[Federal Register Volume 83, Number 111 (Friday, June 8, 2018)]
[Proposed Rules]
[Pages 26752-26785]
[FR Doc No: 2018-12061]

Vol. 83

Friday,

No. 111

June 8, 2018

Part II

 Environmental Protection Agency

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

40 CFR Part 50

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

Federal Register / Vol. 83 , No. 111 / Friday, June 8, 2018 /
Proposed Rules

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

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 50

[EPA-HQ-OAR-2013-0566; FRL-9979-00-OAR]
RIN 2060-AT68

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

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed action.

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

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 proposing to retain the current standard,
without revision.

DATES: Comments must be received on or before July 23, 2018.
    If, by June 15, 2018, the EPA receives a request from a member of
the public to speak at a public hearing concerning the proposed
decision (see SUPPLEMENTARY INFORMATION below), we will hold a public
hearing, with information about the hearing provided in a subsequent
notice in the Federal Register.

ADDRESSES: You may submit comments, identified by Docket ID No. EPA-HQ-
OAR-2013-0566, to the Federal eRulemaking Portal: http://www.regulations.gov.
    Instructions: Follow the online instructions for submitting
comments. Once submitted to the Federal eRulemaking Portal, comments
cannot be edited or withdrawn. The EPA may publish any comment received
to its public docket. Do not submit electronically any information you
consider to be Confidential Business Information (CBI) or other
information whose disclosure is restricted by statute. Multimedia
submissions (audio, video, etc.) must be accompanied by a written
comment. The written comment is considered the official comment and
should include discussion of all points you wish to make. The EPA will
generally not consider comments or comment contents located outside of
the primary submission (i.e., on the web, the cloud, or other file
sharing system). For additional submission methods, the full EPA public
comment policy, information about CBI or multimedia submissions, and
general guidance on making effective comments, please visit http://www2.epa.gov/dockets/commenting-epa-dockets.
    If a public hearing is to be held on this proposed action (see
SUPPLEMENTARY INFORMATION below), in addition to publishing a Federal
Register notice, the EPA will post information regarding it, including
date and time, online at https://www.epa.gov/so2-pollution/primary-national-ambient-air-quality-standard-naaqs-sulfur-dioxide.
    Docket: All documents in the dockets pertaining to this action are
listed on the www.regulations.gov website. This includes documents in
the docket for the proposed decision (Docket ID No. EPA-HQ-OAR-2013-
0566) and a separate docket, established for the Integrated Science
Assessment (ISA) for this review (Docket ID No. EPA-HQ-ORD-2013-0357)
that has been incorporated by reference into the docket for this
proposed decision. Although listed in the index, some information is
not publicly available, e.g., 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<PHONE_NUMBER> and the telephone
number for the Air and Radiation Docket Information Center is (202)
566-1742.

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 protected].

SUPPLEMENTARY INFORMATION:

General Information

Preparing Comments for the EPA

1. Submitting CBI
    Do not submit this information to the EPA through
www.regulations.gov or email. Clearly mark the part or all of the
information that you claim to be CBI. For CBI information in a disk or
CD-ROM that you mail to the EPA, mark the outside of the disk or CD-ROM
as CBI and then identify electronically within the disk or CD-ROM the
specific information that is claimed as CBI. In addition to one
complete version of the comment that includes information claimed as
CBI, a copy of the comment that does not contain the information
claimed as CBI must be submitted for inclusion in the public docket.
Information so marked will not be disclosed except in accordance with
procedures set forth in 40 Code of Federal Regulations (CFR) part 2.
2. Tips for Preparing Your Comments
    When submitting comments, remember to:
     Identify the action by docket number and other identifying
information (subject heading, Federal Register date and page number).
     Follow directions--the agency may ask you to respond to
specific questions or organize comments by referencing a CFR part or
section number.
     Explain why you agree or disagree, suggest alternatives,
and substitute language for your requested changes.
     Describe any assumptions and provide any technical
information and/or data that you used.
     Provide specific examples to illustrate your concerns, and
suggest alternatives.
     Explain your views as clearly as possible, avoiding the
use of profanity or personal threats.
     Make sure to submit your comments by the comment period
deadline identified.
    Public Hearing: If, by June 15, 2018, the EPA receives a request
from a member of the public to speak at a public hearing concerning the
proposed decision, we will hold a public hearing, with information
about the hearing provided in a subsequent notice in the Federal
Register. To request a hearing, to register to speak at a hearing or to
inquire if a hearing will be held, please contact Ms. Regina Chappell
at<PHONE_NUMBER> or by email at [email protected]. If a public
hearing is to be held on this proposed action, the EPA will also post
information regarding it, including, date and time, online at https://www.epa.gov/so2-pollution/primary-national-ambient-air-quality-standard-naaqs-sulfur-dioxide.

Availability of Information Related to This Action

    A number of the documents that are relevant to this proposed
decision 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 (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 (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
(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.

Table of Contents

    The following topics are discussed in this preamble:

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 Proposed Decision
    A. General Approach
    1. Approach in the Last Review
    2. Approach for the Current Review
    B. Health Effects Information
    1. Nature of Effects
    2. At-Risk Populations
    3. Exposure Concentrations Associated With Health Effects
    4. Potential Impacts on Public Health
    C. Summary of Risk and Exposure Information
    1. Key Design Aspects
    2. Key Limitations and Uncertainties
    3. Summary of Exposure and Risk Estimates
    D. Proposed Conclusions on the Current Standard
    1. Evidence- and Exposure and Risk-Based Considerations in the
Policy Assessment
    2. CASAC Advice
    3. Administrator's Proposed Conclusions on the Current 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 and Safety Risks
    I. Executive Order 13211: Actions 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)
References

