,
likely to experience the health effects included in the assessment. As
expected, the risk estimates exhibit the same general patterns in
comparing alternative standards as was observed in the results of the
exposure analyses. Estimated risk varied significantly across the urban
areas examined, with greater variability associated with the 1-hour
NAAQS than with alternative 8-hour standards, and, within any given
urban area, the differences in risk estimated for the various 1-hour
and 8-hour standards analyzed were statistically significant.
In looking more specifically at a comparison between 8-hour
standards at the 0.09 ppm and 0.08 ppm levels, aggregate estimates of
the number of outdoor children in the nine areas likely to experience
moderate ( 15 percent) and large ( 20 percent)
FEV1 decreases and moderate or severe PDI are summarized in the 1997
final rule.\37\ For example, for large FEV 1 decreases
( 20 percent), approximately 2 percent of outdoor children
(58,000 children) would likely experience this effect one or more times
per year (100,000 occurrences) at the 0.08 ppm standard level,
increasing to approximately 3 percent of outdoor children (97,000
children and 220,000 occurrences) at the 0.09 ppm standard level. Based
on this assessment, a standard set at 0.09 ppm would allow
approximately 40-65 percent more outdoor children to experience these
functional and symptomatic effects than would a 0.08 ppm standard, and
approximately 70-120 percent more occurrences of such effects in
outdoor children per year.
---------------------------------------------------------------------------
\37\ Based on the supplemental analyses that used the third-
highest concentration-based form of the standards (Richmond, 1997).
---------------------------------------------------------------------------
In considering these observations, the Administrator and CASAC have
recognized that there are many uncertainties inherent in such
assessments, not all of which can be quantified. Some of the most
important caveats and limitations in this assessment include: (1) The
uncertainties and limitations associated with the exposure analyses
discussed above; (2) the extrapolation of exposure-response functions,
consistent with CASAC's recommendation, that projects some biological
responses 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).\38\
---------------------------------------------------------------------------
\38\ A more complete discussion of assumptions and uncertainties
is presented in the Staff Paper and the technical support documents
(Whitfield et al., 1996; Richmond, 1997).
---------------------------------------------------------------------------
(ii) Excess respiratory-related hospital admissions. A separate
risk assessment was done for increased respiratory-related hospital
admissions as reported in several epidemiologic studies.\39\ The
assessment looked only at one urban area, New York City, for which
adequate air quality information was available to assess population
risk. Increased respiratory-related hospital admissions for individuals
with asthma were modeled using a probabilistic concentration-response
function based on the results of an epidemiologic study in New York
City (Thurston et al., 1992) and estimated distributions of daily
maximum 1-hour average O3 concentrations upon attainment of
alternative standards at various monitors in New York City (developed
as part of the exposure analysis discussed above).\40\ The resulting
risk estimates are for excess respiratory-related hospital admissions
(i.e., those attributable to O3 concentrations above an
estimated background O3 level of 0.04 ppm) for asthmatic
individuals over an O3 season.
---------------------------------------------------------------------------
\39\ Several studies, mainly conducted in the northeastern U.S.
and southeastern Canada have reported excess daily respiratory-
related hospital admissions associated with elevated O3
levels within the general population and, more specifically, for
individuals with asthma.
\40\ The model is described in more detail in Whitfield et al.
(1996) and results from the supplemental analysis are presented in
Richmond (1997).
---------------------------------------------------------------------------
Similar to the risk assessment discussed above for lung function
and respiratory symptom effects, reductions in hospital admissions for
respiratory causes for asthmatic individuals and the general population
are estimated to occur with each change in the level of alternative 8-
hour standards from 0.09 ppm to 0.07 ppm. In looking more specifically
at a comparison between 8-hour standards at 0.09 ppm and 0.08 ppm
levels, a standard set at 0.09 ppm is estimated to allow approximately
40 more excess hospital admissions of asthmatics within an
O3 season in New York City for respiratory causes as
compared to a 0.08 ppm standard, which represents approximately a 40
percent increase in excess O3-related admissions, but only
approximately a 0.3 percent increase in total admissions of asthmatics.
The EPA believes that while these numbers of hospital admissions are
relatively small from a public health perspective, they are indicative
of a pyramid of much larger numbers of related O3-induced
effects, including respiratory-related hospital admissions among the
general population, emergency and outpatient department visits, doctors
visits, and asthma attacks and related increased use of medication that
are important public health considerations.
In taking these observations into account, the Administrator
recognizes the uncertainties and limitations associated with this
assessment. These include: (1) The inability at this time to
quantitatively extrapolate the risk estimates for New York City to
other urban areas; (2) uncertainty associated with the underlying
epidemiologic study from which the concentration-response relationship
used in the analysis was drawn; and (3) uncertainties associated with
the air quality adjustment procedure used to simulate attainment of
alternative standards for the New York City area.\41\
---------------------------------------------------------------------------
\41\ A more complete discussion of these uncertainties and
limitations is presented in the Staff Paper and technical support
documents (Whitfield et al., 1996; Richmond, 1997).
---------------------------------------------------------------------------
B. Potential Indirect Beneficial Health Effects Associated With Ground-
level O3
This section is drawn from information in the record of the 1997
review with regard to the effect of ground-level O3 on the
attenuation of UV-B radiation and potential associated health benefits.
All relevant record information was reviewed, including EPA documents,
published articles, oral testimony at public meetings, and written
comments submitted during the rulemaking. This section summarizes
information on the health effects associated with UV-B radiation
exposure and the relationship between ground-level O3 and
UV-B radiation, and evaluates estimates of UV-B radiation risks that
have been attributed to reductions in ground-level O3
projected to result from attainment of the 1997 O3 NAAQS.
1. Health Effects Associated With UV-B Radiation Exposure
It has long been recognized that exposure to sunlight has a
positive effect on health. Sunlight is essential to the human body
because of its biosynthetic action. More specifically, UV radiation
induces the conversion of ergosterol and other vitamin precursors
[[Page 57279]]
present in normal skin to vitamin D, an essential factor for normal
calcium deposition in growing bones.\42\ Sunlight is also an important
controlling agent of recurrent daily physiological alterations known as
circadian rhythms. Lighting cycles have been shown to be important in
regulating several types of endocrine function. However, it is also
recognized that excessive exposure to solar radiation can result in
adverse health effects, which are particularly associated with UV-B
radiation.
---------------------------------------------------------------------------
\42\ Evidence of this effect is found in Galindo et al., (1995),
who reported on the increased risk of rickets associated with
decreased incident UV-B radiation due to air pollution.
---------------------------------------------------------------------------
The following summary of information on the adverse human health
effects associated with exposure to UV-B radiation focuses on the three
major organ systems whose tissues are commonly exposed to solar
radiation: the skin, eyes, and immune system.\43\ It is these three
systems that are potentially subject to damage from increased UV-B
radiation as a result of the absorption of solar energy by molecules
present in the cells and tissues of these organs. The biologically
effective dose of radiation that actually reaches target molecules
generally depends on the duration of exposure at particular locations,
time of day, time of year, behavior (i.e., ``sun avoidance,'' which is
an intentional decrease in exposure, for example, by using clothing,
sunscreens, and sunglasses to shield from solar radiation; and ``sun
seeking,'' which is an intentional increase in exposure to solar
radiation, for example, by sunbathing), and, for the skin,
characteristics that include pigmentation and temporal variations
(e.g., changes in the pigmentation due to tanning).
---------------------------------------------------------------------------
\43\ The reference document available in the record for the
information in this section is the EPA document ``Assessing the Risk
of Trace Gasses that Can Modify the Stratosphere'' (U.S. EPA, 1987.)
---------------------------------------------------------------------------
a. Effects on the Skin
The most common form of solar damage to the skin is sunburn.
Susceptibility to sunburn and the ability to tan are the basis for a
classification system of six skin phenotypes. The most sensitive
individuals (skin type I) are very light-skinned, with red or blonde
hair and blue or green eyes (U.S. EPA, 1987, ES-33). The most resistant
individuals (skin type VI) are darkly pigmented even without exposure
to solar radiation. Susceptibility to sunburn may be a risk factor for
skin cancer.
Among light-skinned populations, skin cancer is among the most
common kinds of cancer. The three types of skin cancer that have been
associated with exposure to solar radiation include two common types of
nonmelanoma skin cancers, squamous cell carcinoma (SCC) and basal cell
carcinoma (BCC), and melanoma, a far less common form of cancer.
Various types of evidence support the conclusion that increases in
solar radiation in general, and UV-B radiation in particular, increase
skin cancer morbidity and mortality. Epidemiological studies are the
primary source of information providing evidence of associations
between UV-B radiation and the occurrence of skin cancer in humans. In
addition, experimental studies on animals, and animal and bacterial
cells, have helped define the action spectra for particular biological
endpoints, which describe how effective radiation of specific
wavelengths is in causing a biological effect, and also the possible
mechanisms by which damage can occur.
(i) Nonmelanoma skin cancer (NMSC). Based on surveys, particularly
in the U.S. and Australia, prolonged exposure to the sun is considered
to be the dominant risk factor for NMSC (U.S. EPA, 1987, ES-33). It has
been observed that NMSC tends to develop on sites that are most
frequently exposed to the sun (e.g., head, face, and neck). Outdoor
workers, who are subject to greater exposure to solar radiation, tend
to have higher incidence rates of NMSC. A latitudinal gradient exists
for the flux of UV-B radiation (i.e., the amount of radiation
transmitted through the atmosphere), with fluxes generally higher in
lower latitudes. A similar latitudinal gradient is generally seen in
incidence rates of NMSC. Skin pigmentation provides a protective
barrier that reduces the risk of developing NMSC, such that light-
skinned individuals, who are more susceptible to sunburn and have blue
or green eyes, are more likely to develop NMSC. The risk of NMSC is
highest among individuals with a genetic predisposition to abnormal
skin pigmentation (e.g., people with xeroderma pigmentosum).
Both types of NMSC result from the malignant transformation of
keratinocytes, the major structural cells of the skin. Cumulative long-
term exposure to UV radiation is the exposure of concern for both types
of NMSC. More specifically, the incremental increase in cumulative
lifetime exposure to UV-B radiation is the metric used to estimate the
risk of increased incidence of NMSC (U.S. EPA, 1987, ES-3).
Epidemiological evidence, however, also indicates that exposure to
solar radiation may play different roles in the etiology of SCC and
BCC. In particular, SCC is more likely to develop on sites receiving
the highest cumulative UV radiation doses (e.g., nose), and the
development of SCC is more strongly associated with cumulative exposure
to UV radiation. Relative to SCC, BCC is more likely to develop on
sites that are not normally exposed to the sun, such as the trunk. For
a given cumulative level of exposure to solar radiation, the risk of
developing SCC may be greater than the risk of developing BCC.
