[Federal Register Volume 84, Number 52 (Monday, March 18, 2019)]
[Rules and Regulations]
[Pages 9866-9907]
[FR Doc No: 2019-03855]

Vol. 84

Monday,

No. 52

March 18, 2019

Part II

Environmental Protection Agency

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40 CFR Part 50

Review of the Primary National Ambient Air Quality Standards for Sulfur
Oxides; Final Rule

Federal Register / Vol. 84 , No. 52 / Monday, March 18, 2019 / Rules
and Regulations

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 50

[EPA-HQ-OAR-2013-0566; FRL-9990-28-OAR]
RIN 2060-AT68

Review of the Primary National Ambient Air Quality Standards for
Sulfur Oxides

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final action.

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SUMMARY: Based on the Environmental Protection Agency's (EPA's) review
of the air quality criteria addressing human health effects and the
primary national ambient air quality standard (NAAQS) for sulfur oxides
(SOX), the EPA is retaining the current standard, without
revision.

DATES: This final action is effective on April 17, 2019.

ADDRESSES: The EPA has established a docket for this action under
Docket ID No. EPA-HQ-OAR-2013-0566. Incorporated into this docket is a
separate docket established for the Integrated Science Assessment for
this review (Docket ID No. EPA-HQ-ORD-2013-0357). All documents in
these dockets are listed on the www.regulations.gov website. Although
listed in the index, some information is not publicly available, e.g.,
Confidential Business Information (CBI) or other information whose
disclosure is restricted by statute. Certain other material, such as
copyrighted material, is not placed on the internet and may be viewed,
with prior arrangement, at the EPA Docket Center. Publicly available
docket materials are available either electronically in
www.regulations.gov or in hard copy at the Air and Radiation Docket
Information Center, EPA/DC, WJC West Building, 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 (202)
566-1744 and the telephone number for the Air and Radiation Docket
Information Center is<PHONE_NUMBER>.

Availability of Information Related to This Action

    A number of the documents that are relevant to this action are
available through the EPA's website at https://www.epa.gov/naaqs/sulfur-dioxide-so2-primary-air-quality-standards. These documents
include the Integrated Review Plan for the Primary National Ambient Air
Quality Standard for Sulfur Dioxide (U.S. EPA, 2014a), available at
https://www3.epa.gov/ttn/naaqs/standards/so2/data/20141028so2reviewplan.pdf, the Integrated Science Assessment for Sulfur
Oxides--Health Criteria (ISA [U.S. EPA, 2017a]), available at https://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=338596, the Risk and
Exposure Assessment for the Review of the National Ambient Air Quality
Standard for Sulfur Oxides (REA [U.S. EPA, 2018a]), available at
https://www.epa.gov/naaqs/sulfur-dioxide-so2-standards-risk-and-exposure-assessments-current-review and the Policy Assessment for the
Review of the Primary National Ambient Air Quality Standard for Sulfur
Oxides (PA [U.S. EPA, 2018b]), available at https://www.epa.gov/naaqs/sulfur-dioxide-so2-standards-policy-assessments-current-review. These
and other related documents are also available for inspection and
copying in the EPA docket identified above.

FOR FURTHER INFORMATION CONTACT: Dr. Nicole Hagan, 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; email<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

Table of Contents

Executive Summary
I. Background
    A. Legislative Requirements
    B. Related SO2 Control Programs
    C. Review of the Air Quality Criteria and Standard for Sulfur
Oxides
    D. Air Quality Information
    1. Sources and Emissions of Sulfur Oxides
    2. Ambient Concentrations
II. Rationale for Decision
    A. Introduction
    1. Background on the Current Standard
    2. Overview of Health Effects Evidence
    3. Overview of Risk and Exposure Information
    B. Conclusions on Standard
    1. Basis for Proposed Decision
    2. CASAC Advice in This Review
    3. Comments on the Proposed Decision
    4. Administrator's Conclusions
    C. Decision on the Primary Standard
III. Statutory and Executive Order Reviews
    A. Executive Order 12866: Regulatory Planning and Review and
Executive Order 13563: Improving Regulation and Regulatory Review
    B. Executive Order 13771: Reducing Regulations and Controlling
Regulatory Costs
    C. Paperwork Reduction Act (PRA)
    D. Regulatory Flexibility Act (RFA)
    E. Unfunded Mandates Reform Act (UMRA)
    F. Executive Order 13132: Federalism
    G. Executive Order 13175: Consultation and Coordination With
Indian Tribal Governments
    H. Executive Order 13045: Protection of Children From
Environmental Health Risks and Safety Risks
    I. Executive Order 13211: Actions Concerning Regulations That
Significantly Affect Energy Supply, Distribution or Use
    J. National Technology Transfer and Advancement Act
    K. Executive Order 12898: Federal Actions To Address
Environmental Justice in Minority Populations and Low-Income
Populations
    L. Determination Under Section 307(d)
    M. Congressional Review Act
References

Executive Summary

    The EPA has completed its current review of the primary (health-
based) NAAQS for SOX, a group of closely related gaseous
compounds that include sulfur dioxide (SO2). Of these
compounds, SO2 (the indicator for the current standard) is
the most prevalent in the atmosphere and the one for which there is a
large body of scientific evidence on health effects. The current
primary standard is set at a level of 75 parts per billion (ppb), as
the 99th percentile of daily maximum 1-hour SO2
concentrations, averaged over 3 years. Based on the EPA's review of key
aspects of the currently available health effects evidence,
quantitative risk and exposure information, advice from the Clean Air
Scientific Advisory Committee (CASAC), and public comments, the EPA is
retaining the current standard, without revision.
    Reviews of the NAAQS are required by the Clean Air Act (CAA) on a
periodic basis. The last review of the primary SO2 NAAQS was
completed in 2010 (75 FR 35520, June 22, 2010). In that review, the EPA
significantly strengthened the primary standard, establishing a 1-hour
standard and revoking the 24-hour and annual standards. The 1-hour
standard was established to provide protection from respiratory effects
associated with exposures as short as a few minutes based on evidence
from health studies that documented respiratory effects in people with
asthma exposed to SO2 for 5 to 10 minutes while breathing at
elevated rates. Revisions to the NAAQS in 2010 were accompanied by
revisions to the ambient air monitoring and reporting regulations,
requiring the reporting of hourly maximum 5-minute SO2
concentrations, in addition to the hourly concentrations.

    Emissions of SO2 and associated concentrations in
ambient air have declined appreciably since 2010 and over the longer
term. For example, as summarized in the PA, emissions nationally are
estimated to have declined by 82% over the period from 2000 to 2016,
with a 64% decline from 2010 to 2016. Such declines in SO2
emissions are likely related to the implementation of national control
programs developed under the Clean Air Act Amendments of 1990, as well
as changes in market conditions, e.g., reduction in energy generation
by coal. One-hour concentrations of SO2 in ambient air in
the U.S. declined more than 82% from 1980 to 2016 at locations
continuously monitored over this period. The decline since 2000 has
been 69% at a larger number of locations continuously monitored since
that time. Daily maximum 5-minute concentrations have also consistently
declined from 2011 to 2016.
    In this review, as in past reviews of the primary NAAQS for
SOX, the health effects evidence evaluated in the ISA is
focused on SO2. The health effects of particulate
atmospheric transformation products of SOX, such as
sulfates, are addressed in the review of the NAAQS for particulate
matter (PM). Additionally, the welfare effects of SOX and
the ecological effects of particulate atmospheric transformation
products are being considered in the review of the secondary NAAQS for
oxides of nitrogen, oxides of sulfur, and PM, while the visibility,
climate, and materials damage-related welfare effects of particulate
sulfur compounds are being evaluated in the review of the secondary
NAAQS for PM.
    The health effects evidence newly available in this review, as
critically assessed in the ISA in conjunction with the full body of
evidence, reaffirms the conclusions from the last review. The health
effects evidence continues to support the conclusion that respiratory
effects are causally related to short-term SO2 exposures,
including effects related to asthma exacerbation in people with asthma,
particularly children with asthma. The clearest evidence for this
conclusion comes from controlled human exposure studies, available at
the time of the last review, that show that people with asthma
experience respiratory effects following very short (e.g., 5-10 minute)
exposures to SO2 while breathing at elevated rates.
Epidemiologic evidence, including that from studies not available in
the last review, also supports this conclusion, primarily due to
studies reporting positive associations between ambient air
concentrations and emergency department visits and hospital admissions,
specifically for children.
    Quantitative analyses of population exposure and risk also inform
the final decision. These analyses expand and improve upon the
quantitative analyses available in the last review. Unlike the REA
available in the last review, which analyzed single-year air quality
scenarios for potential standard levels bracketing the now-current
level, the current REA assesses an air quality scenario for 3 years of
air quality conditions that just meet the now-current standard,
considering all of its elements, including its 3-year form. Other ways
in which the current REA analyses are improved and expanded include
improvements to models, model inputs and underlying databases,
including the vastly expanded ambient air monitoring dataset for 5-
minute concentrations, available as a result of changes in the last
review to data reporting requirements.
    Based on this evidence and quantitative information, as well as
CASAC advice and consideration of public comment, the Administrator has
concluded that the current primary SO2 standard is requisite
to protect public health, with an adequate margin of safety, from
effects of SOX in ambient air and should be retained,
without revision. Therefore, the EPA is retaining the current 1-hour
primary SO2 standard, without revision. This decision is
consistent with CASAC recommendations.

I. Background

    This review focuses on the presence in ambient air of
SOX, a group of closely related gaseous compounds that
includes SO2 and sulfur trioxide (SO3) and of
which SO2 (the indicator for the current standard) is the
most prevalent in the atmosphere and the one for which there is a large
body of scientific evidence on health effects. The health effects of
particulate atmospheric transformation products of SOX, such
as sulfates, as well as visibility, climate, and materials damage-
related welfare effects of such particulate sulfur compounds are being
addressed in the review of the NAAQS for particulate matter (PM) (U.S.
EPA, 2014a, 2016a, 2018c). Additionally, the ecological welfare effects
of SOX and their particulate atmospheric transformation
products are being considered in the review of the secondary NAAQS for
oxides of nitrogen, oxides of sulfur, and PM (U.S. EPA, 2014a,
2017b).\1\
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    \1\ Additional information on the review of secondary NAAQS for
oxides of nitrogen, oxides of sulfur, and PM with regard to
ecological welfare effects is available at: https://www.epa.gov/naaqs/nitrogen-dioxide-no2-and-sulfur-dioxide-so2-secondary-air-quality-standards. Additional information on the review of the PM
NAAQS is available at: https://www.epa.gov/naaqs/particulate-matter-pm-air-quality-standards.
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A. Legislative Requirements

    Two sections of the Clean Air Act (CAA or the Act) govern the
establishment and revision of the NAAQS. Section 108 (42 U.S.C. 7408)
directs the Administrator to identify and list certain air pollutants
and then to issue air quality criteria for those pollutants. The
Administrator is to list those air pollutants that in his ``judgment,
cause or contribute to air pollution which may reasonably be
anticipated to endanger public health or welfare;'' ``the presence of
which in the ambient air results from numerous or diverse mobile or
stationary sources;'' and ``for which . . . [the Administrator] plans
to issue air quality criteria . . . .'' Air quality criteria are
intended to ``accurately reflect the latest scientific knowledge useful
in indicating the kind and extent of all identifiable effects on public
health or welfare which may be expected from the presence of [a]
pollutant in the ambient air . . .'' 42 U.S.C. 7408(a)(2). Section 109
(42 U.S.C. 7409) directs the Administrator to propose and promulgate
``primary'' and ``secondary'' NAAQS for pollutants for which air
quality criteria are 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 such criteria and allowing an
adequate margin of safety, [is] requisite to protect the public
health.'' \2\ As provided in section 109(b)(2), a secondary standard
must ``specify a level of air quality the attainment and maintenance of
which, in the judgment of the Administrator, based on such criteria, is
requisite to protect the public welfare from any known or anticipated
adverse effects associated with the presence of [the] pollutant in the
ambient air.'' \3\
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    \2\ 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 Lead
Industries Association v. EPA, 647 F.2d 1130, 1152 (D.C. Cir 1980);
American Lung Association v. EPA, 134 F.3d 388, 389 (D.C. 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.'').
    \3\ As specified in section 302(h) of the CAA (42 U.S.C.
7602(h)) effects on welfare include, but are not limited to,
``effects on soils, water, crops, vegetation, manmade materials,
animals, wildlife, weather, visibility, and climate, damage to and
deterioration of property, and hazards to transportation, as well as
effects on economic values and on personal comfort and well-being.''