Executive Summary

    This document presents the Administrator's proposed decision in the
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 ppb, as the 99th percentile of daily maximum 1-hour
SO2 concentrations, averaged over 3 years. This document
summarizes the background and rationale for the Administrator's
proposed decision to retain the current standard, without revision, and
solicits comment on this proposed decision and on the array of issues
associated with review of this standard, including public health and
science policy judgments inherent in the proposed decision. The EPA
solicits comment on the four basic elements of the current NAAQS
(indicator, averaging time, level, and form), including whether there
are appropriate alternative approaches for the averaging time or
statistical form that provide comparable public health protection, and
the rationale upon which such views are based.
    This review of the primary SO2 standard is required by
the Clean Air Act (CAA) on a periodic basis. The schedule for
completing this review is established by a consent decree, which
established May 25, 2018 as the deadline for signature of a notice
setting forth the proposed decision in this review and January 28, 2019
as the deadline for signature on a final decision notice.
    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 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, emissions nationally 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 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, 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). One-hour
concentrations of SO2 in ambient air the U.S. declined more
than 82% from 1980 to 2016 at locations continuously monitored over
this period (PA, Figure 2-4). The decline since 2000 has been 69% at a
larger number of locations continuously monitored since that time (PA,
Figure 2-5). Daily maximum 5-minute concentrations have also
consistently declined from 2011 to 2016 (PA, Figure 2-6).
    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 sulfur oxides 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 proposed decision to retain the current primary NAAQS for
SOX, without revision, has been informed by careful
consideration of the key aspects

of the currently available health effects evidence and conclusions
contained in the ISA, quantitative risk and exposure information
presented in the REA, considerations of this evidence and information
discussed in the Policy Assessment, advice from the Clean Air
Scientific Advisory Committee (CASAC), and public input received as
part of the ongoing review of the primary NAAQS for SOX.
    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 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.
    The quantitative analyses of population exposure and risk also
inform the proposed 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 three 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 public comment thus far in this review, the
Administrator proposes to conclude 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. These proposed
conclusions are consistent with CASAC recommendations. In its advice to
the Administrator, the CASAC concurred with the preliminary conclusions
in the draft PA that ``the current scientific literature does not
support revision of the primary NAAQS for SO2'' (Cox and
Diez Roux, 2018b, p. 1 of letter). The CASAC further stated that it
``supports retaining the current standard, and specifically recommends
that all four elements (indicator, averaging time, form, and level)
should remain the same'' (Cox and Diez Roux, 2018b, p. 1 of letter).
The Administrator solicits comment on the proposed conclusion that the
current standard is requisite to protect public health, with an
adequate margin of safety, and on the proposed decision to retain the
standard, without revision. The Administrator also solicits comment on
the array of issues associated with review of this standard, including
public health and science policy judgments inherent in the proposed
decision, as discussed in detail in section II below. The EPA solicits
comment on the four basic elements of the current NAAQS (indicator,
averaging time, level, and form), including whether there are
appropriate alternative approaches for the averaging time or
statistical form that provide comparable public health protection, and
the rationale upon which such views are based.

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 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, are addressed in the review of the NAAQS for PM (U.S. EPA
2014a, 2016a). Additionally, the ecological welfare effects of sulfur
oxides and 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), 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.\1\
---------------------------------------------------------------------------

    \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.
---------------------------------------------------------------------------

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(b). 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\ A secondary standard, as defined in section 109(b)(2),
must ``specify a level of air quality the attainment and maintenance of
which, in the judgment of the Administrator, based on 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\
---------------------------------------------------------------------------

    \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.''
See 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) (42 U.S.C. 7602(h)) effects
on welfare include, but are not limited to, ``effects on soils,
water, crops, vegetation, man-made materials, animals, wildlife,
weather, visibility, and climate, damage to and deterioration of
property, and hazards to transportation, as well as effects on
economic values and on personal comfort and well-being.''

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

    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.
---------------------------------------------------------------------------

    \4\ As used here and similarly throughout this notice, 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.B.2 below describes the
identification of sensitive groups (called at-risk groups or at-risk
populations) in this review.
---------------------------------------------------------------------------

    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 v. Costle, 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 Clean
Air Scientific Advisory Committee (CASAC).\5\
---------------------------------------------------------------------------

    \5\ Lists of CASAC members and members of the CASAC Sulfur
Oxides Review Panel are available at: https://yosemite.epa.gov/sab/sabpeople.nsf/WebCommitteesSubcommittees/CASAC%20Sulfur%20Oxides%20Panel.
---------------------------------------------------------------------------

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
program that covers these 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;
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.

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

    The initial air quality criteria for SOX were issued in
1969 (34 FR 1988, February 11, 1969). Based on these criteria, the EPA,
in initially promulgating NAAQS for SOX in 1971, established
the indicator as SO2. The SOX are a group of
closely related gaseous compounds that include sulfur dioxide and
sulfur trioxide and of which sulfur dioxide (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
and the U.S. Court of Appeals for the District of Columbia Circuit
(D.C. Circuit) 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 most recent review, 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.\6\ 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 SO2 concentrations,
and with 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; \7\ 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 was challenged in court, and the D.C. Circuit 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).
---------------------------------------------------------------------------

    \6\ Timing and related requirements for the implementation of
the revocation are specified in 40 CFR 50.4(e).
    \7\ 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).
---------------------------------------------------------------------------

    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 standards (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) 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).
    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 Policy
Assessment (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 schedule for completion of this review is governed by a consent
decree resolving a lawsuit filed in July 2016 by a group of plaintiffs
which included a claim that the EPA had failed to complete its review
of the primary SO2 NAAQS within five 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, notices
setting forth proposed and final decisions concerning its review of the
primary NAAQS for SOX no later than May 25, 2018 and January
28, 2019, respectively.\9\
---------------------------------------------------------------------------

    \8\ See Complaint, Center for Biological Diversity et al. v.
McCarthy, 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. McCarthy, No. 3:16-cv-03796-VC (N.D. Cal., entered April 28,
2017), Doc. No. 37.
---------------------------------------------------------------------------

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 SO2 sources and emissions (II.B.1) and ambient
concentrations (II.B.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.\10\ Sulfur oxides known to occur

in the troposphere include SO2 and sulfur trioxide
(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).\11\
---------------------------------------------------------------------------

    \10\ 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, 2-24).
    \11\ 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).
---------------------------------------------------------------------------

    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).\12\ 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).
---------------------------------------------------------------------------

    \12\ 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).
---------------------------------------------------------------------------

    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 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,\13\ 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).\14\ 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.\15\ 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).
---------------------------------------------------------------------------

    \13\ When established, the MATS Rules 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).
    \14\ 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).
    \15\ See https://www.epa.gov/diesel-fuel-standards/diesel-fuel-standards-and-rulemakings#nonroad-diesel.
---------------------------------------------------------------------------

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 99th percentile daily maximum 1-hour
concentrations averaged over three years) at locations continuously
monitored over this period (PA, Figure 2-4).\16\ The decline since 2000
has been 69% at the larger number of locations continuously monitored
since that time (PA, Figure 2-5).\17\
---------------------------------------------------------------------------

    \16\ This decline is the average of observations at 24
monitoring sites that have been continuously operating from 1980-
2016.
    \17\ This decline is the average of observations at 193
monitoring sites that have been continuously operating across 2000-
2016.
---------------------------------------------------------------------------

