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

Federal RegisterMar 18, 2019

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 50

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

RIN 2060-AT68

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

AGENCY:

Environmental Protection Agency (EPA).

ACTION:

Final action.

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 (SO

), the EPA is retaining the current standard, without revision.

DATES:

This final action is effective on April 17, 2019.

ADDRESSES:

The EPA has established a docket for this action under Docket ID No. EPA-HQ-OAR-2013-0566. Incorporated into this docket is a separate docket established for the Integrated Science Assessment for this review (Docket ID No. EPA-HQ-ORD-2013-0357). All documents in these dockets are listed on the

www.regulations.gov

website. Although listed in the index, some information is not publicly available,

e.g.,

Confidential Business Information (CBI) or other information whose disclosure is restricted by statute. Certain other material, such as copyrighted material, is not placed on the internet and may be viewed, with prior arrangement, at the EPA Docket Center. Publicly available docket materials are available either electronically in

www.regulations.gov

or in hard copy at the Air and Radiation Docket Information Center, EPA/DC, WJC West Building, Room 3334, 1301 Constitution Ave. NW, Washington, DC. The Public Reading Room is open from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal holidays. The telephone number for the Public Reading Room is (202) 566-1744 and the telephone number for the Air and Radiation Docket Information Center is (202) 566-1742.

Availability of Information Related to This Action

A number of the documents that are relevant to this action are available through the EPA's website at

https://www.epa.gov/naaqs/sulfur-dioxide-so2-primary-air-quality-standards.

These documents include the Integrated Review Plan for the Primary National Ambient Air Quality Standard for Sulfur Dioxide (U.S. EPA, 2014a), available at

https://www3.epa.gov/ttn/naaqs/standards/so2/data/20141028so2reviewplan.pdf,

the Integrated Science Assessment for Sulfur Oxides—Health Criteria (ISA [U.S. EPA, 2017a]), available at

https://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=338596,

the Risk and Exposure Assessment for the Review of the National Ambient Air Quality Standard for Sulfur Oxides (REA [U.S. EPA, 2018a]), available at

https://www.epa.gov/naaqs/sulfur-dioxide-so2-standards-risk-and-exposure-assessments-current-review

and the Policy Assessment for the Review of the Primary National Ambient Air Quality Standard for Sulfur Oxides (PA [U.S. EPA, 2018b]), available at

https://www.epa.gov/naaqs/sulfur-dioxide-so2-standards-policy-assessments-current-review.

These and other related documents are also available for inspection and copying in the EPA docket identified above.

FOR FURTHER INFORMATION CONTACT:

Dr. Nicole Hagan, Health and Environmental Impacts Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency, Mail Code C504-06, Research Triangle Park, NC 27711; telephone: (919) 541-3153; fax: (919) 541-0237; email:

hagan.nicole@epa.gov.

SUPPLEMENTARY INFORMATION:

Table of Contents

Executive Summary

I. Background

A. Legislative Requirements

B. Related SO

Control Programs

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

D. Air Quality Information

1. Sources and Emissions of Sulfur Oxides

2. Ambient Concentrations

II. Rationale for Decision

A. Introduction

1. Background on the Current Standard

2. Overview of Health Effects Evidence

3. Overview of Risk and Exposure Information

B. Conclusions on Standard

1. Basis for Proposed Decision

2. CASAC Advice in This Review

3. Comments on the Proposed Decision

4. Administrator's Conclusions

C. Decision on the Primary Standard

III. Statutory and Executive Order Reviews

A. Executive Order 12866: Regulatory Planning and Review and Executive Order 13563: Improving Regulation and Regulatory Review

B. Executive Order 13771: Reducing Regulations and Controlling Regulatory Costs

C. Paperwork Reduction Act (PRA)

D. Regulatory Flexibility Act (RFA)

E. Unfunded Mandates Reform Act (UMRA)

F. Executive Order 13132: Federalism

G. Executive Order 13175: Consultation and Coordination With Indian Tribal Governments

H. Executive Order 13045: Protection of Children From Environmental Health Risks and Safety Risks

I. Executive Order 13211: Actions Concerning Regulations That Significantly Affect Energy Supply, Distribution or Use

J. National Technology Transfer and Advancement Act

K. Executive Order 12898: Federal Actions To Address Environmental Justice in Minority Populations and Low-Income Populations