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    The requirement that primary standards provide an adequate margin
of safety was intended to address uncertainties associated with
inconclusive scientific and technical information available at the time
of standard setting. It was also intended to provide a reasonable
degree of protection against hazards that research has not yet
identified. See Lead Industries Association v. EPA, 647 F.2d 1130, 1154
(D.C. Cir. 1980); American Petroleum Institute v. Costle, 665 F.2d
1176, 1186 (D.C. Cir. 1981); American Farm Bureau Federation v. EPA,
559 F.3d 512, 533 (D.C. Cir. 2009); Association of Battery Recyclers v.
EPA, 604 F.3d 613, 617-18 (D.C. Cir. 2010). 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 provide an adequate margin of safety, the Administrator is seeking
not only to prevent pollution levels that have been demonstrated to be
harmful but also to prevent lower pollutant levels that may pose an
unacceptable risk of harm, even if the risk is not precisely identified
as to nature or degree. However, the CAA does not require the
Administrator to establish a primary NAAQS at a zero-risk level or at
background concentrations, 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 an adequate margin of safety, the
EPA considers such factors as the nature and severity of the health
effects involved, the size of sensitive population(s) at risk,\4\ 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. See Lead Industries Association v. EPA, 647 F.2d at 1161-62.
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    \4\ As used here and similarly throughout this document, the
term population (or group) refers to persons having a quality or
characteristic in common, such as a specific pre-existing illness or
a specific age or lifestage. Section II.A.2.b below describes the
identification of sensitive groups (called at-risk groups or at-risk
populations) in this review.
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    In setting primary and secondary standards that are ``requisite''
to protect public health and welfare, respectively, as provided in
section 109(b), the EPA's task is to establish standards that are
neither more nor less stringent than necessary for these purposes. In
so doing, the EPA may not consider the costs of implementing the
standards. See generally Whitman v. American Trucking Associations, 531
U.S. 457, 465-472, 475-76 (2001). Likewise, ``[a]ttainability and
technological feasibility are not relevant considerations in the
promulgation of national ambient air quality standards.'' American
Petroleum Institute, 665 F.2d at 1185.
    Section 109(d)(1) requires that ``not later than December 31, 1980,
and at 5-year intervals thereafter, the Administrator shall complete a
thorough review of the criteria published under section 108 and the
national ambient air quality standards . . . and shall make such
revisions in such criteria and standards and promulgate such new
standards as may be appropriate . . . .'' Section 109(d)(2) requires
that an independent scientific review committee ``shall complete a
review of the criteria . . . and the national primary and secondary
ambient air quality standards . . . and shall recommend to the
Administrator any new . . . standards and revisions of existing
criteria and standards as may be appropriate . . . .'' Since the early
1980s, this independent review function has been performed by the
CASAC.

B. Related SO2 Control Programs

    States are primarily responsible for ensuring attainment and
maintenance of ambient air quality standards once the EPA has
established them. Under section 110 of the Act, 42 U.S.C. 7410, and
related provisions, states are to submit, for EPA approval, state
implementation plans (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 the
EPA, also administer the prevention of significant deterioration
permitting program that covers these and other air pollutants. See 42
U.S.C. 7470-7479. In addition, federal programs provide for nationwide
reductions in emissions of these and other air pollutants under Title
II of the Act, 42 U.S.C. 7521-7574, which involves controls for
automobile, truck, bus, motorcycle, nonroad engine and equipment, and
aircraft emissions. Furthermore, the EPA establishes emission standards
for stationary sources under other provisions of the CAA; these
standards, which include the new source performance standards (under
section 111 of the Act, 42 U.S.C. 7411), and the national emission
standards for hazardous air pollutants (under section 112 of the Act,
42 U.S.C. 7412) may also contribute to SO2 emissions
controls and reductions, including through controls aimed at reducing
other pollutants.

C. Review of the Air Quality Criteria and Standard for Sulfur Oxides

    The initial air quality criteria for SOX were issued in
1967 and reevaluated in 1969 (34 FR 1988, February 11, 1969; U.S. DHEW,
1967, 1969). Based on the 1969 criteria, the EPA, in initially
promulgating NAAQS for SOX in 1971, established the
indicator as SO2. SOX are a group of closely
related gaseous compounds that include SO2 and
SO3 and of which SO2 (the indicator for the
current standard) is the most prevalent in the atmosphere and the one
for which there is a large body of scientific evidence on health
effects. The two primary standards set in 1971 were 0.14 parts per
million (ppm) averaged over a 24-hour period, not to be exceeded more
than once per year, and 0.03 ppm, as an annual arithmetic mean (36 FR
8186, April 30, 1971).
    The first review of the air quality criteria and primary standards
for SOX was initiated in the early 1980s and concluded in
1996 with the decision to retain the standards without revision (61 FR
25566, May 22, 1996). In reaching this decision, the Administrator
considered the evidence newly available since the standards were set
that documented asthma-related respiratory effects in people with
asthma exposed for very short periods, such as 5 to 10 minutes. Based
on his consideration of an exposure analysis using the then-limited
monitoring data and early exposure modeling methods, the Administrator
judged that revisions to the standards were not needed to provide
requisite public health protection from SOX in ambient air
at that time (61 FR 25566, May 22, 1996). This decision was challenged
in the U.S. Court of Appeals for the District of Columbia Circuit (D.C.
Circuit), which found that the EPA had failed to adequately explain its
determination that no revision to the primary SO2 standards
was appropriate and remanded the determination back to the EPA for
further explanation. American Lung Association v. EPA, 134 F.3d 388
(D.C. Cir. 1998).
    This remand was addressed in the last review of the air quality
criteria and primary standards for SOX, which was completed
in 2010. In that review, the

EPA promulgated a new 1-hour standard and also promulgated provisions
for the revocation of the then-existing 24-hour and annual primary
standards.\5\ The new 1-hour standard was set with a level of 75 parts
per billion (ppb), a form of the 3-year average of the annual 99th
percentile of daily maximum 1-hour average SO2
concentrations, and SO2 as the indicator. The Administrator
judged that such a standard would provide the requisite protection for
at-risk populations, such as people with asthma, against the array of
adverse respiratory health effects related to short-term SO2
exposures, including those as short as 5 minutes. With regard to
longer-term exposures, the new standard was expected to maintain 24-
hour and annual concentrations generally well below the levels of the
previous standards, and the available evidence did not indicate the
need for separate standards designed to protect against longer-term
exposures (75 FR 35520, June 22, 2010). The EPA also revised the
SO2 ambient air monitoring regulations to require that
monitoring agencies using continuous SO2 methods report the
highest 5-minute concentration for each hour of the day; \6\ agencies
may report all twelve 5-minute concentrations for each hour, including
the maximum, although it is not required (75 FR 35568, June 22, 2010).
This rule and the EPA's denial of several petitions for administrative
reconsideration were challenged in the D.C. Circuit, and the court
denied or dismissed on jurisdictional grounds all the claims in the
petitions for review. National Environmental Development Association's
Clean Air Project v. EPA, 686 F.3d 803, 805 (D.C. Cir. 2012) (``NEDA/
CAP'').
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    \5\ Timing and related requirements for the implementation of
the revocation are specified in 40 CFR 50.4(e).
    \6\ The rationale for this requirement was described as
providing additional monitoring data for use in subsequent reviews
of the primary standard, particularly for use in considering the
extent of protection provided by the 1-hour standard against 5-
minute peak SO2 concentrations of concern (75 FR 35568,
June 22, 2010). In establishing this requirement, the EPA described
such data as being ``of high value to inform future health studies
and, subsequently, future SO2 NAAQS reviews'' (75 FR
35568, June 22, 2010).
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    In May 2013, the EPA initiated the current review by issuing a call
for information in the Federal Register and also announcing a public
workshop to inform the review (78 FR 27387, May 10, 2013). As was the
case for the prior review, this review is focused on health effects
associated with SOX and the public health protection
afforded by the existing standard. Participants in the kickoff workshop
included a wide range of external experts as well as EPA staff
representing a variety of areas of expertise (e.g., epidemiology, human
and animal toxicology, statistics, risk/exposure analysis, atmospheric
science, and biology). Workshop discussions focused on key policy-
relevant issues around which the Agency would structure the review and
the newly available scientific information related to these issues.
Based in part on the workshop discussions, the EPA developed the draft
Integrated Review Plan (IRP) outlining the schedule, process, and key
policy-relevant questions to guide this review of the SOX
air quality criteria and primary standard (U.S. EPA, 2014b). The draft
IRP was released for public comment and was reviewed by the CASAC at a
public teleconference on April 22, 2014 (79 FR 14035, March 12, 2014;
Frey and Diez Roux, 2014). The final IRP was developed with
consideration of comments from the CASAC and the public (U.S. EPA,
2014a; 79 FR 16325, March 25, 2014; 79 FR 66721, November 10, 2014).
    As an early step in development of the Integrated Science
Assessment (ISA) \7\ for this review, the EPA's National Center for
Environmental Assessment (NCEA) hosted a public workshop at which
preliminary drafts of key ISA chapters were reviewed by subject matter
experts (79 FR 33750, June 12, 2014). Comments received from this
review as well as comments from the public and the CASAC on the draft
IRP were considered in preparation of the first draft ISA (U.S. EPA,
2015), released in November 2015 (80 FR 73183, November 24, 2015). The
first draft ISA was reviewed by the CASAC at a public meeting in
January 2016 and a public teleconference in April 2016 (80 FR 79330,
December 21, 2015; 80 FR 79330, December 21, 2015; Diez Roux, 2016).
The EPA released the second draft ISA in December 2016 (U.S. EPA,
2016b; 81 FR 89097, December 9, 2016), which was reviewed by the CASAC
at a public meeting in March 2017 and a public teleconference in June
2017 (82 FR 11449, February 23, 2017; 82 FR 23563, May 23, 2017; Diez
Roux, 2017a). The final ISA was released in December 2017 (U.S. EPA,
2017a; 82 FR 58600, December 13, 2017).
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    \7\ The ISA for this review provides a comprehensive assessment
of the current scientific literature useful in indicating the kind
of and extent of all identifiable effects on public health
associated with the presence of the pollutant in the ambient air, as
described in section 108 of the CAA, emphasizing information that
has become available since the last air quality criteria review in
order to reflect the current state of knowledge. As such, the ISA
forms the scientific foundation for this NAAQS review and is
intended to provide information useful in forming policy relevant
judgments about air quality indicator(s), form(s), averaging time(s)
and level(s) for the NAAQS. The ISA functions in the current NAAQS
review process as the Air Quality Criteria Document (AQCD) did in
reviews completed prior to 2009.
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    In considering the need for quantitative exposure and risk analyses
in this review, the EPA completed the Risk and Exposure Assessment
(REA) Planning Document in February 2017 (U.S. EPA, 2017c; 82 FR 11356,
February 22, 2017) and held a consultation with the CASAC at a public
meeting in March 2017 (82 FR 11449, February 23, 2017; Diez Roux,
2017b). In consideration of the CASAC's comments at that consultation
and public comments, the EPA developed the draft REA and draft PA,
which were released on August 24, 2017 (U.S. EPA, 2017d, e; 82 FR
43756, September 19, 2017). The draft REA and draft PA were reviewed by
the CASAC on September 18-19, 2017 (82 FR 37213, August 9, 2017; Cox
and Diez Roux, 2018a, b). The EPA considered the advice and comments
from the CASAC on the draft REA and draft PA, as well as public
comments, in developing the final REA and final PA, which were released
in early May 2018 (U.S. EPA, 2018a, b).
    The proposed decision (henceforth ``proposal'') to retain the
primary SO2 NAAQS was signed on May 25, 2018, and published
in the Federal Register on June 8, 2018 (83 FR 26752). The EPA held a
public hearing in Washington, DC on July 10, 2018 (83 FR 28843, June
21, 2018). At the public hearing, the EPA heard testimony from three
individuals representing specific interested organizations. The
transcript from this hearing and written testimony provided at the
hearing are in the docket for this review. The EPA extended the 45-day
comment period by 17 days, until August 9, 2018 (83 FR 28843, June 21,
2018), and comments were received from various government, industry,
and environmental groups, as well as members of the general public.
    The schedule for completion of this review is governed by a consent
decree resolving a lawsuit filed in July 2016 that included a claim
that the EPA had failed to complete its review of the primary
SO2 NAAQS within 5 years, as required by the CAA.\8\ The
consent decree, which was entered by the court on April 28, 2017,
provides that the EPA will sign, for publication, a notice setting
forth the final decision concerning its review of the primary NAAQS for
SOX no later than January

28, 2019, with such date to be extended automatically one day for each
day of a lapse in appropriations if such a lapse were to occur within
120 days of this deadline.\9\ The EPA experienced such a lapse in
appropriations in late December 2018 and January 2019, which led to the
automatic extension of the January 28, 2019 deadline to February 25,
2019.\10\
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    \8\ See Complaint, Center for Biological Diversity et al. v.
Wheeler, No. 3:16-cv-03796-VC (N.D. Cal., filed July 7, 2016), Doc.
No. 1.
    \9\ Consent Judgment at 4, Center for Biological Diversity et
al. v. Wheeler, No. 3:16-cv-03796-VC (N.D. Cal., entered April 28,
2017), Doc. No. 37.
    \10\ Joint Notice of Automatic Deadline Extension in Light of
Lapse in Appropriations, Center for Biological Diversity et al. v.
Wheeler, No. 3:16-cv-03796-VC (N.D. Cal., filed February 15, 2019),
Doc. No. 39.
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D. Air Quality Information

