[Federal Register: June 22, 2010 (Volume 75, Number 119)]
[Rules and Regulations]
[Page 35519-35603]
[DOCID:fr22jn10-14]

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Part II

Environmental Protection Agency

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40 CFR Parts 50, 53, and 58

Primary National Ambient Air Quality Standard for Sulfur Dioxide; Final
Rule

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Parts 50, 53, and 58

[EPA-HQ-OAR-2007-0352; 9160-4]
RIN 2060-A048

Primary National Ambient Air Quality Standard for Sulfur Dioxide

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: Based on its review of the air quality criteria for oxides of
sulfur and the primary national ambient air quality standard (NAAQS)
for oxides of sulfur as measured by sulfur dioxide (SO2),
EPA is revising the primary SO2 NAAQS to provide requisite
protection of public health with an adequate margin of safety.
Specifically, EPA is establishing a new 1-hour SO2 standard
at a level of 75 parts per billion (ppb), based on the 3-year average
of the annual 99th percentile of 1-hour daily maximum concentrations.
The EPA is also revoking both the existing 24-hour and annual primary
SO2 standards.

DATES: This final rule is effective on August 23, 2010.

ADDRESSES: EPA has established a docket for this action under Docket ID
No. EPA-HQ-OAR-2007-0352. All documents in the docket are listed on the
http://www.regulations.gov Web site. Although listed in the index, some
information is not publicly available, e.g., confidential business
information or other information whose disclosure is restricted by
statute. Certain other material, such as copyrighted material, will be
publicly available only in hard copy form. Publicly available docket
materials are available either electronically through http://
www.regulations.gov or in hard copy at the Air and Radiation Docket and
Information Center, EPA/DC, EPA West, Room 3334, 1301 Constitution
Ave., NW., Washington, DC. The Public Reading Room is open from 8:30
a.m. to 4:30 p.m., Monday through Friday, excluding legal holidays. The
telephone number for the Public Reading Room is<PHONE_NUMBER> and the
telephone number for the Air and Radiation Docket and Information
Center is<PHONE_NUMBER>.

FOR FURTHER INFORMATION CONTACT: Dr. Michael J. Stewart, Health and
Environmental Impacts Division, Office of Air Quality Planning and
Standards, U.S. Environmental Protection Agency, Mail code C504-06,
Research Triangle Park, NC 27711; telephone:<PHONE_NUMBER>; fax: 919-
541-0237; e-mail<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

Table of Contents

    The following topics are discussed in this preamble:

I. Background
    A. Summary of Revisions to the SO2 Primary NAAQS
    B. Statutory Requirements
    C. Related SO2 Control Programs
    D. History of Reviews of the Primary NAAQS for Sulfur Oxides
    E. Summary of Proposed Revisions to the SO2 Primary
NAAQS
    F. Organization and Approach to Final SO2 Primary
NAAQS Decisions
II. Rationale for Decisions on the Primary Standards
    A. Characterization of SO2 Air Quality
    1. Anthropogenic Sources and Current Patterns of SO2
Air Quality
    2. SO2 Monitoring
    B. Health Effects Information
    1. Short-Term (5-Minute to 24-Hour) SO2 Exposure and
Respiratory Morbidity Effects
    a. Adversity of Short-Term Respiratory Morbidity Effects
    2. Health Effects and Long-Term Exposures to SO2
    3. SO2-Related Impacts on Public Health
    C. Human Exposure and Health Risk Characterization
    D. Approach for Determining Whether To Retain or Revise the
Current Standards
    E. Adequacy of the Current Standards
    1. Rationale for Proposed Decision
    2. Comments on the Adequacy of the Current Standards
    a. Comments on EPA's Interpretation of the Epidemiologic
Evidence
    b. Comments on EPA's Interpretation of the Controlled Human
Exposure Evidence
    c. Comments on EPA's Characterization of SO2-
Associated Exposures and Health Risks
    3. Conclusions Regarding the Adequacy of the Current 24-Hour and
Annual Standards
    F. Conclusions on the Elements of a New Short-Term Standard
    1. Indicator
    a. Rationale for Proposed Decision
    b. Comments on Indicator
    c. Conclusions on Indicator
    2. Averaging Time
    a. Rationale for Proposed Decision
    b. Comments on Averaging Time
    c. Conclusions on Averaging Time
    3. Form
    a. Rationale for Proposed Decision
    b. Comments on Form
    c. Conclusions on Form
    4. Level
    a. Rationale for Proposed Decision
    b. Comments on Level
    c. Conclusions on Level
    5. Retaining or Revoking the Current 24-Hour and Annual
Standards
    a. Rationale for Proposed Decision
    b. Comments on Retaining or Revoking the Current 24-Hour and
Annual Standards
    c. Conclusions on Retaining or Revoking the Current 24-Hour and
Annual Standards
    G. Summary of Decisions on Primary Standards
III. Overview of the Approach for Monitoring and Implementation
IV. Amendments to Ambient Monitoring and Reporting Requirements
    A. Monitoring Methods
    1. Requirements for SO2 Federal Reference Method
(FRM)
    a. Proposed Ultraviolet Fluorescence SO2 FRM and
Implementation
    b. Public Comments
    c. Conclusions on Ultraviolet Fluorescence SO2 FRM
and Implementation
    2. Requirements for Automated SO2 Methods
    a. Proposed Performance Specifications for Automated Methods
    b. Public Comments
    c. Conclusions for Performance Specifications for SO2
Automated Methods
    B. Network Design
    1. Approach for Network Design
    a. Proposed Approach for Network Design
    b. Alternative Network Design
    c. Public Comments
    2. Modeling Ambient SO2 Concentrations
    3. Monitoring Objectives
    a. Proposed Monitoring Objectives
    b. Public Comments
    c. Conclusions on Monitoring Objectives
    4. Final Monitoring Network Design
    5. Population Weighted Emissions Index
    a. Proposed Use of the Population Weighted Emissions Index
    b. Public Comments
    c. Conclusions on the Use of the Population Weighted Emissions
Index
    6. Regional Administrator Authority
    a. Proposed Regional Administrator Authority
    b. Public Comments
    c. Conclusions on Regional Administrator Authority
    7. Monitoring Network Implementation
    a. Proposed Monitoring Network Implementation
    b. Public Comments
    c. Conclusions on Monitoring Network Implementation
    C. Data Reporting
    1. Proposed Data Reporting
    2. Public Comments
    3. Conclusions on Data Reporting
V. Initial Designation of Areas for the 1-Hour SO2 NAAQS
    A. Clean Air Act Requirements
    1. Approach Described in Proposal
    2. Public Comments
    B. Expected Designations Process
VI. Clean Air Act Implementation Requirements
    A. How This Rule Applies to Tribes
    B. Nonattainment Area Attainment Dates
    1. Attaining the NAAQS
    2. Consequences of a Nonattainment Area Failing To Attain by the
Statutory Attainment Date
    C. Section 110(a)(1) and (2) NAAQS Maintenance/Infrastructure
Requirements
    1. Section 110(a)(1)-(2) Submission

    D. Attainment Planning Requirements
    1. SO2 Nonattainment Area SIP Requirements
    2. New Source Review and Prevention of Significant Deterioration
Requirements
    3. General Conformity
    E. Transition From the Existing SO2 NAAQS to a
Revised SO2 NAAQS
VII. Appendix T--Interpretation of the Primary NAAQS for Oxides of
Sulfur and Revisions to the Exceptional Events Rule
    A. Interpretation of the NAAQS for Oxides of Sulfur
    1. Proposed Interpretation of the Standard
    2. Comments on Interpretation of the Standard
    3. Conclusions on Interpretation of the Standard
    B. Exceptional Events Information Submission Schedule
VIII. Communication of Public Health Information
IX. Statutory and Executive Order Reviews
    A. Executive Order 12866: Regulatory Planning and Review
    B. Paperwork Reduction Act
    C. Regulatory Flexibility Act
    D. Unfunded Mandates Reform Act
    E. Executive Order 13132: Federalism
    F. Executive Order 13175: Consultation and Coordination With
Indian Tribal Governments
    G. Executive Order 13045: Protection of Children From
Environmental Health & Safety Risks
    H. Executive Order 13211: Actions That Significantly Affect
Energy Supply, Distribution or Use
    I. National Technology Transfer and Advancement Act
    J. Executive Order 12898: Federal Actions To Address
Environmental Justice in Minority Populations and Low-Income
Populations
References

I. Background

A. Summary of Revisions to the SO2 Primary NAAQS

    Based on its review of the air quality criteria for oxides of
sulfur and the primary national ambient air quality standard (NAAQS)
for oxides of sulfur as measured by sulfur dioxide (SO2),
EPA is making revisions to the primary SO2 NAAQS so the
standards are requisite to protect public health with an adequate
margin of safety, as appropriate under section 109 of the Clean Air Act
(Act or CAA). Specifically, EPA is replacing the current 24-hour and
annual standards with a new short-term standard based on the 3-year
average of the 99th percentile of the yearly distribution of 1-hour
daily maximum SO2 concentrations. EPA is setting the level
of this new standard at 75 ppb. EPA is adding data handling conventions
for SO2 by adding provisions for this new 1-hour primary
standard. EPA is also establishing requirements for an SO2
monitoring network. These new provisions require monitors in areas
where there is an increased coincidence of population and
SO2 emissions. EPA is also making conforming changes to the
Air Quality Index (AQI).

B. Statutory Requirements

    Two sections of the Clean Air Act (Act or CAA) govern the
establishment and revision of National Ambient Air Quality Standards
NAAQS. Section 108 of the Act directs the Administrator to identify and
list air pollutants that meet certain criteria, including that the air
pollutant ``in his judgment, cause[s] or contribute[s] to air pollution
which may reasonably be anticipated to endanger public health and
welfare'' and ``the presence of which in the ambient air results from
numerous or diverse mobile or stationary sources.'' CAA section
108(a)(1)(A) and (B). For those air pollutants listed, section 108
requires the Administrator to issue air quality criteria that
``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 ambient air * * *'' Section 108(a)(2).
    Section 109(a) of the Act directs the Administrator to promulgate
``primary'' and ``secondary'' NAAQS for pollutants for which air
quality criteria have been issued. 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 air quality] criteria and
allowing an adequate margin of safety, are requisite to protect the
public health.'' \1\ Section 109(b)(1). A secondary standard, in turn,
must ``specify a level of air quality the attainment and maintenance of
which, in the judgment of the Administrator, based on [the air quality]
criteria, is requisite to protect the public welfare from any known or
anticipated adverse effects associated with the presence of such
pollutant in the ambient air.'' \2\ Section 109(b)(2) This rule
concerns exclusively the primary NAAQS for oxides of sulfur.
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    \1\ The legislative history of section 109 indicates that a
primary standard is to be set at ``the maximum permissible ambient
air level * * * which will protect the health of any [sensitive]
group of the population,'' and that for this purpose ``reference
should be made to a representative sample of persons comprising the
sensitive group rather than to a single person in such a group.'' S.
Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970). See also American
Lung Ass'n v. EPA, 134 F. 3d 388, 389 (DC Cir. 1998) (``NAAQS must
protect not only average healthy individuals, but also `sensitive
citizens'--children, for example, or people with asthma, emphysema,
or other conditions rendering them particularly vulnerable to air
pollution. If a pollutant adversely affects the health of these
sensitive individuals, EPA must strengthen the entire national
standard.''); Coalition of Battery Recyclers Ass'n v. EPA, No. 09-
1011 (DC Cir. May 14, 2010) slip op. at 7 (same).
    \2\ EPA is currently conducting a separate review of the
secondary SO2 NAAQS jointly with a review of the
secondary NO2 NAAQS (see http://www.epa.gov/ttn/naaqs/
standards/no2so2sec/index.html for more information).
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    The requirement that primary standards include an adequate margin
of safety is intended to address uncertainties associated with
inconclusive scientific and technical information available at the time
of standard setting. It is also intended to provide a reasonable degree
of protection against hazards that research has not yet identified.
Lead Industries Association v. EPA, 647 F.2d 1130, 1154 (DC Cir 1980),
cert. denied, 449 U.S. 1042 (1980); American Petroleum Institute v.
Costle, 665 F.2d 1176, 1186 (DC Cir. 1981), cert. denied, 455 U.S. 1034
(1982). Both kinds of uncertainties are components of the risk
associated with pollution at levels below those at which human health
effects can be said to occur with reasonable scientific certainty.
Thus, in selecting primary standards that include an adequate margin of
safety, the Administrator is seeking not only to prevent pollution
levels that have been demonstrated to be harmful but also to prevent
lower pollutant levels that may pose an unacceptable risk of harm, even
if the risk is not precisely identified as to nature or degree. The CAA
does not require the Administrator to establish a primary NAAQS at a
zero-risk level or at background concentration levels, see Lead
Industries Association v. EPA, 647 F.2d at 1156 n. 51, but rather at a
level that reduces risk sufficiently so as to protect public health
with an adequate margin of safety.
    In addressing the requirement for a margin of safety, EPA considers
such factors as the nature and severity of the health effects involved,
the size of the at-risk population(s), and the kind and degree of the
uncertainties that must be addressed. The selection of any particular
approach to providing an adequate margin of safety is a policy choice
left specifically to the Administrator's judgment. Lead Industries
Association v. EPA, 647 F.2d at 1161-62.
    In setting standards that are ``requisite'' to protect public
health and welfare, as provided in section 109(b), EPA's task is to
establish standards that are neither more nor less stringent than
necessary for these purposes. In so doing, EPA may not consider the
costs of implementing the standards. Whitman v. American Trucking

Associations, 531 U.S. 457, 471, 475-76 (2001).
    Section 109(d)(1) of the Act requires the Administrator to
periodically undertake a thorough review of the air quality criteria
published under section 108 and the NAAQS and to revise the criteria
and standards as may be appropriate. The Act also requires the
Administrator to appoint an independent scientific review committee
composed of seven members, including at least one member of the
National Academy of Sciences, one physician, and one person
representing State air pollution control agencies, to review the air
quality criteria and NAAQS and to ``recommend to the Administrator any
new * * * standards and revisions of existing criteria and standards as
may be appropriate under section 108 and subsection (b) of this
section.'' CAA section 109(d)(2). This independent review function is
performed by the Clean Air Scientific Advisory Committee (CASAC) of
EPA's Science Advisory Board.