Results from experimental studies suggest that UV-B radiation may
be the most important component of solar radiation that causes
variations in the incidence of NMSC. UV radiation has been demonstrated
to produce nonmelanoma skin tumors in animals, and UV-B wavelengths
have been shown to be the most effective part of the UV spectrum in
producing these tumors. Mechanisms by which this damage can occur have
been demonstrated in laboratory animals. UV-B radiation has been shown
to cause a variety of DNA lesions, to induce neoplastic transformation
in cells, and to be a mutagen in both animal and bacterial cells.
Dose-response relationships for NMSC are generally estimated in
terms of a biological amplification factor (BAF), which is defined as
the percent change in tumor incidence that results from a 1 percent
change in UV-B radiation. While there is considerable uncertainty in
such estimates, results from several studies have produced an overall
BAF range that is 1.8 to 2.85 for all nonmelanoma skin tumors (U.S.
EPA, 1987, ES-34). The BAF estimates are generally higher for males
than females and for SCC than BCC, and generally increase with
decreasing latitude. Key uncertainties in these estimates include, for
example, uncertainties in the actual doses of UV-B radiation received
and in the underlying baseline incidence rates in populations.
Additional uncertainty is introduced in estimating the change in
mortality from NMSC associated with changes in UV-B radiation,
reflecting in part discrepancies of reporting between death
certificates and hospital diagnoses. Based on published estimates,
rates of metastasis among SCCs and BCCs varied by one to two orders of
magnitude, with rates estimated to be approximately 2 to 20 percent for
SCC and 0.0028 to 0.55 percent for BCC. The overall fatality rate for
NMSC has been estimated to be approximately 1 to 2 percent, with three-
fourths to four-fifths of the deaths
[[Page 57280]]
attributable to SCC (U.S. EPA, 1987, ES-34).\44\
---------------------------------------------------------------------------
\44\ More recent estimates or mortality rates from NMSC may be
found on the American Cancer Society's Web site http://www.cancer.org, under cancer type ``Skin, Nonmelanoma,'' then under
``Nonmelanoma Skin Cancer--Overview.''
---------------------------------------------------------------------------
(ii) Melanoma. Melanoma is a serious, life-threatening skin cancer
that is far rarer and generally much more aggressive than NMSC.
Melanoma is a malignant cancer of the melanocytes, the pigment
producing cells in the skin. While the development of melanoma is
associated with cumulative lifetime exposure to UV radiation, there are
several histological forms of melanoma that vary in their relationships
to exposure to solar and UV-B radiation, sites on the body, skin
pigmentation, and possibly in precursor lesions. Assessment of
incidence by type is not consistent among registries, thus complicating
attempts to evaluate the relationship between melanoma and solar
radiation (U.S. EPA, 1987, ES-36).
The relationship between exposure to UV-B radiation and melanoma is
not as clear as the relationship between exposure to UV-B radiation and
NMSC. The EPA (1987) noted limitations in the evidence linking solar
radiation to melanoma. For example, no animal models were identified in
which exposure to UV-B radiation experimentally induces melanoma, and
no in vitro models for malignant transformation of melanocytes. Despite
these limitations, EPA (1987) recognizes that a large array of evidence
does support the conclusion that solar radiation is one of the causes
of melanoma. Melanin, the principal pigment in the skin, effectively
absorbs UV radiation, such that darker skin provides more protection
from UV radiation. Light-skinned races, whose skin contains less
protective melanin, have higher incidence and mortality rates from
melanoma than do dark-skinned races. Lighter members of light-skinned
races, including those who are unable to tan or who tan poorly, have a
higher incidence of melanoma than do darker members of light-skinned
races. In addition, as was the case in NMSC, the risk of melanoma is
highest among individuals with a genetic predisposition to abnormal
skin pigmentation (e.g., people with xeroderma pigmentosum).
Sun exposure seems to induce freckling, which is an important risk
factor for melanoma, and sun exposure leading to sunburn apparently
induces melanocytic moles, which are also a risk factor for melanoma.
Additional evidence suggests that melanoma risk may be associated with
childhood sunburn. However, other evidence suggests that childhood
sunburn may be a surrogate for an individual's pigmentation
characteristics or be related to mole development, rather than being a
separate risk factor (U.S. EPA, 1987, ES-37).
Most studies that have used latitude as a surrogate for sunlight or
UV-B exposure have found an increase in melanoma incidence or mortality
correlated with proximity to the equator. Other evidence, however,
creates uncertainty about the relationship between solar radiation and
melanoma. Some ecologic epidemiology studies, conducted primarily in
Europe or in countries close to the equator, have failed to find a
latitudinal gradient for melanoma. In addition, outdoor workers
generally have lower incidence and mortality rates from melanoma than
indoor workers, which appears to be incompatible with the hypothesis
that the cumulative dose from exposure to solar radiation causes
melanoma. Unlike SCC and BCC, most melanoma occurs on sites of the body
that are not habitually exposed to sunlight. This evidence suggests
that exposure to solar radiation, or UV-B, is not solely responsible
for variations in the incidence and mortality from melanoma (U.S. EPA
1987, ES-37).
Considering the available evidence, EPA (1987) concluded that UV-B
radiation is a likely component of solar radiation that causes
melanoma, either through the initiation of tumors or through
suppression of the immune system. The EPA (1987) also recognized that
significant uncertainties exist in characterizing associations between
solar radiation and melanoma, including the appropriate action spectrum
to be used in estimating doses, the best functional form for a dose-
response relationship, and the best way to characterize dose (e.g.,
peak value, cumulative summer exposure).
b. Effects on the Eyes
Evidence suggests that adverse effects on the eye are associated
with exposure to UV-B radiation. Effects likely include increases in
cataract incidence or severity and increased incidence of retinal
disorders and retinal degeneration. Cataracts are characterized by the
gradual loss of transparency of the lens due to the accumulation of
oxidized lens proteins. Many possible mechanisms exist for the
formation of cataracts, and UV-B radiation may play an important role
in some mechanisms. Epidemiological and laboratory evidence indicates
that the exposure of concern in the development of cataracts is the
cumulative lifetime exposure to UV-B radiation.
Although the cornea and aqueous humor of the human eye screen out
significant amounts of ultraviolet-A (UV-A) and UV-B radiation, nearly
50 percent of radiation at 320 nm is transmitted to the lens.
Transmittance declines substantially below 320 nm, so that less than 1
percent is transmitted below approximately 290 to 300 nm. However,
results of laboratory experiments on animals indicate that short-
wavelength UV-B (i.e., below 290 nm) is perhaps 250 times more
effective than long-wavelength UV-B (i.e., 320 nm) in inducing
cataracts. Thus, while epidemiological studies indicate that the
prevalence of human cataracts varies with latitude and UV radiation in
general (U.S. EPA, 1987, ES-40), significant uncertainty exists about
the action spectrum to be used in any estimation of dose associated
with variations in solar radiation.
c. Effects on the Immune System
Information on the effects of UV-B radiation on the immune system
comes primarily from laboratory animal studies. High doses of UV
radiation cause a depression in systemic hypersensitivity reactions,
resulting in an inability of the animal to respond to an antigen
presented to the animal through unirradiated skin, whereas relatively
lower doses cause a depression in local contact hypersensitivity,
resulting in an inability to respond to an antigen presented through
UV-irradiated skin. Both of these immunosuppressive effects of UV
radiation have been found to reside almost entirely in the UV-B portion
of the solar spectrum (U.S. EPA, 1987, ES-39).
Information about the effects of UV radiation on the human immune
system, however, is much more limited. Preliminary studies indicate the
UV radiation may prevent an effective immune response to micro-
organisms that infect via the skin. Because UV-B can produce systemic
immunologic change, the possibility exists that changes in UV-B
radiation exposure could result in effects on diseases whose control
requires systemic rather than local immunity. Without more complete
information from laboratory or epidemiological studies, the nature of
an exposure of concern cannot be estimated. Immunologic studies have
not assessed the effects of long-term, low-dose UV-B irradiation, such
that the magnitude of risk from this type of exposure cannot be
assessed (U.S. EPA, 1987, ES-40).
[[Page 57281]]
2. Relationship Between Ground-level O3 and UV-B Radiation
Exposure
a. Relevant Atmospheric Factors
The relationships between ground-level O3 and UV
radiation occur in the context of a much larger dynamic of the earth's
atmospheric systems. The sun is, of course, overwhelmingly the main
source of a wide band of electromagnetic radiation, including the
ultraviolet. The total atmosphere blocks a significant portion of the
range of this incoming solar radiation before it reaches ground level,
including much of the more energetic wavelengths that are shorter than
visible light. The UV spectrum (100-400 nm) is comprised of UV-C (100-
280 nm), UV-B (280-320 nm), and UV-A (320-400 nm). The most energetic
component, UV-C, is completely blocked or absorbed by oxygen
(O2) and O3 in the atmosphere. The middle range,
UV-B, is efficiently but not completely absorbed by total column
O3. Ultraviolet-A radiation (320-400 nm) in wavelengths
above 350 nm is not absorbed by O2 or O3, nor is
visible light (4000-900 nm) \45\ (U.S. EPA, 1987, ES 35). The
absorption of UV-B by O3 varies across the spectrum, being
much stronger for wavelengths of 300 nm and below than for the upper
region near 320 nm (Cupitt, 1994). Because the amount of atmospheric
O3 traversed by sunlight varies with the sun angle,
atmospheric absorption is more complete in winter months and both early
and late in the day, as compared to the absorption around mid-day near
the summertime solar zenith. Therefore, a decrease in total column
O3 from naturally occurring conditions is of greater concern
during times of higher sun angles, and for the more energetic portion
of the UV-B range.
---------------------------------------------------------------------------
\45\ The shorter (blue) wavelengths of visible light are,
however, scattered by atmospheric gases, which is responsible for
the ``blue'' sky characteristic of days with low pollution and less
than full cloud cover.
---------------------------------------------------------------------------
The underlying annual and diurnal patterns of UV-B penetration to
the ground layer are driven primarily by three factors: (1) The change
in apparent sun angle with the surface that occurs as the earth travels
around the sun; (2) the diurnal change in apparent sun angle caused by
the earth's rotation; and (3) the solar/meteorologically driven annual
change in the amount of O3 in the stratosphere.
Stratospheric O3 over U.S. latitudes shows a characteristic
peak in the spring months, falling steadily thereafter through summer
and fall (Fishman et al., 1990; Frederic et al., 1993). The combination
of the annual sun cycle and the stratospheric O3 cycle means
that peak UV-B radiation reaching the troposphere tends to occur in
late June to early July, and falls steadily thereafter (Frederick et
al., 1993). The annual peak in ground-level O3
concentrations, which extends in most areas from May through September,
generally overlaps the UV-B radiation peak (e.g., U.S. EPA, 1996a,
Figure 4-23).