    This section presents information on sources and emissions of
SO2 and ambient concentrations, with a focus on information
that is most relevant for the review of the primary SO2
standard. This section is drawn from the more detailed discussion of
SO2 air quality in the PA and the ISA. It presents a summary
of SOX sources and emissions (section I.D.1) and ambient
concentrations (section I.D.2).
1. Sources and Emissions of Sulfur Oxides
    Sulfur oxides are emitted into air from specific sources (e.g.,
fuel combustion processes) and are also formed in the atmosphere from
other atmospheric compounds (e.g., as an oxidation product of reduced
sulfur compounds, such as sulfides). Sulfur oxides are also transformed
in the atmosphere to particulate sulfur compounds, such as
sulfates.\11\ Sulfur oxides known to occur in the troposphere include
SO2 and SO3 (ISA, section 2.3). With regard to
SO3, it ``is known to be present in the emissions of coal-
fired power plants, factories, and refineries, but it reacts with water
vapor in the stacks or immediately after release into the atmosphere to
form H2SO4'' and ``gas-phase
H2SO4 . . . quickly condenses onto existing
atmospheric particles or participates in new particle formation'' (ISA,
section 2.3). Thus, as a result of rapid atmospheric chemical reactions
involving SO3, the most prevalent sulfur oxide in the
atmosphere is SO2 (ISA, section 2.3).\12\
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    \11\ Some sulfur compounds formed from or emitted with
SOX are very short-lived (ISA, pp. 2-23 to 2-24). For
example, studies in the 1970s and 1980s identified particle-phase
sulfur compounds, including inorganic SO3-2
complexed with Fe(III) in the particles emitted by a smelter near
Salt Lake City, UT. Subsequent studies reported rapid oxidation of
such compounds, ``on the order of seconds to minutes'' and ``further
accelerated by low pH'' (ISA, p. 2-24). Thus, ``[t]he highly acidic
aqueous conditions that arise once smelter plume particles
equilibrate with the ambient atmosphere ensure that S(IV)-Fe(III)
complexes have a small probability of persisting and becoming a
matter of concern for human exposure'' (ISA, p. 2-24).
    \12\ The health effects of particulate atmospheric
transformation products of SOX, such as sulfates, are
addressed in the review of the NAAQS for PM (U.S. EPA 2014a, 2016a,
2018c).
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    Fossil fuel combustion is the main anthropogenic source of
SO2 emissions, while volcanoes and landscape fires
(wildfires as well as controlled burns) are the main natural sources
(ISA, section 2.1).\13\ Industrial chemical production, pulp and paper
production, natural biological activity (plants, fungi, and
prokaryotes), and volcanoes are among many sources of reduced sulfur
compounds that contribute, through various oxidation reactions in the
atmosphere, to the formation of SO2 in the atmosphere (ISA,
section 2.1). Anthropogenic SO2 emissions originate
primarily from point sources, including coal-fired electricity
generating units (EGUs) and other industrial facilities (ISA, section
2.2.1). The largest SO2-emitting sector within the U.S. is
electricity generation, and 97% of SO2 from electricity
generation is from coal combustion. Other anthropogenic sources of
SO2 emissions include industrial fuel combustion and process
emissions, industrial processing, commercial marine activity, and the
use of fire in landscape management and agriculture (ISA, section
2.2.1).
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    \13\ A modeling analysis estimated annual mean SO2
concentrations for 2001 in the absence of any U.S. anthropogenic
emissions of SO2 (2008 ISA, section 2.5.3; ISA, section
2.5.5). Such concentrations are referred to as U.S. background or
USB. The 2008 ISA analysis estimated USB concentrations of
SO2 to be below 0.01 ppb over much of the U.S., ranging
up to a maximum of 0.03 ppb (ISA, section 2.5.5).
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    National average SO2 emissions are estimated to have
declined by 82% over the period from 2000 to 2016, with a 64% decline
from 2010 to 2016 (PA, Figure 2-2; 2014 National Emissions Inventory
(NEI)). Such declines in SO2 emissions are likely related to
the implementation of national control programs developed under the
Clean Air Act Amendments of 1990, including Phase I and II of the Acid
Rain Program, the Clean Air Interstate Rule, the Cross-State Air
Pollution Rule, and the Mercury Air Toxic Standards,\14\ as well as
changes in market conditions, e.g., reduction in energy generation by
coal (PA, section 2.1, Figure 2-2; U.S. EIA, 2017).\15\ Regulations on
sulfur content of diesel fuel, both fuel for onroad vehicles and
nonroad engines and equipment, may also contribute to declining trends
in SO2 emissions.\16\ Declines in emissions from all sources
between 1971, when SOX NAAQS were first established, and
1990, when the Amendments were adopted, were on the order of 5,000 tpy
deriving primarily from reductions in emissions from the metals
processing sector (ISA, Figure 2-5).
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    \14\ When established, the MATS Rule was estimated to reduce
SO2 emissions from power plants by 41% beyond the
reductions expected from the Cross-State Air Pollution Rule (U.S.
EPA, 2011).
    \15\ In 2014, the EPA promulgated Tier 3 Motor Vehicle Emission
and Fuel Standards that set emissions standards for new vehicles and
lowered the sulfur content of gasoline. Reductions in SO2
emissions resulting from these standards are expected to be more
than 14,000 tons in 2018 (U.S. EPA, 2014c).
    \16\ See https://www.epa.gov/diesel-fuel-standards/diesel-fuel-standards-and-rulemakings#nonroad-diesel.
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2. Ambient Concentrations
    Ambient air concentrations of SO2 in the U.S. have
declined substantially from 1980 to 2016, more than 82% in terms of the
form of the current standard (the 3-year average of annual 99th
percentile daily maximum 1-hour concentrations) at locations
continuously monitored over this period (PA, Figure 2-4).\17\ The
decline since 2000 has been 69% at the larger number of locations
continuously monitored since that time (PA, Figure 2-5).\18\
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    \17\ This decline is the average of observations at 24
monitoring sites that have been continuously operating from 1980-
2016.
    \18\ This decline is the average of observations at 193
monitoring sites that have been continuously operating across 2000-
2016.
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    As a result of changes to the monitoring data reporting
requirements promulgated in 2010 (as summarized in section I.C above)
maximum hourly 5-minute concentrations of SO2 in ambient air
are available at SO2 NAAQS compliance monitoring sites (PA,
Figure 2-3; 75 FR 35554, June 22, 2010).\19\ These newly available data
document reductions in peak 5-minute concentrations across the U.S. For
example, over the period from 2011 to 2016, the 99th percentile 5-
minute SO2 concentrations at SO2 sites
continuously monitored during this period declined approximately 53%
(PA, Figure 2-6, Appendix B).
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    \19\ Such measurements were available for fewer than 10% of
monitoring sites at the time of the last review. Of the monitors
reporting 5-minute data in 2016, almost 40% are reporting all twelve
5-minute SO2 measurements in each hour while about 60%
are reporting the maximum 5-minute SO2 concentration in
each hour (PA, section 2.2). The expanded dataset has provided a
more robust foundation for the quantitative analyses in the REA for
this review.
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    Concentrations of SO2 vary across the U.S. and tend to
be higher in areas with sources having relatively higher SO2
emissions (e.g., locations influenced by emissions from EGUs).
Consistent with the locations of larger SO2 sources, higher
concentrations are primarily

located in the eastern half of the continental U.S., especially in the
Ohio River valley, upper Midwest, and along the Atlantic coast (PA,
Figure 2-7). The point source nature of SO2 emissions
contributes to the relatively high spatial variability of
SO2 concentrations compared with pollutants such as ozone
(ISA, section 3.2.3). Another factor in the spatial variability is the
dispersion and oxidation of SO2 in the atmosphere, processes
that contribute to decreasing concentrations with increasing distance
from the source. Point source emissions of sulfur oxides create a plume
of appreciably higher concentrations in the air, which may or may not
impact large portions of the surrounding populated areas depending on
specific source characteristics, meteorological conditions and terrain.
    Analyses in the ISA of ambient air monitoring data for 2013-2015 in
six areas indicate that 1-hour daily maximum SO2
concentrations vary across seasons, with the greatest variations seen
in the upper percentile concentrations (versus average or lower
percentiles) for each season (ISA, section <IP_ADDRESS>).\20\ This seasonal
variation as well as month-to-month variations are generally consistent
with month-to-month emissions patterns and the expected atmospheric
chemistry of SO2 for a given season. Consistent with the
nationwide diel patterns reported in the last review, 1-hour average
and 5-minute hourly maximum SO2 concentrations for 2013-2015
in all six areas evaluated were generally low during nighttime and
approached maxima values during daytime hours (ISA, section <IP_ADDRESS>,
Figures 2-23 and 2-24). The timing and duration of daytime maxima in
the six sites evaluated in the ISA were likely related to a combination
of source emissions and meteorological parameters (ISA, section
<IP_ADDRESS>; 2008 ISA [U.S. EPA 2008a], section 2.5.1).
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    \20\ The six ``focus areas'' evaluated in the ISA are:
Cleveland, OH; Pittsburgh, PA; New York City, NY; St. Louis, MO (and
neighboring areas in IL); Houston, TX; and Gila County, AZ (ISA,
section <IP_ADDRESS>). These six locations were selected based on (1)
their relevance to current health studies (i.e., areas with peer-
reviewed, epidemiologic analysis); (2) the existence of four or more
monitoring sites located within the area boundaries; and (3) the
presence of several diverse SO2 sources within a given
focus area boundary.
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II. Rationale for Decision

    This section presents the rationale for the Administrator's
decision to retain the existing primary SO2 standard. This
decision is based on a thorough review in the ISA of the latest
scientific information, published through August 2016 (ISA, p. xlii),
on human health effects associated with SOX in ambient air.
This decision also accounts for analyses in the PA of policy-relevant
information from the ISA and the REA, as well as information on air
quality; the analyses of human exposure and health risks in the REA;
CASAC advice; and consideration of public comments received on the
proposal.
    Section II.A provides background on the general approach for this
review and the basis for the existing standard, and also presents brief
summaries of key aspects of the currently available health effects and
exposure/risk information. Section II.B summarizes the proposed
conclusions and CASAC advice, addresses public comments received on the
proposal and presents the Administrator's conclusions on the adequacy
of the current standard, drawing on consideration of this information,
advice from the CASAC, and comments from the public. Section II.C
summarizes the Administrator's decision on the primary standard.

A. Introduction

    As in prior reviews, the general approach to reviewing the current
primary standard is based, most fundamentally, on using the EPA's
assessment of current scientific evidence and associated quantitative
analyses to inform the Administrator's judgment regarding a primary
SO2 standard that protects public health with an adequate
margin of safety. In drawing conclusions with regard to the primary
standard, the final decision on the adequacy of the current standard is
largely a public health policy judgment to be made by the
Administrator. The Administrator's final decision draws upon scientific
information and analyses about health effects, population exposure and
risks, as well as judgments about how to consider the range and
magnitude of uncertainties that are inherent in the scientific evidence
and exposure/risk analyses. The approach to informing these judgments,
discussed more fully below, is based on the recognition that the
available health effects evidence generally reflects a continuum,
consisting of levels 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.
This approach is consistent with the requirements of the NAAQS
provisions of the Clean Air Act and with how the EPA and the courts
have historically interpreted the Act. These provisions require the
Administrator to establish primary standards that, in his judgment, are
requisite to protect public health with an adequate margin of safety.
In so doing, the Administrator seeks to establish standards that are
neither more nor less stringent than necessary for this purpose. The
Act does not require that primary standards be set at a zero-risk
level, but rather at a level that avoids unacceptable risks to public
health including the health of sensitive groups.\21\ The four basic
elements of the NAAQS (indicator, averaging time, level, and form) are
considered collectively in evaluating the health protection afforded by
a standard.
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    \21\ As noted in section I.A above, such protection is specified
for the sensitive group of individuals and not to a single person in
the sensitive group (see S. Rep. No. 91-1196, 91st Cong., 2d Sess.
10 [1970]).
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    In evaluating the appropriateness of retaining or revising the
current primary SO2 standard, the EPA has adopted an
approach that builds upon the general approach used in the last review
and reflects the body of evidence and information now available. As
summarized in section II.A.1 below, the Administrator's decisions in
the prior review were based on an integration of information on health
effects associated with exposure to SO2 with information on
the public health significance of key health effects, as well as on
policy judgments as to when the standard is requisite to protect public
health with an adequate margin of safety and on consideration of advice
from the CASAC and public comments. These decisions were also informed
by air quality and related analyses and quantitative exposure and risk
information.
    Similarly, in this review, as described in the PA, the proposal,
and elsewhere in this document, we draw on the current evidence and
quantitative assessments of exposure and risk pertaining to the public
health risk of SO2 in ambient air. The past and current
approaches are both based, most fundamentally, on the EPA's assessments
of the current scientific evidence and associated quantitative
analyses. The EPA's assessments are primarily documented in the ISA,
REA and PA, all of which have received CASAC review and public comment
(80 FR 73183, November 24, 2015; 80 FR 79330, December 21, 2015; 81 FR
89097, December 9, 2016; 82 FR 11356, February 22, 2017; 82 FR 11449,
February 23, 2017; 82 FR 23563, May 23, 2017; 82 FR 37123, August 9,
2017; 82 FR 43756, September 19, 2017; 83 FR 14638, April 5, 2018). To
bridge the gap between the scientific assessments of the ISA and REA
and the judgments required of the Administrator in determining whether
the current standard remains requisite to protect