    As a result of the reporting requirements promulgated in 2010 (as
summarized in section I.C above) maximum hourly five-minute
concentrations of SO2 in ambient air are available at
SO2 NAAQS compliance monitoring sites (PA, Figure 2-3; FR 75
35554, June 22, 2010).\18\ 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 declined approximately 53% (PA, Figure 2-
6, Appendix B).
---------------------------------------------------------------------------

    \18\ 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.
---------------------------------------------------------------------------

    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 higher concentrations, which may or may not
impact large portions of surrounding populated areas depending on
meteorological conditions and terrain.
    Analyses in the ISA of 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>).\19\ 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>; U.S. EPA 2008a, section 2.5.1).
---------------------------------------------------------------------------

    \19\ The six ``focus areas'' evaluated in the ISA are:
Cleveland, OH; Pittsburgh, PA; New York City, NY; St. Louis, MO-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.
---------------------------------------------------------------------------

II. Rationale for Proposed Decision

    This section presents the rationale for the Administrator's
proposed decision to retain the current primary SO2
standard. This rationale is based on a thorough review of the latest
scientific information generally published through August 2016,\20\ as
presented in the ISA, on human health effects associated with
SO2 and pertaining to the presence of SOX in
ambient air. The Administrator's rationale also takes into account: (1)
The PA evaluation of the policy-relevant information in the ISA and
quantitative analyses of air quality, human exposure and health risks
in the REA; (2) CASAC advice and recommendations, as reflected in
discussions of drafts of the ISA, REA, and PA at public meetings and in
the CASAC's letters to the Administrator; and (3) public comments
received during the development of these documents.
---------------------------------------------------------------------------

    \20\ In addition to the review's opening ``call for
information'' (78 FR 27387, May 10, 2013), ``the U.S. EPA routinely
conducted literature searches to identify relevant peer-reviewed
studies published since the previous ISA (i.e., from January 2008
through August 2016)'' (ISA, p. 1-3). References that are cited in
the ISA, the references that were considered for inclusion but not
cited, and electronic links to bibliographic information and
abstracts can be found at: https://hero.epa.gov/hero/sulfur-oxides.
---------------------------------------------------------------------------

    In presenting the rationale for the Administrator's proposed
decision and its foundations, section II.A provides background on the
general approach for review of the primary SO2 standard,
including a summary of the approach used in the last review (section
II.A.1) and the general approach for the current review (section
II.A.2). Section II.B summarizes the currently available health effects
evidence, focusing on consideration of key policy-relevant aspects.
Section II.C summarizes the exposure and risk information for this
review, drawing on the quantitative analyses for SO2,
presented in the REA. Section II.D presents the Administrator's
proposed conclusions on the current standard (section II.D.3), drawing
on both evidence-based and exposure/risk-based considerations (section
II.D.1) and advice from the CASAC (section II.D.2).

A. General Approach

    The past and current approaches described below are both based,
most fundamentally, on using the EPA's assessments of the current
scientific evidence and associated quantitative analyses to inform the
Administrator's judgment regarding a primary standard for
SOX that protects public health with an adequate margin of
safety. 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; 81 FR 89097, December 9, 2016; 82 FR
11356, February 22, 2017; 82 FR 43756, September 19, 2017). In bridging
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 policy implications of the
evaluation of the current evidence in ISA and the quantitative analyses
in the REA. In evaluating the health protection afforded by the current
standard, the four basic elements of the NAAQS (indicator, averaging
time, level, and form) are considered collectively.
    We note that 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 will draw 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 analyses. This approach 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 the judgment of the Administrator, 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 or
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\
---------------------------------------------------------------------------

    \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]).
---------------------------------------------------------------------------

1. Approach in the Last Review
    The last review of the primary NAAQS for SOX was
completed in 2010 (75 FR 35520, June 22, 2010). The decision in that
review to substantially revise the standards (establishing a 1-hour
standard and revoking the 24-hour and annual standards) was based on
the extensive body of evidence of respiratory effects in people with
asthma that has expanded in this area over the four decades since the
first SO2 standards were set in 1971 (U.S. EPA 1982, 1986,
1994, 2008a). In so doing, the 2010 decision considered the full body
of evidence, as assessed in the 2008 ISA; the 2009 REA, which included
the staff assessment of the policy-relevant information contained in
the ISA and analyses of air quality, exposure and risk; the advice and
recommendations of the CASAC; and public comment. In addition to
epidemiologic evidence linking respiratory outcomes in people with
asthma to short-term SO2 air quality metrics, a key element
of the expanded evidence base in the 2010 review was a series of
controlled human exposure studies which document bronchoconstriction-
related effects on lung function in people with asthma exposed while
breathing at elevated rates \22\ for periods as short as five minutes.
Another key element was the air quality database, expanded since the
previous review (completed in 1996), which documented the then-recent
pattern of peak 5-minute SO2 concentrations. The EPA used
these data in the quantitative exposure and risk assessments to provide
an up-to-date ambient air quality context for interpreting the health
effects evidence in the 2010 review. Together these aspects of the 2010
review additionally addressed the issues raised in the court remand to
the EPA of the Agency's 1996 decision not to revise the standards at
that time to specifically address 5-minute exposures (75 FR 35523, June
22, 2010). In so doing, the EPA strengthened the primary NAAQS for

SOX to provide the requisite protection of public health
with an adequate margin of safety and to specifically afford increased
protection for at-risk populations, such as people with asthma, against
adverse respiratory health effects related to short-term SO2
exposures (75 FR 35550, June 22, 2010).
---------------------------------------------------------------------------

    \22\ The phrase ``elevated ventilation'' (or ``moderate or
greater exertion'') was used in the 2009 REA and Federal Register
notices in the last review to refer to activity levels that in
adults 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'' to refer to the same situation.
---------------------------------------------------------------------------

    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 Administrator gave particular attention to the robust evidence
base, comprised of findings from controlled human exposure,
epidemiologic, and animal toxicological studies that collectively were
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 a
broader range of respiratory outcomes, with uncertainty noted about the
magnitude of the study effect estimates, quantification of the exposure
concentration-response relationship, potential confounding by
copollutants, and other areas (75 FR 35535-36, June 22, 2010; 2008 ISA,
section 5.3).
    The conclusions reached in the last review were based primarily on
interpretation of the short-term health effects evidence, particularly
the 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 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 recommendations,\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, 2000).
Based on these considerations, the Administrator, in reaching decisions
in the last review, gave weight to the findings of respiratory effects
in exercising people with asthma after 5- to 10-minute exposures as low
as 200 ppb. With regard to higher exposures, at or above 400 ppb, she
noted their association with respiratory symptoms as indication of
their clear adversity, as well as the greater number of study subjects
responding with lung function decrements. Moreover, she took note of
the greater severity of the response, recognizing effects associated
with exposures as low as 200 ppb to be less severe (75 FR 35547, June
22, 2010).
---------------------------------------------------------------------------