As noted in the EPA's SunWise Program communications, UV-B
radiation exposure is of most concern between the hours of 10 am and 4
pm, peaking around mid-day. Ground-level O3 patterns vary,
but in urban areas, summertime peaks tend to occur between noon and 4
pm (U.S. EPA, 1996a, Section 4.4). This obviously overlaps with peak
incoming UV-B radiation. The pattern of vertical mixing in the
atmosphere is such that morning ground-level measurements probably do
not accurately reflect ``mixing-layer'' concentrations (U.S. EPA,
1996a, p. 3-44).\46\
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\46\ The mixing layer (relevant to the vertical ``thickness'' of
ground-level O3) develops and grows in height through the
day.
---------------------------------------------------------------------------
The relationship between ground-level O3 and solar
radiation, including UV-B radiation, is complex and mediated by a
number of atmospheric factors. It is not limited to the simple
absorption of energy. At a fundamental level, the variation in apparent
solar radiation is a primary cause of meteorological fluctuations that
strongly influence the build-up and transport of anthropogenic air
pollution. Further, as discussed in Chapter 3 of the Criteria Document,
UV-B radiation that penetrates the stratosphere to the mixing layer
plays a key role in the processes leading to the formation of
photochemical smog, including the formation of ground-level
O3. In fact, increased penetration of UV-B radiation to the
troposphere due to stratospheric O3 depletion would likely
increase ground-level concentrations of O3 in most urban and
many rural areas of the U.S. (U.S. EPA, 1996a, p. 3-5). The chain of
indirect events triggered by increased penetration of UV-B radiation
can result in both increases and decreases in aerosol and acid rain
formation (U.S. EPA, 1996a; pp. 3-38 to 39), with attendant further
feedbacks through heterogeneous chemistry and aerosol scattering of UV-
B radiation. All of these complex processes could, under varying
conditions, increase or decrease the amount of UV-B radiation that
actually reaches ground level relative to an unperturbed case. The
reactions can further affect the concentrations of radiatively
important substances such as methane, ozone, and particles, and could
affect local, regional, and global climate.
Setting aside the direction and magnitude of these complex indirect
effects of UV-B radiation penetration on ground-level air pollution,
and assuming appropriate sun angles and cloud density, the marginal
effect of ground-level O3 on the absorption of UV-B
radiation by the earth's atmosphere can be considered separately.
Because of increased scattering of incident UV-B radiation by the
denser layer air molecules, droplets, and particles nearer the surface,
tropospheric O3 can absorb somewhat more UV-B radiation than
an equal amount of O3 in the stratosphere (Bruhl and
Creutzen, 1989). The extent to which this increase in unit effect
occurs depends on the relative concentrations and character of aerosols
in the troposphere as compared to the stratosphere.
A further consideration is the relative effectiveness of ground-
level O3 in absorbing those spectra of UV-B radiation
wavelengths most likely to cause health effects. The ``effective dose''
of UV-B radiation can be expressed as a function of two factors, the
intensity of radiation (by wavelength) reaching the earth's surface and
the action spectrum. The wavelength-dependent effect of O3
on reducing the intensity of radiation in the UV-B range is summarized
above. The action spectrum describes how effective radiation at
particular wavelengths is at causing a particular biological effect or
a response in an instrument. Action spectra allow the estimation of the
potential effects of simultaneously changing radiation at different
wavelengths by different amounts, as happens with changing
O3 levels. Laboratory and field studies have been used to
estimate and adopt action spectra conventions for various biological
endpoints (e.g., Madronich, 1992). As noted above, uncertainty exists
about the action spectra as well as how to specify appropriate dose
metrics for particular health endpoints. Even estimates of the range of
wavelengths considered to be generally biologically active vary within
the UV-B radiation spectrum. These different action spectra have
different sensitivities to changes in total column O3, which
are formalized as numerical radiation amplification factors (RAF).\47\
In general, a 1 percent change in total column O3 will
produce greater than a 1 percent change (e.g., 1.1
[[Page 57282]]
to 1.8 percent) in effective radiation dose for particular effects.
---------------------------------------------------------------------------
\47\ The RAF is defined as the percent increase in effective
dose divided by the percent decrease in total column zone
(Madronich, 1992).
---------------------------------------------------------------------------
Nevertheless, as noted above, typical summertime ground-level
O3 pollution in the eastern U.S. is less than 1 percent of
total column O3. Even considering the relative effectiveness
of ground-level O3 in reducing UV-B radiation and the
amplification of effective dose, such pollution could add a few percent
at most to naturally occurring biologically effective UV-B radiation
shielding.\48\ Viewed from one perspective and holding all other
factors constant, the assumed typical O3 pollution level is
providing some ``improvement'' or incremental UV-B radiation shielding
above the natural conditions that would otherwise exist in the mixing
layer. It should also be noted that, if typical summertime
O3 levels were assumed to approximate the estimated
continental background of about 40 ppb for daylight hours (U.S. EPA,
1996b, p. 20-21), this too would represent an ``improvement'' over the
natural conditions that would exist in the mixing layer without the
influence of international transport of O3.\49\
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\48\ For reasons discussed below, any such shielding would vary
widely from day to day, even in the summer O3 season.
\49\ This estimated continental background is due in part to
natural sources of emissions in North America and in part to the
long-range transport of emissions from both anthropogenic and
natural sources outside of North America.
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The extent to which changes in ground-level O3
concentrations would translate into changes in UV-B radiation-related
health effects in various locations cannot, however, be adequately
viewed by reference to uniform assumptions applicable for specific sun
angle, latitude, time of day, cloud cover, and the presence of other
pollutants. \50\ In the real world, all of these factors vary with
location, season, meteorology, and time of day. Moreover, the complex
causal relationships noted above among all of these factors mean that
neither static calculations holding other factors constant (e.g.,
Cupitt, 1994) nor simple empirical associations between measured
ground-level O3 and UV-B radiation (e.g., Frederick et al.,
1993) provide an adequate basis for assessing the ``net'' shielding
associated with control strategy driven changes in ground-level
pollution in various locations over an extended time period. Moreover,
as for the direct effects of O3, the extent of resultant UV-
B radiation-related health effects is also heavily dependent on the
variation of these physical changes superimposed on the activity
patterns and other factors that determine population exposures and
sensitivities to UV-B radiation, and on the extent to which significant
biological responses can be attributed in part to episodic peak
exposures as well as to long-term cumulative exposures.
---------------------------------------------------------------------------
\50\ Adding to the complexity of understanding this relationship
are the results of high-dose animal toxicology studies that suggest
more research is needed into the direct effects of ground-level
O3 on the skin. Tests by Thiele et al. (1997) suggest
that long-term exposure to O3 can deplete vitamin E in
the skin, and this could make the skin more susceptible to the
effects of UV-B radiation (U.S. EPA, 1997). Therefore, reducing
long-term ground-level O3 exposure might serve to reduce
skin problems. Even a relatively small O3 effect here
could partially or completely offset any small UV-B radiation
mediated effect estimated based on O3--UV-B interactions
alone.
---------------------------------------------------------------------------
Assessing the effective O3 layer shielding is
considerably more difficult for ground-level O3 than for
stratospheric O3 because of its far greater spatial and
temporal variability and the much smaller contribution made by ground-
level O3. Some insights into the relative variability of
these two layers are provided in Fishman et al. (1990), which compares
satellite measurements of stratospheric O3 with ``residual''
tropospheric O3, a measure that actually excludes the lowest
portion of the ground-layer O3 in the mixing layer. For the
summer months, the long-term spatial variability in the amount of ozone
in the stratosphere across the lower 48 U.S. States is about 7 percent
(Figure 8c), while the variability in the tropospheric ``residual'' is
nearly 4 times greater, at about 25 percent (Figure 9c). By comparison,
the spatial variability in ground-level O3 measurements
across regions and cities in the U.S. is far greater (U.S. EPA, 1996a,
Chapter 4) reaching 200 percent and higher for comparable long-term
measurements. Within an area as small as the Los Angeles basin alone,
for example, the median ground-level 8-hour O3 values in
different locations varied by more than a factor of 2 (Table 28;
Johnson et al., 1996c). The satellite information also shows a marked
contrast in the seasonal variations in O3 for these two
layers. The variation in the summer/winter stratospheric O3
column over the U.S. is only about 2 to 4 percent, while the variation
in seasonal ``residual'' tropospheric O3 is about 50 to 80
percent (Figures 8a,c;9a,c; Fishman et al., 1990). Again, the
variability is even greater for ground-level measurements (e.g., U.S.
EPA, 1996a, Figure 4-23; Frederick et al., 1993)
Although Fishman et al. (1990) do not compare daily variations in
stratospheric O3 above the U.S., it is reasonable to
conclude that the spatial and annual/seasonal temporal stability
evidenced by this large stratospheric reservoir would result in far
more stable day-to-day and diurnal patterns as compared to ground-level
O3. The high variability of daytime O3
concentrations for these temporal scales is amply documented in the
Criteria Document (U.S. EPA, 1996a, Figure 4-23).
The spatial and temporal stability of the expansive and deep
stratospheric O3 reservoir means that assessments of the
effects of long-term declines or restoration can reasonably assume that
short-term and local-scale variations in important factors such as
cloud cover, other pollutants, temperature, and activity patterns
beneath this layer will tend to ``even out'' over time, permitting more
confidence in the magnitude and direction of such assessments. In
contrast to the stability of the stratospheric O3 layer, the
large spatial and day-to-day variability outlined above for ground-
level O3 means that geographical or temporal variations in
other factors such as weather, other pollutants, and human activity
patterns may not ``even out'' in particular areas under assessment.
Moreover, it is reasonable to assume that the variations in ground-
level O3 are not independent of the variations in many of
these other factors. Such variability may have a substantial impact on
the outcome of any assessment of the relative effects of a change in
ground-level O3 strategies or standards. This, combined with
the many local- and regional-scale interactions among all of these
factors, would complicate any such ground-level O3
assessment.
b. Factors Related to Area-Specific Assessment
An enumeration of factors that would be important in assessing the
potential UV-B radiation-related consequences of a more stringent
O3 NAAQS in any geographical area serves to illustrate the
complexities discussed above. Analogous to the factors that were
important in the respiratory effects exposure and risk assessments
discussed above section II.A.2, these UV-B radiation-related factors
include: the temporal and spatial patterns of ground-level
O3 concentrations throughout a geographic area where
reductions are likely to occur, and the variations in O3
concentrations within a comprehensive set of ``microenvironments''
relevant to UV-B radiation exposures; the associated temporal and
spatial patterns of UV-B radiation flux in such microenvironments; the
temporal and spatial patterns of movement of people throughout the
microenvironments within the geographic area; and the effects of
variable behaviors (e.g., the use of sunscreen, hats, sunglasses)
within the range of activities that people
[[Page 57283]]
regularly engage in, on the effective dose of UV-B radiation that
reaches target organs such as the skin.