C. Related SO2 Control Programs

    States are primarily responsible for ensuring attainment and
maintenance of ambient air quality standards once EPA has established
them. Under section 110 of the Act, and related provisions, States are
to submit, for EPA approval, State implementation plans (SIPs) that
provide for the attainment and maintenance of such standards through
control programs directed to sources of the pollutants involved. The
States, in conjunction with EPA, also administer the prevention of
significant deterioration program that covers these pollutants. See CAA
sections 160-169. In addition, Federal programs provide for nationwide
reductions in emissions of these and other air pollutants through the
Federal motor vehicle and motor vehicle fuel control program under
title II of the Act (CAA sections 202-250) which involves controls for
emissions from all moving sources and controls for the fuels used by
these sources; new source performance standards under section 111; and
title IV of the Act (CAA sections 402-416), which specifically provides
for major reductions in SO2 emissions. EPA has also
promulgated the Clean Air Interstate Rule (CAIR) to require additional
SO2 emission reductions needed in the eastern half of the
United States to address emissions which contribute significantly to
nonattainment with, or interfere with maintenance of, the PM NAAQS by
downwind States in the CAIR region. This rule was remanded by the DC
Circuit, and although it remains in effect, EPA is reevaluating it
pursuant to the court remand.
    Currently, there are several areas designated as being in
nonattainment of the primary SO2 NAAQS (see section VI).
Moreover, as a result of this final rule, additional areas could be
classified as non-attainment. Certain States would then be required to
develop SIPs that identify and implement specific air pollution control
measures to reduce ambient SO2 concentrations to attain and
maintain the revised SO2 NAAQS, most likely by requiring air
pollution controls on sources that emit oxides of sulfur
(SOx).

D. History of Reviews of the Primary NAAQS for Sulfur Oxides

    On April 30, 1971, the EPA promulgated primary SO2 NAAQS
(36 FR 8187). These primary standards, which were based on the findings
outlined in the original 1969 Air Quality Criteria for Sulfur Oxides,
were set at 0.14 parts per million (ppm) averaged over a 24-hour
period, not to be exceeded more than once per year, and 0.030 ppm
annual arithmetic mean. In 1982, EPA published the Air Quality Criteria
for Particulate Matter and Sulfur Oxides (EPA, 1982) along with an
addendum of newly published controlled human exposure studies, which
updated the scientific criteria upon which the initial standards were
based (EPA, 1982). In 1986, EPA published a second addendum presenting
newly available evidence from epidemiologic and controlled human
exposure studies (EPA, 1986). In 1988, EPA published a proposed
decision not to revise the existing standards (53 FR 14926) (April 26,
1988). However, EPA specifically requested public comment on the
alternative of revising the current standards and adding a new 1-hour
primary standard of 0.4 ppm (400 ppb) to protect asthmatics against 5-
10 minute peak SO2 concentrations.
    As a result of public comments on the 1988 proposal and other post-
proposal developments, EPA published a second proposal on November 15,
1994 (59 FR 58958). The 1994 re-proposal was based in part on a
supplement to the second addendum of the criteria document, which
evaluated new findings on 5-10 minute SO2 exposures in
asthmatics (EPA, 1994a; EPA, 1994b). As in the 1988 proposal, EPA
proposed to retain the existing 24-hour and annual standards. EPA also
solicited comment on three regulatory alternatives to further reduce
the health risk posed by exposure to high 5-minute peaks of
SO2 if additional protection were judged to be necessary.
The three alternatives were: (1) Revising the existing primary
SO2 NAAQS by adding a new 5-minute standard of 0.6 ppm (600
ppb) SO2; (2) establishing a new regulatory program under
section 303 of the Act to supplement protection provided by the
existing NAAQS, with a trigger level of 0.6 ppm (600 ppb)
SO2, one expected exceedance; and (3) augmenting
implementation of existing standards by focusing on those sources or
source types likely to produce high 5-minute peak concentrations of
SO2.
    On May 22, 1996, EPA announced its final decision not to revise the
NAAQS for SOx (61 FR 25566). EPA found that asthmatics--a
susceptible population group--could be exposed to short-term
SO2 bursts resulting in repeated `exposure events' such that
tens or hundreds of thousands of asthmatics could be exposed annually
to lung function effects ``distinctly exceeding * * * [the] typical
daily variation in lung function'' that asthmatics routinely
experience, and found further that repeated occurrences should be
regarded as significant from a public health standpoint. 61 FR at
25572, 25573. Nonetheless, the agency concluded that ``the likelihood
that asthmatic individuals will be exposed * * * is very low when
viewed from a national perspective'', that ``5-minute peak
SO[2] levels do not pose a broad public health problem when
viewed from a national perspective'', and that ``short-term peak
concentrations of SO[2] do not constitute the type of
ubiquitous public health problem for which establishing a NAAQS would
be appropriate.'' Id. at 25575. EPA concluded, therefore, that it would
not revise the existing standards or add a standard to specifically
address 5-minute exposures. EPA also announced an intention to propose
guidance, under section 303 of the Act, to assist States in responding
to short-term peaks of SO2 and later initiated a rulemaking
to do so (62 FR 210 (Jan. 2, 1997).
    The American Lung Association and the Environmental Defense Fund
challenged EPA's decision not to establish a 5-minute standard. On
January 30, 1998, the Court of Appeals for the District of Columbia
Circuit found that EPA had failed to adequately explain its
determination that no revision to the SO2 NAAQS was
appropriate and remanded the determination back to EPA for further
explanation. American Lung Ass'n v. EPA, 134 F. 3d 388 (DC Cir. 1998).
Specifically, the court held that EPA had failed to adequately explain
the basis for its conclusion that short-term SO2 exposures
to asthmatics do not constitute a public health problem,

noting that the agency had failed to explain the link between its
finding that repeated short-term exposures were significant, and that
there would be tens to hundreds of thousands of such exposures annually
to a susceptible subpopulation. 134 F. 3d at 392. The court also
rejected the explanation that short-term SO2 bursts were
``localized, infrequent, and site-specific'' as a rational basis for
the conclusion that no public health problem existed for purposes of
section 109: ``[N]othing in the Final Decision explains why
`localized', `site-specific', or even `infrequent' events might
nevertheless create a public health problem, particularly since, in
some sense, all pollution is local and site-specific * * *''. Id. The
court accordingly remanded the case to EPA to adequately explain its
determination or otherwise take action in accordance with the opinion.
In response, EPA has collected and analyzed additional air quality data
focused on 5-minute concentrations of SO2. These air quality
analyses conducted since the last review helped inform the current
review, which (among other things) address the issues raised in the
court's remand of the Agency's last decision.
    EPA formally initiated the current review of the air quality
criteria for oxides of sulfur and the SO2 primary NAAQS on
May 15, 2006 (71 FR 28023) with a general call for information. EPA's
draft Integrated Review Plan for the Primary National Ambient Air
Quality Standards for Sulfur Dioxide (EPA, 2007a) was made available in
April 2007 for public comment and was discussed by the CASAC via a
publicly accessible teleconference on May 11, 2007. As noted in that
plan, SOX includes multiple gaseous (e.g., SO3)
and particulate (e.g., sulfate) species. Because the health effects
associated with particulate species of SOX have been
considered within the context of the health effects of ambient
particles in the Agency's review of the NAAQS for particulate matter
(PM), the current review of the primary SO2 NAAQS is focused
on the gaseous species of SOX and does not consider health
effects directly associated with particulate species.
    The first draft of the Integrated Science Assessment for Oxides of
Sulfur-Health Criteria (ISA) and the Sulfur Dioxide Health Assessment
Plan: Scope and Methods for Exposure and Risk Assessment (EPA, 2007b)
were reviewed by CASAC at a public meeting held on December 5-6, 2007.
Based on comments received from CASAC and from the public, EPA
developed the second draft of the ISA and the first draft of the Risk
and Exposure Assessment to Support the Review of the SO2
Primary National Ambient Air Quality Standard (Risk and Exposure
Assessment (REA)). These documents were reviewed by CASAC at a public
meeting held on July 30-31, 2008. Based on comments received from CASAC
and the public at this meeting, EPA released the final ISA in September
of 2008 (EPA, 2008a; henceforth referred to as ISA). In addition,
comments received were considered in developing the second draft of the
REA. Importantly, the second draft of the REA contained a draft staff
policy assessment that considered the evidence presented in the final
ISA and the air quality, exposure, and risk characterization results
presented in the second draft REA, as they related to the adequacy of
the current SO2 NAAQS and potential alternative primary
SO2 standards. This document was reviewed by CASAC at a
public meeting held on April 16-17, 2009. In preparing the final REA
report, which included the final staff policy assessment, EPA
considered comments received from CASAC and the public at and
subsequent to that meeting. The final REA containing the final staff
policy assessment was completed in August 2009 (EPA 2009a; henceforth
referred to as REA)).
    On December 8, 2009 EPA published its proposed revisions to the
primary SO2 NAAQS. 74 FR 64810 presented a number of
conclusions, findings, and determinations proposed by the
Administrator. EPA invited general, specific, and/or technical comments
on all issues involved with this proposal, including all such proposed
judgments, conclusions, findings, and determinations. EPA invited
specific comment on the level, or range of levels, appropriate for such
a standard, as well as on the rationale that would support that level
or range of levels. These comments were carefully considered by the
Administrator as she made her final decisions, as described in this
notice, on the primary SO2 NAAQS
    The schedule for completion of this review is governed by a
judicial order resolving a lawsuit filed in September 2005, concerning
the timing of the current review. Center for Biologic Diversity v.
Johnson (Civ. No. 05-1814) (D.D.C. 2007). The order that now governs
this review, entered by the court in August 2007 and amended in
December 2008, provides that the Administrator will sign, for
publication, a final rulemaking concerning the review of the primary
SO2 NAAQS no later than June 2, 2010.

E. Summary of Proposed Revisions to the SO2 Primary NAAQS

    For the reasons discussed in the preamble of the proposal for the
SO2 primary NAAQS, EPA proposed to make revisions to the
primary SO2 NAAQS (and to add SO2 data handling
conventions) so the standards provide requisite protection of public
health with an adequate margin of safety. Specifically, EPA proposed to
replace the current 24-hour and annual standards with a new short-term
SO2 standard. EPA proposed that this new short-term standard
would be based on the 3-year average of the 99th percentile (or 4th
highest) of the yearly distribution of 1-hour daily maximum
SO2 concentrations. EPA proposed to set the level of this
new 1-hour standard within the range of 50 to 100 ppb and solicited
comment on standard levels as high as 150 ppb. EPA also proposed to
establish requirements for an SO2 monitoring network at
locations where maximum SO2 concentrations are expected to
occur and to add a new Federal Reference Method (FRM) for measuring
SO2 in the ambient air. Finally, EPA proposed to make
corresponding changes to the Air Quality Index for SO2.

F. Organization and Approach to Final SO2 Primary NAAQS Decisions

    This action presents the Administrator's final decisions regarding
the need to revise the current SO2 primary NAAQS, and what
those revisions should be. Revisions to the primary NAAQS for
SO2, and the rationale supporting those revisions, are
described below in section II.
    An overview of the approach for monitoring and implementation is
presented in section III. Requirements for the SO2 ambient
monitoring network and for a new, additional FRM for measuring
SO2 in the ambient air are described in section IV. EPA's
current plans for designations and for implementing the revised
SO2 primary NAAQS are discussed in sections V and VI
respectively. Related requirements for data completeness, data
handling, data reporting, rounding conventions, and exceptional events
are described in section VII. Communication of public health
information through the AQI is discussed in section VIII. A recitation
of statutory authority and a discussion of those executive order
reviews which are relevant are provided in section IX.
    Today's final decisions are based on a thorough review in the ISA
of scientific information on known and potential human health effects
associated with exposure to SO2 in the

air. These final decisions also take into account: (1) Assessments in
the REA of the most policy-relevant information in the ISA as well as
quantitative exposure and risk analyses based on that information; (2)
CASAC Panel advice and recommendations, as reflected in its letters to
the Administrator and its public discussions of the ISA and REA; (3)
public comments received during the development of the ISA and REA; and
(4) public comments received on EPA's notice of proposed rulemaking.