public health with an adequate margin of safety, the PA evaluates the
policy implications of the current evidence in the ISA and of the
quantitative analyses in the REA.
    In considering the scientific and technical information, we
consider both the information available at the time of the last review
and information newly available since the last review, including most
particularly that which has been critically analyzed and characterized
in the current ISA. We additionally consider the quantitative exposure
and risk information described in the REA that estimated
SO2-related exposures and lung function decrements
associated with air quality conditions just meeting the current
standard in simulated at-risk populations in multiple case study areas
(REA, chapter 5). The evidence-based discussions presented below (and
summarized more fully in the proposal) draw upon evidence from studies
evaluating health effects related to exposures to SO2, as
discussed in the ISA. The exposure/risk-based discussions also
presented below (and summarized more fully in the proposal) have been
drawn from the quantitative analyses for SO2, as discussed
in the REA. Sections II.A.2 and II.A.3 below provide an overview of the
current health effects and quantitative exposure and risk information
with a focus on the specific policy-relevant questions identified for
these categories of information in the PA (PA, chapter 3).
1. Background on the Current Standard
    The current primary standard was established in the last review of
the primary NAAQS for SOX, which was completed in 2010 (75
FR 35520, June 22, 2010). The decision in that review to revise the
primary standards (establishing a 1-hour standard and providing for
revocation of the 24-hour and annual standards) reflected the extensive
body of evidence of respiratory effects in people with asthma, which
has expanded over the four decades since the first SO2
standards were established in 1971 (U.S. EPA, 1982, 1986, 1994, 2008a).
This evidence was assessed in the 2008 ISA.
    A key element of the expanded evidence base was a series of
controlled human exposure studies documenting effects on lung function
associated with bronchoconstriction in people with asthma exposed while
breathing at elevated rates \22\ for periods as short as minutes (U.S.
EPA, 1982, 1986, 1994, 2008a). Another aspect of the information
available in the 2010 review was the air quality database, which had
expanded since the previous review (completed in 1996), and which
provided data on the pattern of peak 5-minute SO2
concentrations occurring at that time. The EPA used these data in the
2009 quantitative exposure and risk assessments to provide an up-to-
date ambient air quality context for interpreting the health effects
evidence. In addition to providing support for decisions in the 2010
review, these aspects of that review provided support to the EPA in
addressing the issues raised in the court remand of the Agency's 1996
decision not to revise the standards to specifically address 5-minute
exposures with that decision (75 FR 35523, June 22, 2010). Together,
the evidence characterized in the 2008 ISA, which included
epidemiologic and animal toxicologic studies as well as the extensive
set of controlled human exposure studies, and the quantitative
assessments in the 2009 REA, as well as advice from the CASAC and
public comment, formed the basis for the EPA's 2010 action to
strengthen the primary NAAQS for SOX to provide the
requisite protection of public health with an adequate margin of
safety, and to provide increased protection for at-risk populations,
such as people with asthma (75 FR 35550, June 22, 2010).
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    \22\ The phrase ``elevated ventilation'' (or ``moderate or
greater exertion'') was used in the 2009 REA and Federal Register
notifications in the last review to refer to activity levels in
adults that would be associated with ventilation rates at or above
40 liters per minute; an equivalent ventilation rate was derived in
order to identify corresponding rates for the range of ages and
sizes of the simulated populations (U.S. EPA, 2009, section
<IP_ADDRESS>). Accordingly, these phrases are used in the current review
when referring to REA analyses from the last review. Otherwise,
however, the documents for this review generally use the phrase
``elevated breathing rates'' in place of those phrases.
---------------------------------------------------------------------------

    Thus, the 2010 decision focused on the effects most pertinent to
SOX in ambient air and recognized the long-standing evidence
regarding the sensitivity of some people with asthma to brief
SO2 exposures experienced while breathing at elevated rates.
The robust evidence base, comprised of findings from controlled human
exposure, epidemiologic, and animal toxicological studies, was judged
``sufficient to infer a causal relationship'' between short-term
SO2 exposures ranging from 5 minutes to 24 hours and
respiratory morbidity (75 FR 35535, June 22, 2010). The ``definitive
evidence'' for this conclusion came from studies of 5- to 10-minute
controlled exposures that reported respiratory symptoms and decreased
lung function in exercising individuals with asthma (2008 ISA, section
5.3). Supporting evidence was provided by epidemiologic studies of
associations of a broader range of health outcomes with ambient air
concentrations of SO2, with uncertainty noted about the
magnitude of the study effect estimates, quantification of the
concentration-response relationship, potential confounding by
copollutants, and other aspects (75 FR 35535-36, June 22, 2010; 2008
ISA, section 5.3).
    Accordingly, conclusions reached in the last review were based
primarily on consideration of the health effects evidence for short-
term exposures, and particularly on interpretation of the evidence from
controlled human exposure studies within the context of the
quantitative exposure and risk analyses. The epidemiologic evidence
also provided support for various aspects of the decision. In making
judgments on the public health significance of health effects related
to short-term ambient air-related SO2 exposures, the
Administrator considered statements from the American Thoracic Society
(ATS) regarding adverse effects of air pollution,\23\ the CASAC's
written advice and comments,\24\ and judgments made by the EPA in
considering similar effects in previous NAAQS reviews (75 FR 35526 and
35536, June 22, 2010; ATS, 1985, 2000a). Based on these considerations,
the Administrator, in 2010, gave weight to the findings of respiratory
effects in exercising people with asthma after 5- to 10-minute
exposures as low as 200 ppb, and further recognized that higher
exposures (at or above 400 ppb) were associated with respiratory
symptoms and with a greater number of study subjects experiencing lung
function decrements. Moreover, she took note of the greater severity of
the response at and above 400 ppb, recognizing effects associated

with exposures as low as 200 ppb to be less severe (75 FR 35547, June
22, 2010).
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    \23\ The 1999 statement of the ATS (published in 2000) on ``What
Constitutes an Adverse Health Effect of Air Pollution?'' is
``intended to provide guidance to policy makers and others who
interpret the scientific evidence on the health effects of air
pollution for the purpose of risk management'' and describes
``principles to be used in weighing the evidence'' when considering
what may be adverse and nonadverse effects on health (ATS, 2000a).
For example, the ATS statements recognized a distinction between
reversible and irreversible effects, recommending that reversible
loss of lung function in combination with the presence of symptoms
be considered adverse (ATS 1985, 2000a; 75 FR 35526, June 22, 2010).
    \24\ For example, the CASAC letter on the first draft
SO2 REA to the Administrator stated: ``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'' (Henderson, 2008).
---------------------------------------------------------------------------

    As a result and based on consideration of the entire body of
evidence and information available in the review, with particular
attention to the exposure and risk estimates from the 2009 REA, as well
as the advice from the CASAC and public comments, the Administrator
concluded that the then-existing 24-hour standard did not adequately
protect public health (75 FR 35536, June 22, 2010). The 2009 REA
estimated that substantial percentages of children with asthma might be
expected to experience exposures at least once annually that had been
associated with moderate or greater lung function decrements \25\ in
the controlled human exposure studies (75 FR 35536, June 22, 2010). The
Administrator judged that such exposures can result in adverse health
effects in people with asthma and found that the estimated population
frequencies for such exposures (24% of the at-risk population with at
least one occurrence per year at or above 400 ppb and 73% with at least
one occurrence per year at or above 200 ppb) were significant from a
public health perspective and that the then-existing primary standards
did not adequately protect public health (75 FR 35536, June 22,
2010).\26\ In order to provide the requisite protection to people with
asthma from the adverse health effects of 5-minute to 24-hour
SO2 exposures, she replaced the 24-hour standard with a new,
1-hour standard (75 FR 35536, June 22, 2010). Further, upon reviewing
the evidence with regard to the potential for effects from long-term
exposures,\27\ the Administrator revoked the annual standard based on
her recognition of the lack of sufficient health evidence to support a
long-term standard and on air quality information indicating that the
new short-term standard would have the effect of generally maintaining
annual SO2 concentrations well below the level of the
revoked annual standard (75 FR 35550, June 22, 2010).
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    \25\ In assessments for NAAQS reviews, the magnitude of lung
function responses described as indicative of a moderate response
include increases in specific airway resistance (sRaw) of at least
100% (e.g., 2008 ISA; U.S. EPA, 1994, Table 8; U.S. EPA, 1996, Table
8-3). The moderate category has also generally included reductions
in forced expiratory volume in 1 second (FEV1) of 10 to
20% (e.g., U.S. EPA, 1996, Table 8). For the 2008 ISA, the midpoint
of that range (15%) was used to indicate a moderate response. A
focus on 15% reduction in FEV1 was also consistent with
the relationship observed between sRaw and FEV1 responses
in the Linn et al. studies (1987, 1990) for which ``a 100% increase
in sRaw roughly corresponds to a 12 to 15% decrease in
FEV1'' (U.S. EPA, 1994, p. 20). Thus, in the 2008 review,
moderate or greater SO2-related bronchoconstriction or
decrements in lung function referred to the occurrence of at least a
doubling in sRaw or at least a 15% reduction in FEV1
(2008 ISA, p. 3-5).
    \26\ In giving particular attention to the exposure and risk
estimates from the 2009 REA for air quality just meeting the then-
existing standards, the Administrator also noted epidemiologic study
findings of associations with respiratory-related health outcomes in
studies of locations where maximum 24-hour average SO2
concentrations were below the level of the then-existing 24-hour
standard, while also recognizing uncertainties associated with the
epidemiologic evidence (75 FR 35535-36, June 22, 2010).
    \27\ In evaluating the health effects studies in the ISA, the
EPA has generally categorized exposures of durations longer than a
month to be ``long-term'' (ISA, p. 1-2; 2008 ISA, p. 3-1).
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    The Administrator selected a 1-hour averaging time for the new
standard based on available air quality analyses in the REA that
indicated that a 1-hour averaging time would be effective in addressing
5-minute peak SO2 concentrations such that the requisite
protection from 5- to 10-minute exposure events could be provided
without having a standard with a 5-minute averaging time (75 FR 35539,
June 22, 2010).\28\ The analyses suggested that, compared to a 24-hour
averaging time, a 1-hour averaging time would more efficiently and
effectively limit 5-minute peak concentrations of SO2 that
had been shown in controlled human exposure studies to result in
increased prevalence of respiratory symptoms and/or decrements in lung
function in exercising people with asthma (2009 REA, section <IP_ADDRESS>;
75 FR 35539, June 22, 2010). The analyses found that a 1-hour standard
could substantially reduce the upper end of the distribution of
SO2 concentrations in ambient air that were more likely to
be associated with respiratory effects, while the longer averaging time
was shown to lack effectiveness and efficiency in addressing 5-minute
peak SO2 concentrations, likely over-controlling in some
areas while under-controlling in others (75 FR 35539, June 22, 2010;
2009 REA, section <IP_ADDRESS>). The CASAC additionally advised that ``a
one-hour standard is the preferred averaging time'' (Samet, 2009, pp.
15, 16), finding the REA to provide a ``convincing rationale'' that
supported ``a one-hour standard as protective of public health''
(Samet, 2009, pp. 1, 15 and 16). Thus, in consideration of the
available information summarized here and CASAC advice, the
Administrator judged that a 1-hour standard (given the appropriate
level and form) was the appropriate means for controlling short-term
exposures to SO2 ranging from 5 minutes to 24 hours (75 FR
35539, June 22, 2010).
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    \28\ The Administrator judged that a standard with a 5-minute
averaging time would result in significant and unnecessary
instability in public health protection (75 FR 35539, June 22,
2010). Such instability could reduce public health protection by
disrupting an area's ongoing implementation plans and associated
control programs (75 FR 35537, June 22, 2010).
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    The statistical form for the 1-hour standard, the 99th percentile
daily maximum 1-hour average concentrations averaged over 3 years, is
based on consideration of the health effects evidence, stability in the
public health protection provided by the programs implementing the
standard, and advice from the CASAC, as well as results of the 2009 REA
for alternative standard forms (75 FR 35541, June 22, 2010). With
regard to stability, the concentration-based form averaged over 3 years
was concluded to be appreciably more stable than a no-exceedance based
form, which had been the form of the then-existing 24-hour standard (75
FR 35541, June 22, 2010). The Administrator's objective in selecting
the specific concentration-based form was for the form of the new
standard to be especially focused on limiting the upper end of the
distribution of ambient SO2 concentrations (i.e., above 90th
percentile SO2 concentrations) in order to provide
protection with an adequate margin of safety against effects observed
in controlled human exposure studies and associated with ambient air
SO2 concentrations in epidemiologic studies (75 FR 35541,
June 22, 2010). Based on results of air quality and exposure analyses
in the REA which indicated the 99th percentile form likely to be
appreciably more effective at achieving the desired control of 5-minute
peak exposures than a 98th percentile form, the Administrator decided
the form should be the 99th percentile of daily maximum 1-hour
concentrations averaged over 3 years (75 FR 35541, June 22, 2010).
    The level for the new standard was set primarily based on
consideration of the findings of the 2009 REA exposure analyses with
regard to the varying degrees of protection that different levels of a
1-hour daily maximum SO2 standard might be expected to
provide against 5-minute exposures to concentrations of 200 ppb and 400
ppb.\29\ For example, the single-year