While analogous to the respiratory-related factors, there are a
number of important differences between these sets of factors that
arise, for example: (1) Due to the indirect nature of the relationship
between changes in ground-level O3 and UV-B radiation-
related health effects (in contrast to the direct relationship between
ground-level O3 and inhalation-related health effects); (2)
the long-term nature of the relevant exposures that are associated with
UV-B radiation's chronic health effects (in contrast to the short-term
exposures associated with acute inhalation effects); (3) the different
types of parameters that are relevant to assessing dermal exposures (in
contrast to those that are important in assessing inhalation
exposures); and (4) the importance of skin type in characterizing the
sensitive populations (in contrast to characterizing sensitive
populations in terms of activity levels and respiratory health status).
Further, as was done in EPA's assessment of respiratory effects, it is
important to characterize the exposure-related factors specifically to
address the relevant at-risk sensitive population groups. As noted in
section II.B.1, the sensitivity to UV-B radiation effects varies among
U.S. demographic groups, such that it could be important to incorporate
census data on relevant characteristics (e.g., age at time of exposure,
skin pigmentation) that affect an individual's susceptibility.
Aspects of each of these factors are discussed briefly below, and
areas where current information or modeling tools are insufficient to
address these factors at this time are noted.
(i) Estimation of area-specific and microenvironment changes in
ground-level O3. Implementation of a more stringent
O3 standard would, over time, further reduce O3
concentrations across the U.S., but would affect various areas in
different ways. Depending on the strategies adopted, in some locations
peak concentrations would be reduced significantly during the
O3 season, while the lower concentrations that occur on far
more numerous days could increase. In such areas, the long-term
cumulative effect could be little net change, or even a small increase
in cumulative shielding. In other areas, the entire distribution of
O3 could be reduced. The assessment of the acute respiratory
health effects of O3 appropriately focused on the higher
portion of this distribution, using a simple roll-back approach
discussed above (section II.A.2.a) to simulate changes in air quality
patterns during the O3 season based on available air quality
monitoring data. For assessment of chronic effects such as those
associated with UV-B radiation, however, where long-term cumulative
exposures are of central importance, the mid to lower portion of the
distribution would also be important. Also the distribution across the
entire year, for which O3 monitoring data is not generally
available in many parts of the country, could potentially be important.
The mid to lower portion of the distribution is much more strongly
influenced by complex atmospheric chemistry, such that more
sophisticated, area-specific modeling may be needed.
In addition, although not relevant to assessing direct respiratory
effects, the vertical distribution of O3 concentrations up
through the mixing layer becomes important in assessing the effect of
O3 in shielding UV-B radiation. The current lack of routine
vertical profile measurements means that little is known about the
relative effect of ground-level control strategies on O3 in
the mixing layer.
With regard to characterizing changes in O3
concentrations within microenvironments relevant to UV-B radiation
exposure, it is clear that this set of microenvironments would differ
in some respects from the set of microenvironments that were relevant
for respiratory effects. For example, while indoor microenvironments
can reduce exposure to both ambient O3 and UV-B radiation,
outdoor microenvironments that are relevant for inhalation exposure do
not reflect the characteristics that are important for UV-B radiation
exposure. For example, while not relevant to inhalation exposure,
microenvironments shaded by the presence of trees, buildings, and other
structures in many heavily occupied areas could be important to
characterize because they would tend to have greatly reduced UV-B
radiation exposures even when at the same ground-level O3
concentration as a sunny microenvironment.
(ii) Estimation of temporal and spatial patterns of UV-B radiation
flux. Relative to the assessment of respiratory effects, the assessment
of the effect of O3 shielding on UV-B radiation-related
health effects requires the additional step of estimating how changes
in the temporal and spatial patterns of O3 concentrations
result in changes in the patterns of UV-B radiation. Given a three-
dimensional pattern of O3 levels, a first-order
approximation of UV-B penetration to the Earth's surface can be readily
made. The factors that influence radiation flux through the
stratosphere are fairly well characterized, and most directly related
to the modest changes in stratospheric O3 and large
variations in sun angle that depend on latitude, time of year, and time
of day (U.S. EPA, 1987). Nevertheless, beyond these factors, and in
addition to changes in ground-level O3, a number of other
(second-order) factors in the boundary layer and the rest of the
troposphere can affect the amount of UV-B radiation reaching
potentially affected populations. One such factor is cloud cover, which
can reduce UV-B radiation reaching the earth's surface by 50 percent or
more (Cupitt, 1994). Another such factor is the presence of UV-B
radiation scattering and absorbing aerosols. Depending on local
circumstances and the strategy chosen, aerosol-related UV-B radiation
exposure might increase or decrease as a result of ground-level
O3 reductions (U.S. EPA, 1996a, Chapter 3). Both
O3 and aerosols can affect local climate as well as UV-B
radiation, and this could affect cloud cover as a further indirect
consequence of a reduction strategy. While any such indirect effects
might be expected to be small for modest O3 changes, it is
not currently possible to predict the magnitude or the sign of their
net effect on UV-B radiation penetration.
(iii) Estimation of temporal and spatial patterns of movement of
people throughout microenvironments. While population densities are
high in areas with the highest ground-level O3
concentrations, people may not receive their highest exposure to UV-B
radiation in such locations. Reductions in O3 shielding
would presumably be most significant in outdoor recreational areas such
as the beach or rural open areas where many people likely receive a
disproportionate share of their cumulative sun exposure. Local or
regional meteorological factors can, however, cause ground-level
O3 concentrations to be lower in many such areas,
particularly in the western United States. For example, O3
concentrations in the heavily populated Los Angeles area tend to be
lowest at the coast and increase inland; in this case, smog-related
O3 would be providing the least shielding where the
potential for exposure to UV-B radiation is the highest. The extensive
database on human activity patterns, which was used in the assessment
of respiratory effects, does not include parameters that relate to
people's movement through the types of outdoor microenvironments that
are relevant to the assessment of UV-B radiation exposure. For example,
additional data would be needed to conduct an exposure analysis that
could account for the fraction of UV-B
[[Page 57284]]
radiation exposure that is incurred during outdoor recreational
activities in non-shaded microenvironments. EPA believes that reliable
estimation of the change in UV-B radiation exposure associated with
reducing ground-level O3 would be hindered by not taking
such factors into account.
(iv) Effects of variable behaviors on effective dose of UV-B
radiation. Another important factor to be considered in assessing the
potential UV-B radiation-related effects of a change in ground-level
O3 is that human behavior affects UV-B radiation exposures.
When people choose to shield themselves from UV-B radiation exposure
with clothing and sunscreens, and by timing their outdoor activities to
avoid peak sun conditions, they are affecting a parameter that is
important in assessing UV-B radiation-related effects. The generally
well-known risks associated with too much sun exposure are such that
many people limit their own as well as their children's exposure
through such measures, regardless of the status of the protective
stratospheric O3 layer or variable amounts of ground-level
O3 pollution. While some sun exposure is generally
beneficial to health, limiting excessive sun exposure would remain
important for a person's health even if the stratospheric O3
layer were fully restored to its natural state.\51\
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\51\ Because of the high baseline risk of effects under natural
conditions, as well as the increased risk posed by stratospheric
O3 depletion, medical authorities and governmental bodies
have developed campaigns to effect such changes in behavior. The EPA
and the National Weather Service (NWS) developed the UV Index. The
Index provides a forecast of the expected risk of overexposure to
the sun and indicates the degree of caution that should be taken
when working, playing, or exercising outdoors. The EPA also
developed the SunWise School Program to be used in conjunction with
the UV Index. This program is designed to educate the public,
especially children and their care givers, about the health risks
associated with overexposure to UV radiation and encourage simple
and sensible behaviors that can reduce the risk of sun-related
health problems later in life (U.S. EPA, 1995a, b).
---------------------------------------------------------------------------
Since sun-seeking or sun-avoidance behaviors can tend to maximize
or minimize exposure to UV-B radiation, not factoring such behavioral
data into an area-specific exposure assessment would hinder reliable
estimation of the increased exposure associated with reducing ground-
level O3. Changes in behavior in the past, specifically
increases in sun-seeking behaviors, are believed to be the primary
reason for the increases in skin cancer incidence and mortality
observed in the U.S. by the 1980's (U.S. EPA, 1987). Conversely, future
rates of skin cancer could be reduced to the extent that people choose
to change their behavior by increasing sun-avoidance behaviors.
Public awareness of the risks associated with overexposure to UV
radiation seems to be having an effect on behavior. In 1987, EPA noted
that behaviors causing increased UV-B radiation exposure were
apparently reaching an upper limit (U.S. EPA, 1987, ES-35). The effect
of increased awareness of the health consequences of UV-B radiation
exposure on decreasing the number of harmful exposures is not likely to
show up, in terms of reducing the incidence and mortality rates of skin
cancers, for many years. Nevertheless, ignoring its effects would tend
to bias exposure estimates in an area-specific assessment of the UV-B
radiation-related effects of smog reduction strategies.
Based on the discussion of factors above, the Administrator
believes that more information is needed to address these factors
before reliable area-specific quantitative assessment of potential UV-B
radiation-related consequences of a more stringent O3 NAAQS
would be possible. EPA intends to seek additional information relevant
to such quantitative assessment. EPA is now requesting comment on the
factors discussed above.
3. Evaluation of UV-B Radiation-Related Risk Estimates for Ground-level
O3 Changes
As should be clear from the discussion above, a full risk
assessment of UV-B radiation-related effects resulting from a moderate
change in ground-level O3 would be an extremely challenging
enterprise that appears to be beyond current data and modeling
capabilities. Nevertheless, three analyses (Cupitt, 1994; U.S. DOE,
1995; Lutter and Wolz, 1997) have developed estimates that attempt to
bound the potential indirect UV-B radiation related effects associated
with replacing the former 1-hour O3 NAAQS with an 8-hour
O3 standard. All three analyses essentially reflect a static
comparison of two separate O3 concentrations on a national
basis, and include, either explicitly or implicitly, numerous
assumptions needed while excluding the important area-specific issues
and factors outlined above.
The most thoroughly documented calculations are those provided in
Cupitt (1994), an EPA white paper developed as an initial scoping
analysis of the issues, in preparation for potential consideration in
the Regulatory Impact Analysis (RIA) that would accompany the
O3 NAAQS regulatory package. The paper discusses many of the
important factors and uncertainties outlined above, summarizes key
background information to provide perspective, and includes a
discussion and table summarizing the many simplifying assumptions that
were needed to permit the development of quantitative estimates.
Cupitt's analysis evaluates changes resulting from cumulative exposures
under two scenarios, including one that compares estimates of NMSC
incidence associated with an assumed reduction of daytime summer
O3 of 10 ppb in O3 that would occur uniformly
throughout 30 eastern States and the District of Columbia and within an
assumed atmospheric mixing layer that ranged up to 2 km in altitude.