II. Rationale for Decisions on the Primary Standards

    This section presents the rationale for the Administrator's
decision to revise the existing SO2 primary standards by
replacing the current 24-hour and annual standards with a new 1-hour
SO2 standard at a level of 75 ppb, based on the 3-year
average of the annual 99th percentile of 1-hour daily maximum
concentrations. As discussed more fully below, this rationale takes
into account: (1) Judgments and conclusions presented in the ISA and
the REA; (2) CASAC advice and recommendations as reflected in the CASAC
panel's discussions of drafts of the ISA and REA at public meetings, in
separate written comments, and in letters to the Administrator
(Henderson 2008a; Henderson 2008b; Samet, 2009); (3) public comments
received at CASAC meetings during the development of the ISA and the
REA; and (4) public comments received on the notice of proposed
rulemaking.
    In reaching this decision, EPA has drawn upon an integrative
synthesis of the entire body of evidence on human health effects
associated with the presence of SO2 in the ambient air, and
upon the results of the quantitative exposure and risk assessments
reflecting this evidence. As discussed below, this body of evidence
addresses a broad range of health endpoints associated with exposure to
SO2 in the ambient air. In considering this entire body of
evidence, EPA chose to focus most on those health endpoints for which
the ISA found the strongest evidence of an association with
SO2 (see section II.B below). Thus, the rationale for this
final decision on the SO2 NAAQS focused primarily on
respiratory morbidity following short-term (5-minutes to 24-hours)
exposure to SO2, for which the ISA found a causal
relationship.
    As discussed below, a substantial amount of new research has been
conducted since EPA's last review of the SO2 NAAQS, with
important new information coming from epidemiologic studies in
particular. In addition to the substantial amount of new epidemiologic
research, the ISA considered a limited number of new controlled human
exposure studies and re-evaluated key older controlled human exposure
studies. In evaluating both the new and key older controlled human
exposure studies, the ISA utilized updated guidelines published by the
American Thoracic Society (ATS) on what constitutes an adverse effect
of air pollution (see ISA, section 3.1.3; p. 3-4). Importantly, all
controlled human exposure and epidemiologic studies evaluated in the
ISA have undergone intensive scrutiny through multiple layers of peer
review and opportunities for public review and comment. Thus, the
review of this information has been extensive and deliberate.
    After a background discussion of the principal emitting sources and
current patterns of SO2 air quality and a description of the
current SO2 monitoring network from which those air quality
patterns are obtained (section II.A), the remainder of this section
discusses the Administrator's rationale for her final decisions on the
primary standards. Section II.B includes an overview of the scientific
evidence related to the respiratory effects associated with ambient
SO2 exposure. This overview includes a discussion of the at-
risk populations considered in the ISA. Section II.C summarizes the key
approaches taken by EPA to assess exposures and health risks associated
with exposure to ambient SO2. Section II.D summarizes the
approach that was used in the current review of the SO2
NAAQS with regard to consideration of the scientific evidence and the
air quality, exposure, and risk-based results related to the adequacy
of the current standards and potential alternative standards. Sections
II.E and II.F discuss, respectively, the Administrator's decisions
regarding the adequacy of the current standards and the elements of a
new short-term standard, taking into consideration public comments on
the proposed decisions. Section II.G summarizes the Administrator's
decisions with regard to the SO2 primary NAAQS.

A. Characterization of SO2 Air Quality

1. Anthropogenic Sources and Current Patterns of SO2 Air
Quality
    Anthropogenic SO2 emissions originate chiefly from point
sources, with fossil fuel combustion at electric utilities (~66%) and
other industrial facilities (~29%) accounting for the majority of total
emissions (ISA, section 2.1). Other anthropogenic sources of
SO2 include both the extraction of metal from ore as well as
the burning of high sulfur-containing fuels by locomotives, large
ships, and equipment utilizing diesel engines. SO2 emissions
and ambient concentrations follow a strong east to west gradient due to
the large numbers of coal-fired electric generating units in the Ohio
River Valley and upper Southeast regions. In the 12 Consolidated
Metropolitan Statistical Areas (CMSAs) that had at least four
SO2 regulatory monitors from 2003-2005, 24-hour average
concentrations in the continental U.S. ranged from a reported low of ~1
ppb in Riverside, CA and San Francisco, CA to a high of ~12 ppb in
Pittsburgh, PA and Steubenville, OH (ISA, section 2.5.1). In addition,
outside or inside all CMSAs from 2003-2005, the annual average
SO2 concentration was 4 ppb (ISA, Table 2-8). However,
spikes in hourly concentrations occurred. The mean 1-hour maximum
concentration outside or inside CMSAs was 13 ppb, with a maximum value
of greater than 600 ppb outside CMSAs and greater than 700 ppb inside
CMSAs (ISA, Table 2-8).
    Temporal and spatial patterns of 5-minute peaks of SO2
are also important given that controlled human exposure studies have
demonstrated that exposure to these peaks can result in adverse
respiratory effects in exercising asthmatics (see section II.B below).
For those monitors which voluntarily reported 5-minute block average
data,\3\ when maximum 5-minute concentrations were reported, the
absolute highest concentration over the ten-year period exceeded 4000
ppb, but for all individual monitors, the 99th percentile was below 200
ppb (ISA, section 2.5.2 Table 2-10). Median concentrations from these
monitors reporting 5-minute data ranged from 1 ppb to 8 ppb, and the
average for each maximum 5-minute level ranged from 3 ppb to 17 ppb.
Delaware, Pennsylvania, Louisiana, and West Virginia had mean values
for maximum 5-minute data exceeding 10 ppb. Among aggregated within-
State data for the 16 monitors from which all 5-minute average
intervals were reported, the median values ranged from 1 ppb to 5 ppb,
and the means ranged from 3 ppb to 11 ppb (ISA, section 2.5.2 at 2-43).
The highest reported concentration was 921 ppb, but the 99th percentile
values

for aggregated within-State data were all below 90 ppb (id).
---------------------------------------------------------------------------

    \3\ A small number of sites, 98 total from 1997 to 2007 of the
approximately 500 SO2 monitors, and not the same sites in
all years, voluntarily reported 5-minute block average data to AQS
(ISA, section 2.5.2). Of these, 16 reported all twelve 5-minute
averages in each hour for at least part of the time between 1997 and
2007. The remainder reported only the maximum 5-minute average in
each hour.
---------------------------------------------------------------------------

2. SO2 Monitoring
    Although EPA established the SO2 standards in 1971,
uniform minimum monitoring network requirements for SO2
monitoring were only adopted in May 1979. From the time of the
implementation of the 1979 monitoring rule through 2008, the
SO2 monitoring network has steadily decreased in size from
approximately 1496 sites in 1980 to the approximately 488 sites
operating in 2008. At present, except for SO2 monitoring
required at National Core Monitoring Stations (NCore stations), there
are no minimum monitoring requirements for SO2 in 40 CFR
part 58 Appendix D, other than a requirement for EPA Regional
Administrator approval before removing any existing monitors and a
requirement that any ongoing SO2 monitoring must have at
least one monitor sited to measure the maximum concentration of
SO2 in that area. EPA removed the specific minimum
monitoring requirements for SO2 in the 2006 monitoring rule
revisions, except for monitoring at NCore stations, based on the fact
that there were no SO2 nonattainment areas at that time,
coupled with trends showing an increasing gap between national average
SO2 concentrations and the current 24-hour and annual
standards. The rule was also intended to provide State, local, and
Tribal air monitoring agencies flexibility in meeting perceived higher
priority monitoring needs for other pollutants, or to implement the new
multi-pollutant sites (NCore network) required by the 2006 rule
revisions (71 FR 61236, (October 6, 2006)). More information on
SO2 monitoring can be found in section IV.

B. Health Effects Information

    The ISA concluded that there was sufficient evidence to infer a
``causal relationship'' between respiratory morbidity and short-term
(5-minutes to 24-hours) exposure to SO2 (ISA, section 5.2).
Importantly, we note that a ``causal relationship'' is the strongest
finding the ISA can make.\4\ This conclusion was based on the
consistency, coherence, and plausibility of findings observed in
controlled human exposure studies of 5-10 minutes, epidemiologic
studies mostly using 1-hour daily maximum and 24-hour average
SO2 concentrations, and animal toxicological studies using
exposures of minutes to hours (ISA, section 5.2). This evidence is
briefly summarized below and discussed in more detail in the proposal
(see sections II.B.1 to II.B.5, see 74 FR at 64815-821). We also note
that the ISA judged evidence of an association between SO2
exposure and other health categories to be less convincing; other
associations were judged to be suggestive but not sufficient to infer a
causal relationship (i.e., short-term exposure to SO2 and
mortality) or inadequate to infer the presence or absence of a causal
relationship (i.e., short-term exposure to SO2 and
cardiovascular morbidity, and long-term exposure to SO2 and
respiratory morbidity, other morbidity, and mortality). Key conclusions
from the ISA are described in greater detail in Table 5-3 of the ISA.
---------------------------------------------------------------------------

    \4\ A causal relationship is based on ``[e]vidence [that] is
sufficient to conclude that there is a causal relationship between
relevant pollutant exposures and the health outcome. That is, a
positive association has been observed between the pollutant and the
outcome in studies in which chance, bias, and confounding could be
ruled out with reasonable confidence. Evidence includes, for
example, controlled human exposure studies; or observational studies
that cannot be explain by plausible alternatives or are supported by
other lines of evidence (e.g. animal studies or mechanism of action
information). Evidence includes replicated and consistent high-
quality studies by multiple investigators.'' ISA Table 1-2, at 1-11.
---------------------------------------------------------------------------

1. Short-Term (5-minute to 24-hour) SO2 Exposure and
Respiratory Morbidity Effects
    The ISA examined numerous controlled human exposure studies and
found that moderate or greater decrements in lung function (i.e.,
[gteqt] 15% decline in Forced Expiratory Volume (FEV1) and/
or [gteqt] 100% increase in specific airway resistance (sRaw)) occur in
some exercising asthmatics exposed to SO2 concentrations as
low as 200-300 ppb for 5-10 minutes. The ISA also found that among
asthmatics, both the percentage of individuals affected, and the
severity of the response increased with increasing SO2
concentrations. That is, at 5-10 minute concentrations ranging from
200-300 ppb, the lowest levels tested in free breathing chamber
studies, approximately 5-30% percent of exercising asthmatics
experienced moderate or greater decrements in lung function (ISA, Table
3-1). At concentrations of 400-600 ppb, moderate or greater decrements
in lung function occurred in approximately 20-60% of exercising
asthmatics, and compared to exposures at 200-300 ppb, a larger
percentage of asthmatics experienced severe decrements in lung function
(i.e., [gteqt] 20% decrease in FEV1 and/or [gteqt] 200%
increase in sRaw; ISA, Table 3-1). Moreover, at SO2
concentrations [gteqt] 400 ppb (5-10 minute exposures), moderate or
greater decrements in lung function were often statistically
significant at the group mean level and frequently accompanied by
respiratory symptoms. Id.
    The ISA also found that in locations meeting the current
SO2 NAAQS, numerous epidemiologic studies reported positive
associations between ambient SO2 concentrations and
respiratory symptoms in children, as well as emergency department
visits and hospitalizations for all respiratory causes and asthma
across multiple age groups. Moreover, the ISA concluded that these
epidemiologic studies were consistent and coherent. This evidence was
consistent in that associations were reported in studies conducted in
numerous locations and with a variety of methodological approaches
(ISA, section 5.2; p. 5-5). It was coherent in that respiratory symptom
results from epidemiologic studies of short-term (predominantly 1-hour
daily maximum or 24-hour average) SO2 concentrations were
generally in agreement with respiratory symptom results from controlled
human exposure studies of 5-10 minutes. These results were also
coherent in that the respiratory effects observed in controlled human
exposure studies of 5-10 minutes further provided a basis for a
progression of respiratory morbidity that could lead to the increased
emergency department visits and hospital admissions observed in
epidemiologic studies (ISA, section 5.2; p. 5-5). In addition, the ISA
found that when evaluated as a whole, SO2 effect estimates
in multi-pollutant models generally remained positive and relatively
unchanged when co-pollutants were included. Therefore, although
recognizing the uncertainties associated with separating the effects of
SO2 from those of co-occurring pollutants, the ISA concluded
that ``the limited available evidence indicates that the effect of
SO2 on respiratory health outcomes appears to be generally
robust and independent of the effects of gaseous co-pollutants,
including NO2 and O3, as well as particulate co-
pollutants, particularly PM2.5'' (ISA, section 5.3; p. 5-9).
    The ISA also found that the respiratory effects of SO2
were consistent with the mode of action as it is currently understood
from animal toxicological and controlled human exposure studies (ISA,
section 5.2; p. 5-2). The immediate effect of SO2 on the
respiratory system is bronchoconstriction. This response is mediated by
chemosensitive receptors in the tracheobronchial tree. Activation of
these receptors triggers central nervous system reflexes that result in