L. Determination Under Section 307(d)

M. Congressional Review Act

References

Executive Summary

The EPA has completed its current review of the primary (health-based) NAAQS for SO

, a group of closely related gaseous compounds that include sulfur dioxide (SO

). Of these compounds, SO

(the indicator for the current standard) is the most prevalent in the atmosphere and the one for which there is a large body of scientific evidence on health effects. The current primary standard is set at a level of 75 parts per billion (ppb), as the 99th percentile of daily maximum 1-hour SO

concentrations, averaged over 3 years. Based on the EPA's review of key aspects of the currently available health effects evidence, quantitative risk and exposure information, advice from the Clean Air Scientific Advisory Committee (CASAC), and public comments, the EPA is retaining the current standard, without revision.

Reviews of the NAAQS are required by the Clean Air Act (CAA) on a periodic basis. The last review of the primary SO

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 SO

for 5 to 10 minutes while breathing at elevated rates. Revisions to the NAAQS in 2010 were accompanied by revisions to the ambient air monitoring and reporting regulations, requiring the reporting of hourly maximum 5-minute SO

concentrations, in addition to the hourly concentrations.

Emissions of SO

and associated concentrations in ambient air have declined appreciably since 2010 and over the longer term. For example, as summarized in the PA, emissions nationally are estimated to have declined by 82% over the period from 2000 to 2016, with a 64% decline from 2010 to 2016. Such declines in SO

emissions are likely related to the implementation of national control programs developed under the Clean Air Act Amendments of 1990, as well as changes in market conditions,

e.g.,

reduction in energy generation by coal. One-hour concentrations of SO

in ambient air in the U.S. declined more than 82% from 1980 to 2016 at locations continuously monitored over this period. The decline since 2000 has been 69% at a larger number of locations continuously monitored since that time. Daily maximum 5-minute concentrations have also consistently declined from 2011 to 2016.

In this review, as in past reviews of the primary NAAQS for SO

, the health effects evidence evaluated in the ISA is focused on SO

. The health effects of particulate atmospheric transformation products of SO

, such as sulfates, are addressed in the review of the NAAQS for particulate matter (PM). Additionally, the welfare effects of SO

and the ecological effects of particulate atmospheric transformation products are being considered in the review of the secondary NAAQS for oxides of nitrogen, oxides of sulfur, and PM, while the visibility, climate, and materials damage-related welfare effects of particulate sulfur compounds are being evaluated in the review of the secondary NAAQS for PM.

The health effects evidence newly available in this review, as critically assessed in the ISA in conjunction with the full body of evidence, reaffirms the conclusions from the last review. The health effects evidence continues to support the conclusion that respiratory effects are causally related to short-term SO

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 SO

while breathing at elevated rates. Epidemiologic evidence, including that from studies not available in the last review, also supports this conclusion, primarily due to studies reporting positive associations between ambient air concentrations and emergency department visits and hospital admissions, specifically for children.

Quantitative analyses of population exposure and risk also inform the final decision. These analyses expand and improve upon the quantitative analyses available in the last review. Unlike the REA available in the last review, which analyzed single-year air quality scenarios for potential standard levels bracketing the now-current level, the current REA assesses an air quality scenario for 3 years of air quality conditions that just meet the now-current standard, considering all of its elements, including its 3-year form. Other ways in which the current REA analyses are improved and expanded include improvements to models, model inputs and underlying databases, including the vastly expanded ambient air monitoring dataset for 5-minute concentrations, available as a result of changes in the last review to data reporting requirements.

Based on this evidence and quantitative information, as well as CASAC advice and consideration of public comment, the Administrator has concluded that the current primary SO

standard is requisite to protect public health, with an adequate margin of safety, from effects of SO

in ambient air and should be retained, without revision. Therefore, the EPA is retaining the current 1-hour primary SO

standard, without revision. This decision is consistent with CASAC recommendations.

I. Background

This review focuses on the presence in ambient air of SO

, a group of closely related gaseous compounds that includes SO

and sulfur trioxide (SO

) and of which SO

(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 SO

, such as sulfates, as well as visibility, climate, and materials damage-related welfare effects of such particulate sulfur compounds are being addressed in the review of the NAAQS for particulate matter (PM) (U.S. EPA, 2014a, 2016a, 2018c). Additionally, the ecological welfare effects of SO

and their particulate atmospheric transformation products are being considered in the review of the secondary NAAQS for oxides of nitrogen, oxides of sulfur, and PM (U.S. EPA, 2014a, 2017b).