exposure assessment for St. Louis \30\ estimated that a 1-hour standard
at 100 ppb would likely protect more than 99% of children with asthma
in that city from experiencing any days in a year with at least one 5-
minute exposure at or above 400 ppb while at moderate or greater
exertion, and approximately 97% of those children with asthma from
experiencing any days in a year with at least one exposure at or above
200 ppb while at moderate or greater exertion (75 FR 35546-47, June 22,
2010). The St. Louis study area results for the air quality scenario
representing a 1-hour standard level of 50 ppb suggested that such a
standard would further limit exposures, such that more than 99% of
children at moderate or greater exertion would likely be protected from
experiencing any days in a year with a 5-minute exposure at or above
the 200 ppb benchmark concentration (75 FR 35542, June 22, 2010). In
considering the implications of these estimates, and the substantial
reduction in 5-minute exposures at or above 200 ppb, the Administrator
did not judge that a standard level as low as 50 ppb \31\ was warranted
(75 FR 35547, June 22, 2010). Before reaching her conclusion with
regard to level for the 1-hour standard, the Administrator additionally
considered the epidemiologic evidence, placing relatively more weight
on those U.S. epidemiologic studies (some conducted in multiple
locations) reporting mostly positive and sometimes statistically
significant associations between ambient SO2 concentrations
and emergency department visits or hospital admissions related to
asthma or other respiratory symptoms, and noting a cluster of three
studies for which 99th percentile 1-hour daily maximum concentrations
were estimated to be between 78-150 ppb and for which the
SO2 effect estimate remained positive and statistically
significant in copollutant models with PM (75 FR 35547-48, June 22,
2010).\32\
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    \29\ The Administrator additionally noted the results of the
analysis of the limited available air quality data for 5-minute
SO2 concentrations with regard to prevalence of higher 5-
minute concentrations at monitor sites when data were adjusted to
just meet a standard level of 100 ppb. This 40-county analysis,
which compared 5-minute concentrations estimated to occur in these
air quality scenarios to benchmark levels, indicated for a 1-hour
standard level of 100 ppb, there would be a maximum annual average
of 2 days per year with 5-minute concentrations above 400 ppb and 13
days with 5-minute concentrations above 200 ppb (75 FR 35546, June
22, 2010).
    \30\ Of the two study areas assessed in the 2009 REA (St. Louis
and Greene County, Missouri), the EPA considered the St. Louis
results to be more informative to consideration of the adequacy of
protection associated with the then-current and alternative
standards (75 FR 35528, June 22, 2010; 74 FR 64840, December 8,
2009). The St. Louis study area included several counties and had
population size and magnitudes of emissions density (on a spatial
scale) similar to other urban areas in the U.S., while the second
study area (Greene County, Missouri) was a rural county with much
lower population and emissions density.
    \31\ In the 2009 REA results for the St. Louis single year
scenario with a level of 50 ppb (the only level below 100 ppb that
was analyzed), 99.9% of children with asthma would be expected to be
protected from a day with a 5-minute exposure at or above 200 ppb,
and 100% from a day with a 5-minute exposure at or above 400 ppb
(2009 REA, Appendix, p. B-62).
    \32\ Regarding the monitor concentrations in these studies, the
EPA noted that although they may be a reasonable approximation of
concentrations occurring in the areas, the monitored concentrations
were likely somewhat lower than the absolute highest 99th percentile
1-hour daily maximum SO2 concentrations occurring across
these areas (75 FR 35547, June 22, 2010).
---------------------------------------------------------------------------

    Based on the above considerations and the comments received on the
proposal, advice from the CASAC, the entire body of evidence and
information available in that review, and the related
uncertainties,\33\ the Administrator selected a standard level of 75
ppb. She concluded that such a standard, with a 1-hour averaging time
and 99th percentile form, would provide an increase in public health
protection compared to the then-existing standards and would be
expected to provide the desired degree of protection against the
respiratory effects elicited by SO2 exposures in controlled
human exposure studies and associated with ambient air concentrations
in epidemiologic studies (75 FR 35548, June 22, 2010).\34\ The
Administrator emphasized the latter in judging that the level of 75 ppb
provided an adequate margin of safety (75 FR 35548, June 22, 2010).
Thus, she concluded that a NAAQS for SOX of 75 ppb, as the
99th percentile of daily maximum 1-hour average SO2
concentrations averaged over 3 years, would provide the requisite
protection of public health with an adequate margin of safety (75 FR
35547-35548, June 22, 2010).
---------------------------------------------------------------------------

    \33\ Such uncertainties included both those with regard to the
epidemiologic evidence, including potential confounding and exposure
measurement error, and also those with regard to the information
from controlled human exposure studies for at-risk groups, including
the extent to which the results would be expected to be similar for
individuals with more severe asthma than that in study subjects (75
FR 35546, June 22, 2010).
    \34\ For example, such a standard was considered likely ``to
maintain SO2 concentrations below those in locations
where key U.S. epidemiologic studies have reported that ambient
SO2 is associated with clearly adverse respiratory health
effects, as indicated by increased hospital admissions and emergency
department visits'' and also was ``expected to substantially limit
asthmatics' exposure to 5-10 minute SO2 concentrations
>=200 ppb, thereby substantially limiting the adverse health effects
associated with such exposures'' (75 FR 35548, June 22, 2010).
---------------------------------------------------------------------------

2. Overview of Health Effects Evidence
    In this section, we provide an overview of the policy-relevant
aspects of the health effects evidence available for consideration in
this review. Section II.B of the proposal provides a detailed summary
of key information contained in the ISA and in the PA on the health
effects associated with SO2 exposures, and the related
public health implications, focusing particularly on the information
most relevant to consideration of effects associated with the presence
of SO2 in ambient air (83 FR 26761, June 8, 2018). The
subsections below briefly outline this information in the four topic
areas addressed in section II.B of the proposal.
a. Nature of Effects
    Sulfur dioxide is a highly reactive and water-soluble gas that once
inhaled is absorbed almost entirely in the upper respiratory tract \35\
(ISA, sections 4.2 and 4.3). Brief exposures to SO2 can
elicit respiratory effects, particularly in individuals with asthma
when breathing at elevated rates (ISA, p. 1-17). Under conditions of
elevated breathing rates (e.g., while exercising), SO2
penetrates the upper respiratory tract, entering the tracheobronchial
region,\36\ where, in sufficient concentration, it results in responses
linked to asthma exacerbation in individuals with asthma (ISA, sections
4.2, 4.3, and 5.2). People with asthma have an increased propensity for
the airways to narrow in response to certain inhaled stimuli, as
compared to people without asthma or allergies (ISA, section
<IP_ADDRESS>).\37\ This narrowing or constriction of the airways in the
respiratory tract, termed bronchoconstriction, is characteristic of an
asthma attack and is the most sensitive indicator of SO2-
induced lung function effects (ISA, p. 5-8). Bronchoconstriction causes
an increase in airway resistance, often assessed by measurement of
specific airway resistance (sRaw). Exercising individuals without
asthma have also been found to exhibit increased sRaw or related
responses, such as reduced forced expiratory volume in 1 second
(FEV1), but at much higher SO2

exposure concentrations than exercising individuals with asthma (ISA,
section <IP_ADDRESS>). For example, the ISA finds that ``healthy adults are
relatively insensitive to the respiratory effects of SO2
below 1 ppm'' (ISA, p. 5-9).
---------------------------------------------------------------------------

    \35\ The term ``upper respiratory tract'' refers to the portion
of the respiratory tract--including the nose, mouth and larynx--that
precedes the tracheobronchial region (ISA, sections 4.2 and 4.3).
    \36\ The term ``tracheobronchial region'' refers to the region
of the respiratory tract subsequent to the larynx and preceding the
deep lung (or alveoli). This region includes the trachea, bronchi,
and bronchioles.
    \37\ The propensity for airways to narrow following inhalation
of some stimuli is termed bronchial or airway responsiveness (ISA,
section <IP_ADDRESS>, p. 5-8). In clinical situations where airway
responsiveness to methacholine or histamine is assessed and the
concentration resulting in a specific reduction in lung function
(the provocative concentration) meets the ATS criteria for
classification of the subject as hyperresponsive, the terms airway
hyperresponsiveness (AHR) or bronchial hyperresponsiveness (BHR) are
used (ATS, 2000b). Along with symptoms, variable airway obstruction,
and airway inflammation, AHR (or BHR) is a primary feature in the
clinical definition and characterization of asthma severity (ISA,
section <IP_ADDRESS>; Reddel et al., 2009).
---------------------------------------------------------------------------

    Based on assessment of the currently available evidence, as in the
last review, the ISA concludes that there is a causal relationship
between short-term SO2 exposures (as short as a few minutes)
and respiratory effects (ISA, section 5.2.1). The clearest evidence
comes from the long-standing evidence base of controlled human exposure
studies demonstrating effects related to asthma exacerbation including
lung function decrements \38\ and respiratory symptoms (e.g., cough,
shortness of breath, chest tightness and wheeze) in people with asthma
exposed to SO2 for 5 to 10 minutes at elevated breathing
rates (U.S. EPA, 1994; 2008 ISA; ISA, section 5.2.1).
Bronchoconstriction, evidenced by decrements in lung function, that are
sometimes accompanied by respiratory symptoms, occurs in these studies
at SO2 concentrations as low as 200 ppb in some people with
asthma exposed while breathing at elevated rates, such as during
exercise (ISA, section <IP_ADDRESS>). In contrast, respiratory effects are
not generally observed in other people with asthma (nonresponders \39\)
and healthy adults exposed to SO2 concentrations below 1000
ppb while exercising (ISA, sections <IP_ADDRESS> and <IP_ADDRESS>). Across
studies, bronchoconstriction in response to SO2 exposure is
seen during respiratory conditions of elevated breathing rates, such as
exercise, or with mouthpiece exposures that involve laboratory-
facilitated rapid, deep breathing.\40\ With these breathing conditions,
breathing shifts from nasal breathing to oral (with mouthpiece) or
oronasal breathing, which increases the concentrations of
SO2 reaching the tracheobronchial airways, where, depending
on dose and the exposed individual's susceptibility, it may cause
bronchoconstriction (ISA, sections <IP_ADDRESS>, 4.2.2, and <IP_ADDRESS>).
---------------------------------------------------------------------------

    \38\ The specific responses reported in the evidence base that
are described in the ISA as lung function decrements are increased
sRaw and FEV1 (ISA, section <IP_ADDRESS>).
    \39\ The data from controlled human exposure studies of people
with asthma indicate that there are two subpopulations that differ
in their airway responsiveness to SO2, with the second
subpopulation (non-responders) being insensitive to SO2
bronchoconstrictive effects at concentrations as high as 1000 ppb
(ISA, pp. 5-14 to 5-21; Johns et al., 2010).
    \40\ Laboratory-facilitated rapid deep breathing involves rapid,
deep breathing through a mouthpiece that provides a mixture of
oxygen with enough carbon dioxide to prevent an imbalance of gases
in the blood usually resulting from hyperventilation. Breathing in
the laboratory with this technique is referred to as eucapnic
hypernea (ISA, p. 5-6).
---------------------------------------------------------------------------