bronchoconstriction and respiratory symptoms that are often followed by
rapid shallow breathing (id). The ISA noted that asthmatics are likely
more sensitive to the respiratory effects of SO2 due to pre-
existing inflammation associated with the disease. For example, pre-
existing inflammation may lead to enhanced release of inflammatory
mediators, and/or enhanced sensitization of the chemosensitive
receptors (id).
    Taken together, the ISA concluded that the controlled human
exposure, epidemiologic, and toxicological evidence supported its
determination of a causal relationship between respiratory morbidity
and short-term (5-minutes to 24-hours) exposure to SO2.
a. Adversity of Short-Term Respiratory Morbidity Effects
    As discussed more fully in the proposal (section II.B.1.c, 74 FR at
64817) and in section II.E.2.b below, based on: (1) American Thoracic
Society (ATS) guidelines; (2) advice and recommendations from CASAC
(see specific consensus CASAC comments in sections II.E.2.b and
II.F.4.b below); and (3) conclusions from previous NAAQS reviews, EPA
found that 5-10 minute exposures to SO2 concentrations at
least as low as 200 ppb can result in adverse health effects in some
asthmatics (i.e., 5-30% of the tested individuals in controlled human
exposure studies of 200-300 ppb). As just mentioned, at SO2
concentrations >= 400 ppb, controlled human exposure studies have
reported decrements in lung function that are often statistically
significant at the group mean level, and that are frequently
accompanied by respiratory symptoms. Being mindful that the ATS
guidelines specifically indicate decrements in lung function with
accompanying respiratory symptoms as being adverse (see proposal
section II.B.1.c, 74 FR at 64817 and section II.E.2.b below), exposure
to 5-10 minute SO2 concentrations >= 400 ppb can result in
health effects that are clearly adverse.
    The ATS also indicated that exposure to air pollution that
increases the risk of an adverse effect to a population is adverse,
even though it may not increase the risk of any individual to an
unacceptable level (ATS 2000; see proposal section II.B.1.c, 74 FR at
64817). As an example, ATS states:

    A population of children with asthma could have a distribution
of lung function such that no individual child has a level
associated with significant impairment. Exposure to air pollution
could shift the distribution toward lower levels without bringing
any individual child to a level that is associated with clinically
relevant consequences. Individuals within the population would,
however, have diminished reserve function and are at potentially
increased risk if affected by another agent, e.g., a viral
infection. Assuming that the relationship between the risk factor
and the disease is causal, the committee considered that such a
shift in the risk factor distribution, and hence the risk profile of
the exposed population, should be considered adverse, even in the
absence of the immediate occurrence of frank illness (ATS 2000, p.
668).

    As mentioned above, the ISA reported that exposure to
SO2 concentrations as low as 200-300 ppb for 5-10 minutes
results in approximately 5-30% of exercising asthmatics experiencing
moderate or greater decrements in lung function (defined in terms of a
>= 15% decline in FEV1 or 100% increase in sRaw; ISA, Table
3-1). Even though these results were not statistically significant at
the group mean level, in light of EPA's interpretation of how to apply
the ATS guidelines for defining an adverse effect, as described above,
the REA found that these results could reasonably indicate an
SO2-induced shift in these lung function measurements for
this subset of the population. As a result, an appreciable percentage
of exercising asthmatics exposed to SO2 concentrations as
low as 200 ppb would be expected to have diminished reserve lung
function and would be expected to be at greater risk if affected by
another respiratory agent, for example, viral infection. Importantly,
as explained immediately above, diminished reserve lung function in a
population that is attributable to air pollution is considered an
adverse effect under ATS guidance. In addition to the 2000 ATS
guidelines, the REA was also mindful of previous CASAC recommendations
(Henderson 2006) and NAAQS review conclusions (EPA 2006, EPA 2007d)
indicating that moderate decrements in lung function can be clinically
significant in some asthmatics (discussed in detail below, see section
II.E.2.b). The REA further considered that subjects participating in
these controlled human exposure studies do not include severe
asthmatics and that it was reasonable to presume that persons with more
severe asthma than the study participants would have a more serious
health effect from short-term exposure to 200 ppb SO2.\5\
Taken together, the REA concluded that exposure to SO2
concentrations at least as low as 200 ppb can result in adverse health
effects in asthmatics and that this conclusion was in agreement with
consensus CASAC comments and recommendations expressed during the
current SO2 NAAQS review (see sections II.E.2.b and II.F.4.b
below).
---------------------------------------------------------------------------

    \5\ We also note that very young children were not included in
the controlled human exposure studies and this absence of data on
what is likely to be a sensitive life stage is a source of
uncertainty for children's susceptibility to SO2.
---------------------------------------------------------------------------

    In addition to the controlled human exposure evidence,
epidemiologic studies also indicate that adverse respiratory morbidity
effects are associated with SO2 (REA, section 4.3). As
mentioned above, in reaching the conclusion of a causal relationship
between respiratory morbidity and short-term SO2 exposure,
the ISA generally found positive associations between ambient
SO2 concentrations and emergency department visits and
hospitalizations for all respiratory causes and asthma. Notably,
emergency department visits, hospitalizations, episodic respiratory
illness, and aggravation of respiratory diseases (e.g. asthma)
attributable to air pollution are considered adverse health effects
under ATS guidelines.
2. Health Effects and Long-Term Exposures to SO2
    There were numerous studies published since the last review
examining possible associations between long-term SO2
exposure and mortality and morbidity (respiratory morbidity,
carcinogenesis, adverse prenatal and neonatal outcomes) endpoints.
However, the ISA concluded that the evidence relating long-term (weeks
to years) SO2 exposure to adverse health effects was
``inadequate to infer the presence or absence of a causal
relationship'' (ISA, Table 5-3). That is, the ISA found the long-term
health evidence to be of insufficient quantity, quality, consistency,
or statistical power to make a determination as to whether
SO2 was truly associated with these health outcomes (ISA,
Table 1-2).
3. SO2-Related Impacts on Public Health
    Interindividual variation in human responses to air pollutants
indicates that some populations are at increased risk for the
detrimental effects of ambient exposure to SO2. The NAAQS
are intended to provide an adequate margin of safety for both the
general population and susceptible populations that are potentially at
increased risk for health effects in response to exposure to ambient
air pollution (see footnote 1 above). To facilitate the identification
of populations at increased risk for SO2-related health
effects, studies have identified factors that contribute to the
susceptibility of individuals to SO2. Susceptible
individuals are broadly defined as those with a greater

likelihood of an adverse outcome given a specific exposure in
comparison with the general population (American Lung Association,
2001). The susceptibility of an individual to SO2 can
encompass a multitude of factors which represent normal developmental
phases or life stages (e.g., age) or biologic attributes (e.g.,
gender); however, other factors (e.g., socioeconomic status (SES)) may
influence the manifestation of disease and also increase an
individual's susceptibility (American Lung Association, 2001). In
addition, populations may be at increased risk to SO2 due to
an increase in their exposure during certain life stages (e.g.,
childhood or old age) or as a result of external factors (e.g., SES)
that contribute to an individual being disproportionately exposed to
higher concentrations than the general population.\6\ It should be
noted that in some cases specific populations may be affected by
multiple susceptibility factors. For example, a population that is
characterized as having low SES may have less access to healthcare
resulting in the manifestation of a disease, which increases their
susceptibility to SO2, while they may also reside in a
location that results in disproportionately high exposure to
SO2.
---------------------------------------------------------------------------

    \6\ This aspect of susceptibility is referred to as
vulnerability in the proposal and in the ISA.
---------------------------------------------------------------------------

    To examine whether SO2 differentially affects certain
populations, stratified analyses are often conducted in epidemiologic
investigations to identify the presence or absence of effect
modification. A thorough evaluation of potential effect modifiers may
help identify susceptible populations that are at increased risk to
SO2 exposure. These analyses are based on the proper
identification of confounders and subsequent adjustment for them in
statistical models, which helps separate a spurious from a true causal
association. Although the design of toxicological and human clinical
studies does not allow for an extensive examination of effect
modifiers, the use of animal models of disease and the study of
individuals with underlying disease or genetic polymorphisms do allow
for comparisons between subgroups. Therefore, the results from these
studies, combined with those results obtained through stratified
analyses in epidemiologic studies, contribute to the overall weight of
evidence for the increased susceptibility of specific populations to
SO2. Those populations identified in the ISA to be
potentially at greater risk of experiencing an adverse health effect
from SO2 were described in detail in the proposal (section
II.B.5) and include: (1) Those with pre-existing respiratory disease;
(2) children and older adults; (3) persons who spend increased time
outdoors or at elevated ventilation rates; (4) persons with lower SES;
and (5) persons with certain genetic factors.
    As discussed in the proposal (section II.B.5.g, 74 FR at 64821),
large proportions of the U.S. population are likely to be at increased
risk of experiencing SO2-related health effects. In the
United States, approximately 7% of adults and 9% of children have been
diagnosed with asthma. Notably, the prevalence and severity of asthma
is higher among certain ethnic or racial groups such as Puerto Ricans,
American Indians, Alaskan Natives, and African Americans (EPA 2008b).
Furthermore, a higher prevalence of asthma among persons of lower SES
and an excess burden of asthma hospitalizations and mortality in
minority and inner-city communities have been observed (EPA, 2008b). In
addition, population groups based on age comprise substantial segments
of individuals that may be potentially at risk for SO2-
related health impacts. Based on U.S. census data from 2000, about 72.3
million (26%) of the U.S. population are under 18 years of age, 18.3
million (7.4%) are under 5 years of age, and 35 million (12%) are 65
years of age or older. There is also concern for the large segment of
the population that is potentially at risk to SO2-related
health effects because of increased time spent outdoors at elevated
ventilation rates (those who work or play outdoors). Overall, the
considerable size of the population groups at risk indicates that
exposure to ambient SO2 could have a significant impact on
public health in the United States.

C. Human Exposure and Health Risk Characterization

    To put judgments about SO2-associated health effects
into a broader public health context, EPA has drawn upon the results of
the quantitative exposure and risk assessments. Judgments reflecting
the nature of the evidence and the overall weight of the evidence are
taken into consideration in these quantitative exposure and risk
assessments. These assessments include estimates of the likelihood that
asthmatic children at moderate or greater exertion (e.g. while
exercising) in St. Louis or Greene County, Missouri would experience
SO2 exposures of potential concern. In addition, these
analyses include an estimate of the number and percent of exposed
asthmatic children in these locations likely to experience
SO2-induced lung function responses (i.e., moderate or
greater decrements in lung function defined in terms of sRaw or
FEV1) under varying air quality scenarios (i.e., current air
quality and air quality simulated to just meet the current or potential
alternative standards). These assessments also characterize the kind
and degree of uncertainties inherent in such estimates.
    As previously mentioned, the ISA concluded that the evidence for an
association between respiratory morbidity and short-term SO2
exposure was ``sufficient to infer a causal relationship'' (ISA,
section 5.2) and that the ``definitive evidence'' for this conclusion
was from the results of 5-10 minute controlled human exposure studies
demonstrating decrements in lung function and/or respiratory symptoms
in exercising asthmatics (ISA, section 5.2). Accordingly, the air
quality and exposure analyses and their associated risk
characterizations focused on 5-minute concentrations of SO2
in excess of potential health effect benchmark values derived from the
controlled human exposure literature (see proposal section II.C.1, 74
FR at 64821, and REA, section 6.2). These benchmark levels are not
potential standards, but rather are SO2 exposure
concentrations which represent ``exposures of potential concern'' which
are used in these analyses to estimate potential exposures and risks
associated with 5-minute concentrations of SO2. The REA
considered 5-minute benchmark levels of 100, 200, 300, and 400 ppb in
these analyses, but especially noted exceedances or exposures with
respect to the 200 and 400 ppb 5-minute benchmark levels. These
benchmark levels were highlighted because (1) 400 ppb represents the
lowest concentration in free-breathing controlled human exposure
studies where moderate or greater lung function decrements occurred
which were often statistically significant at the group mean level and
were frequently accompanied by respiratory symptoms; and (2) 200 ppb is
the lowest level at which moderate or greater decrements in lung
function in free-breathing controlled human exposure studies were found
in some individuals, although these lung function changes were not
statistically significant at the group mean level. Notably, 200 ppb is
also the lowest level that has been tested in free-breathing controlled
human exposure studies (REA, section 4.2.2).\7\
---------------------------------------------------------------------------

    \7\ The ISA cites one chamber study with intermittent exercise
where healthy and asthmatic children were exposed to 100 ppb
SO2 in a mixture with ozone and sulfuric acid. The ISA
notes that compared to exposure to filtered air, exposure to the
pollutant mix did not result in statistically significant changes in
lung function or respiratory symptoms (ISA, section <IP_ADDRESS>).