Assuming no other relevant factors changed over the several decade
exposure period that would be required, the resulting increase in NMSC
incidence for this extreme scenario was estimated eventually to reach
``between 0.6% and 1%.'' While these percentages are small--indeed too
small to be measurable (Cupitt, 1994)--if taken at face value, they
would not necessarily be judged as trivial because of the large
baseline of NMSC. For reasons outlined below, however, even these small
percentage estimates appear to be substantially overstated and cannot
be considered reliable.
The Cupitt paper was never formally published, but it was subjected
to internal agency peer review and commentary by experts at EPA's
Office of Research and Development (ORD) (Childs, 1994; Altshuller,
1994). While finding the exposition, including recognition of the
difficulties in such an approach, to be ``very acceptable,'' the
reviewers noted substantial uncertainties in basic data and concerns
about the numerous simplifying assumptions that called the numerical
results into significant question. Examples of data uncertainties noted
by the reviewers include: (1) The accuracy of column O3 (in
Dobson units) and UV measurements used; (2) the fact, recognized in
Cupitt (1994), that the predicted UV-B radiation flux changes are at
the ``noise'' level and could not be reliably detected statistically or
attributed to the change in ground-level O3 concentration;
(3) data on effects of aerosols are limited, yet ignoring such effects
in estimating the O3--UV-B radiation relationship was
``erroneous;'' and (4) data to permit dynamic assessment of the
feedback between increased UV radiation and increased O3 is
limited to uncertain models, and this potential feedback mechanism was
ignored in the analysis (Childs, 1994).
Reviewers also questioned a number of the simplifying assumptions
that
[[Page 57285]]
could have ``substantial impact'' on the resulting risk estimates.
Among these were: (1) The assumed mixing height of 2 km, which
reviewers considered too high on average, especially for the eastern
United States (By overstating the thickness of the pollution-related
layer of the atmosphere that is the focus of the control strategies
designed to attain the NAAQS, this factor would bias the estimates
upwards by as much as a factor of 2.); (2) the assumption that the
ozone mixing ratio is the same at the earth's surface as it is at 2 km,
when the vertical profile varies through the diurnal cycle (Because
vertical mixing increases through the day, this assumption would be
most important in the earlier portion of daylight hours.); (3) the
assumption that neither aerosols nor O3 production cycles
themselves exert either positive or negative feedback on UV-B
penetration (As noted in the previous section, a dynamic consideration
of these factors could change the direction of the result in particular
areas.); (4) the assumption that NMSC might result from episodic
exposures, when, in fact, NMSC results from cumulative doses (This
assumption affects only separate and far smaller estimates Cupitt made
for episodic changes, essentially invalidating those results.); (5) the
assumption that all people would be susceptible based on assumed
exposure factors; and (6) the assumption that behavioral patterns,
demographic patterns, and meteorological factors and other factors
related to actual exposures remain constant over time (Childs, 1994;
Altschuller, 1994).
These reviewers capsulized their conclusions regarding the
quantitative results of this analysis as follows:
In summary, (1) the numbers resulting from these calculations
are quite small, and (2) the limitations of the accuracy and
reliability of the input to the calculations produces numbers that
cannot be defended, whether large or small. (Childs, 1994).
As noted in the discussion above, this is not simply a matter of
uncertain and small risk estimates. On balance, several of the problems
noted above served to inflate the overall estimates, and, depending
upon local conditions and the control strategy assumed, could even call
the direction of the results into question for some locations. Further,
a significant bias, not highlighted in the cited reviews, is how well
the assumed 10 ppb change in daytime O3 levels averaged over
an entire summer season (and over half the U.S.) reflects what might
occur in response to the revised O3 NAAQS.\52\ In fact, this
assumed change, as well as the assumptions regarding its spatial and
vertical extent, are significantly larger than could reasonably be
expected based on the revisions to the O3 standard
promulgated in 1997.
---------------------------------------------------------------------------
\52\ Cupitt provides no rationale for the selection for this
value where it first appears in a Table, which is characterized as
addressing ``questions from OMB.''
---------------------------------------------------------------------------
To provide a fair comparison, it is necessary to convert the 1-hour
standard into its nearest 8-hour equivalent. As documented in the Staff
Paper (U.S. EPA, 1996b), the nearest equivalent 8-hour standard would
have a level of about 0.09 ppm. Superficially, this might appear to
support a 10 ppb difference compared to the 0.08 ppm 8-hour standard
set in 1997, until considering that these standards are stated in
reference to extreme high values in the distribution (e.g., the average
of the 4th-highest daily maximum concentrations). Cupitt's analysis
assumed that a ``mixing layer'' up to 2 km deep over a very large
geographical region would experience a change of 10 ppb in daylight
average O3 for an entire O3 season. This scenario
would require a challenging regional strategy that would, on average,
reduce each day for the over 150 day O3 season by 10 ppb.
Yet, the 0.08 ppm 8-hour O3 standard would require that only
the fourth-highest day of the ozone season be reduced by about 10 ppb,
as compared to the previous standard. Based on available O3
trends information, strategies that reduce peak O3 days
would have far less effect on the far more numerous days toward the
middle and lower-parts of the O3 season distribution (e.g.,
U.S. EPA, 1996a, Figures 4-2, 4-3). In fact, as reported in the
Response to Comments document, based on earlier RIA projections of
long-term O3 reductions that might occur with the 0.08 ppm
8-hour O3 standard, the magnitude of the assumed average
change appears to be overstated by more than a factor of 3 (U.S. EPA,
1997). When considered with the excessively high assumed mixing layer,
the overly large geographical area requiring reductions (over 30
States), and the assumption that the entire population would be at the
same risk as the more sensitive subpopulations, it is EPA's judgment,
based on the record, that these readily identified biases could well be
on the order of a factor of 10. EPA solicits comment on the assumptions
discussed above.
More subtle are the uncertainties and potential bias inherent in an
essentially static comparison of two different O3 values
that are assumed to be uniform over a very large area. Dynamic, real-
world strategies would involve a number of alternative local and
regional scale approaches that vary significantly in time and space,
with a variety of possible outcomes with respect to the middle and
lower portions of the distribution that is most relevant to estimating
long-term summer averages over a period of decades into the future. An
example of such local strategy-dependent outcomes would be control of
NOX emissions across a metropolitan area, which could reduce
O3 concentrations at downwind peak monitors, but also result
in localized increases in lower concentrations in the center city area
(National Academy of Sciences, 1991, Figure 11-2). As noted in section
II.B.2 above and in Altshuller (1994), the interrelated indirect
results from reduced O3 and UV-B radiation could trigger
feedbacks through increased O3, aerosol, or cloud cover that
could partially or fully offset the initial O3 effects on
UV-B radiation. Available data and assessment tools do not permit a
reasonable quantitative assessment of these second-and third-order
indirect effects (Altshuller, 1994; Childs, 1994).
Other potential problems associated with ignoring area-specific
considerations in an O3/UV-B risk analysis summarized in the
previous section include the assessment of local physical factors
(e.g., buildings) that reduce UV-B radiation exposure in outdoor
microenvironments, meteorological conditions (e.g., sea breeze) or
local emissions patterns that reduce pollution in high UV-B radiation
exposure microenvironments, behavioral adjustments to information
concerning UV-B radiation risk over time, and local differences in the
proportion of sensitive populations. Even Cupitt's assumption that 90
percent of exposure occurs during the summer O3 season
embeds an assumption about long-term personal behavior for which little
empirical evidence exists.
In summary, the Cupitt (1994) white paper was useful for its
intended purpose as a scoping analysis to identify the potential issues
arising in any attempt to assess the potential shielding provided by
changes in ground-level O3. It established that any effects
of even fairly large long-term O3 reductions in ground-level
O3 would be quite small, but as evidenced in the comments of
the peer review and the discussion above, available data and modeling
tools fall far short of permitting reliable quantitative risk estimates
for
[[Page 57286]]
consideration in standard setting or benefits assessments.
The analysis of this issue by U.S. Department of Energy (DOE) staff
(1995) is summarized in a statement submitted as a part of public
comments at a CASAC meeting. The exposition is far less complete than
that of Cupitt, and it is quite difficult to reconcile the range of
estimates for NMSC, the lower bound of which are less than Cupitt,
while the upper bound estimates are more than double his. The analysis
apparently starts with the same assumptions regarding a constant change
in summertime O3 of 10 ppb through a 2 km mixing layer, but
important information about the other assumptions is lacking. In any
event, the paper does not appear to improve upon the methodology in the
Cupitt analysis.\53\ Given that the U.S. DOE statement must share the
limitations outlined above for Cupitt and the fact that the analytical
approach is not well documented nor peer reviewed, no reliance is
placed on the quantitative results presented in the U.S. DOE
submission.
---------------------------------------------------------------------------
\53\ In addition to estimates for NMSC, the U.S. DOE statements
also provided estimates for melanoma skin cancers and cataracts. As
discussed above, the quantitative relationship between cumulative
UV-B exposure and the latter effects are not as well established as
for NMSC. Given the lack of documentation and the additional
uncertainties over those for NMSC, neither the U.S. DOE estimates of
such effects nor the uncritical reliance on them by Lutter and Wolz
(1997) should not given quantitative credence.
---------------------------------------------------------------------------
The work of economic analysts Lutter and Wolz (1997) provides a
``preliminary analysis'' of UV-B radiation screening by tropospheric
O3. Here, the exposition permits a more direct comparison
with that of Cupitt, and it appears that many of the same simplifying
assumptions were used--either explicitly or implicitly. This paper
relied upon Cupitt's assumption that the NAAQS revision might bring
about a summertime average of 10 ppb reduction in O3 in
areas not attaining the standard. As discussed above, based on the
record, EPA believes this substantially overstates the likely effect of
the NAAQS revision. Their assumption of a constant mixing ratio for the
10 ppb change that would extend well above the planetary boundary
layer, up to 10 km, also introduces upward bias into their upper-bound
risk estimates. The resultant apparent dose appears to be a factor of 4
larger than the upper bound used by Cupitt and U.S. DOE staff. The
other quantitative inputs to the analysis differed to a more modest
degree from those used by Cupitt. In the end, the upper bound estimate
of NMSC is more than double that of Cupitt, due largely to the
unwarranted assumption of a 10 km mixing height.
Again, because the quantitative assessment shares most of the
limitations cited above for Cupitt, and actually adds substantial bias
in a key assumption, EPA has placed no reliance on the quantitative
risk estimates for NMSC from Lutter and Wolz (1997) or to the secondary
estimates derived in the U.S. DOE analyses. EPA solicits comment on the
assessments discussed above.
At the end of the 1997 O3 NAAQS review, EPA published
the final RIA, containing, among other requirements, an analysis
addressing all of the quantifiable benefits of the O3 NAAQS.