    The current evidence base of controlled human exposure studies of
individuals with asthma,\41\ is consistent with the evidence base from
the last review, and is summarized in the ISA (ISA, section <IP_ADDRESS>,
Tables 5-1 and 5-2). With regard to effects related to asthma
exacerbation, the main responses observed include increases in specific
airway resistance (sRaw) and reductions in forced expiratory volume in
one second (FEV1) after 5- to 10-minute exposures. As
recognized in the last review, the results of these studies indicate
that among individuals with asthma, some individuals (e.g., responders)
have a greater response to SO2 than others, or a measurable
response at lower exposure concentrations (ISA, p. 5-14). The
SO2-induced bronchoconstriction in these studies occurs
rapidly (in just a few minutes) when individuals are exposed while
breathing at an elevated rate, and is transient, with recovery
occurring with a return to resting breathing rate or cessation of
exposure, generally within an hour (ISA, p. 5-14, Table 5-2; Linn et
al., 1984; Johns et al., 2010).
---------------------------------------------------------------------------

    \41\ The subjects in these studies have primarily been adults.
The exception has been a few studies conducted in adolescents aged
12 to 18 years of age (ISA, pp. 5-22 to 5-23; PA, sections <IP_ADDRESS>
and <IP_ADDRESS>).
---------------------------------------------------------------------------

    The currently available epidemiologic evidence includes studies
reporting positive associations with short-term SO2
exposures for asthma-related hospital admissions of children or
emergency department visits by children (ISA, section 5.2.1). These
findings provide supporting evidence of the EPA's conclusion of a
causal relationship between short-term SO2 exposures and
respiratory effects, for which the controlled human exposure studies
are the primary basis (ISA, section <IP_ADDRESS>). Among the epidemiologic
studies newly available in this review, there are a limited number that
have investigated SO2 effects related to asthma
exacerbation, with the most supportive evidence coming from studies of
asthma-related hospital admissions of children or emergency department
visits by children (ISA, section <IP_ADDRESS>). As in the last review, areas
of uncertainty in the epidemiologic evidence are related to the
characterization of exposure based on the use of ambient air
concentrations at fixed site monitors as surrogates for population
exposure (often over a substantially sized area and for durations
greater than an hour) and the potential for confounding by PM \42\ or
other copollutants (ISA, section 5.2.1). In general, the pattern of
associations across the newly available studies is consistent with the
studies available in the last review (ISA, p. 5-75).
---------------------------------------------------------------------------

    \42\ The potential for confounding by PM is of particular
interest given that SO2 is a precursor to PM (ISA, p. 1-
7).
---------------------------------------------------------------------------

    For long-term SO2 exposure and respiratory effects, the
evidence base is somewhat augmented since the last review such that the
current ISA concludes it to be suggestive of, but not sufficient to
infer, a causal relationship (ISA, section 5.2.2). The support for this
conclusion comes mainly from the limited epidemiologic findings of
associations between long-term SO2 concentrations and
increases in asthma incidence combined with findings of laboratory
animal studies involving newborn rodents that indicate a potential for
SO2 exposure to contribute to the development of asthma,
especially allergic asthma, in children (ISA, section <IP_ADDRESS>). The
evidence showing increases in asthma incidence is coherent with results
of animal toxicological studies that provide a pathophysiologic basis
for the development of asthma. The overall body of evidence, however,
lacks consistency (ISA, sections <IP_ADDRESS> and <IP_ADDRESS>). Further, there
are uncertainties associated with the epidemiologic evidence across the
respiratory effects examined for long-term exposure (ISA, section
<IP_ADDRESS>).
    For effects other than those involving the respiratory system, the
current evidence is generally similar to the evidence available in the
last review and leads to similar conclusions about the totality of
adverse health effects. With regard to a relationship between short-
term SO2 exposure and total mortality, the ISA reaches the
same conclusion as the previous review that the evidence is suggestive
of, but not sufficient to infer, a causal relationship (ISA, section
5.5.1). This conclusion is based on the findings of previously and
newly available multicity epidemiologic studies that report positive
associations, accompanied by uncertainty with respect to the potential
for SO2 to have an independent effect on mortality. While
recent studies have analyzed some key uncertainties and addressed data
gaps from the previous review, uncertainties still exist. These
uncertainties include that: The number of studies that examined
copollutant confounding is limited; there is evidence of a reduction in
the SO2-mortality effect estimates (i.e., relative risks) in
copollutant models with

nitrogen dioxide and PM with mass median aerodynamic diameter nominally
below 10 microns (PM10); and a potential biological
mechanism for mortality following short-term SO2 exposures
is lacking (ISA, section <IP_ADDRESS>).
    For other categories of health effects,\43\ the currently available
evidence is inadequate to infer the presence or absence of a causal
relationship, mainly due to inconsistent evidence across specific
outcomes and uncertainties regarding exposure measurement error, the
potential for copollutant confounding, and potential modes of action
(ISA, sections 5.3.1, 5.3.2, 5.4, 5.5.2, 5.6). These conclusions are
consistent with those made in the previous review (ISA, p. xlviii).
---------------------------------------------------------------------------

    \43\ The other categories evaluated in the ISA include
cardiovascular effects with short- or long-term exposures;
reproductive and developmental effects; and cancer and total
mortality with long-term exposures (ISA, section 1.6.2 and Table 1-
1).
---------------------------------------------------------------------------

    Thus, given the strength of the evidence supporting the conclusion
of a causal relationship between short-term exposure to SO2
in ambient air and respiratory effects, in particular, asthma
exacerbation in individuals with asthma, the focus in this review, as
in prior reviews, is on such effects.
b. At-Risk Populations
    In this review, we use the term ``at-risk populations'' to
recognize populations with a quality or characteristic in common (e.g.,
a specific pre-existing illness or specific age or lifestage) that
contributes to them having a greater likelihood of experiencing
SO2-related health effects. People with asthma are at
increased risk for SO2-related health effects, specifically
for respiratory effects, and specifically asthma exacerbation elicited
by short-term exposures while breathing at elevated rates (ISA,
sections <IP_ADDRESS> and 6.3.1). This conclusion of the at-risk status of
people with asthma, as was the case in 2010, is based on the well-
established and well-characterized evidence from controlled human
exposure studies, supported by the evidence related to mode of action
for SO2 and evidence from epidemiologic studies (ISA,
sections <IP_ADDRESS> and 6.3.1). Further, some individuals with asthma have
a greater response to SO2 than others with similar disease
status (ISA, section <IP_ADDRESS>; Horstman et al., 1986; Johns et al.,
2010). The ISA also finds the evidence to be suggestive of increased
risk for children and older adults, while noting some limitations and
inconsistencies (ISA, sections <IP_ADDRESS> and <IP_ADDRESS>).\44\ Children with
asthma, however, may be particularly at risk compared to adults with
asthma (ISA, section 6.3.1). This conclusion reflects several
characteristics of children as compared to adults, as summarized in
section II.B of the proposal, that may put children with asthma at
greater risk of SO2-related bronchoconstrictive effects than
adults with asthma.\45\
---------------------------------------------------------------------------

    \44\ The current evidence for risk to older adults relative to
other lifestages comes from epidemiologic studies, for which the
findings are somewhat inconsistent, and studies with which there are
uncertainties in the association with the health outcome (ISA,
section <IP_ADDRESS>).
    \45\ There are few controlled human exposure studies to inform
our understanding of any differences in exposure concentrations
associated with bronchoconstrictive effects in young children as
compared to adults or adolescents as those studies have not included
subjects younger than 12 years (ISA, p. 5-22). The ISA does not find
the evidence to be adequate to conclude differential risk status for
subgroups of children with asthma (ISA, sections <IP_ADDRESS> and 6.6).
In consideration of the limited information regarding factors
related to breathing habit, however, the ISA suggests that children
with asthma approximately 5 to 11 years of age, and ``particularly
boys and perhaps obese children, might be expected to experience
greater responsiveness (i.e., larger decrements in lung function)
following exposure to SO2 than normal-weight adolescents
and adults'' (ISA, pp. 5-36 and 4-7).
---------------------------------------------------------------------------

    The finding that some individuals with asthma have a greater
response to SO2 than others with similar disease status is
quantitatively analyzed in a study, newly available in this review,
that examined differences in lung function response using individual
subject data available from five studies of individuals with asthma
exposed to multiple concentrations of SO2 for 5 to 10
minutes while breathing at elevated rates (Johns et al., 2010). As
noted in the ISA, ``these data demonstrate a bimodal distribution of
airway responsiveness to SO2 in individuals with asthma,
with one subpopulation that is insensitive to the bronchoconstrictive
effects of SO2 even at concentrations as high as 1.0 ppm,
and another subpopulation that has an increased risk for
bronchoconstriction at low concentrations of SO2'' (ISA, p.
5-20). In analyses focused on the more sensitive subpopulation, the
study demonstrated statistically significant increases in
bronchoconstriction with exposures as low as 0.3 ppm (Johns et al.,
2010). While such information provides documentation that some
individuals with asthma have a greater response to SO2 than
others, the factors contributing to this greater susceptibility are not
yet known (ISA, pp. 5-14 to 5-21).
c. Exposure Concentrations Associated With Health Effects
    Our understanding of exposure duration and concentrations
associated with SO2-related health effects is largely based,
as it was in the last review, on the longstanding evidence base of
controlled human exposure studies. These studies in individuals with
asthma exposed to SO2 for 5 to 10 minutes while breathing at
elevated rates demonstrate clear and consistent increases in magnitude
and occurrence of decrements in lung function (e.g., increased sRaw and
reduced FEV1) and in occurrence of respiratory symptoms with
increasing SO2 exposure (ISA, section <IP_ADDRESS>, Table 5-2 and
pp. 5-35, 5-39). Further, the evidence base demonstrates the occurrence
of SO2-related effects resulting from peak exposures on the
order of minutes \46\ and other short-term exposures have been found to
elicit a similar bronchoconstrictive response for somewhat longer
(e.g., 30-minute) exposure durations (ISA, p. 5-14; Kehrl et al.,
1987).
---------------------------------------------------------------------------

    \46\ While the air quality metrics in the epidemiologic studies
are for time periods longer than the 5- to 10-minute exposures
eliciting effects in the controlled human exposure studies, these
studies may not adequately capture the spatial and temporal
variation in SO2 concentrations and cannot address
whether observed associations of asthma-related emergency room
visits or hospital admissions with 1-hour to 24-hour ambient air
concentration metrics are indicative of a potential response to
exposure on the order of hours or much shorter-term exposure to
peaks in SO2 concentration (ISA, pp. 5-49, 5-59, 5-25).
---------------------------------------------------------------------------

    The controlled human exposure studies of people with asthma further
demonstrate \47\ that SO2 concentrations as low as 200 to
300 ppb for 5 to 10 minutes elicited moderate or greater lung function
decrements (a decrease in FEV1 of at least 15% or an
increase in sRaw of at least 100%) in a subset of the study subjects
(ISA, sections <IP_ADDRESS> and 5.2.1). The percent of individuals affected,
the severity of response, and the accompanying occurrence of
respiratory symptoms increased with increasing SO2 exposure
concentrations (ISA, section 5.2.1). At concentrations ranging from 200
to 300 ppb, the lowest levels for which the ISA describes the
occurrence of moderate or greater SO2-related lung function
decrements, as many as 33% of exercising study subjects with asthma
experienced such decrements in lung function (ISA,

section 5.2.1, Table 5-2).\48\ At concentrations at or above 400 ppb,
moderate or greater decrements in lung function occurred in as many as
approximately 30 to 60% of exercising individuals with asthma, and
compared to the results for exposures at 200 to 300 ppb, a larger
percentage of individuals with asthma experienced the more severe
decrements in lung function (i.e., an increase in sRaw of at least
200%, and/or a 20% or more decrease in FEV1) at these higher
concentrations (ISA, section <IP_ADDRESS>, p. 5-9 and Table 5-2).
Additionally, at concentrations at or above 400 ppb, moderate or
greater decrements in lung function were frequently accompanied by
respiratory symptoms, such as cough, wheeze, chest tightness, or
shortness of breath, with some of these findings reaching statistical
significance at the study group level (ISA, Table 5-2 and section
5.2.1).
---------------------------------------------------------------------------

    \47\ The findings summarized in Table 5-2 of the ISA and in
Table 3-1 of the PA are based on results that have been adjusted for
effects of exercise in clean air so that they have separated out any
effect of exercise in causing bronchoconstriction and reflect only
the SO2-specific effect.
    \48\ Additionally, analyses of data from the full set of these
studies that focused only on the results for the study subjects that
are responsive to SO2 at exposure concentrations below
1000 ppb found there to be statistically significant increases in
lung function decrements occurring at 300 ppb (ISA, p. 153; Johns et
al., 2010).
---------------------------------------------------------------------------