---------------------------------------------------------------------------

    The REA utilized three approaches to characterize health risks. In
the first approach, for each air quality scenario, statistically
estimated 5-minute SO2 concentrations \8\ and measured
ambient 5-minute SO2 concentrations were compared to the 5-
minute potential health effect benchmark levels discussed above (REA,
chapter 7). This air quality analysis included all available ambient
monitoring data as well as a more detailed analysis in 40 counties. The
air quality analysis was considered a broad characterization of
national air quality and human exposures that might be associated with
these 5-minute SO2 concentrations. An advantage of the air
quality analysis is its relative simplicity; however, there is
uncertainty associated with the assumption that SO2 air
quality can serve as an adequate surrogate for total exposure to
ambient SO2. Actual exposures might be influenced by factors
not considered by this approach, including small-scale spatial
variability in ambient SO2 concentrations (which might not
be represented by the current fixed-site ambient monitoring network)
and spatial/temporal variability in human activity patterns. A more
detailed overview of the air quality analysis and its associated
limitations and uncertainties is provided in the proposal (see sections
II.C.2, 74 FR at 64822 and II.C.3, 74 FR at 64823, respectively) and
the air quality analysis is thoroughly described in the REA (chapter
7).
---------------------------------------------------------------------------

    \8\ Benchmark values derived from the controlled human exposure
literature were associated with a 5-minute averaging time. However,
as noted in footnote 3 above, only 98 ambient monitors located in 13
States from 1997-2007 reported measured 5-minute SO2
concentrations since such monitoring is not required (see section
II.A.2 and section IV). In contrast, 809 monitors in 48 States, DC,
Puerto Rico, and the Virgin Islands reported 1-hour SO2
concentrations over a similar time period. Therefore, to broaden
analyses to areas where measured 5-minute SO2
concentrations were not available, the REA utilized a statistical
relationship to estimate the highest 5-minute level in an hour,
given a reported 1-hour average SO2 concentration (REA,
section 6.4). Then, similar to measured 5-minute SO2
concentrations, statistically estimated 5-minute SO2
concentrations were compared to 5-minute potential health effect
benchmark values (REA, chapters 7 and 8, respectively).
---------------------------------------------------------------------------

    In the second approach, an inhalation exposure model was used to
generate more realistic estimates of personal exposures in asthmatics
(REA, chapter 8). This analysis estimated temporally and spatially
variable microenvironmental 5-minute SO2 concentrations and
simulated asthmatics' contact with these pollutant concentrations while
at moderate or greater exertion (i.e., while at elevated ventilation
rates). The approach was designed to estimate exposures that are not
necessarily represented by the existing ambient monitoring data and to
better represent the physiological conditions corresponding with the
respiratory effects reported in controlled human exposure studies.
AERMOD, an EPA dispersion model, was used to estimate 1-hour ambient
SO2 concentrations using emissions estimates from
stationary, non-point, and where applicable, port sources. The Air
Pollutants Exposure (APEX) model, an EPA human exposure model, was then
used to estimate population exposures using the estimated hourly census
block level SO2 concentrations. From the 1-hour census block
concentrations, 5-minute maximum SO2 concentrations within
each hour were estimated by APEX (REA, section 8.7.1) using the
statistical relationship mentioned above in footnote 8. Estimated
exposures to 5-minute SO2 levels were then compared to the
5-minute potential health effect benchmark levels discussed above. This
approach to assessing exposures was more resource intensive than using
ambient levels as an indicator of exposure; therefore, the final REA
included the analysis of two locations: St. Louis and Greene County,
MO. Although the geographic scope of this analysis was limited, the
approach provided estimates of SO2 exposures in asthmatics
and asthmatic children in St. Louis and Greene Counties, and thus
served to complement the broader air quality characterization. A more
detailed overview of this exposure analysis and its associated
limitations and uncertainties is provided in the proposal (see sections
II.C.2, 74 FR at 64822 and II.C.3, 74 FR at 64823, respectively) and
the exposure analysis is thoroughly described in the REA (chapter 8).
    The third approach was a quantitative risk assessment. This
approach combined results from the exposure analysis (i.e., the number
of exposed total asthmatics or asthmatic children while at moderate or
greater exertion) with exposure-response functions derived from
individual level data from controlled human exposure studies (see ISA,
Table 3-1 and Johns (2009) \9\) to estimate the percentage and number
of exposed asthmatics and asthmatic children in St. Louis and Greene
County likely to experience a moderate or greater lung function
response (i.e., decrements in lung function defined in terms of
FEV1 and sRaw) under the air quality scenarios mentioned
above (REA, chapter 9). A more detailed overview of this analysis and
its associated limitations and uncertainties is provided in the
proposal (see sections II.C.2, 74 FR at 64822 and II.C.3, 74 FR at
64823, respectively) and the quantitative risk analysis is thoroughly
described in the REA (chapter 9).
---------------------------------------------------------------------------

    \9\ EPA recently conducted a complete quality assurance review
of all individual subject data. The results of this review did not
substantively change any of the entries in ISA, Table 3-1, and did
not in any way affect the conclusions of the ISA (see Johns and
Simmons, 2009).
---------------------------------------------------------------------------

    Notably, for the reasons described in the REA (REA, section 10.3.3)
and the proposal (see section II.E.1.b, 74 FR at 64827), when
considering the St. Louis and Greene County exposure and risk results
as they relate to the adequacy of the current standards, the REA
concluded that the St. Louis results were more informative in terms of
ascertaining the extent to which the current standards protect against
health effects linked to the various benchmarks (linked in turn to 5-
minute SO2 exposures). The results in fact suggested that
the current standards may not adequately protect public health (REA,
section 10.3.3, p. 364). Moreover, the REA judged that the exposure and
risk estimates for the St. Louis study area provided useful insights
into exposures and risks for other urban areas in the U.S. with similar
population and SO2 emissions densities (id.). For similar
reasons, the St. Louis results were more informative for ascertaining
the adequacy of the potential alternative standards under
consideration.
    Key results of the air quality, exposure, and risk analyses were
presented in the policy assessment chapter of the REA (chapter 10) and
summarized in the proposal (see Tables 2-4 in the preamble to the
proposed rule). In considering these results, the proposal noted that
these analyses support that 5-minute SO2 exposures,
reasonably judged important from a public health perspective, were
associated with air quality adjusted upward to simulate just meeting
the current standards (see proposal, section II.E.1.c, 74 FR at 64828).
Moreover, these results indicated that 99th percentile 1-hour daily
maximum standard levels in the range of 50-100 ppb could substantially
limit exposures of asthmatic children at moderate or greater exertion
from 5-minute SO2 concentrations >=400 ppb, and appreciably
limit exposures of these children from 5-minute SO2
concentrations >=200 ppb (REA, p. 392-393). Results of these analyses
also indicated that a 1-hour standard at 150

ppb could still substantially limit exposures of asthmatic children at
moderate or greater exertion from 5-minute SO2
concentrations >=400 ppb, but would provide these children appreciably
less protection from exposure to 5-minute SO2 concentrations
>=200 ppb (REA, p. 395-396).

D. Approach for Determining Whether To Retain or Revise the Current
Standards

    EPA notes that the final decision on retaining or revising the
current primary SO2 standards is a public health policy
judgment to be made by the Administrator. This judgment has been
informed by a recognition that the available health effects evidence
reflects a continuum consisting of ambient levels of SO2 at
which scientists generally agree that health effects are likely to
occur, through lower levels at which the likelihood and magnitude of
the response become increasingly uncertain. The Administrator's final
decisions draw upon scientific information and analyses related to
health effects, population exposures and risks; judgments about the
appropriate response to the range of uncertainties that are inherent in
the scientific evidence and analyses; and comments received from CASAC
and the public.
    To evaluate whether the current primary SO2 standards
are adequate or whether revisions are appropriate, EPA has used an
approach in this review described in chapter 10 of the REA which builds
upon the approaches used in reviews of other criteria pollutants,
including the most recent reviews of the NO2, Pb,
O3, and PM NAAQS (EPA, 2008c; EPA, 2007c; EPA, 2007d; EPA,
2005), and reflects the latest body of evidence and information that is
currently available, as reflected by the ISA. As in other recent
reviews, EPA considered the implications of placing more or less weight
or emphasis on different aspects of the scientific evidence and the
exposure-/risk-based information, recognizing that the weight to be
given to various elements of the evidence and exposure/risk information
is part of the public health policy judgments that the Administrator
will make in reaching decisions on the standard.
    A series of general questions framed this approach to considering
the scientific evidence and exposure-/risk-based information. First,
EPA's consideration of the scientific evidence and exposure/risk
information with regard to the adequacy of the current standards has
been framed by the following questions:

     To what extent does evidence that has become available
since the last review reinforce or call into question evidence for
SO2-associated effects that were identified in the last
review?
     To what extent has evidence for different health
effects and/or susceptible populations become available since the
last review?
     To what extent have uncertainties identified in the
last review been reduced and/or have new uncertainties emerged?
     To what extent does evidence and exposure-/risk-based
information that has become available since the last review
reinforce or call into question any of the basic elements
(indicator, averaging time, form, and level) of the current
standard?

    To the extent that the available evidence and exposure-/risk-based
information suggests it may be appropriate to consider revision of the
current standards, EPA considers that evidence and information with
regard to its support for consideration of a standard that is either
more or less stringent than the current standards. This evaluation is
framed by the following questions:

     Is there evidence that associations, especially causal
or likely causal associations, extend to ambient SO2
concentrations as low as, or lower than, the concentrations that
have previously been associated with health effects? If so, what are
the important uncertainties associated with that evidence?
     Are exposures above benchmark levels and/or health
risks estimated to occur in areas that meet the current standard? If
so, are the estimated exposures and health risks important from a
public health perspective? What are the important uncertainties
associated with the estimated risks?

    To the extent that there is support for consideration of a revised
standard, EPA then considers the specific elements of the standard
(indicator, averaging time, form, and level) within the context of the
currently available information. In so doing, the Agency addresses the
following questions regarding the elements of the standard:

     Does the evidence provide support for considering a
different indicator for gaseous SOX?
     Does the evidence provide support for considering
different, or additional averaging times?
     What ranges of levels and forms of alternative
standards are supported by the evidence, and what are the associated
uncertainties and limitations?
     To what extent do specific averaging times, levels, and
forms of alternative standards reduce the estimated exposures above
benchmark levels and risks attributable to exposure to ambient
SO2, and what are the uncertainties associated with the
estimated exposure and risk reductions?

    The questions outlined above have been addressed in the REA. The
following sections present considerations regarding the adequacy of the
current standards and conclusions on the elements of a new short-term
standard in terms of indicator, averaging time, form, and level.

E. Adequacy of the Current Standards

    This section discusses considerations related to the decision as to
whether the current 24-hour and annual SO2 primary NAAQS are
requisite to protect public health with an adequate margin of safety.
Specifically, section II.E.1 provides an overview of the rationale
supporting the Administrator's proposal that the current standards do
not provide adequate public health protection; section II.E.2 discusses
public comments received on the adequacy of the current standards; and
section II.E.3 discusses the Administrator's final decision on whether
the current SO2 primary NAAQS is requisite to protect public
health with an adequate margin of safety, as required by sections
109(d) and (b) of the Act.
1. Rationale for Proposed Decision
    In the proposal, the Administrator initially concluded that the
current 24-hour and annual SO2 NAAQS were not adequate to
protect public health with an adequate margin of safety (see section
II.E.4, 74 FR at 64829). In reaching this conclusion, she considered
the: (1) Scientific evidence and conclusions in the ISA; (2) exposure
and risk information presented in the REA; (3) conclusions of the
policy assessment chapter of the REA; and (4) views expressed by CASAC.
These considerations are discussed in detail in the proposal (see
section II.E., 74 FR at 64826) and are summarized in this section.
    In the proposal the Administrator noted the following in
considering the adequacy of the current 24-hour and annual primary
SO2 standards:
     The conclusion of the ISA that the results of controlled
human exposure and epidemiologic studies form a plausible and coherent
data set that supports a causal relationship between short-term (5-
minutes to 24-hours) SO2 exposures and adverse respiratory
effects, and that the epidemiologic evidence (buttressed by the
clinical evidence) indicates that the effects seen in the epidemiologic
studies are attributable to exposure to SO2 (ISA, section
5.2).
     The conclusion of the ISA that ``[i]n the epidemiologic
studies, respiratory effects were observed in areas where the maximum
ambient 24-h avg SO2 concentration was below the current 24-