This analysis, which was reviewed by other Federal agencies and
approved for release by the Office of Management and Budget (OMB),
concluded that the available scientific and technical information would
not permit reliable quantitative estimates of any effect of changing
the O3 NAAQS on UV-B radiation-related effects. Based on the
present examination of all of the available information in the record,
the Administrator believes that this remains a sound conclusion.
C. Consideration of Net Adverse Health Effects of Ground-Level
O3
In considering the net adverse health effects of ground-level
O3, EPA has focused on characterizing and weighing the
comparative importance of the potential indirect beneficial health
effects associated with the attenuation of UV-B radiation by ground-
level O3 (section II.B above) and the direct adverse health
effects associated with breathing O3 in the ambient air
(section II.A above). The same key factors considered by EPA in its
1997 review of the O3 standard are again considered here in
characterizing the additional information on potential beneficial
effects and in comparatively weighing this information relative to the
direct adverse effects. Beyond quantitative assessments of exposure and
risk that were central to EPA's 1997 review, these factors include the
nature and severity of the effects, the types of available evidence,
the size and nature of the sensitive populations at risk, and the kind
and degree of uncertainties in the evidence and assessments. In
recognition of the complexity and multidimensional nature of such a
comparison, no attempt is made to characterize all the relevant effects
or associated risks to public health with a common metric.
The available record information on the potential indirect
beneficial health effects associated with ground-level O3
includes information from studies of health effects caused by exposure
to UV-B radiation and studies that focus on the consequences of
unnaturally high exposures to UV-B radiation due to depletion of the
stratospheric O3 layer, as well as analyses that attempt to
focus specifically on the consequences of assumed changes in
tropospheric O3 levels. The nature and severity of the
effects of UV-B radiation exposure on the skin, eye, and immune system
are discussed above (section II.B.1), as is the nature of sensitive
populations at risk for these effects. These effects, especially on the
skin and eye, are generally understood to be associated with long-term
cumulative exposure to UV-B radiation and to have long latency periods
from cumulative exposures, especially those early in life. People with
light skin pigmentation make up the primary at-risk population for
effects on the skin, especially for NMSC, while at-risk populations for
other effects are not as well understood. For NMSC, uncertainties in
the evidence generally relate to uncertainties in the relevant action
spectra and BAFs, as well as in factors related to characterizing the
severity of the different types of NMSC. Based on the record
information, for the other effects, the role of UV-B radiation is less
well understood (e.g., as to relevant action spectra, BAFs, the nature
of exposures of concern), although cumulative exposure to UV-B
radiation is thought to play a causal role. These characterizations are
derived from the large body of epidemiologic and toxicologic evidence
that served as the basis for the reference document by EPA (1987).
The record includes a quantitative assessment conducted by EPA
(1987, App. E) of the health risks associated with changes in exposure
to UV-B radiation attributable to changes in the stratospheric
O3 layer. This assessment models the relationship between
wide-scale changes in global/regional levels of stratospheric
O3, resulting from emissions of O3 depleting
substances with long-atmospheric lifetimes, and changes in UV-B
radiation flux as a function of latitude for three broad regions across
the United States.\54\ As discussed above (section II.B.2), because
changes in the stratospheric O3 layer are relatively uniform
across broad regions, varying across the U.S. primarily with
[[Page 57287]]
latitude, information on localized spatial and temporal patterns of
exposure-related variables (e.g., changes in ground-level
O3, meteorological conditions, human activity patterns) are
not relevant in producing credible estimates of risk associated with
changes in stratospheric O3. This is in sharp contrast to
the nature of the information necessary to produce credible estimates
of risk associated with changes in exposures to UV-B radiation
projected to result from changes in ground-level O3 that
would be associated with attainment of alternative 8-hour standards for
O3.
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\54\ Since the EPA's 1987 risk assessment on stratospheric ozone
depletion, numerous changes have been made to the model to reflect
the commitments made since 1987 by the United States, under
amendments to the Montreal Protocol, for reductions in production of
various ozone depleting chemicals and to incorporate more accurately
the latest scientific information.
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An evaluation of the available analyses that have produced
estimates of health risks associated with changes in ground-level
O3 (section II.B.3 above) identifies major limitations in
available information that resulted in the need for the analyses to
incorporate broad and unsupportable assumptions. These limitations are
particularly important with regard to information on spatial and
temporal patterns of changes in ground-level O3 likely to
result from various future emission control strategies, relevant
meteorological conditions and atmospheric chemistry leading to a
cascade of broader indirect effects, and human demographic and activity
patterns likely to result in exposures of concern. For the reasons
discussed above, these limitations are judged to be of central
importance in any such analysis. Thus, in light of such limitations,
the Administrator agrees with internal and external reviewers in
proposing to conclude that the available scientific and technical
information would not permit credible quantitative estimates of these
potential beneficial effects.\55\ Thus, available analyses based on
such limited information cannot serve as credible estimates of
potential beneficial effects associated with the presence of ground-
level O3 due to man-made emissions of O3 forming
substances.
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\55\ This conclusion was also reached by the Health and
Ecological Effects Subcommittee of the Advisory Council on Clean Air
Compliance Analysis, a part of EPA's Science Advisory Board, in
conjunction with their review of the ``The Benefits and Costs of the
Clean Air Act 1990 to 2010'' (EPA, 1999b)
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Further, in setting aside the available quantitative analyses, EPA
notes that our above evaluation of a number of critical factors in the
analyses provides reasons for believing that the public health impacts
of any potential beneficial effects associated with ground-level
O3 are likely very small, albeit unquantifiable at this time
(section II.B.2). In giving qualitative consideration to the available
evidence on potential indirect beneficial effects of ground-level
O3, EPA believes it is appropriate to weigh this information
in the context of the body of evidence on adverse effects caused by
direct inhalation exposures to ground-level O3 that formed
the basis for the 1997 O3 primary standard.
As an initial matter, as discussed in the 1997 final rule, the
Administrator focused primarily on quantitative comparisons of risk,
exposure, and air quality in selecting both the level (62 FR 38867-8)
and form (62 FR 38869-72) of the 1997 O3 primary standard.
More specifically, she looked at comparisons of both those risks to
public health that can be explicitly quantified in terms of estimated
incidences and the size of the at-risk population (e.g., children)
likely to experience adverse effects, as well as those for which
quantitative risk information is more limited, but for which
quantitative estimates of the number of children likely to experience
exposures of concern could be developed (as discussed in section II.A.2
above). In considering these comparisons, she recognized that although
there were inherent uncertainties in these estimates, the underlying
assessments took into account extensive data bases on the spatial and
temporal patterns of air quality and directly relevant human activity
patterns likely to result in inhalation exposures of concern. Further,
the Administrator took into account CASAC's advice that the assessment
methods were appropriate and state-of-the-art, and that the results
should play a central role in her decision.
Beyond the quantitative information on direct adverse effects, with
regard to the qualitative evidence suggestive of potential serious,
chronic adverse effects on public health associated with long-term
inhalation exposures, the Administrator judged that such information
was too uncertain and not well enough understood at the time to serve
as the basis for establishing a more restrictive 8-hour standard in
terms of either level (62 FR 38868) or form (62 FR 38871). This
conclusion was consistent with CASAC's advice that further research
into potential chronic adverse effects in humans should be continued,
and the results considered in the next review (62 FR 38871).
In weighing the available information on potential indirect
beneficial effects of ground-level O3, the Administrator
considers this information in the same light as the information on
potential direct chronic adverse effects associated with long-term
inhalation exposures to ground-level O3. In both instances,
the potential health effects are serious and likely to develop over
many years, with important periods of exposure likely occurring in
childhood. Different population groups are likely affected, however, by
these potential adverse and beneficial effects. Urban populations and
people with impaired respiratory systems (e.g., people with asthma),
who are disproportionately from certain minority groups, are most at-
risk for the direct inhalation-related effects, whereas fair-skinned
populations are most generally, but not exclusively, at-risk for the
indirect beneficial effects related to exposure to UV-B radiation.
Although different types of uncertainties are inherent in the record
information on these effects, in both cases, the uncertainties related
to ground-level O3 are so great as to preclude the
development of credible estimates of the size of the affected
population or the probability of the occurrence of such effects. In the
case of indirect effects related to ground-level O3, EPA
believes that the use of plausible but unsubstantiated assumptions
would likely lead to the conclusion that the potential impacts on
public health are likely very small; no such conclusions have yet been
drawn with regard to the public health impacts of potential direct
chronic adverse effects related to inhalation exposures. After
considering these factors, the Administrator now provisionally
concludes that, much like the qualitative evidence on direct adverse
effects potentially associated with long-term inhalation exposures, the
newly considered available evidence on potential indirect beneficial
effects is not well enough understood at this time to serve as the
basis for establishing a less restrictive 8-hour standard than was
promulgated in 1997. Rather, the Administrator believes that the most
recent evidence and analyses of potential long-term, indirect
beneficial effects should be considered in the next review in
conjunction with the most recent information on long-term, direct
adverse effects.
D. Proposed Response to Remand on the Primary O3 NAAQS
After carefully considering the scientific information available in
the record on adverse effects on public health associated with direct
inhalation exposures to O3 in the ambient air and on the
potential for indirect benefits to public health associated with the
presence of ground-level O3 and the resultant attenuation of
naturally occurring UV-B radiation from the sun, taking into account
the weight of that evidence in assessing the net adverse
[[Page 57288]]
health effects of ground-level O3, and for the reasons
discussed above, the Administrator proposes to respond to the remand by
reaffirming the 8-hour primary O3 standard promulgated in
1997. In proposing to leave unchanged the 1997 O3 standard
at this time, the Administrator has fully considered the available
information in the record of the 1997 O3 NAAQS review on
potential beneficial health effects of ground-level O3.
Based on such consideration, she has provisionally determined that the
information linking changes in patterns of ground-level O3
concentrations likely to occur as a result of programs implemented to
attain the 1997 O3 NAAQS to changes in relevant exposures to
UV-B radiation of concern to public health is too uncertain at this
time to warrant any relaxation in the level of public health protection
previously determined to be requisite to protect against the
demonstrated direct adverse respiratory effects of exposure to
O3 in the ambient air. Further, the Administrator notes that
it is the Agency's view that associated changes in UV-B radiation
exposures of concern, using plausible but highly uncertain assumptions
about likely changes in patterns of ground-level ozone concentrations,
would likely be very small from a public health perspective.
In the past, the Administrator has been confronted with situations
where there has been both quantifiable and unquantifiable evidence, and
has moved forward with a NAAQS decision. The inability to quantify all
related effects does not preclude the Agency from making a NAAQS
decision, particularly in situations where there is strong quantifiable
evidence of significant adverse health effects. Moreover, in this case,
as noted above, EPA believes the potential beneficial effects are not
quantifiable at this time and likely very small from a public health
perspective. Accordingly, the Administrator believes it is
inappropriate to wait for additional information on such effects prior
to responding to this remand.