    \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, 2000).
    \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).
---------------------------------------------------------------------------

    In reaching her conclusion on the adequacy of the then-existing
primary standards, the Administrator gave particular attention to the
exposure and risk estimates from the 2009 REA for air quality
conditions just meeting the then-existing (24-hour and annual)
standards. In so doing, the Administrator also noted epidemiologic
study findings of associations with respiratory outcomes in studies of
locations where maximum 24-hour average SO2 concentrations
were below the level of the then existing 24-hour standard. The 2009
REA estimated that substantial percentages of children with asthma
might be expected to experience at least once annually, exposures 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 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).
---------------------------------------------------------------------------

    \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).
---------------------------------------------------------------------------

    Based on consideration of the entire body of evidence and
information available in the review, as well as the advice from the
CASAC and public comments, the Administrator concluded that the
appropriate approach to revising the standards was to replace the then-
existing 24-hour standard with a new, short-term standard set to
provide requisite protection with an adequate margin of safety to
people with asthma and afford protection from the adverse health
effects of 5-minute to 24-hour SO2 exposures (75 FR 35536,
June 22, 2010). Accordingly, the available information was then
considered in reaching conclusions on the four elements of such a new
standard: indicator, averaging time, form, and level. Further, upon
reviewing the evidence with regard to the potential for effects from
long-term exposures, the Administrator revoked the annual standard. In
so doing, she recognized the lack of sufficient health evidence to
support a long-term standard and that the new short-term standard would
have the effect of generally maintaining the annual SO2
concentrations well below the level of the revoked annual standard (75
FR 35550, June 22, 2010).
    With regard to the indicator for the new short-term standard, the
EPA continued to focus on SO2 as the most appropriate
indicator for SOX because the available scientific
information regarding health effects was overwhelmingly indexed by
SO2. Furthermore, although the presence of SOX
species other than SO2 in ambient air had been recognized,
no alternative to SO2 had been advanced as a more
appropriate surrogate for SOX (75 FR 35536, June 22, 2010).
Controlled human exposure studies and animal toxicological studies
provided specific evidence for health effects following exposures to
SO2, and epidemiologic studies typically analyzed
associations of health outcomes with concentrations of SO2.
Based on the information available in the last review and consistent
with the views of the CASAC that ``for indicator, SO2 is
clearly the preferred choice'' (Samet, 2009, p. 14), the Administrator
concluded it was appropriate to continue to use SO2 as

the indicator for a standard that was intended to address effects
associated with exposure to SO2, alone or in combination
with other SOX (75 FR 35536, June 22, 2010). In so doing,
the EPA recognized that measures leading to reductions in population
exposures to SO2 will also likely reduce exposures to other
SOX (75 FR 35536, June 22, 2010).
    With regard to the averaging time for the new standard, the
Administrator judged 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). She further 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).\26\ Accordingly, she considered longer
averaging times.
---------------------------------------------------------------------------

    \26\ 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).
---------------------------------------------------------------------------

    Results of air quality analyses in the REA suggested that a
standard based on 24-hour average SO2 concentrations would
not likely be an effective or efficient approach for addressing 5-
minute peak SO2 concentrations, likely over-controlling in
some areas while under-controlling in others (2009 REA, section
<IP_ADDRESS>). In contrast, these same analyses suggested that a 1-hour
averaging time would be more efficient and would be effective at
limiting 5-minute peaks of SO2 (2009 REA, section
<IP_ADDRESS>.). Drawing on this information, the Administrator concluded
that a 1-hour standard, with the appropriate form and level, would be
likely to substantially reduce 5- to 10-minute peaks 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 (75 FR 35539, June 22, 2010).
Further, she 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
outcomes (75 FR 35539, June 22, 2010).
    The Administrator additionally took note of advice from the CASAC.
The CASAC stated that the REA had presented a ``convincing rationale''
for a 1-hour standard and that ``a one-hour standard is the preferred
averaging time'' (Samet, 2009, pp. 15, 16). The CASAC further stated
that it was ``in agreement with having a short-term standard'' and
found that ``the REA supports a one-hour standard as protective of
public health'' (Samet, 2009, p. 1). Thus, in consideration of the
available information summarized here and the CASAC's advice, the
Administrator concluded that a 1-hour standard (given the appropriate
level and form) was an appropriate means of controlling short-term
exposures to SO2 ranging from 5 minutes to 24 hours (75 FR
35539, June 22, 2010).
    With regard to the statistical form for the new 1-hour standard,
the Administrator judged that the form of the standard should reflect
the health effects evidence presented in the ISA that indicated that
the percentage of people with asthma affected and the severity of the
response increased with increasing SO2 concentrations (75 FR
35541, June 22, 2010). She additionally found it reasonable to consider
stability (e.g., to avoid disruption of programs implementing the
standard and the related public health protections from those programs)
as part of her consideration of the form for the standard (75 FR 35541,
June 22, 2010). In so doing, she noted that a concentration-based form
averaged over three years would likely 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 CASAC
additionally stated that ``[t]here is adequate information to justify
the use of a concentration-based form averaged over 3 years'' (Samet,
2009, p. 16). In consideration of this information, the Administrator
judged a concentration-based form averaged over three years to be most
appropriate (75 FR 35541, June 22, 2010).
    In selecting a specific concentration-based form, the Administrator
considered health evidence from the ISA as well as air quality,
exposure, and risk information from the REA. In so doing, the
Administrator concluded that the form of a new 1-hour standard should
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).
The Administrator further noted that, based on results of air quality
and exposure analyses in the REA, a 99th percentile form was likely to
be appreciably more effective at achieving the desired control of 5-
minute peak exposures than a 98th percentile form (75 FR 35541, June
22, 2010). Thus, the Administrator selected a 99th percentile form
averaged over three years (75 FR 35541, June 22, 2010).
    Lastly, based on the body of scientific evidence and information
available, as well as CASAC recommendations and public comment, the
Administrator decided on a standard level that, in combination with the
specified choice of indicator, averaging time and form, would be
requisite to protect public health, including the health of at-risk
populations, with an adequate margin of safety. In reaching the
decision on a level for the new 1-hour standard, the Administrator gave
primary emphasis to the body of health effects evidence assessed in the
ISA. In so doing, she noted that the controlled human exposure studies
provided the most direct evidence of respiratory effects from exposure
to SO2 (75 FR 35546, June 22, 2010). The Administrator drew
on evidence from these studies in reaching judgments on the magnitude
of adverse respiratory effects and associated potential public health
significance for the air quality exposure and risk analysis results of
air quality scenarios for conditions just meeting alternative levels
for a new 1-hour standard (described in the 2009 REA).
    In light of judgments regarding the health effects evidence, the
Administrator considered what the findings of the 2009 REA exposure
analyses indicated with regard to varying degrees of protection that
different 1-hour standard levels might be expected to provide against
5-minute exposures to concentrations of 200 ppb and 400 ppb, given the
specified choice of indicator, averaging time, and form.\27\ For
example, the single-year exposure assessment for St. Louis \28\
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). Results
for the air quality scenario for a 1-hour standard level of 50 ppb
suggested that such a standard would further limit exposures, such that
more than 99% \29\ 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 \30\ 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 the 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).\31\
---------------------------------------------------------------------------