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(a)(2). Section 109 (42 U.S.C. 7409) directs the Administrator to propose and promulgate “primary” and “secondary” NAAQS for pollutants for which air quality criteria are issued. Section 109(b)(1) defines a primary standard as one “the attainment and maintenance of which in the judgment of the Administrator, based on such criteria and allowing an adequate margin of safety, [is] requisite to protect the public health.”

As provided in section 109(b)(2), a secondary standard must “specify a level of air quality the attainment and maintenance of which, in the judgment of the Administrator, based on such criteria, is requisite to protect the public welfare from any known or anticipated adverse effects associated with the presence of [the] pollutant in the ambient air.”

The legislative history of section 109 indicates that a primary standard is to be set at “the maximum permissible ambient air level . . . which will protect the health of any [sensitive] group of the population,” and that for this purpose “reference should be made to a representative sample of persons comprising the sensitive group rather than to a single person in such a group.” S. Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970).

See also Lead Industries Association

EPA,

647 F.2d 1130, 1152 (D.C. Cir 1980);

American Lung Association

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.”).

As specified in section 302(h) of the CAA (42 U.S.C. 7602(h)) effects on welfare include, but are

not limited to, “effects on soils, water, crops, vegetation, manmade materials, animals, wildlife, weather, visibility, and climate, damage to and deterioration of property, and hazards to transportation, as well as effects on economic values and on personal comfort and well-being.”

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

EPA,

647 F.2d 1130, 1154 (D.C. Cir. 1980);

American Petroleum Institute

Costle,

665 F.2d 1176, 1186 (D.C. Cir. 1981);

American Farm Bureau Federation

EPA,

559 F.3d 512, 533 (D.C. Cir. 2009);

Association of Battery Recyclers

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

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,

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

EPA,

647 F.2d at 1161-62.

As used here and similarly throughout this document, the term population (or group) refers to persons having a quality or characteristic in common, such as a specific pre-existing illness or a specific age or lifestage. Section II.A.2.b below describes the identification of sensitive groups (called at-risk groups or at-risk populations) in this review.

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

American Trucking Associations,

531 U.S. 457, 465-472, 475-76 (2001). Likewise, “[a]ttainability and technological feasibility are not relevant considerations in the promulgation of national ambient air quality standards.”

American Petroleum Institute,

665 F.2d at 1185.

Section 109(d)(1) requires that “not later than December 31, 1980, and at 5-year intervals thereafter, the Administrator shall complete a thorough review of the criteria published under section 108 and the national ambient air quality standards . . . and shall make such revisions in such criteria and standards and promulgate such new standards as may be appropriate . . . .” Section 109(d)(2) requires that an independent scientific review committee “shall complete a review of the criteria . . . and the national primary and secondary ambient air quality standards . . . and shall recommend to the Administrator any new . . . standards and revisions of existing criteria and standards as may be appropriate . . . .” Since the early 1980s, this independent review function has been performed by the CASAC.

B. Related SO

Control Programs

States are primarily responsible for ensuring attainment and maintenance of ambient air quality standards once the EPA has established them. Under section 110 of the Act, 42 U.S.C. 7410, and related provisions, states are to submit, for EPA approval, state implementation plans (SIPs) that provide for the attainment and maintenance of such standards through control programs directed to sources of the pollutants involved. The states, in conjunction with the EPA, also administer the prevention of significant deterioration permitting program that covers these and other air pollutants.

See

42 U.S.C. 7470-7479. In addition, federal programs provide for nationwide reductions in emissions of these and other air pollutants under Title II of the Act, 42 U.S.C. 7521-7574, which involves controls for automobile, truck, bus, motorcycle, nonroad engine and equipment, and aircraft emissions. Furthermore, the EPA establishes emission standards for stationary sources under other provisions of the CAA; these standards, which include the new source performance standards (under section 111 of the Act, 42 U.S.C. 7411), and the national emission standards for hazardous air pollutants (under section 112 of the Act, 42 U.S.C. 7412) may also contribute to SO

emissions controls and reductions, including through controls aimed at reducing other pollutants.