h avg NAAQS level * * *.'' (ISA, section 5.2, p. 5-2.) and so would
occur at ambient SO2 concentrations that are present in
locations meeting the current 24-hour NAAQS.
     These respiratory effects also occurred in areas with
annual air quality levels considerably lower than those allowed by the
current annual standard, indicating that the current annual standard is
also not providing protection against short-term health effects
reported in epidemiologic studies (ISA, section 5.2).
     Analyses in the REA supporting that 5-minute exposures,
reasonably judged important from a public health perspective (i.e.,
respiratory effects judged to be adverse to the health of asthmatics,
see sections II.B.1.c above, and II.E.2.b below), were associated with
air quality adjusted upward to simulate just meeting the current 24-
hour and annual standards.
     CASAC advice ``that the current 24-hour and annual
standards are not adequate to protect public health, especially in
relation to short term exposures to SO2 (5-10 minutes) by
exercising asthmatics'' (Samet, 2009, p. 15).
    Based on these considerations (discussed in more detail in the
proposal, see sections II.E.1 and II.E.2), the Administrator proposed
that the current 24-hour and annual SO2 standards are not
requisite to protect public health with an adequate margin of safety
against adverse respiratory effects associated with short-term (5-
minute to 24-hour) SO2 exposures. In considering approaches
to revising the current standards, the Administrator initially
concluded it appropriate to consider setting a new 1-hour standard. The
Administrator noted that a 1-hour standard would likely provide
increased public health protection, especially for members of at-risk
groups, from the respiratory effects described in both epidemiologic
and controlled human exposure studies.
2. Comments on the Adequacy of the Current Standards
    This section discusses public comments on the proposal that either
supported or opposed the Administrator's proposed decision to revise
the current SO2 primary NAAQS. Comments on the adequacy of
the current standards that focused on the scientific and/or the
exposure/risk basis for the Administrator's proposed conclusions are
discussed in sections II.E.2.a-II.E.2.c. Comments on the epidemiologic
evidence are considered in section II.E.2.a. Comments on the controlled
human exposure evidence are considered in section II.E.2.b. Comments on
human exposure and health risk assessments are considered in section
II.E.2.c. To the extent these comments on the evidence and information
are also used to justify commenters' conclusions on decisions related
to indicator, averaging time, form, or level, they are noted as well in
the appropriate sections below (II.F.1-II.F.4, respectively). The
summaries of comments, and responses thereto, presented below are not
exclusive: other comments and responses are being included in the
Response to Comment (RTC) Document which is part of the record for this
rulemaking (EPA, 2010).
    Many public commenters agreed with the proposal that based on the
available information, the current SO2 standards are not
requisite to protect public health with an adequate margin of safety
and that revisions to the standards are therefore appropriate. Among
those calling for revisions to the standards were environmental groups
(e.g., Sierra Club, WEACT for Environmental Justice, Center for
Biological Diversity, (CBD) Environmental Defense Fund (EDF), Natural
Resources Defense Council (NRDC)); medical/public health organizations
(e.g., American Lung Association (ALA), American Thoracic Society
(ATS)); State environmental organizations (e.g., National Association
of Clean Air Agencies (NACAA), Northeast States for Coordinated Air Use
Management (NESCAUM); State environmental agencies (e.g., such agencies
in DE, IA, IL, MI, NY, NM, OH, PA, TX, VT); the Fond du Lac Band of
Lake Superior Chippewa (Fond du Lac) Tribe, local groups (e.g.,
Houston-Galveston Area Council, Alexandria Department of Transportation
and Environmental Services) and most individual commenters (~13,000).
These commenters generally concluded that the current SO2
standards need to be revised and that a more stringent standard is
needed to protect the health of susceptible population groups. In
supporting the need to adopt a more stringent NAAQS for SO2,
these commenters often referenced the conclusions of CASAC, as well as
evidence and information presented in the proposal. As such, the
rationale offered by these commenters was consistent with that
presented in the proposal to support the Administrator's proposed
decision to revise the current SO2 NAAQS.
    Most industry commenters (e.g., Utility Air Regulatory Group
(UARG), American Petroleum Institute (API), Arizona Public Service,
National Petrochemical & Refiners Association (NPRA), Montana-Dakota
Utilities Co., Dominion Resources, Council of Industrial Boiler Owners
(CIBO), Edison Electric Institute (EEI), Duke Energy, National Mining
Association (NMA)); and some organizations (e.g., Texas Association of
Business, The Annapolis Center for Science-Based Public Policy
(ACSBPP), South Carolina Chamber of Commerce) opposed the proposed
revisions to the SO2 primary NAAQS. In supporting their
views, industry commenters generally concluded that EPA did not
appropriately consider uncertainties associated with the epidemiologic
and controlled human exposure evidence.
    More specifically, with respect to the epidemiologic studies, many
of these commenters concluded that results of these studies are
confounded by co-pollutants and thus too uncertain to determine whether
SO2 is truly associated with the health outcomes being
measured (e.g., hospital admissions; Federal Register see below). With
respect to the controlled human exposure studies, many commenters were
critical of the 5-minute benchmark levels that were derived from these
studies and subsequently used by EPA in the air quality, exposure, and
risk analyses. These groups were particularly concerned about the
Administrator's reliance on the 200 ppb 5-minute benchmark level in
assessing the adequacy of the current and potential alternative
standards. In general, many industry groups maintained that adverse
respiratory effects did not occur following 5-10 minute SO2
exposures < 400 ppb (e.g., API, EEI, CIBO) and some groups stated that
even at SO2 concentrations >= 400 ppb, reported effects may
not be of clinical concern, and thus are likely not adverse (e.g.,
UARG). Many industry groups (e.g., API, UARG) also disagreed with EPA's
(and CASAC's) conclusions that severe asthmatics were not included in
these controlled human exposure studies, and that severe asthmatics
would likely have a more pronounced response to SO2
exposures at a given level, or would respond to even lower levels of
SO2.
    In responding to these specific comments, we note that the
Administrator relied in the proposal on the evidence, information, and
judgments contained in the ISA and the REA (including the policy
assessment chapter), as well as on the advice of CASAC. In considering
the evidence, information, and judgments of the ISA and the REA, the
Agency notes that these documents have been reviewed and discussed
extensively by CASAC at multiple public meetings (see above, section
I.D) and in their letters to the

EPA Administrator. Thus, it is important to note that CASAC generally
accepted the key findings and conclusions presented in both the ISA and
REA (see Henderson 2008a, Henderson 2008b, and Samet, 2009).
a. Comments on EPA's Interpretation of the Epidemiologic Evidence
    Many industry groups (e.g., API, UARG, American Chemistry Council
(ACC), Dominion Resources, ExxonMobil, Progress Energy, CIBO, The
Fertilizer Institute, EEI, Dow Chemical Company (Dow), MeadWestvaco
Corporation (MWV), (NMA) and some organizations (e.g., ACSBPP)
commented that, given the presence of numerous co-pollutants in the
air, the epidemiologic studies do not support the contention that
SO2 itself is causing health effects. For example, UARG
stated: ``The epidemiological evidence cannot determine that
SO2 is a cause of or a contributor to hospital admissions
(``HA''), emergency department (``ED'') visits or respiratory symptoms,
the effects cited in the Proposed Rule.''
    Although EPA has recognized that multiple factors can contribute to
the etiology of respiratory disease and that more than one air
pollutant could independently impact respiratory health, we continue to
judge, as discussed in the ISA, that the available evidence supports
the conclusion that there is an independent effect of SO2 on
respiratory morbidity. In reaching this judgment, we recognize that a
major methodological issue affecting SO2 epidemiologic
studies concerns the evaluation of the extent to which other air
pollutants, particular PM2.5,\10\ may confound or modify
SO2-related effect estimates. The use of multi-pollutant
regression models is a common approach for evaluating potential
confounding by co-pollutants in epidemiologic studies. It is therefore
important to note that when the ISA evaluated U.S. and international
epidemiologic studies employing multi-pollutant models, SO2
effect estimates generally remained positive and relatively unchanged
when co-pollutants, including PM, were included (see ISA, p. 5-5).
Therefore, although recognizing the uncertainties associated with
separating the effects of SO2 from those of co-occurring
pollutants, the ISA concluded that the limited available evidence
indicates that the effect of SO2 on respiratory health
outcomes appears to be generally robust and independent of the effects
of gaseous co-pollutants, including NO2 and O3,
as well as particulate co-pollutants, particularly PM2.5
(ISA, section 5.2; p. 5-9).
---------------------------------------------------------------------------

    \10\ As noted in the proposal (see sections II.D.1, 74 FR at
64824-64825 and II.F.4.a, 74 FR at 64835), there is special
sensitivity in this review in disentangling SO2-related
effects from PM-related effects (especially sulfate PM).
---------------------------------------------------------------------------

    In considering questions of confounding and causation, the
epidemiologic studies should not be considered in a vacuum. As
emphasized by the ISA, and endorsed by CASAC, controlled human exposure
studies provide support for the plausibility of the associations
reported in epidemiologic studies (ISA, section 5-5; Henderson 2008a;
Henderson 2008b). These controlled human exposure studies exposed
exercising asthmatics to 5-10 minute peaks of SO2 and
reported decrements in lung function and/or respiratory symptoms in up
to 60% of these individuals (depending on exposure concentration; see
ISA, Table 5-3; p. 5-11). Thus, these experimental study results
provide strong support for an independent contribution of
SO2 to the respiratory health effects reported in
epidemiologic studies: ``The effects of SO2 on respiratory
symptoms, lung function, and airway inflammation observed in the human
clinical studies using peak exposures further provides a basis for a
progression of respiratory morbidity resulting in increased emergency
department visits and hospital admissions. Collectively, these findings
provide biological plausibility for the observed association between
ambient SO2 levels and emergency department visits and
hospitalizations for all respiratory diseases and asthma, notably in
children and older adults. * * *'' (ISA, section 5.2 at p. 5-5). Thus,
EPA is not relying solely on the epidemiologic studies to evaluate
whether associations reported in these studies (e.g., associations with
emergency department visits) are likely the result of ambient
SO2 exposure.
b. Comments on EPA's Interpretation of the Controlled Human Exposure
Evidence
    Many industry groups (e.g., API, ACC, Progress Energy, EEI, CIBO)
commented that adverse health effects do not occur following 5-10
minute SO2 exposures < 400 ppb. In addition, some groups
(e.g., UARG) commented that adverse respiratory effects do not occur in
exercising asthmatics following SO2 exposures below 600 ppb.
The disagreement is not whether effects occur in exercising asthmatics
at these exposure levels and exposure durations. Rather, the issue is
whether the effects experienced can properly be regarded as adverse. In
general, these groups conclude that EPA's judgment of adverse health
effects at SO2 exposure levels below 600 or 400 ppb is
inappropriately based on an unsound interpretation of ATS guidelines.
More specifically, these groups generally contend that decrements in
lung function without accompanying respiratory symptoms are not adverse
effects of SO2 exposure, and that decrements in lung
function in a percentage of exercising asthmatics does not represent a
shift in lung function at the population level. Some of these groups
also contend that EPA followed the advice of individual CASAC members,
rather than consensus CASAC written comments on the ISA and REA when
concluding respiratory effects associated with SO2 exposures
below 600 or 400 ppb are adverse. Furthermore, some groups contend that
effects below 400 ppb should not be considered adverse because compared
to the number of asthmatics experiencing decrements in lung function,
there were similar numbers of asthmatics experiencing increases in lung
function. EPA disagrees with these comments, and believes that the
clinical evidence also supports the conclusion that the current
standards are not requisite to protect public health with and adequate
margin of safety.
    The Agency disagrees that adverse respiratory effects do not occur
in exercising asthmatics following 5-10 minute SO2 exposures
ranging from 400-600 ppb. As previously mentioned, at SO2
concentrations ranging from 400-600 ppb, moderate or greater decrements
in lung function occur in approximately 20-60% of exercising asthmatics
(again, defined in terms of a >= 15% decline in FEV1 or 100%
increase in sRaw; ISA, Table 3-1). Moreover, at concentrations >= 400
ppb, decrements in lung function are often statistically significant at
the group mean level, and are frequently accompanied by respiratory
symptoms (ISA, Table 5-1). ATS guidelines on what constitutes an
adverse health effect of air pollution clearly state that reversible
loss of lung function in combination with the presence of symptoms
should be considered adverse (ATS 1985, 2000). Moderate or greater
decrements in lung function accompanied by respiratory symptoms fit
this description. Thus, the Agency's conclusion of adverse health
effects associated with SO2 concentrations >= 400 ppb is
consistent with ATS guidelines.
    The Agency also disagrees with industry commenters regarding the
adversity of the respiratory effects seen in exercising asthmatics
following 5-10 minute SO2 exposures ranging from 200-300
ppb. As mentioned above (section II.B.1), and discussed more

fully in the proposal (see section II.B.3, 74 FR at 64819), the ISA
reported that exposure to SO2 concentrations as low as 200-
300 ppb for 5-10 minutes results in approximately 5-30% of exercising
asthmatics experiencing moderate or greater decrements in lung
function. In 2000, the ATS updated its guidelines on ``what constitutes
an adverse health effect of air pollution.'' These guidelines indicated
that exposure to air pollution that increases the risk of an adverse
effect to the entire population is adverse, even though it may not
increase the risk of any individual to an unacceptable level (ATS
2000). For example, ATS notes that a population of asthmatics could
have a distribution of lung function such that no individual has a
level associated with significant impairment. Exposure to air pollution
could shift the distribution to lower levels that still do not bring
any individual to a level that is associated with clinically relevant
effects. However, this would be considered adverse because individuals
within the population would have diminished reserve function, and
therefore would be at increased risk if affected by another agent (ATS
2000).
    Considering the 2000 ATS guidelines, the results of the clinical
studies conducted at 200-300 ppb were reasonably interpreted by EPA to
indicate an SO2-induced shift in these lung function
measurements for a subset of this population. That is, an appreciable
percentage of this population of exercising asthmatics would be
expected to experience moderate or greater decrements in lung function
in response to SO2 concentrations as low as 200 ppb, and
thus would be expected to have diminished reserve lung function. As a
result, this sub-population would be at greater risk of a more severe
response if affected by another respiratory agent (e.g., viral
infection, or O3).
    EPA is also mindful of CASAC comments on this issue following the
second draft ISA. The second draft ISA placed relatively little weight
on health effects associated with SO2 exposures at 200-300
ppb. CASAC strongly disagreed with this characterization of the health
evidence. Their consensus letter following the second draft ISA states:

    Our major concern is the conclusions in the ISA regarding the
weight of the evidence for health effects for short-term exposure to
low levels of SO2. Although the ISA presents evidence
from both clinical and epidemiological studies that indicate health
effects occur at 0.2 ppm or lower, the final chapter emphasizes
health effects at 0.4 ppm and above * * * CASAC believes the
clinical and epidemiological evidence warrants stronger conclusions
in the ISA regarding the available evidence of health effects at 0.2
ppm or lower concentrations of SO2. The selection of a
lower bound concentration for health effects is very important
because the ISA sets the stage for EPA's risk assessment decisions.
In its draft Risk and Exposure Assessment (REA) to Support the
Review of the SO2 Primary National Ambient Air Quality Standards
(July 2008), EPA chose a range of 0.4 ppm-0.6 ppm SO2
concentrations for its benchmark analysis. As CASAC will emphasize
in a forthcoming letter on the REA, we recommend that a lower bound
be set at least as low as 0.2 ppm. (Henderson 2008a)

    EPA also notes the similar CASAC comments on the first draft of the
REA. The consensus CASAC letter following the 1st draft REA states:

    The CASAC believes strongly that the weight of clinical and
epidemiology evidence indicates there are detectable clinically
relevant health effects in sensitive subpopulations down to a level
at least as low as 0.2 ppm SO2. These sensitive
subpopulations represent a substantial segment of the at-risk
population. (Henderson 2008b; p. 1)

See Coalition of Battery Recyclers Association v. EPA, No. 09-1011 (DC
Cir., May 14, 2010), slip opinion at 9, holding that it was reasonable
for EPA to conclude that a two IQ point mean population loss is an
adverse effect based in part on CASAC advice that such a decrement is
significant. CASAC's strong advice regarding the adversity of effects
at the 200 ppb level similarly supports EPA's conclusion that the
observed lung decrements are adverse.
    In addition to the considerations described above, we also note the
following key points:
     In the current SO2 NAAQS review, clinicians on
the CASAC Panel advised that moderate or greater decrements in lung
function can be clinically significant in some individuals with
respiratory disease.\11\
---------------------------------------------------------------------------

    \11\ See hearing transcripts from EPA Clean Air Scientific
Advisory Committee (CASAC), July 30-31 2008, Sulfur Oxides-Health
Criteria (part 3 of 4) pages 211-213). These transcripts can be
found in Docket ID No. EPA-HQ-ORD-2006-0260. Available at http://
www.regulations.gov.
---------------------------------------------------------------------------

     In the last O3 NAAQS review, CASAC indicated
that moderate decrements in lung function can be clinically significant
in some asthmatics (Henderson 2006), and that in the context of
standard setting, a focus on the lower end of the range of moderate
functional responses is most appropriate for estimating potentially
adverse lung function decrements in people with lung disease (e.g.,
asthma; see 73 FR at 16463).
     In the last O3 NAAQS review, the Criteria
Document and the Staff Paper indicated that for many people with lung
disease (e.g., asthma), even moderate decrements in lung function or
respiratory symptoms would likely interfere with normal activities and
result in additional and more frequent use of medication (EPA 2006, EPA
2007d).
     Subjects participating controlled human exposure studies
do not include severe asthmatics, and it is reasonable to presume that
persons with more severe asthma than the study participants would have
a more serious health effect from short-term exposure to 200 ppb
SO2.
    Considering these key points along with the ATS guidelines and
consensus CASAC comments on the draft ISA and REA described above, we
reasonably conclude that 5-10 minute exposures to SO2
concentrations at least as low as 200 ppb can result in adverse health
effects in exercising asthmatics.
    In addition, as noted above some groups (e.g., API) contend that
effects below 400 ppb should not be considered adverse because compared
to the number of asthmatics experiencing decrements in lung function,
there were similar numbers of asthmatics experiencing increases in lung
function.
    The commenters correctly point out that at the lowest concentration
tested in free-breathing chamber studies (200 ppb), there are a similar
number of asthmatics experiencing a moderate or greater decrease in
lung function (i.e., >= 100 increase in sRaw or >= 15 decrease in
FEV1) and experiencing what might be called a moderate
improvement in lung function (i.e., >= 100 decrease in sRaw or >= 15
increase in FEV1). This observation is consistent with data
presented in Figures 4-2 and 4-3 of the ISA showing essentially no
SO2 -induced change in lung function at 200 ppb when
averaged across asthmatics participating in the three Lin et al.,
controlled human exposure studies. However, these figures also
demonstrate that asthmatics who are sensitive to SO2 at a
higher concentration (600 ppb) experience, on average, a greater
decrement in lung function at lower concentrations, including 200 ppb,
when compared with all subjects combined. Therefore, while some
asthmatics are relatively insensitive to SO2-induced
respiratory effects even at concentrations >= 600 ppb, there is clear
empirical evidence that others experience significant
bronchoconstriction following exposures to both relatively high (600
ppb) and low (200 ppb) SO2 concentrations. Among these
SO2-sensitive asthmatics, Figures 4-2 and 4-3 of the ISA
show a clear increase in

bronchoconstriction with increasing SO2 concentrations from
200-400 ppb. Given this clear relationship of exposure and effect at
all levels in the sensitive asthmatics (i.e. those who experienced
significant decrements in lung function at the highest exposure
concentration used (600 ppb)), EPA does not accept the commenter's
premise that controlled human exposure studies do not demonstrate
adverse effects in some asthmatics at 5-10 minute levels below 400 ppb.
    In addition to disagreeing with EPA's proposed finding of adverse
health effects following 5- 10 minute SO2 exposures as low
as 200 ppb, many industry groups (e.g., API, UARG, ACC, ExxonMobil)
also disagreed with EPA that severe asthmatics were not included in
controlled human exposure studies. That is, these groups contend that
EPA is incorrect in assuming that severe asthmatics would likely have a
more pronounced response to SO2 exposures at a given level,
or would respond to even lower levels of SO2 and that this
should be taken into account when judging the adequacy of the current
standards. As support for their assertion, multiple industry groups
cite controlled human exposure studies in the ISA stating that they
included ``severe asthmatics'' and also cite a study by Linn et al.
(1987) which concluded that among asthmatics, responses to
SO2 exposure are not dependent on the clinical severity of
asthma and that ``the subjects with the highest risk [of temporary
respiratory disturbances from ambient SO2] can be identified
only by actually measuring their responses to SO2''.
    We disagree with the assertion that severe asthmatics have been
evaluated in 5-10 minute controlled human exposure studies. Although
studies cited in the ISA referred to a group of subjects as ``moderate/
severe'' asthmatics, these individuals had well-controlled asthma, were
able to withhold medication, were not dependent on corticosteroids, and
were able to engage in moderate to heavy levels of exercise. By today's
standards, these individuals would clearly be classified as moderate
asthmatics. EPA therefore concludes that persons with asthma that is
more severe than moderate asthma, as that term is currently understood,
were not included in the controlled human exposure studies (and
understandably so, for ethical reasons).
    In addition, EPA agrees with the commenters that there is little
evidence from controlled human exposure studies to suggest that the
respiratory effects of SO2 differ between mild and moderate
asthmatics (see Linn et al., 1987). However, this may very well be due,
at least in part, to persistence of medication among the moderate
asthmatic subjects. More importantly, the moderate asthmatics began the
exposure with compromised lung function relative to the mild
asthmatics. Therefore, similar functional declines from different
baselines between mild and moderate asthmatics would clearly not have
the same physiological importance. CASAC specifically addressed the
issue of asthma severity in a letter to the Administrator: ``For
ethical reasons severe asthmatics were not part of these clinical
studies, but it is not unreasonable to presume that they would have
responded to even a greater degree (Henderson 2008a; p. v).'' It is
also important to note that in addition to the strict health-specific
inclusion and exclusion criteria for a given controlled human exposure
study, many asthmatics who might otherwise be able to participate
choose not to participate because of anxiety related to what they
viewed as potential adverse health risks. EPA concludes that it is
appropriate to assume, as CASAC suggested, that persons with more
severe asthma would respond to an even greater degree than the moderate
asthmatics in the clinical studies.
c. Comments on EPA's Characterization of SO2-Associated
Exposures and Health Risks
    Several commenters discussed the analyses of SO2-
associated exposures and health risks presented in the REA. As in past
reviews (EPA 2005, 2007c, 2007d), EPA has estimated risks associated
with the current standards to inform judgments on the public health
risks that could exist under different standard options. Some industry
commenters (e.g., API, UARG, Lignite Energy Council (LEC), Jackson
Walker, ASARCO, the National Rural Electric Cooperative Association)
concluded that when considering the adequacy of the current standards,
the Administrator should consider exposures and risks associated with
actual SO2 air quality rather than air quality allowed by
the current NAAQS. They consequently challenged the relevance and
appropriateness of EPA's use of SO2 concentrations that have
been simulated to just meet the current standards in assessing the
adequacy of the current standards.
    In addition to the objections noted above, we note that UARG
generally concluded that the results of EPA's quantitative risk
assessment are fundamentally flawed in that they substantially
overestimate risks associated with the various air quality scenarios.
UARG contends that this is because EPA did not use proper exposure-
response functions in estimating risks associated with SO2
exposure. Moreover, UARG contends EPA further overestimates risk
because of the use of 50 ppb exposure bins in estimating the number of
occurrences of an adverse lung function response (see below).
    With respect to comments that when considering the adequacy of the
current standards, the Administrator should consider exposures and
risks associated with actual SO2 air quality rather than
that simulated to just meet the current standards, these commenters
generally concluded: (1) It is more relevant to assess exposures and
risks associated with actual SO2 air quality since adjusting
air quality to just meet the current standards require large
adjustments to air quality that are highly uncertain; and (2) NAAQS are
intended to address actual, rather than highly improbable, risks to
human health. In addition, these groups generally concluded that
exposure and risk estimates presented in the REA suggest relatively
little health risk associated with current levels of SO2,
and thus, there is no need to revise the current SO2
standards.
    We disagree with these commenters that exposure- and risk-related
considerations in the NAAQS reviews should rely only on actual air
quality, and that EPA therefore improperly adjusted air quality in its
risk and exposure analyses to simulate air quality allowed by the
current primary SO2 NAAQS. EPA is required to review whether
the present standards--not present air quality--are requisite to
protect public health with an adequate margin of safety. Section
109(b)(1). In making this determination it is relevant to consider
exposures and risks which could be permissible under the current
standards. See American Trucking Associations v. EPA, 283 F.3d 355, 370
(DC Cir. 2002) (existence of evidence showing adverse effects occurring
at levels allowed by the current standards justifies finding that it is
appropriate to revise the existing NAAQS). Consequently, it is at the
very least reasonable for EPA, in its REA, to make air quality
adjustments to estimate SO2-related exposures and health
risks that could exist in areas that just meet the present standards.
Thus, although we acknowledge that exposure and health risk estimates
associated with current ambient concentrations are substantially
smaller than those associated with air quality adjusted to just meet
the current standards, we also note that this is

irrelevant to the question of whether the current standards are
requisite to protect public health with an margin of safety.
    In both of these cases, EPA is not trying to evaluate whether areas
would or would not be in attainment of the current standards. Those are
issues that are addressed during the implementation of the NAAQS.
Instead, in this rulemaking EPA is evaluating what NAAQS would be
appropriate under section 109(b)(1), by evaluating the impact on or
risks to public health from air quality that is at the level of the
current standards, as well as evaluating air quality that is at the
level of various alternative standards. EPA uses this information to
inform the decision on what NAAQS would be requisite to protect public
health with an adequate margin of safety.
    If EPA determines that the current standards require revision, EPA
is further required to determine what revisions are appropriate in
light of the requirement that primary NAAQS be requisite to protect
public health with an adequate margin of safety. Section 109(d)(1). It
is thus similarly reasonable for EPA to make air quality adjustments to
simulate different potential alternative standards to provide
information on exposures and risks under these potential alternative
standards.\12\
---------------------------------------------------------------------------

    \12\ In conducting these analyses, EPA is not trying to evaluate
whether areas would or would not be in attainment of the current
standards. Again, those issues are addressed during the
implementation of the NAAQS.
---------------------------------------------------------------------------

    We agree that there are uncertainties inherent in making air
quality adjustments. These uncertainties are discussed thoroughly in
the REA (REA, sections 6.5 and <IP_ADDRESS>). For example, the REA noted the
following regarding adjustment of SO2 concentrations:

    This procedure for adjusting either the ambient concentrations
(i.e., in the air quality characterization) or health effect
benchmark levels (i.e., in the exposure assessment) was necessary to
provide insight into the degree of exposure and risk which would be
associated with an increase in ambient SO2 levels such
that the levels were just at the current standards in the areas
analyzed. Staff recognizes that it is extremely unlikely that
SO2 concentrations in any of the selected areas where
concentrations have been adjusted would rise to meet the current
NAAQS and that there is considerable uncertainty associated with the
simulation of conditions that would just meet the current standards.
Nevertheless, this procedure was necessary to assess the ability of
the current standards, not current ambient SO2
concentrations, to protect public health (REA, section 6.5; p. 64)