The 0.08 ppm, 8-hour primary standard is met at an ambient air
quality monitoring site when the 3-year average of the annual fourth-
highest daily maximum 8-hour average O3 concentration is
less than or equal to 0.08 ppm. Data handling conventions are specified
in a new appendix I to 40 CFR part 50, as discussed in the 1996
proposal and 1997 final rule.\56\
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\56\ Subsequent to the 1997 final rule, EPA has promulgated
further revisions to 40 CFR part 50 with regard to the applicability
of the 1-hour O3 standards (65 FR 45182; July 20, 2000).
In addition, EPA notes that recent legislation addresses the timing
of future actions on nonattainment designations with regard to the
8-hour O3 standards (Pub. L. No. 106-377, 114 Stat. 1441
(2000)).
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In proposing to respond to the remand by reaffirming the 1997
primary O3 standard at this time, the Administrator
recognizes, however, that relevant information on indirect potentially
beneficial health effects of ground-level O3 is now
available that was not part of this rulemaking record. In addition, she
notes that the next periodic review of the O3 NAAQS has now
been initiated by EPA's ORD with a call for information (65 FR 57810;
September 26, 2000). Thus, to ensure that the next review of the
O3 criteria and standards can be based on a comprehensive
and current body of relevant scientific information, EPA encourages the
submission of new scientific information on the relationships between
ground-level O3, associated attenuation of UV-B radiation
and other indirect effects of the presence of O3 in the
ambient air, and effects on public health such as those associated with
changes in relevant exposures to UV-B radiation.
In looking ahead to the next review, EPA anticipates that the
available information may warrant a fuller examination of relevant
public health policy factors in weighing the net adverse health effects
associated with ground-level O3. Such factors could include,
for example, the extent to which the proximate cause of the effects is
natural or man-made; the extent to which the effects are in excess of
naturally occurring background levels; the extent to which the
exposures of concern are affected by human behavior patterns; the time
course of exposure-response relationships; and environmental justice
issues that arise in any analysis of risk trade-offs involving
different sensitive populations. To help inform this aspect of the next
review, EPA also solicits comments on whether these and other factors
should be considered to be relevant in weighing the net adverse health
effects of ground-level O3.
III. Rationale for Proposed Response To Remand on the Secondary O3
Standard
This notice also presents the Administrator's proposed response to
the remand, reaffirming the 8-hour O3 secondary standard
promulgated in 1997, based on: (1) Information from the 1997 criteria
and standards review that served as the basis for the 1997 secondary
O3 standard, including the scientific information on welfare
effects associated with direct exposures to O3 in the
ambient air, with a focus on vegetation effects, and assessments of
vegetation exposure, risk, and economic values and (2) a review of the
scientific information in the record of the 1997 review (but not
considered as part of the basis for the 1997 standard) on the welfare
effects associated with changes in UV-B radiation, the association
between changes in ground-level O3 and changes in UV-B
radiation, and predictions of changes in ground-level O3
levels likely to result from attainment of alternative O3
standards.
A. Direct Adverse Welfare Effects
As discussed in the 1997 final rule, direct exposures to
O3 have been associated quantitatively and qualitatively
with a wide range of vegetation effects such as visible foliar injury,
growth reductions and yield loss in annual crops, growth reductions in
tree seedlings and mature trees, and effects that can have impacts at
the forest stand and ecosystem level. Visible foliar injury can
represent a direct loss of the intended use of the plant, ranging from
reduced yield and/or marketability for some agricultural species to
impairment of the aesthetic value of urban ornamental species. On a
larger scale, foliar injury is occurring on native vegetation in
national parks, forests, and wilderness areas, and may be degrading the
aesthetic quality of the natural landscape, a resource important to
public welfare. Growth and yield effects of O3 have been
well documented for numerous species, including commodity crops, fruits
and vegetables, and seedlings of both coniferous and deciduous tree
species. Although data from tree seedling studies could not be
extrapolated to quantify responses to O3 in mature trees,
long-term observational studies of mature trees have shown growth
reductions in the presence of elevated O3 concentrations.
Even where these growth reductions are not attributed to O3
alone, it has been reported that O3 is a significant
contributor that potentially exacerbates the effects of other
environmental stresses (e.g., pests). In addition, growth reductions
can indicate that plant vigor is being compromised such that the plant
can no longer compete effectively for essential nutrients, water,
light, and space. When many O3-sensitive individuals make up
a population, the whole population may be affected. Changes occurring
within sensitive populations, or stands, if they are severe enough,
ultimately can change community and ecosystem structure. Structural
changes that alter the ecosystem functions of energy flow and nutrient
cycling can alter ecosystem succession.
[[Page 57289]]
Based on key studies and other biological effects information
reported in the Criteria Document and Staff Paper, it was recognized
that peak O3 concentrations equal to or greater than 0.10
ppm can be phytotoxic to a large number of plant species, and can
produce acute foliar injury and reduced crop yield and biomass
production. In addition, O3 concentrations within the range
of 0.05 to 0.10 ppm have the potential over a longer duration of
creating chronic stress on vegetation that can result in reduced plant
growth and yield, shifts in competitive advantages in mixed
populations, decreased vigor leading to diminished resistance to pest
and pathogens, and injury from other environmental stresses. Some
sensitive species can experience foliar injury and growth and yield
effects even when O3 concentrations never exceed 0.08 ppm.
Further, the available scientific information supports the conclusion
that a cumulative seasonal exposure index is more biologically relevant
than a single event or mean index.
To put judgments about these vegetation effects into a broader
national perspective, the Administrator has taken into account the
extent of exposure of O3-sensitive species, potential risks
of adverse effects to such species, and monetized and non-monetized
categories of increased vegetation protection associated with
reductions in O3 exposures. In so doing, the Administrator
recognized that markedly improved air quality, and thus significant
reductions in O3 exposures would result from attainment of
the 0.08 ppm, 8-hour primary standard. In looking further at the
incremental protection associated with attainment of a seasonal
secondary standard, she recognized that areas that would likely be of
most concern for effects on vegetation, as measured by the seasonal
exposure index, would also be addressed by the 0.08 ppm, 8-hour primary
standard.
B. Potential Indirect Beneficial Welfare Effects
This section is drawn from the limited information in the record of
the 1997 review with regard to the effect of ground-level O3
on the attenuation of UV-B radiation and potential associated welfare
benefits.\57\ While this information suggests the potential for effects
on plants and aquatic organisms, EPA (1987, ES-40--ES-43) recognizes
that relevant studies are limited and the uncertainties are great due
in part to problems in study designs, such that quantitative
conclusions cannot be drawn.
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\57\ The information in this section is drawn primarily from the
EPA document ``Assessing the Risk of Trace Gasses that Can Modify
the Stratosphere'' (U.S. EPA, 1987).
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With regard to effects on vegetation, while some plant cultivars
tested in the laboratory were determined to be sensitive to UV-B
radiation exposure, these experiments have been shown to inadequately
replicate effects in the field, such that they do not reflect the
complex interactions between plants and their environment. The only
long-term field studies of crops involved soybeans, producing
suggestive evidence of reduced yields under conditions simulating
changes in total column O3 over an order of magnitude
greater than those projected to occur as a result of changes in ground-
level O3 associated with attainment of the 1997
O3 NAAQS. Beyond the limited studies of crops, EPA (1987,
ES-41) notes that little or no data exist on UV-B radiation effects on
trees and other types of natural vegetation, or on possible
interactions with pathogens. While it is noted that changes in UV-B
radiation levels could alter the results of competition in natural
ecosystems, no evidence is available to evaluate this effect. Further,
it is recognized that UV-B radiation may both inhibit and stimulate
plant flowering, depending on the species and growth conditions.
Recognizing that interactions between UV-B radiation and other
environmental factors are important in determining potential UV-B
radiation effects on plants, EPA (1987, ES-42) notes that extensive,
long-term studies would be required to address these interactions.
With regard to effects on aquatic organisms, EPA (1987, ES-42)
notes that while initial experiments show that increased UV-B radiation
has the potential to harm aquatic life, difficulties in experimental
designs and the limited scope of the studies prevent the quantification
of potential risks. Some study results suggest that most zooplankton
show no effect due to increased exposure to UV-B radiation up to some
threshold exposure level, with exposures above such threshold levels
eliciting notable effects. For species under UV-B stress, such effects
could include reduced time spent at the surface of the water, which is
critical for breeding in some species, possibly leading to changes in
species diversity. It is also noted that, as do all other living
organisms, aquatic biota cope with exposure to UV-B radiation by
avoidance, shielding, and repair mechanisms, although uncertainty
exists as to the extent to which such mitigation mechanisms would occur
(U.S. EPA, 1987, ES-43). It is recognized that determination of UV-B
radiation exposure in aquatic systems is complex because of the
variable attenuation of UV-B radiation in the water column, and that
further research is needed to improve our understanding of how UV-B
radiation exposure affects marine species, particularly given their
world-wide importance as a source of protein.
C. Proposed Response To Remand on the Secondary O3 NAAQS
After considering the scientific information available in the
record on adverse welfare effects associated with direct exposure to
O3 in the ambient air and on the potential indirect benefits
to public welfare related to attenuation of naturally occurring UV-B
radiation, the Administrator provisionally concludes that there is
insufficient information available on UV-B radiation-related effects to
warrant any relaxation in the level of public welfare protection
previously determined to be requisite to protect against the
demonstrated direct adverse effects of exposure to O3 in the
ambient air. Thus, the Administrator proposes to respond to the remand
by reaffirming the 8-hour secondary O3 standard promulgated
in 1997, which is identical to the 8-hour primary O3
standard.
As recognized above in section II.B.4 with regard to consideration
of health effects, the Administrator also recognizes that relevant
information on indirect potentially beneficial welfare effects of
ground-level O3 is now available that was not part of this
rulemaking record. In addition, as previously noted, the next periodic
review of the O3 NAAQS is now being initiated by EPA's ORD
with a call for information. Thus, to ensure that the next review of
the O3 criteria and standards can be based on a
comprehensive and current body of relevant scientific information, EPA
encourages the submission of new scientific information on the
relationships between ground-level O3, associated
attenuation of UV-B radiation and other indirect effects of the
presence of O3 in the ambient air, and effects on public
welfare such as those associated with changes in relevant exposures to
UV-B radiation.
IV. Administrative Requirements
A. Executive Order 12866: OMB Review of ``Significant Actions''
Under Executive Order 12866, the Agency must determine whether a
regulatory action is ``significant'' and, therefore, subject to OMB
review and
[[Page 57290]]
the requirements of the Executive Order. The order defines
``significant regulatory action'' as one that may:
(1) Have an annual effect on the economy of $100 million or more or
adversely affect in a material way the economy, a sector of the
economy, productivity, competition, jobs, the environment, public
health or safety, or State, local, or tribal governments or
communities;
(2) Create a serious inconsistency or otherwise interfere with an
action taken or planned by another Agency;
(3) Materially alter the budgetary impact of entitlements, grants,
user fees, or loan programs or the rights and obligations or recipients
thereof; or
(4) Raise novel legal or policy issues arising out of legal
mandates, the President's priorities, or the principles set forth in
the Executive Order.