    Two hundred ppb is the lowest exposure concentration for which
individual study subject data for percent changes in sRaw and
FEV1 are available from studies that have assessed the
SO2 effect versus the effect of exercise in clean air (ISA,
Table 5-2 and Figure 5-1). In nearly all of these studies (and all of
these studies with such data for concentrations from 200 to 400 ppb),
study subjects breathed freely (e.g., without using a mouthpiece).\49\
In studies that tested 200 ppb exposures, a portion of the exercising
study subjects with asthma (approximately 8 to 9%) responded with at
least a doubling in sRaw or an increase in FEV1 of at least
15% (ISA, Table 5-2 and Figure 5-2; PA, Table 3-1; Linn et al., 1983a;
Linn et al., 1987).
---------------------------------------------------------------------------

    \49\ Studies of free-breathing subjects generally make use of
small rooms in which the atmosphere is experimentally controlled
such that study subjects are exposed by freely breathing the
surrounding air (e.g., Linn et al., 1987).
---------------------------------------------------------------------------

    With regard to exposure concentrations below 200 ppb, very limited
evidence is available for concentrations as low as 100 ppb. Some
differences in methodology and the reporting of results complicate
comparison of the studies with 100 ppb exposure to studies using higher
exposures. In the studies evaluating the 100 ppb concentration level,
subjects were exposed by mouthpiece rather than freely breathing in an
exposure chamber (Sheppard et al., 1981; Sheppard et al., 1984; Koenig
et al., 1989; Koenig et al., 1990; Trenga et al., 2001; ISA, section
<IP_ADDRESS>; PA, section <IP_ADDRESS>). Additionally, only a few of these
studies included an exposure to clean air while exercising that would
have allowed for distinguishing the effect of SO2 from the
effect of exercise in causing bronchoconstriction (Sheppard et al.,
1981; Sheppard et al., 1984; Koenig et al., 1989). In those few cases,
a limited number of adult and adolescent study subjects were reported
to experience small changes in sRaw, with the magnitudes of change
appearing to be smaller than responses reported from studies at
exposures of 200 ppb or more.50 51 Thus, while the studies
evaluating 100 ppb exposures are limited and their interpretation is
complicated by the use of different reporting of results and exposure
methods that differ from those used in studies of higher
concentrations, the 100 ppb studies do not indicate that exposure at
100 ppb results in as much as a doubling in sRaw, based on the
extremely few adults and adolescents tested (Sheppard et al., 1981;
Sheppard et al., 1984; Koenig et al., 1989).
---------------------------------------------------------------------------

    \50\ For example, although individual study subject data for
SO2-attributable changes in sRaw in these studies are not
available in the terms needed to summarize the responses consistent
with the study result summaries in the ISA, Table 5-2 (e.g., percent
change), the increase in sRaw reported for two young adult subjects
exposed to 100 ppb in the study by Sheppard et al. (1981) was
slightly less than half the response of these subjects at 250 ppb,
and the results for the study by Sheppard et al. (1984) indicate
that none of the eight study subjects experienced as much as a
doubling in sRaw in response to the mouthpiece exposure to 125 ppb
while exercising (in Table 2 of Sheppard et al., 1984,
concentrations calculated to cause a doubling of sRaw in all
subjects are higher than 125 ppb, the lowest exposure
concentration). In the study of adolescents (aged 12 to 18 years),
among the three individual study subjects for which total
respiratory resistance appears to have increased with SO2
exposure, the magnitude of increase in that metric after
consideration of the response to exercise appears to be less than
100% in each subject (Koenig et al., 1989).
    \51\ In a mouthpiece exposure system, the inhaled breath
completely bypasses the nasal passages where SO2 is
efficiently removed, thus allowing more of the inhaled
SO2 to penetrate the tracheobronchial airways (2008 ISA,
p. 3-4; ISA, section <IP_ADDRESS>). This allowance of deeper penetration
of SO2 into the tracheobronchial airways, as well as
limited evidence comparing responses by mouthpiece and chamber
exposures, leads to the expectation that SO2-responsive
people with asthma breathing SO2 using a mouthpiece,
particularly while breathing at elevated rates, would experience
greater lung function responses than if exposed to the same test
concentration while freely breathing in an exposure chamber (ISA, p.
5-23; Linn et al., 1983b).
---------------------------------------------------------------------------

    Specific exposure concentrations that may be eliciting respiratory
responses are not available from the epidemiologic evidence base, which
includes studies that find associations with outcomes such as asthma-
related emergency department visits and hospital admissions. For
example, in noting limitations of epidemiologic studies with regard to
uncertainties in SO2 exposure estimates, the ISA recognized
that ``[it] is unclear whether SO2 concentrations at the
available fixed site monitors adequately represent variation in
personal exposures especially if peak exposures are as important as
indicated by the controlled human exposure studies'' (ISA, p. 5-37).
This extends the observation of the 2008 ISA that ``it is possible that
these epidemiologic associations are determined in large part by peak
exposures within a 24-h[our] period'' (2008 ISA, p. 5-5). Another key
uncertainty in the epidemiologic evidence available in this review, as
in the last review, is potential confounding by copollutants,
particularly PM, given the important role of SO2 as a
precursor to PM in ambient air (ISA, p. 5-5). Among the U.S.
epidemiologic studies reporting mostly positive and sometimes
statistically significant associations between ambient SO2
concentrations and emergency department visits or hospital admissions
(some conducted in multiple locations), few studies have attempted to
address the uncertainty of potential copollutant confounding. For
example, as in the last review, there are three U.S. studies for which
the SO2 effect estimate remained positive and statistically
significant in copollutant models with PM. No additional such studies
have been newly identified in this review that might inform this issue
(83 FR 26765, June 8, 2018). Thus, such uncertainties regarding
copollutant confounding, as well as exposure measurement error, remain
in the currently available epidemiologic evidence base (ISA, p. 5-6).
d. Potential Impacts on Public Health
    In general, the magnitude and implications of potential impacts on
public health are dependent upon the type and severity of the effect,
as well as the size and other features of the population affected (ISA,
section 1.7.4; PA, <IP_ADDRESS>). The information discussed in this section
indicates the potential for exposures to SO2 in ambient air
to be of public health importance. Such considerations contributed to
the basis for the 2010 decision to appreciably strengthen the primary
SO2 NAAQS and to establish a 1-hour standard to provide the
requisite public health protection for at-risk populations from short-
term exposures of concern.
    The potential public health impacts of SO2
concentrations in ambient air relate to respiratory effects of short-
term exposures and particularly those effects

associated with asthma exacerbation in people with asthma. As
summarized above in section II.A.2.a, these effects include
bronchoconstriction resulting in decrements in lung function and
elicited by short-term exposures during periods of elevated breathing
rate. Consistent with these SO2-related effects, asthma-
related health outcomes such as emergency department visits and
hospital admissions have been positively associated with ambient air
concentrations of SO2 in epidemiologic studies (ISA, section
<IP_ADDRESS>).
    As summarized in section II.A.2.b above, people with asthma are the
population at risk for SO2-related effects and children with
asthma are considered to be at relatively greater risk than other age
groups (ISA, section 6.3.1). The evidence supporting this conclusion
comes primarily from studies of individuals with mild to moderate
asthma,\52\ with very little evidence available for individuals with
severe asthma. The evidence base of controlled human exposure studies
of exercising people with asthma provides very limited information
indicating that there are similar responses (in terms of relative
decrements in lung function in response to SO2 exposures)
across individuals with asthma of differing severity.\53\ However, the
two available studies ``suggest that adults with moderate/severe asthma
may have more limited reserve to deal with an insult compared with
individuals with mild asthma'' (ISA, p. 5-22; Linn et al., 1987; Trenga
et al., 1999). Consideration of such baseline differences among members
of at-risk populations and of the relative transience or persistence of
these responses (e.g., as noted in section II.A.2.a above), as well as
other factors, is important to characterizing implications for public
health, as recognized by the ATS in their recent statement on
evaluating adverse health effects of air pollution (Thurston et al.,
2017).
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    \52\ These studies categorized asthma severity based mainly on
the individual's use of medication to control asthma, such that
individuals not regularly using medication were classified as
minimal/mild, and those regularly using medication as moderate/
severe (Linn et al., 1987). The ISA indicates that the moderate/
severe grouping would likely be classified as moderate by today's
asthma classification standards due to the level to which their
asthma was controlled and their ability to engage in moderate to
heavy levels of exercise (ISA, p. 5-22; Johns et al., 2010; Reddel,
2009).
    \53\ The ISA identifies two studies that have investigated the
influence of asthma severity on responsiveness to SO2,
with one finding that a larger change in lung function observed in
the moderate/severe asthma group was attributable to the exercise
component of the study protocol while the other did not assess the
role of exercise in differences across individuals with asthma of
differing severity (Linn et al., 1987; Trenga et al., 1999). Based
on the criteria used in the study by Linn et al. (1987) for placing
individuals in the ``moderate/severe'' group, however, the asthma of
these individuals ``would likely be classified as moderate by
today's classification standards'' (ISA, p. 5-22; Johns et al.,
2010; Reddel, 2009).
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    Multiple statements by the ATS on what constitutes an adverse
health effect of air pollution inform the Administrator's judgment on
the public health significance of SO2-related effects,
particularly those with the potential to occur under air quality
conditions allowed by the current standard. Building on the earlier
statement by the ATS that was considered in the last review (ATS,
2000a), the recent policy statement by the ATS provides a general
framework for interpreting evidence that proposes a ``set of
considerations that can be applied in forming judgments'' for this
context (Thurston et al., 2017). The earlier ATS statement, in addition
to emphasizing clinically relevant effects (e.g., the adversity of
small transient changes in lung function metrics in combination with
respiratory symptoms), also emphasized both the need to consider
changes in ``the risk profile of the exposed population'' and effects
on the portion of the population that may have a diminished reserve
that could put its members at potentially increased risk of effects
from another agent (ATS, 2000a). The consideration of effects on
individuals with preexisting diminished lung function continues to be
recognized as important in the more recent ATS statement (Thurston et
al., 2017). All of these concepts, including the consideration of the
magnitude or severity of effects occurring in just a subset of study
subjects, as well as the consideration of persistence or transience of
effects,\54\ are recognized as important considerations in the more
recent ATS statement (Thurston et al., 2017) and continue to be
relevant to consideration of the evidence base for SO2.
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    \54\ In speaking of transient effects, the recent statement
refers to effects lasting on the order of hours (Thurston et al.,
2017).
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    Such concepts are routinely considered by the Agency in weighing
public health implications for decisions on primary NAAQS, as
summarized in section I.A above. For example, in deliberations on a
standard that provides the requisite public health protection under the
Act, the EPA traditionally recognizes the nature and severity of the
health effects involved, recognizing the greater public health
significance of more severe health effects, including, for example,
responses that have been documented to be accompanied by respiratory
symptoms, and of the risk of repeated occurrences of effects (76 FR
54308, August 31, 2011; 80 FR 65292, October 26, 2015). Another area of
consideration is characterization of the population at risk, including
its size and, as pertinent, the exposure/risk estimates in this regard.
Such factors related to public health significance, and the kind and
degree of associated uncertainties, are considered by the EPA in
addressing the CAA requirement that the primary NAAQS be requisite to
protect public health, including an adequate margin of safety, as
summarized in section I.A above.
    Ambient air concentrations of SO2 vary considerably in
areas near sources, but concentrations in the vast majority of the U.S.
are well below the current standard (PA, Figure 2-7). Thus, while the
population counts discussed below may convey information and context
regarding the size of populations living near sizeable sources of
SO2 emissions in some areas, the concentrations in most
areas of the U.S. are well below the conditions assessed in the REA.
    With regard to the size of the U.S. population at risk of
SO2-related effects, the National Center for Health
Statistics data from the 2015 National Health Interview Survey (NHIS)
\55\ indicate that approximately 8% of the U.S. population has asthma
(PA, Table 3-2; CDC, 2017). The estimated prevalence is greater in
children (8.4% for children less than 18 years of age) than adults
(7.6%) (PA, Table 3-2; CDC, 2017). Asthma was the leading chronic
illness affecting children in 2012, the most recent year for which such
an evaluation is available (Bloom et al., 2013). As noted in the PA,
there are more than 24 million people with asthma currently in the
U.S., including more than 6 million children (PA, sections <IP_ADDRESS> and
3.2.4). Among populations of different races or ethnicities, black non-
Hispanic and Puerto Rican Hispanic children are estimated to have the
highest