    \27\ 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
indicated for a 1-hour standard level of 100 ppb a maximum annual
average of two 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).
    \28\ With regard to the results for the two study areas assessed
in the 2009 REA, 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.
    \29\ The 2009 REA indicated this percentage to be 99.9% (2009
REA, Appendix B, p. B-62).
    \30\ 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).
    \31\ 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).
---------------------------------------------------------------------------

    Given the above considerations and the comments received on the
proposal, the Administrator judged, based on the entire body of
evidence and information available in that review (concluded in 2010),
and the related uncertainties,\32\ that a standard level of 75 ppb was
appropriate. She concluded that such a standard, with a 1-hour
averaging time and 99th percentile form, would provide a significant
increase in public health protection compared to the then-existing
standards and would be expected to provide protection, with an adequate
margin of safety, 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). The Administrator found that ``a 1-hour
standard at a level of 75 ppb is 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). Such a
standard was also 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'' (75 FR 35548,
June 22, 2010). Lastly, the Administrator noted ``that a standard level
of 75 ppb is consistent with the consensus recommendation of CASAC''
(75 FR 35548, June 22, 2010). The Administrator also considered the
likelihood of public health benefits at lower standard levels, and
judged a 1-hour standard at 75 ppb to be sufficient to protect public
health with an adequate margin of safety (75 FR 35547-35548, June 22,
2010).
---------------------------------------------------------------------------

    \32\ Such uncertainties included both those with regard to the
epidemiologic evidence, including potential confounding and exposure
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).
---------------------------------------------------------------------------

2. Approach for the Current Review
    To evaluate whether it is appropriate to consider retaining the now
current primary SO2 standard, or whether consideration of
revision is appropriate, the EPA has adopted an approach in this review
that builds upon the general approach used in the last review and
reflects the body of evidence and information now available.
Accordingly, the approach in this review takes into consideration the
approach used in the last review, addressing key policy-relevant
questions in light of currently available scientific and technical
information. As summarized above, the Administrator's decisions in the
prior review were based on an integration of SO2 health
effects information with judgments on the adversity and public health
significance of key health effects, policy judgments as to when the
standard is requisite to protect against public health with an adequate
margin of safety, consideration of CASAC advice, and consideration of
public comments.
    Similarly, in this review, we draw on the current evidence and
quantitative assessments of exposure pertaining to the public health
risk of SO2 in ambient air. In considering the scientific
and technical information here, we consider both the information
available at the time of the last review and information newly
available since the last review, including that which has been
critically analyzed and characterized in the current ISA. The
quantitative exposure and risk analyses provide a context for
interpreting the evidence of lung function decrements in people with
asthma breathing at elevated rates and the potential public health
significance of exposures associated with air quality conditions that
just meet the current standard.

B. Health Effects Information

    The information summarized here is based on our scientific
assessment of the health effects evidence available in this review;
this assessment is documented in the ISA and its policy implications
are further discussed in the PA. More than 400 studies are newly
available and considered in the ISA, including more than 200 health
studies. They are consistent with the evidence that was available in
the last review. As in the last review, the key evidence comes from the
body of controlled human exposure studies that document effects in
people with asthma. Policy implications of the currently available
evidence are discussed in the PA (as summarized in section II.D.1
below). The subsections below briefly summarize the following aspects
of the evidence: The nature of SO2-related health effects
(section II.B.1), the populations at risk (section II.B.2), exposure
concentrations associated with health effects (section II.B.3), and
potential public health implications (section II.B.4).
1. Nature of Effects
    In this review, as in past reviews, the health effects evidence
evaluated in the ISA for SOX is focused on SO2
(ISA, p. 5-1). As summarized in section I.D.1 above, atmospheric
chemistry as well as emissions contribute to SO2 being the
most prevalent sulfur oxide in the atmosphere. As concluded in the ISA,
``[o]f the sulfur oxides, SO2 is the most

abundant in the atmosphere, the most important in atmospheric
chemistry, and the one most clearly linked to human health effects''
(ISA, p. 2-1). Accordingly, the ISA states that ``only SO2
is present at concentrations in the gas phase that are relevant for
chemistry in the atmospheric boundary layer and troposphere, and for
human exposures'' (ISA, p. 2-18). Thus, the current health effects
evidence and the Agency's review of the evidence, including the
evidence newly available in this review, continues to focus on
SO2.
    Sulfur dioxide is a highly reactive and water-soluble gas that once
inhaled is absorbed almost entirely in the upper respiratory tract \33\
(ISA, sections 4.2 and 4.3). Short exposures to SO2 can
elicit respiratory effects, particularly in individuals with asthma
(ISA, p. 1-17). Under conditions of elevated breathing rates (e.g.,
while exercising), SO2 penetrates into the tracheobronchial
region,\34\ 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). More specifically, bronchoconstriction,\35\ which
is characteristic of an asthma attack, is the most sensitive indicator
of SO2-induced lung function effects (ISA, p. 5-8).
Associated with this bronchoconstriction response is an increase in
airway resistance which is an index of airway hyperresponsiveness
(AHR).\36\ Exercising individuals without asthma have also been found
to exhibit such responses, but at much higher SO2 exposure
concentrations (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).
---------------------------------------------------------------------------

    \33\ 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).
    \34\ 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 and
bronchii.
    \35\ The term bronchoconstriction refers to constriction or
narrowing of the airways in the respiratory tract.
    \36\ Airway hyperresponsiveness, which is an increased
propensity of the airways to narrow in response to
bronchoconstrictive stimuli, is a characteristic feature of people
with asthma (ISA, section <IP_ADDRESS>).
---------------------------------------------------------------------------