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

The initial air quality criteria for SO

were issued in 1967 and reevaluated in 1969 (34 FR 1988, February 11, 1969; U.S. DHEW, 1967, 1969). Based on the 1969 criteria, the EPA, in initially promulgating NAAQS for SO

in 1971, established the indicator as SO

. SO

are a group of closely related gaseous compounds that include SO

and SO

and of which SO

(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 SO

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 SO

in ambient air at that time (61 FR 25566, May 22, 1996). This decision was challenged in the U.S. Court of Appeals for the District of Columbia Circuit (D.C. Circuit), which found that the EPA had failed to adequately explain its determination that no revision to the primary SO

standards was appropriate and remanded the determination back to the EPA for further explanation.

American Lung Association

EPA,

134 F.3d 388 (D.C. Cir. 1998).

This remand was addressed in the last review of the air quality criteria and primary standards for SO

, 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.

The new 1-hour standard was set with a level of 75 parts per billion (ppb), a form of the 3-year average of the annual 99th percentile of daily maximum 1-hour average SO

concentrations, and SO

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 SO

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 SO

ambient air monitoring regulations to require that monitoring agencies using continuous SO

methods report the highest 5-minute concentration for each hour of the day;

agencies may report all twelve 5-minute concentrations for each hour, including the maximum, although it is not required (75 FR 35568, June 22, 2010). This rule and the EPA's denial of several petitions for administrative reconsideration were challenged in the D.C. Circuit, and the court denied or dismissed on jurisdictional grounds all the claims in the petitions for review.

National Environmental Development Association's Clean Air Project

EPA,

686 F.3d 803, 805 (D.C. Cir. 2012) (“

NEDA/CAP”

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

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 SO

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 SO

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 SO

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 SO

air quality criteria and primary standard (U.S. EPA, 2014b). The draft IRP was released for public comment and was reviewed by the CASAC at a public teleconference on April 22, 2014 (79 FR 14035, March 12, 2014; Frey and Diez Roux, 2014). The final IRP was developed with consideration of comments from the CASAC and the public (U.S. EPA, 2014a; 79 FR 16325, March 25, 2014; 79 FR 66721, November 10, 2014).

As an early step in development of the Integrated Science Assessment (ISA)

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).

The ISA for this review provides a comprehensive assessment of the current scientific literature useful in indicating the kind of and extent of all identifiable effects on public health associated with the presence of the pollutant in the ambient air, as described in section 108 of the CAA, emphasizing information that has become available since the last air quality criteria review in order to reflect the current state of knowledge. As such, the ISA forms the scientific foundation for this NAAQS review and is intended to provide information useful in forming policy relevant judgments about air quality indicator(s), form(s), averaging time(s) and level(s) for the NAAQS. The ISA functions in the current NAAQS review process as the Air Quality Criteria Document (AQCD) did in reviews completed prior to 2009.

In considering the need for quantitative exposure and risk analyses in this review, the EPA completed the Risk and Exposure Assessment (REA) Planning Document in February 2017 (U.S. EPA, 2017c; 82 FR 11356, February 22, 2017) and held a consultation with the CASAC at a public meeting in March 2017 (82 FR 11449, February 23, 2017; Diez Roux, 2017b). In consideration of the CASAC's comments at that consultation and public comments, the EPA developed the draft REA and draft PA, which were released on August 24, 2017 (U.S. EPA, 2017d, e; 82 FR 43756, September 19, 2017). The draft REA and draft PA were reviewed by the CASAC on September 18-19, 2017 (82 FR 37213, August 9, 2017; Cox and Diez Roux, 2018a, b). The EPA considered the advice and comments from the CASAC on the draft REA and draft PA, as well as public comments, in developing the final REA and final PA, which were released in early May 2018 (U.S. EPA, 2018a, b).

The proposed decision (henceforth “proposal”) to retain the primary SO

NAAQS was signed on May 25, 2018, and published in the

Federal Register

on June 8, 2018 (83 FR 26752). The EPA held a public hearing in Washington, DC on July 10, 2018 (83 FR 28843, June 21, 2018). At the public hearing, the EPA heard testimony from three individuals representing specific interested organizations. The transcript from this hearing and written testimony provided at the hearing are in the docket for this review. The EPA extended the 45-day comment period by 17 days, until August 9, 2018 (83 FR 28843, June 21, 2018), and comments were received from various government, industry, and environmental groups, as well as members of the general public.