In view of its important policy implications, this proposed action
has been judged to be a ``significant regulatory action'' within the
meaning of the Executive Order. The EPA has submitted this proposed
action to OMB for review. Changes made in response to OMB suggestions
or recommendations will be documented in the public record and made
available for public inspection at EPA's Air and Radiation Docket and
Information Center (Docket No. A-95-58).
Since today's proposed response to the remand is a reaffirmation of
the revisions to the O3 NAAQS previously promulgated in
1997, no new RIA has been prepared. The RIA (1997) prepared in
conjunction with the 1997 revision to the O3 NAAQS is
available in the docket, from EPA at the address under ``Availability
of Related Information,'' and in electronic form as discussed above in
``Electronic Availability.''
The Clean Air Act and judicial decisions make clear that the
economic and technological feasibility of attaining ambient standards
are not to be considered in setting NAAQS, although such factors may be
considered in the development of State plans to implement the
standards. Accordingly, although a RIA was prepared for the 1997
decision to revise the O3 NAAQS, neither that RIA nor the
associated contractor reports have been considered in issuing this
proposal.
B. Executive Order 13045: Children's Health
Executive Order 13045, entitled ``Protection of Children from
Environmental Health Risks and Safety Risks'' (62 FR 19885, April 23,
1997), requires Federal agencies to ensure that their policies,
programs, activities, and standards identify and assess environmental
health and safety risks that may disproportionately affect children. To
respond to this order, agencies must explain why the regulation is
preferable to other potentially effective and reasonably feasible
alternatives considered by the agency.
Today's proposed response to the remand, reaffirming the 1997
primary O3 NAAQS, specifically takes into account children
as the group most at risk to the direct inhalation-related effects of
O3 exposure, and was based on studies of effects on
children's health (U.S. EPA, 1996a; U.S. EPA, 1996b) and assessments of
children's exposure and risk (Johnson et al., 1994; Johnson et al.,
1996a,b; Whitfield et al., 1996; Richmond, 1997). The 1997 revision to
the primary O3 NAAQS was promulgated to provide adequate
protection to the public, especially children, against a wide range of
direct O3-induced health effects, including decreased lung
function, primarily in children who are active outdoors; increased
respiratory symptoms, primarily in highly sensitive individuals;
hospital admissions and emergency room visits for respiratory causes,
among children and adults with respiratory disease; inflammation of the
lung and possible long-term damage to the lungs. This proposed response
to the remand affirming the 1997 primary O3 NAAQS maintains
the level of protection of children's health established by the
standard set in 1997. Therefore, today's proposed action does comply
with the requirements of E.O. 13045.
C. Executive Order 13132: Federalism
Executive Order 13132, entitled ``Federalism'' (64 FR 43255, August
10, 1999), requires EPA to develop an accountable process to ensure
``meaningful and timely input by State and local officials in the
development of regulatory policies that have federalism implications.''
``Policies that have federalism implications'' is defined in the
Executive Order to include regulations that have ``substantial direct
effects on the States, on the relationship between the national
government and the States, or on the distribution of power and
responsibilities among the various levels of government.''
Today's proposed response to the remand does not have federalism
implications. It will not have substantial direct effects on the
States, on the relationship between the national government and the
States, or on the distribution of power and responsibilities among the
various levels of government, as specified in Executive Order 13132.
The proposed response to the remand only reaffirms the previously
promulgated ozone standard and would not alter the relationship that
has existed under the Clean Air Act for 30 years, in which EPA sets
NAAQS and the states implement them through submission of SIPs, in
accordance with the requirements of the Clean Air Act. Thus, Executive
Order 13132 does not apply to this action. In the spirit of Executive
Order 13132, and consistent with EPA policy to promote communications
between EPA and State and local governments, EPA specifically solicits
comment on this proposed action from State and local officials.
D. Executive Order 13175: Consultation and Coordination With Indian
Tribal Governments
Executive Order 13175, entitled ``Consultation and Coordination
with Indian Tribal Governments'' (65 FR 67249, November 6, 2000),
requires EPA to develop an accountable process to ensure ``meaningful
and timely input by tribal officials in the development of regulatory
policies that have tribal implications.'' ``Policies that have tribal
implications'' is defined in the Executive Order to include regulations
that have ``substantial direct effects on one or more Indian tribes, on
the relationship between the Federal government and the Indian tribes,
or on the distribution of power and responsibilities between the
Federal government and Indian tribes.''
This proposed response to the remand does not have tribal
implications. It will not have substantial direct effects on tribal
governments, on the relationship between the Federal government and
Indian tribes, or on the distribution of power and responsibilities
between the Federal government and Indian tribes, as specified in
Executive Order 13175. This is because this proposed response to the
remand leaves unchanged the 1997 final rule. Thus, Executive Order
13175 does not apply to this rule.
E. Unfunded Mandates Reform Act
Title II of the Unfunded Mandates Reform Act of 1995 (UMRA), Public
Law 104-4, establishes requirements for Federal agencies to assess the
effects of their regulatory actions on State, local, and tribal
governments and the private sector. Under section 202 of the UMRA, EPA
generally must prepare a written statement, including a cost-benefit
analysis, for proposed and final rules with ``Federal mandates'' that
may result in expenditures to State, local, and tribal governments, in
the aggregate, or to the private sector, of $100 million
[[Page 57291]]
or more in any one year. Before promulgating an EPA rule for which a
written statement is needed, section 205 of the UMRA generally requires
EPA to identify and consider a reasonable number of regulatory
alternatives and adopt the least costly, most cost-effective or least
burdensome alternative that achieves the objectives of the rule. The
provisions of section 205 do not apply when they are inconsistent with
applicable law. Moreover, section 205 allows EPA to adopt an
alternative other than the least costly, most cost-effective or least
burdensome alternative if the Administrator publishes with the final
rule an explanation why that alternative was not adopted. Before EPA
establishes any regulatory requirements that may significantly or
uniquely affect small governments, including tribal governments, it
must have developed under section 203 of the UMRA a small government
agency plan. The plan must provide for notifying potentially affected
small governments, enabling officials of affected small governments to
have meaningful and timely input in the development of EPA regulatory
proposals with significant Federal intergovernmental mandates, and
informing, educating, and advising small governments on compliance with
the regulatory requirements.
As noted above, EPA cannot consider in setting a NAAQS the economic
or technological feasibility of attaining ambient air quality
standards, although such factors may be considered to a degree in the
development of State plans to implement the standards. Accordingly, and
for the reasons discussed in the 1996 proposal and 1997 final rule, EPA
has determined that the provisions of sections 202, 203, and 205 of the
UMRA do not apply to this proposed action. The EPA acknowledges,
however, that any corresponding revisions to associated State
implementation plan requirements and air quality surveillance
requirements, 40 CFR part 51 and 40 CFR part 58, respectively, might
result in such effects. Accordingly, EPA will address unfunded mandates
as appropriate when it proposes any revisions to 40 CFR parts 51 and
58.
F. Regulatory Flexibility Analysis/Small Business Regulatory
Enforcement Fairness Act
Under the Regulatory Flexibility Act (RFA), 5 U.S.C. 601 et seq.,
EPA must prepare a regulatory flexibility analysis assessing the impact
of any proposed or final rule on small entities. Under 6 U.S.C. 605(b),
this requirement may be waived if EPA certifies that the rule will not
have a significant economic impact on a substantial number of small
entities. Small entities include small businesses, small not-for-profit
enterprises, and governmental entities with jurisdiction over
populations less than 50,000 people.
Today's proposed response to the remand, reaffirming the 1997
primary O3 NAAQS, does not establish any new regulatory
requirements affecting small entities. On the basis of the above
considerations and for the reasons discussed in the 1996 proposal and
1997 final rule, EPA certifies that today's proposed action will not
have a significant economic impact on a substantial number of small
entities within the meaning of the RFA, as affirmed by the D.C. Circuit
in American Trucking Associations v. EPA, 175 F. 3d 1027 (D.C. Cir.
1999). Based on the same considerations, EPA also certifies that the
new small-entity provisions in section 244 of the Small Business
Regulatory Enforcement Fairness Act (SBREFA) do not apply.
G. Paperwork Reduction Act
Today's proposed response to the remand does not establish any new
information collection requirements beyond those which are currently
required under the Ambient Air Quality Surveillance Regulations in 40
CFR part 58 (OMB #2060-0084, EPA ICR No. 0940.15). Therefore, the
requirements of the Paperwork Reduction Act do not apply to today's
proposed action.
H. National Technology Transfer and Advancement Act
Section 12(d) of the National Technology Transfer and Advancement
Act of 1995 (NTTAA), Public Law No. 104-113, Section 12(d) (15 U.S.C.
272 note) directs EPA to use voluntary consensus standards in its
regulatory activities unless to do so would be inconsistent with
applicable law or otherwise impractical. Voluntary consensus standards
are technical standards (e.g., materials specifications, test methods,
sampling procedures, and business practices) that are developed or
adopted by voluntary consensus standards bodies. The NTTAA directs EPA
to provide Congress, through OMB, explanations when the Agency decides
not to use available and applicable voluntary consensus standards.
Today's proposed response to the remand does not involve technical
standards. Therefore, EPA did not consider the use of any voluntary
consensus standards.
I. Executive Order 13211: Energy Effects
This proposed response to remand is not a ``significant energy
action'' as defined in Executive Order 13211, ``Actions Concerning
Regulations That Significantly Affect Energy Supply, Distribution, or
Use'' (66 FR 28355 (May 22, 2001)) because it is not likely to have a
significant adverse effect on the supply, distribution, or use of
energy. This is because this proposed response to the remand leaves
unchanged the 1997 final rule. Thus, Executive Order 13211 does not
apply to this rule.
V. References
Altschuller, A.P. (1994) Memorandum to L.T. Cupitt re: Addendum to
My Review of Your Manuscript ``Calculations of the Impact of
Tropospheric Ozone Changes On UV-B Flux and Potential Skin Cancers''
EPA Docket A-95-54, IV-D-2694, Appendix B 17.
American Thoracic Society. (1985) Guidelines as to what constitutes
an adverse respiratory health effect, with special reference to
epidemiologic studies of air pollution. American Review of
Respiratory Disease. 131: 666-668.
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List of Subjects in 40 CFR Part 50
Environmental protection, Air pollution control, Carbon monoxide,
Lead, Nitrogen dioxide, Ozone, Particulate matter, Sulfur oxides.
Dated: October 31, 2001.
Christine Todd Whitman,
Administrator.
[FR Doc. 01-27820 Filed 11-8-01; 8:45 am]
BILLING CODE 6560-50-P