    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 for
this causal relationship comes from the long-standing evidence base of
controlled human exposure studies (U.S. EPA, 1994; 2008 ISA). These
studies demonstrate asthma exacerbation-related lung function
decrements \37\ and respiratory symptoms (e.g., cough, chest tightness
and wheeze) in people with asthma exposed to SO2 for 5 to 10
minutes at elevated breathing rates (ISA, section 5.2.1).
Bronchoconstriction, evidenced by decrements in lung function, that are
sometimes accompanied by respiratory symptoms (e.g., cough, wheeze,
chest tightening and shortness of breath), is observed to occur 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>).\38\ In contrast, respiratory
effects are not generally observed in other people with asthma
(nonresponders) and healthy adults exposed, while exercising, to
SO2 concentrations below 1000 ppb (ISA, sections <IP_ADDRESS> and
<IP_ADDRESS>). Across studies, bronchoconstriction in response to
SO2 exposure is mainly seen during conditions of elevated
breathing rates, such as exercise or with mouthpiece exposures that
involve laboratory-facilitated rapid, deep breathing.\39\ With these
conditions, breathing shifts from nasal breathing to oral/nasal
breathing, which increases the concentrations of SO2
reaching the tracheobronchial region of lower 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>).
---------------------------------------------------------------------------

    \37\ The specific responses reported in the evidence base that
are described in the ISA as lung function decrements are increased
specific airway resistance (sRaw) and reduced forced expiratory
volume in 1 second (FEV1) (ISA, section <IP_ADDRESS>).
    \38\ 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 being insensitive to SO2
bronchoconstrictive effects at concentrations as high as 1000 ppb
(ISA, pp. 5-14 to 5-21; Johns et al., 2010).
    \39\ 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.
---------------------------------------------------------------------------

    The evidence base of controlled human exposure studies for people
with asthma \40\ is the same in this review as in the last review. Such
studies reporting asthma exacerbation-related effects for individuals
with asthma are summarized in Tables 5-1 and 5-2, as well as section
<IP_ADDRESS> of the ISA. 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 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 as
little as two minutes from exposure start, and is transient, with
recovery occurring upon cessation of exposure (ISA, p. 5-14; Table 5-
2).
---------------------------------------------------------------------------

    \40\ 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 epidemiologic evidence, some of which is newly available since
the time of the last review, includes studies reporting positive
associations for asthma-related hospital admissions of children or
emergency department visits by children with short-term SO2
exposures (ISA, section 5.2.1). These findings provide evidence
supportive 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>). With regard to newly available epidemiologic studies,
there are a limited number of such studies that have investigated
SO2 effects related to asthma exacerbation, with the most
supportive evidence coming from studies on asthma-related emergency
department visits by children and hospital admissions of children (ISA,
section <IP_ADDRESS>). As in the last review, areas of uncertainty in the
epidemiologic evidence relate to the characterization of exposure
through the use of fixed site monitor concentrations 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
\41\ 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).
---------------------------------------------------------------------------

    \41\ The potential for confounding by PM is of particular
interest given that SO2 is a precursor to PM (ISA, p. 1-
7).
---------------------------------------------------------------------------

    The evidence base for long-term \42\ SO2 exposure and
respiratory effects is somewhat augmented since the last review such
that the ISA in the current review 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 study 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,
section <IP_ADDRESS>). Further, there are uncertainties that apply to the
epidemiologic evidence, including newly available evidence, across the
respiratory effects examined for long-term exposure (ISA, section
<IP_ADDRESS>).
---------------------------------------------------------------------------

    \42\ In evaluating the health effects studies in the ISA, the
EPA has generally categorized exposures of durations longer than a
month as ``long-term'' (ISA, p. 1-2).
---------------------------------------------------------------------------

    For effects other than respiratory effects, the current evidence is
generally similar to the evidence available in the last review, and
leads to similar conclusions. 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 evidence of previously
and newly available multicity epidemiologic studies that provide
consistent evidence of positive associations coupled with uncertainty
regarding the potential for SO2 to have an independent
effect on mortality. While recent studies have analyzed some key
uncertainties and data gaps from the previous review, uncertainties
still exist, given the limited number of studies that examined
copollutant confounding, the evidence for a decrease in the size of
SO2-mortality associations in copollutant models with
nitrogen dioxide and particulate matter with mass median aerodynamic
diameter below 10 microns, and the lack of a potential biological
mechanism for mortality following short-term SO2 exposures
(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,
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, the current health effects evidence supports the primary
conclusion that short-term exposure to SO2 in ambient air
causes respiratory effects, in particular, asthma exacerbation in
individuals with asthma; this evidence and these conclusions are also
consistent with that available in the last review. The focus in this
review, as in prior reviews, is on such effects.
2. At-Risk Populations
    In this document, we use the term ``at-risk populations'' \44\ to
recognize populations that have a greater likelihood of experiencing
SO2-related health effects, i.e. groups with characteristics
that contribute to an increased risk of SO2-related health
effects. In identifying factors that increase risk of SO2-
related health effects, we have considered evidence regarding factors
contributing to increased susceptibility, which generally include
intrinsic factors, such as physiological factors that may influence the
internal dose or toxicity of a pollutant, or extrinsic factors, such as
sociodemographic or behavioral factors (ISA, p. 6-1).
---------------------------------------------------------------------------

    \44\ As noted in section I above, we use the term ``at-risk
populations'' to refer to persons having a quality or characteristic
in common, such as a specific pre-existing illness or a specific age
or lifestage for which there is an increased risk of SO2-
related health effects.
---------------------------------------------------------------------------

    The information newly available in this review has not
substantially altered our previous understanding of at-risk populations
for SO2 in ambient air. As in the last review, 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 is based on the well-
established and well-characterized evidence from controlled human
exposure studies, supported by the evidence on mode of action for
SO2 with additional support from epidemiologic studies (ISA,
sections <IP_ADDRESS> and 6.3.1). Somewhat similar to the conclusion in the
last review that children and older adults are potentially susceptible
populations, the ISA (relying on a framework for evaluating the
evidence for risk factors that has been developed since the last
review) \45\ indicates the evidence to be suggestive of increased risk
for these groups, with some limitations and inconsistencies (ISA,
sections <IP_ADDRESS> and <IP_ADDRESS>).\46\
---------------------------------------------------------------------------