The schedule for completion of this review is governed by a consent decree resolving a lawsuit filed in July 2016 that included a claim that the EPA had failed to complete its review of the primary SO

NAAQS within 5 years, as required by the CAA.

The consent decree, which was entered by the court on April 28, 2017, provides that the EPA will sign, for publication, a notice setting forth the final decision concerning its review of the primary NAAQS for SO

no later than January

28, 2019, with such date to be extended automatically one day for each day of a lapse in appropriations if such a lapse were to occur within 120 days of this deadline.

The EPA experienced such a lapse in appropriations in late December 2018 and January 2019, which led to the automatic extension of the January 28, 2019 deadline to February 25, 2019.

See

Complaint,

Center for Biological Diversity et al.

Wheeler,

No. 3:16-cv-03796-VC (N.D. Cal., filed July 7, 2016), Doc. No. 1.

Consent Judgment at 4,

Center for Biological Diversity et al.

Wheeler,

No. 3:16-cv-03796-VC (N.D. Cal., entered April 28, 2017), Doc. No. 37.

Joint Notice of Automatic Deadline Extension in Light of Lapse in Appropriations,

Center for Biological Diversity et al.

Wheeler,

No. 3:16-cv-03796-VC (N.D. Cal., filed February 15, 2019), Doc. No. 39.

D. Air Quality Information

This section presents information on sources and emissions of SO

and ambient concentrations, with a focus on information that is most relevant for the review of the primary SO

standard. This section is drawn from the more detailed discussion of SO

air quality in the PA and the ISA. It presents a summary of SO

sources and emissions (section I.D.1) and ambient concentrations (section I.D.2).

1. Sources and Emissions of Sulfur Oxides

Sulfur oxides are emitted into air from specific sources (

e.g.,

fuel combustion processes) and are also formed in the atmosphere from other atmospheric compounds (

e.g.,

as an oxidation product of reduced sulfur compounds, such as sulfides). Sulfur oxides are also transformed in the atmosphere to particulate sulfur compounds, such as sulfates.

Sulfur oxides known to occur in the troposphere include SO

and SO

(ISA, section 2.3). With regard to SO

, 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 H

” and “gas-phase H

. . . 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 SO

, the most prevalent sulfur oxide in the atmosphere is SO

(ISA, section 2.3).

Some sulfur compounds formed from or emitted with SO

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 SO

−2

complexed with Fe(III) in the particles emitted by a smelter near Salt Lake City, UT. Subsequent studies reported rapid oxidation of such compounds, “on the order of seconds to minutes” and “further accelerated by low pH” (ISA, p. 2-24). Thus, “[t]he highly acidic aqueous conditions that arise once smelter plume particles equilibrate with the ambient atmosphere ensure that S(IV)-Fe(III) complexes have a small probability of persisting and becoming a matter of concern for human exposure” (ISA, p. 2-24).

The health effects of particulate atmospheric transformation products of SO

, such as sulfates, are addressed in the review of the NAAQS for PM (U.S. EPA 2014a, 2016a, 2018c).

Fossil fuel combustion is the main anthropogenic source of SO

emissions, while volcanoes and landscape fires (wildfires as well as controlled burns) are the main natural sources (ISA, section 2.1).

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 SO

in the atmosphere (ISA, section 2.1). Anthropogenic SO

emissions originate primarily from point sources, including coal-fired electricity generating units (EGUs) and other industrial facilities (ISA, section 2.2.1). The largest SO

-emitting sector within the U.S. is electricity generation, and 97% of SO

from electricity generation is from coal combustion. Other anthropogenic sources of SO

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).

A modeling analysis estimated annual mean SO

concentrations for 2001 in the absence of any U.S. anthropogenic emissions of SO

(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 SO

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 SO

emissions are estimated to have declined by 82% over the period from 2000 to 2016, with a 64% decline from 2010 to 2016 (PA, Figure 2-2; 2014 National Emissions Inventory (NEI)). Such declines in SO

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,

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).

Regulations on sulfur content of diesel fuel, both fuel for onroad vehicles and nonroad engines and equipment, may also contribute to declining trends in SO

emissions.

Declines in emissions from all sources between 1971, when SO

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).