    These air quality adjustments are not meant to imply an expectation
that SO2 concentrations will increase broadly across the
United States or in any given area. Rather, as just noted above, they
are meant to estimate SO2-related exposures and health risks
if air quality were at the level of the current and potential
alternative standards. Such estimates can inform decisions on whether
the current standards, or particular potential alternative standards,
provide the requisite protection of public health.
    As mentioned above, UARG generally concluded that under all air
quality scenarios, the results of EPA's quantitative risk assessment
(the third of the analyses conducted in the REA (chapter 9), see
section II.C above) are substantially overestimated because EPA did not
use proper methods to estimate the parameters of the exposure-response
functions used in its analyses. UARG contends this is because many of
the subjects in the controlled human exposure studies from which EPA's
exposure-response functions were derived (see REA, Table 9-3) were
exposed to more than one SO2 concentration, yet EPA treated
each exposure event as being independent (e.g., if the same subject was
exposed to 200 and 300 ppb SO2, EPA considered these as
representing two independent exposure events). UARG contends that
observations from the same subject exposed to different SO2
concentrations are not independent observations and should not be
treated as such. Notably, when UARG derived their own exposure-response
functions taking into account that observations from the same subject
exposed to different SO2 concentrations are not independent
of each other, they estimated appreciably less risk than that estimated
by EPA.
    There are a variety of techniques and/or assumptions that can be
used to fit individual subject data from the controlled human exposure
studies (see REA, Table 9-3) to exposure-response curves. Moreover, any
technique or assumption utilized will have inherent uncertainties. EPA
discussed the uncertainties associated with our quantitative risk
assessment in detail in the REA (REA, section 9.4); we also gave an
overview of key uncertainties in the proposal (see section II.C.3, 74
FR at 64824). The approach used to estimate the exposure-response
functions was not first introduced in the SO2 risk
assessment, it was previously recommended to EPA by an applied
statistician serving on the O3 CASAC Panel and used in the
O3 risk assessment (which had individual controlled human
exposure data similar to that in the current SO2 NAAQS
review; see EPA 2007d and EPA 2007e). Importantly, this approach
allowed EPA to use all the available individual subject data. Moreover,
an inspection of the estimated exposure-response curve and the
underlying data suggest that any biases in the parameter estimates are
likely to be slight (see EPA 2010, section II.C). Consequently, EPA
does not accept UARG's view that the methodology used in EPA's
quantitative risk assessment was inappropriate.
    We further note that UARG's exposure-response functions do not fit
the underlying controlled human exposure data (the proportions of
subjects who responded at each exposure level) nearly as well as the
exposure-response functions estimated using EPA's approach. We believe
this could be due to the methodology used in UARG's reanalysis of the
individual-level data from the controlled human exposure studies used
in the quantitative risk assessment. UARG attempted to estimate
subject-specific exposure-response functions, and to use the results of
these estimates to obtain estimates of the two parameters in the
population-level exposure-response functions. As described in more
detail in section II.C of the RTC document (EPA 2010), EPA does not
believe there are sufficient data to properly estimate the parameters
of subject-specific exposure-response functions. More specifically,
UARG chose a three-parameter quadratic function for the subject-
specific exposure-response functions. However, none of the subjects had
more than three exposures, and many had only one or two. EPA believes
that this information is particularly limited for estimating these
subject-specific exposure-response functions, especially given that a
large percentage of the total number of subjects had fewer exposures
than the number of parameters UARG was attempting to estimate (i.e.,
UARG estimated three parameters in its exposure-response functions, but
over fifty percent of subjects only had one or two exposures). It
appears that UARG's population-level exposure-response function
estimates depended on these subject-specific exposure-response function
estimates and thus could explain why UARG's estimated population-level
exposure-response functions do not fit the underlying controlled human
exposure data nearly as well as the approach used by EPA. A more
detailed response to this comment can be found in section II.C of the
RTC document (EPA 2010).
    As mentioned above, UARG also concluded that EPA further
overestimates the total number of occurrences of an adverse lung
function response (i.e., total number of

occurrences of increases in sRaw >= 100 or 200% and/or declines in
FEV1 >= 15 or 20%) in its quantitative risk assessment. More
specifically, UARG concluded that the use of 50 ppb bins, combined with
assigning all exposures within a bin the probability of an adverse lung
function response at the midpoint of that bin (e.g., all exposures from
0-50 ppb were assigned the probability of an adverse lung function
response occurring at 25 ppb), resulted in a substantial overestimate
of the total number of occurrences of lung function responses in
asthmatics at moderate or greater exertion. UARG generally concludes
that this is because the vast majority of exposures of asthmatics at
moderate or greater exertion are occurring below the midpoint of the 0-
50 ppb exposure bin (i.e., most exposures are occurring below 25 ppb),
yet EPA is assigning these very low SO2 exposures the higher
probability of a lung function response associated with the midpoint of
the 0-50 ppb exposure bin. UARG contends that this results in a
substantial overestimation of the total number of occurrences of lung
function response in asthmatics and asthmatic children at moderate or
greater exertion. UARG further notes that this methodological concern
was raised in its comments on the second draft REA, but EPA failed to
address this issue and relied heavily on this metric in the proposal
with respect to the adequacy of the current and potential alternative
standards. EPA's response to this comment is discussed below and in
more detail in section II.C of the RTC document (EPA 2010).
    EPA generally agrees with UARG's technical comments that there is a
substantial overestimation of the total occurrences of lung function
responses because of the binning issues described above. However, we
strongly disagree that: (1) This issue was not acknowledged in the
final REA; and (2) the metric of total occurrences was relied on
heavily in the policy assessment chapter of the REA (REA, chapter 10)
and in the Administrator's rationale with respect to the adequacy of
the current and potential alternative standards. First, EPA did respond
to this concern in the final REA. More specifically, page 344 of the
final REA states:

    As noted in public comments on the 2nd draft SO2 REA,
the assignment of response probability to the midpoint of the
exposure bin combined with the lack of more finely divided intervals
in this range can lead to significant overestimation of risks based
on total occurrences of a defined lung function response. This is
because the distribution of population exposures for occurrences is
not evenly distributed across the bin, but rather is more heavily
weighted toward the lower range of the bin. Thus, combining all
exposures estimated to occur in the lowest bin with a response
probability assigned to the midpoint of the bin results in a
significant overestimate of the risk. Therefore, staff places less
weight on the estimated number of occurrences of lung function
responses.

    Thus, as noted in the final REA, less weight was placed on this
metric in the quantitative risk assessment chapter (REA, chapter 9),
and importantly, no weight was placed on this metric in either the
policy assessment chapter of the REA (REA, chapter 10) or in the
Administrator's rationale sections of the proposal preamble. Rather,
the policy assessment chapter of the REA and the Administrator's
rationale at the proposal considered the percent of exposed asthmatic
children at moderate or greater exertion estimated to have at least one
defined lung function response per year in St. Louis. Importantly, this
metric is not appreciably affected by the binning issue raised in
UARG's comments. As stated on page 344-345 of the final REA:

    This overestimation of total occurrences does not impact the
risk metric expressed as incidence or percent incidence of a defined
lung function response 1 or more times per year because the bulk of
the exposures contributing to these risk metrics are not skewed
toward the lower range of the reported exposure bins.\13\
---------------------------------------------------------------------------

    \13\ Although in St. Louis, the percent of exposed asthmatic
children at moderate or greater exertion estimated to have at least
one defined lung function response per year was not appreciably
affected, it was found that for this same metric, the already very
low risk estimates in Greene County became appreciably lower when
the binning issue discussed above was considered. However, as noted
above in section II.C and discussed in more detail in the REA (REA,
section 10.3.3) and the proposal (see section II.E.b, 74 FR at
64827), the St. Louis exposure and risk results were found to be
more informative in addressing the adequacy of the current and
potential alternative standards. Moreover, while the Administrator's
rationale in the proposal relied minimally on the St. Louis
quantitative risk results (see above), she importantly placed no
weight on any metric from the Greene County quantitative risk
assessment.

    Finally, it is important to note that the Administrator's rationale
in the proposal regarding the adequacy of the current and potential
alternative standards in general placed only limited reliance on the
results of the quantitative risk assessment in St. Louis, with no
reliance on the estimates of total occurrences. Rather, in addition to
the substantial weight that she placed on the scientific evidence as
described in the ISA, the Administrator placed relatively more weight
on the results of the St. Louis exposure analysis. For example, in
discussing the adequacy of the current standards, the proposal states:
``The Administrator especially notes the results of the St. Louis
exposure analysis which, as summarized above, indicates that
substantial percentages of asthmatic children at moderate or greater
exertion would be exposed, at least once annually, to air quality
exceeding the 400 and 200 ppb benchmarks'' (see 74 FR at 64829). We
note that results of the quantitative risk assessment in St. Louis,
with respect to the percent of asthmatic children estimated to have at
least one lung function response per year (using EPA's exposure-
response functions), supports the Administrator's overall conclusions
in the proposal regarding the adequacy of the current and potential
alternative standards.
3. Conclusions Regarding the Adequacy of the Current 24-Hour and Annual
Standards
    In reviewing the adequacy of the current standards, the
Administrator has considered the scientific evidence assessed in the
ISA, the exposure and risk results presented in the REA, the
conclusions of the policy assessment chapter of the REA, and comments
from CASAC and the public. These considerations are described below.
    As in the proposal, the Administrator accepts and agrees with the
ISA's conclusion that the results of controlled human exposure and
epidemiologic studies form a plausible and coherent data set that
supports a causal relationship between short-term (5 minutes to 24
hours) SO2 exposures and adverse respiratory effects. The
Administrator acknowledges that there are uncertainties associated with
the epidemiologic evidence (e.g., potential confounding by co-
pollutants). However, she agrees that the epidemiologic evidence,
supported by the controlled human exposure evidence, generally
indicates that the effects seen in these studies are attributable to
exposure to SO2, rather than co-pollutants, most notably
PM2.5. She also accepts and agrees with the conclusion of
the ISA that ``[i]n the epidemiologic studies, respiratory effects were
observed in areas where the maximum ambient 24-h avg SO2
concentration was below the current 24-h avg NAAQS level. * * *'' (ISA,
section 5.2, p. 5-2) and so would occur at ambient SO2
concentrations that are present in locations meeting the current 24-
hour NAAQS. The Administrator also notes that these effects occurred in
areas with annual air quality levels considerably lower than those
allowed by the current annual standard, indicating that the annual
standard also

is not providing protection against such effects. Existence of
epidemiologic studies showing adverse effects occurring at levels
allowed by the current standards is an accepted justification for
finding that it is appropriate to revise the existing standards. See,
e.g. American Trucking Associations v. EPA, 283 F. 3d at 370; see also
American Farm Bureau v. EPA, 559 F. 3d.512, 521-23 (DC Cir. 2009)
(effects associated with short-term exposure seen in areas with ambient
concentrations lower than long-term standard, so that without further
explanation, standard does not adequately protect against short-term
exposures).
    With respect to the controlled human exposure studies, the
Administrator judges that effects following 5-10 minute SO2
exposures >= 400 ppb and >= 200 ppb can result in adverse health
effects to asthmatics. This judgment is based on ATS guidelines,
explicit CASAC consensus written advice and recommendations, and
judgments made by EPA in previous NAAQS reviews. Thus, similar to the
proposal, she notes analyses in the REA supporting that 5-minute
exposures >= 400 ppb and >= 200 ppb were associated with air quality
adjusted upward to simulate just meeting the current standards. The
Administrator especially notes the results of the St. Louis exposure
analysis which, as summarized in the proposal (see section II.E.1.b and
Table 3, see 74 FR at 64841), indicates that substantial percentages of
asthmatic children at moderate or greater exertion would be exposed, at
least once annually, to air quality exceeding the 400 and 200 ppb 5-
minute benchmarks given air quality simulated to just meet the current
standards. The Administrator judged these 5-minute exposures to be
significant from a public health perspective due to their estimated
frequency: Approximately 24% of child asthmatics at moderate or greater
exertion in St. Louis are estimated to be exposed at least once per
year to air quality exceeding the 5-minute 400 ppb benchmark, a level
associated with lung function decrements in the presence of respiratory
symptoms. Additionally, approximately 73% of child asthmatics in St.
Louis at moderate or greater exertion would be expected to be exposed
at least once per year to air quality exceeding the 5-minute 200 ppb
benchmark. This health evidence and risk-based information underlie
CASAC's conclusion that the current SO2 standards do not
adequately protect public health. As discussed in the proposal, CASAC
stated: ``the current 24-hour and annual standards are not adequate to
protect public health, especially in relation to short-term exposures
to SO2 (5-10 minutes) by exercising asthmatics'' (Samet,
2009, p. 15). The Administrator agrees with this conclusion.
    In considering approaches to revising the current standards, the
Administrator concludes that it is appropriate to set a new standard,
that such standard must provide requisite protection with an adequate