    \45\ Since the 2010 review of the primary SO2 NAAQS,
the EPA has developed a formal framework to transparently
characterize the strength of the evidence that can inform the
identification of populations and lifestages at increased risk of a
health effect related to exposure to a pollutant. This framework is
part of the systematic approach taken in the ISA for this review
(ISA, section 6.2).
    \46\ The current evidence for risk to older adults relative to
other lifestages comes from epidemiologic studies, for which
findings are somewhat inconsistent, and studies with which there are
uncertainties in the association with the health outcome (ISA,
section <IP_ADDRESS>).
---------------------------------------------------------------------------

    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, which
include their greater responsiveness to methacholine,\47\ a chemical
that can elicit bronchoconstriction in people with asthma, as well as
their greater use of oral breathing, particularly by boys (ISA,
sections <IP_ADDRESS> and 4.1.2). Oral breathing (vs. nasal breathing) and
increased breathing rate are factors that allow for greater
SO2 penetration into the tracheobronchial region of the
lower airways, and reflect conditions of individuals with asthma in
which bronchoconstriction-related responses have been observed in the
controlled exposure studies (ISA, sections 4.2.2, <IP_ADDRESS>, and 6.3.1).
Although the epidemiological evidence includes a number of studies
focused on health outcomes in children that are supportive of the
qualitative conclusions of causality (ISA, section <IP_ADDRESS>), there are
few controlled human exposure studies to inform our

understanding of exposure concentrations associated with effects in
this population group. Those studies have not included subjects younger
than 12 years (ISA, p. 5-22). Some characteristics particular to
school-age children younger than 12 years, such as increased propensity
for mouth breathing (ISA, p. 4-5), however, suggest that this age group
of children with asthma might be expected to experience larger lung
function decrements than adults with asthma (ISA, p. 5-25).\48\
---------------------------------------------------------------------------

    \47\ The ISA concluded that potential differences in airway
responsiveness of children to SO2 relative to adolescents
and adults may be inferred by differences in responses to
methacholine (ISA, section <IP_ADDRESS>). Methacholine is a chemical that
can elicit bronchoconstriction through its action on airway smooth
muscle receptors. It is commonly used to identify people with asthma
and accordingly has been used to screen subjects for studies of
SO2 effects. However, results of studies of the extent to
which airway response to methacholine is predictive of
SO2 responsiveness have varied somewhat. For example, an
analysis of the extent to which airway responsiveness to
methacholine, a history of respiratory symptoms, and atopy were
significant predictors of airway responsiveness to SO2,
found that about 20 to 25% of subjects ranging in age from 20 to 44
years that were hyperresponsive to methacholine were also
hyperresponsive to SO2 (ISA, section <IP_ADDRESS>; Nowak et
al., 1997). Another study focused on individuals with airway
responsiveness to methacholine found only a weak correlation between
airway responsiveness to SO2 and methacholine (ISA,
section <IP_ADDRESS>; Horstman et al., 1986).
    \48\ The ISA does not find the evidence to be adequate to
conclude differential risk status for subgroups of children with
asthma (ISA, Chapter 6). In consideration of the limited information
regarding factors related to breathing habit, however, and
recognizing the lack of evidence from controlled human exposure
studies of SO2-induced lung function decrements in
children, approximately 5 to 11 years of age, with asthma, the ISA
suggests that this age group of children 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, p. 4-7 and 5-36).
---------------------------------------------------------------------------

    Additionally, 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). This occurrence is
quantitatively analyzed in a study newly available in this review. This
study 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). While such information provides documentation that some
individuals have a greater response to SO2 than others with
the same disease status, the factors contributing to this greater
susceptibility are not yet known (ISA, pp. 5-14 to 5-21).
    The current evidence for factors evaluated in the ISA other than
asthma status and lifestage is inadequate to determine whether they
(e.g., sex and SES) might have an influence on risk of SO2-
related effects (ISA, section 6.6).
3. 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 demonstrate a dose-
response relationship between 5- and 10-minute SO2 exposure
concentrations and decrements in lung function (e.g., increased sRaw
and reduced FEV1) and occurrence of respiratory symptoms in
individuals with asthma exposed while breathing at elevated rates (ISA,
section <IP_ADDRESS>). Clear and consistent increases in these effects occur
with increasing SO2 exposure (ISA, Table 5-2 and pp. 5-35,
5-39). Further, the SO2-induced bronchoconstriction occurs
rapidly; exposures as short as 5 minutes have been found to elicit a
similar bronchoconstrictive response as somewhat longer exposures. For
example, during exposure to SO2 over a 30-minute period with
continuous exercise, the response to SO2 has been found to
develop rapidly and is maintained throughout the 30-minute exposure
(ISA, p. 5-14). In a study involving short exercise periods within a 6-
hour exposure period, the effects observed following exercise were
documented to return to baseline levels within one hour after the
cessation of exercise, even with continued exposure (ISA, p. 5-14; Linn
et al., 1984). Thus, the controlled human exposure evidence base
demonstrates the occurrence of SO2-related effects as a
result of peak exposures on the order of minutes.\49\
---------------------------------------------------------------------------

    \49\ As 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 study findings \50\ demonstrate that
SO2 concentrations as low as 200 to 300 ppb for 5 to 10
minutes elicited moderate or greater lung function decrements, measured
as a decrease in FEV1 of at least 15% or an increase in sRaw
of at least 100%, in 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 SO2-related lung function decrements
(in terms of 15% reductions in FEV1 or doubling or tripling
of sRaw), as many as 33% of exercising study subjects with asthma
experienced moderate or greater decrements in lung function (ISA,
section 5.2.1, Table 5-2). Analyses focused on subjects with asthma in
multiple studies 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). At concentrations at or above 400
ppb, moderate or greater decrements in lung function occurred in 20 to
60% of exercising individuals with asthma and a larger percentage of
individuals with asthma experienced 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), compared to exposures at 200 to 300
ppb (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).
---------------------------------------------------------------------------

    \50\ 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.
---------------------------------------------------------------------------

    The lowest exposure concentration for which individual study
subject data are available in terms of the sRaw and FEV1
from studies that have assessed the SO2 effect versus the
effect of exercise in clean air is 200 ppb (ISA, Table 5-2 and Figure
5-1). In nearly all of these studies (and all of the studies for
concentrations below 500 ppb), study subjects breathed freely (e.g.,
without using a mouthpiece).\51\ In studies that tested 200 ppb, 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).
---------------------------------------------------------------------------