prevalence, at 13.4% and 13.9%, respectively. Asthma prevalence is also
increased among populations in poverty, with the prevalence estimated
to be 11.1% among people living in households below the poverty level
compared to 7.2% of those living above it (CDC, 2017).
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    \55\ The NHIS is conducted annually by the U.S. Centers for
Disease Control and Prevention. The NHIS collects health information
from a nationally representative sample of the noninstitutionalized
U.S. civilian population through personal interviews. Participants
(or parents of participants if the survey participant is a child)
who have ever been told by a doctor or other health professional
that the participant had asthma and reported that they still have
asthma were considered to have current asthma. Data are weighted to
produce nationally representative estimates using sample weights;
estimates with a relative standard error greater than or equal to
30% are generally not reported (Mazurek and Syamlal, 2018). The NHIS
estimates described here are drawn from the 2015 NHIS, Table 4-1
(https://www.cdc.gov/asthma/nhis/2015/table4-1.htm).
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    With regard to the potential for exposure of the populations at
risk from exposures to SO2 in ambient air, while
SO2 concentrations have generally declined across the U.S.
since 2010 when the current standard was set (PA, Figures 2-5 and 2-6),
there are numerous areas where SO2 concentrations still
contribute to air quality that is near or above the standard. For
example, the PA noted that the air quality monitoring data for the
2014-2016 period indicated there to be 15 core-based statistical areas
\56\ with air quality exceeding the primary SO2 standard
(design values \57\ were above the existing standard level of 75 ppb),
of which a number have sizeable populations (PA, section <IP_ADDRESS>). In
addition to this evidence of elevated ambient air SO2
concentrations, there are limitations in the monitoring network with
regard to the extent that it might be expected to capture all areas
with the potential to exceed the standard (e.g., 75 FR 35551; June 22,
2010). In recognition of these limitations, we also examined the
proximity of populations to sizeable SO2 point sources using
the recently available emissions inventory information (2014 NEI),
which is also characterized in the ISA (PA, section <IP_ADDRESS>, Appendix
F; ISA, section 2.2.2). This information indicates that there are more
than 300,000 and 60,000 children living within 1 km of facilities
emitting at least 1000 and 2000 tpy of SO2, respectively
(PA, section <IP_ADDRESS>). Within 5 km of such sources, the numbers are
approximately 1.4 million and 700,000, respectively (PA, Table 3-5).
While information on SO2 concentrations in locations of
maximum impact of such sources is not available for all these areas,
and SO2 concentrations vary appreciably near sources, simply
considering the 2015 national estimate of asthma prevalence of
approximately 8% (noted above), this information would suggest there
may be as many as 24,000 to more than 100,000 children with asthma that
live in areas near substantially sized sources of SO2
emissions to ambient air (PA, section <IP_ADDRESS>; Table 3-5).
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    \56\ Core-based statistical area (CBSA) is a geographic area
defined by the U.S. Office of Management and Budget to consist of an
urban area of at least 10,000 people in combination with its
surrounding or adjacent counties (or equivalents) with which there
are socioeconomic ties through commuting (https://www.census.gov/geo/reference/gtc/gtc_cbsa.html). Populations in the 15 CBSAs
referred to in the body of the text range from approximately 30,000
to more than a million (based on 2016 U.S. Census Bureau estimates).
    \57\ A design value is a statistic that describes the air
quality status of a given area relative to the level of the
standard, taking into account the averaging time and form (as well
as indicator). Thus, design values for the SO2 NAAQS are
in terms of 3-year averages of annual 99th percentile 1-hour daily
maximum concentrations of SO2. Design values are
typically used to assess whether the NAAQS is violated, to classify
nonattainment areas, to track air quality trends and progress toward
meeting the NAAQS and to develop control strategies.
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3. Overview of Risk and Exposure Information
    Our consideration of the scientific evidence available in the
current review (summarized in section II.A.2 above), as at the time of
the last review, is informed by results from a quantitative analysis of
estimated population exposure and associated risk of respiratory
effects that the evidence indicates to be elicited in some portion of
exercising people with asthma by short-term exposures to elevated
SO2 concentrations, e.g., such as exposures lasting 5 or 10
minutes. This analysis, for the air quality scenario of just meeting
the current standard, estimates two types of risk metrics in terms of
percentages of the simulated at-risk populations of adults with asthma
and children with asthma (REA, section 4.6). The first of the two risk
metrics is based on comparison of the estimated 5-minute exposure
concentrations for individuals breathing at elevated rates to 5-minute
exposure concentrations of potential concern (benchmark
concentrations). The second risk metric utilizes exposure-response (E-
R) information from studies in which subjects experienced moderate or
greater lung function decrements (specifically a doubling or more in
sRaw) to estimate the portion of the simulated at-risk population
likely to experience one or more days with a SO2-related
increase in sRaw of at least 100% (REA, sections 4.6.1 and 4.6.2). Both
metrics are used in the REA to characterize health risk associated with
5-minute peak SO2 exposures among simulated at-risk
populations during periods of elevated breathing rates. These risk
metrics were also derived in the REA for the last review and the
associated estimates informed the 2010 decision that established the
current standard (75 FR 35546-35547, June 22, 2010).
    The following subsections provide brief overviews of the key
aspects of the design and methods of the quantitative assessment in
this review (section II.A.3.a) and the important uncertainties
associated with these analyses (section II.A.3.b). The results of the
analyses are summarized in section II.A.3.c. These overviews are drawn
from the summary presented in section II.C of the proposal (83 FR
26767, June 8, 2018).
a. Key Design Aspects
    In this section, we provide a brief overview of key aspects of the
quantitative exposure and risk assessment conducted for this review and
summarized in more detail in section II.C.1 of the proposal (83 FR
26767, June 8, 2018), including the study areas, air quality adjustment
approach, modeling tools, at-risk populations simulated, and benchmark
concentrations assessed. The assessment is described in detail in the
REA and summarized in section 3.2.2 of the PA.
    The REA focuses on air quality conditions that just meet the
current standard, and the analyses estimate exposure and risk for at-
risk populations in three urban study areas in: (1) Fall River, MA; (2)
Indianapolis, IN; and (3) Tulsa, OK. The three study areas present a
variety of circumstances related to population exposure to short-term
peak concentrations of SO2 in ambient air, including a range
in total population size, different mixtures of SO2
emissions sources, and three different climate regions of the U.S.: The
Northeast, Ohio River Valley (Central), and South (REA, section 3.1;
Karl and Koss, 1984).\58\ The latter two regions comprise the part of
the U.S. with generally the greatest prevalence of elevated
SO2 concentrations and large emissions sources (PA, Figure
2-7 and Appendix F). Accordingly, the three study areas illustrate
three different patterns of exposure to SO2 concentrations
in a populated area in the U.S. (REA, section 5.1). While the same air
quality scenario is simulated in all three study areas (conditions that
just meet the current standard), study-area-specific characteristics
related to sources, meteorology, topography and population contribute
to variation in the estimated magnitude of exposure and associated risk
across study areas.
---------------------------------------------------------------------------

    \58\ Additionally, continuous 5-minute ambient air monitoring
data (i.e., all 5-minute values for each hour) are available in all
three study areas (REA, section 3.2).
---------------------------------------------------------------------------

    As indicated by this case study approach to assessing exposure and
risk, the analyses in the REA are intended to provide assessments of an
air quality scenario just meeting the current standard for a small,
diverse set of study areas and associated exposed at-risk populations
that will be informative to the EPA's consideration of potential

exposures and risks that may be associated with the air quality
conditions occurring under the current SO2 standard. The REA
analyses are not designed to provide a comprehensive national
assessment of such conditions (REA, section 2.2). The objective of the
REA is not to present an exhaustive analysis of exposure and risk in
areas of the U.S. that currently just meet the standard or an analysis
of exposure and risk associated with air quality adjusted down to just
meet the standard in areas that currently do not meet the standard.\59\
Rather, the purpose is to assess, based on current tools and
information, the potential for exposures and risks beyond those
indicated by the information available at the time the current standard
was established. Accordingly, capturing an appropriate level of
diversity in study areas and air quality conditions (that reflect the
current standard scenario) is important to the role of the REA in
informing the EPA's understanding of, and conclusions on, the public
health protection afforded by the current standard (PA, section
<IP_ADDRESS>).
---------------------------------------------------------------------------

    \59\ Nor is the objective of the REA to provide a comprehensive
assessment of current air quality across the U.S.
---------------------------------------------------------------------------

    A broad variety of spatial and temporal patterns of SO2
concentrations can exist when ambient air concentrations just meet the
current standard. These patterns will vary due to many factors
including the types of emissions sources in a study area and several
characteristics of those sources, such as magnitude of emissions and
facility age, use of various control technologies, patterns of
operation, and local factors, as well as local meteorology. Estimates
derived using the particular analytical approaches and methodologies
for characterizing the study area-specific air quality provide an
indication of this variability in the spatial and temporal patterns of
SO2 concentrations occurring under air quality conditions
just meeting the current standard. In light of the uncertainty
associated with these concentration estimates, the REA presents results
from two different approaches to adjusting air quality to just meet the
current standard (described in more detail in sections 3.4 and <IP_ADDRESS>
of the REA).\60\
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    \60\ The first approach uses the highest design value across all
modeled air quality receptors to estimate the amount of
SO2 concentration reduction needed to adjust the air
quality concentrations in each area to just meet the standard (REA,
section 3.4). In recognition of potential uncertainty in the first
approach, the second approach uses the air quality receptor having
the 99th percentile of the distribution of design values (instead of
the receptor with the maximum design value) to estimate the
SO2 concentration reductions needed to adjust the air
quality to just meet the standard, setting all receptors at or above
the 99th percentile to just meet the standard (REA, section
<IP_ADDRESS>).
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    Consistent with the health effects evidence summarized in section
II.A.2 above, the focus of the REA is on short-term (5-minute)
exposures of individuals with asthma in the simulated populations
during times when they are breathing at an elevated rate. Five-minute
concentrations in ambient air were estimated for the current standard
scenario using a combination of 1-hour concentrations from the EPA's
preferred near-field dispersion model, the American Meteorological
Society/EPA regulatory model (AERMOD), with adjustment such that they
just meet the current standard, and relationships between 1-hour and 5-
minute concentrations occurring in the local ambient air monitoring
data. The air quality modeling step was taken to capture the spatial
variation in ambient SO2 concentrations across each urban
study area. Such variation can be relatively high in areas affected by
large point sources and is unlikely to be captured by the limited
number of monitoring locations in each area. The modeling step yields
1-hour concentrations at model receptor sites across the modeling
domain across the 3-year modeling period (consistent with the 3-year
form of the standard). These concentrations were adjusted such that the
air quality modeling receptor location(s) with the highest
concentrations just met the current standard. Rather than applying the
same adjustment to concentrations at all receptors in a study area, the
adjustment was derived by focusing on reducing emissions from the
source(s) contributing the most to the standard exceedances (REA,
section 3.4 and <IP_ADDRESS>). Relationships between 1-hour and 5-minute
concentrations at local monitors were then used to estimate 5-minute
concentrations associated with the adjusted 1-hour concentrations
across the 3-year period at all model receptor locations in each of the
three study areas (REA, section 3.5). In this way, available continuous
5-minute ambient air monitoring data (datasets with all twelve 5-minute
concentrations in each hour) were used to reflect the fine-scale
temporal variation in SO2 concentrations documented by these
data. This approach was used in recognition of the limitations
associated with air quality modeling at this fine temporal scale, e.g.,
limitations in the time steps of currently available model input data
such as for emissions estimates.
    The estimated 5-minute concentrations in ambient air across each
study area were then used together with the Air Pollutants Exposure
(APEX) model, a probabilistic human exposure model that simulates the
activity of individuals in the population, including their exertion
levels and movement through time and space, to estimate concentrations
of 5-minute SO2 exposure events in indoor, outdoor, and in-
vehicle microenvironments. The use of APEX for estimating exposures
allows for consideration of factors that affect exposures that are not
addressed by consideration of ambient air concentrations alone. These
factors include: (1) Attenuation in SO2 concentrations
expected to occur in some indoor microenvironments; (2) the influence
of human activity patterns on the time series of exposure
concentrations; and (3) accounting for human physiology and the
occurrence of elevated breathing rates concurrent with SO2
exposures (REA, section 2.2). These factors are all key to
appropriately characterizing exposure and associated health risk for
SO2.\61\
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    \61\ The exposure modeling performed for this review, including
ways in which it has been updated since the 2009 REA are summarized
in section II.C of the proposal and described in detail in the REA
(e.g., REA, Chapter 4 and Appendices E through I).
---------------------------------------------------------------------------

    The at-risk populations for which exposure and risk are estimated
(children and adults with asthma) ranges from 8.0 to 8.7% of the total
populations (ages 5-95) in the exposure modeling domains for the three
study areas (REA, section 5.1). The percent of children with asthma in
the simulated populations ranges from 9.7 to 11.2% across the three
study areas (REA, section 5.1). Within each study area the percent
varies with age, sex and whether family income is above or below the
poverty level (REA, section 4.1.2, Appendix E).\62\ This variation is
greatest in the Fall River study area, with census block level, age-
specific asthma prevalence estimates ranging from 7.9 to 18.6% for
girls and from 10.7 to 21.5% for boys (REA, Table 4-1).
---------------------------------------------------------------------------

    \62\ As described in section 4.1.2 and Appendix E of the REA,