    \51\ 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, the very
limited available evidence is for

exposure as low as 100 ppb. Some differences in methodology and the
reporting of results complicate comparisons of the studies of 100 ppb
exposure with studies of higher concentrations. In the studies testing
this concentration, 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 determining the effect of
SO2 versus the effect of exercise in causing
bronchoconstriction (Sheppard et al., 1981, 1984; Koenig et al., 1989).
In those 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 exposure concentrations of 200 ppb or more.52 53 Thus,
the set of studies for the 100 ppb exposure concentration, while
limited and complicated by differences from studies of higher
concentrations with regard to reporting of results and exposure method,
does not indicate this exposure concentration to result in as much as a
doubling in sRaw, based on the extremely few adults and adolescents
tested (Sheppard et al., 1981, 1984; Koenig et al., 1989).
---------------------------------------------------------------------------

    \52\ For example, 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 the study of adolescents (aged 12 to 18
years), among the three individual study subjects for which
respiratory resistance appears to have increased with SO2
exposure, the magnitude of any increase after consideration of the
response to exercise appears to be less than 100% in each subject
(Koenig et al., 1989).
    \53\ 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 into the tracheobronchial airways (2008
ISA, p. 3-4; ISA, section <IP_ADDRESS>). This allowance of greater
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 epidemiological studies that find
associations with outcomes such as asthma-related emergency department
visits and hospitalizations. 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). Given the important role of SO2
as a precursor to PM in ambient air, however, a key uncertainty in the
epidemiologic evidence available in this review, as in the last review,
is potential confounding by copollutants, particularly PM (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 this uncertainty, e.g., through the use of
copollutant models. 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.\54\ No additional such studies have been newly identified in this
review that might inform this issue. Thus, such uncertainties regarding
copollutant confounding, as well as exposure measurement error, remain
in the currently available epidemiologic evidence base (ISA, p. 5-6).
---------------------------------------------------------------------------

    \54\ Based on data available for specific time periods at some
monitors in the areas of these studies, the 99th percentile 1-hour
daily maximum concentrations were estimated in the last review to be
between 78-150 ppb (Thompson and Stewart, 2009; PA, Appendix D).
---------------------------------------------------------------------------

4. 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>). With regard to SO2
concentrations in ambient air, the public health implications and
potential public health impacts relate to the effects causally related
to SO2 exposures of interest in this review. These are
respiratory effects of short-term exposures, and particularly those
effects associated with asthma exacerbation in people with asthma. As
summarized above in section II.B.1, the most strongly demonstrated
effects are bronchoconstriction-related effects resulting in decrements
in lung function elicited by short term exposures during periods of
elevated breathing rate; asthma-related health outcomes such as
emergency department visits and hospital admissions have also been
statistically associated with ambient air SO2 concentration
metrics in epidemiologic studies (ISA, section <IP_ADDRESS>).
    As summarized in section II.B.2 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 within this at-risk population (ISA, section 6.3.1). The
evidence supporting this conclusion comes primarily from studies of
individuals with mild to moderate asthma,\55\ 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) of individuals with differences in
severity of their asthma.\56\ 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.B.3 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).
---------------------------------------------------------------------------

    \55\ 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).
    \56\ 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). The ISA
states, ``[h]owever, both 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). Based
on the criteria used in the study by Linn et al (1987) for placing
individuals in the ``moderate/severe'' group, the ISA concluded that
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).
---------------------------------------------------------------------------

    The Administrator's judgment is informed by statements by the ATS
on what constitutes an adverse health effect of air pollution. Building
on the earlier statement by the ATS that was considered in the last
review (ATS, 2000), the recent policy statement by the ATS on what
constitutes an adverse health effect of air pollution 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, 2000). 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). For example, in adding emphasis in this area, this
statement conveys the view that ``small lung function changes'' in
individuals with compromised function, such as that resulting from
asthma, should be considered adverse, even without accompanying
respiratory symptoms (Thurston et al., 2017). All of these concepts,
including the consideration of the magnitude of effects occurring in
just a subset of study subjects, are recognized as important in the
more recent ATS statement (Thurston et al., 2017) and continue to be
relevant to consideration of the evidence base for SO2.
    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,
effects that have been documented to be accompanied by 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 are requisite to protect public
health, including a 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 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)
\57\ indicate that approximately 8% of the U.S. population has asthma
(PA, Table 3-2; CDC, 2017). Among all U.S. adults, the prevalence is
estimated to be 7.6%, with women having a higher estimate (9.7%) than
men (5.4%). 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).
---------------------------------------------------------------------------

    \57\ 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).
---------------------------------------------------------------------------

    Relatively greater population-level SO2 impacts (i.e.,
greater numbers of individuals affected) might be expected in
population groups with relatively greater asthma prevalence (i.e.,
groups with relatively higher percentages of individuals that have
asthma). Among all U.S. children, the asthma prevalence estimate is
greater for boys than girls (CDC, 2017). Asthma prevalence estimates
from the 2015 NHIS vary for children of different races or ethnicities
and household income, among other factors (CDC, 2017). Among
populations of different races or ethnicities, black non-Hispanic and
Puerto Rican Hispanic children are estimated to have the highest
prevalences, 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.
    The information on which to base estimates of asthma prevalence in
other subgroups of children is much more limited (e.g., as discussed in
the REA, section 4.1.2). For example, the more limited information from
the NHIS for 2011-2015 indicates there to be a greater prevalence of
asthma in children that are obese \58\ compared to those that are not
(REA, section 4.1.2, Figure 4-2).\59\
---------------------------------------------------------------------------

    \58\ Although the CDC does not report NHIS estimates for the
percent of obese adults or children that have asthma, they do report
that that more adults with asthma are obese than adults without
asthma. As discussed in the REA, the NHIS sample size for children
with asthma identified as obese is very limited (REA, section
4.1.2).
    \59\ In consideration of the limited information regarding
factors related to breathing habit (whether one is breathing through
their nose or mouth) and recognizing the lack of evidence from
controlled human exposure studies of SO2-induced lung
function decrements in children, approximately 5 to 11 years of age,
with asthma, the ISA suggests that this age group of children 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. 4-7 and 5-36). However, the ISA
does not find the evidence to be adequate to conclude differential
risk status for subgroups of children with asthma (ISA, Chapter 6).
---------------------------------------------------------------------------

    With regard to the potential for exposure of the populations at
risk from exposures to SO2 in ambient air, the PA recognizes
that 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

most recently available design values for the primary SO2
standard (those based on monitoring data for the 2014-2016 period)
indicate there to be 15 core-based statistical areas \60\ with design
values above the existing standard level of 75 ppb, of which a number
have sizeable populations.\61\ 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).\62\ In recognition of these limitations,
the PA also examined the proximity of populations to sizeable
SO2 point sources using the most recently available