When established, the MATS Rule was estimated to reduce SO

emissions from power plants by 41% beyond the reductions expected from the Cross-State Air Pollution Rule (U.S. EPA, 2011).

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 SO

emissions resulting from these standards are expected to be more than 14,000 tons in 2018 (U.S. EPA, 2014c).

See

https://www.epa.gov/diesel-fuel-standards/diesel-fuel-standards-and-rulemakings#nonroad-diesel.

2. Ambient Concentrations

Ambient air concentrations of SO

in the U.S. have declined substantially from 1980 to 2016, more than 82% in terms of the form of the current standard (the 3-year average of annual 99th percentile daily maximum 1-hour concentrations) at locations continuously monitored over this period (PA, Figure 2-4).

The decline since 2000 has been 69% at the larger number of locations continuously monitored since that time (PA, Figure 2-5).

This decline is the average of observations at 24 monitoring sites that have been continuously operating from 1980-2016.

This decline is the average of observations at 193 monitoring sites that have been continuously operating across 2000-2016.

As a result of changes to the monitoring data reporting requirements promulgated in 2010 (as summarized in section I.C above) maximum hourly 5-minute concentrations of SO

in ambient air are available at SO

NAAQS compliance monitoring sites (PA, Figure 2-3; 75 FR 35554, June 22, 2010).

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 SO

concentrations at SO

sites continuously monitored during this period declined approximately 53% (PA, Figure 2-6, Appendix B).

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 SO

measurements in each hour while about 60% are reporting the maximum 5-minute SO

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 SO

vary across the U.S. and tend to be higher in areas with sources having relatively higher SO

emissions (

e.g.,

locations influenced by emissions from EGUs). Consistent with the locations of larger SO

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 SO

emissions contributes to the relatively high spatial variability of SO

concentrations compared with pollutants such as ozone (ISA, section 3.2.3). Another factor in the spatial variability is the dispersion and oxidation of SO

in the atmosphere, processes that contribute to decreasing concentrations with increasing distance from the source. Point source emissions of sulfur oxides create a plume of appreciably higher concentrations in the air, which may or may not impact large portions of the surrounding populated areas depending on specific source characteristics, meteorological conditions and terrain.

Analyses in the ISA of ambient air monitoring data for 2013-2015 in six areas indicate that 1-hour daily maximum SO

concentrations vary across seasons, with the greatest variations seen in the upper percentile concentrations (versus average or lower percentiles) for each season (ISA, section 2.5.3.2).

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 SO

for a given season. Consistent with the nationwide diel patterns reported in the last review, 1-hour average and 5-minute hourly maximum SO

concentrations for 2013-2015 in all six areas evaluated were generally low during nighttime and approached maxima values during daytime hours (ISA, section 2.5.3.3, 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 2.5.3.3; 2008 ISA [U.S. EPA 2008a], section 2.5.1).

The six “focus areas” evaluated in the ISA are: Cleveland, OH; Pittsburgh, PA; New York City, NY; St. Louis, MO (and neighboring areas in IL); Houston, TX; and Gila County, AZ (ISA, section 2.5.2.2). 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 SO

sources within a given focus area boundary.

II. Rationale for Decision

This section presents the rationale for the Administrator's decision to retain the existing primary SO

standard. This decision is based on a thorough review in the ISA of the latest scientific information, published through August 2016 (ISA, p. xlii), on human health effects associated with SO

in ambient air. This decision also accounts for analyses in the PA of policy-relevant information from the ISA and the REA, as well as information on air quality; the analyses of human exposure and health risks in the REA; CASAC advice; and consideration of public comments received on the proposal.

Section II.A provides background on the general approach for this review and the basis for the existing standard, and also presents brief summaries of key aspects of the currently available health effects and exposure/risk information. Section II.B summarizes the proposed conclusions and CASAC advice, addresses public comments received on the proposal and presents the Administrator's conclusions on the adequacy of the current standard, drawing on consideration of this information, advice from the CASAC, and comments from the public. Section II.C summarizes the Administrator's decision on the primary standard.

A. Introduction

As in prior reviews, the general approach to reviewing the current primary standard is based, most fundamentally, on using the EPA's assessment of current scientific evidence and associated quantitative analyses to inform the Administrator's judgment regarding a primary SO

standard that protects public health with an adequate margin of safety. In drawing conclusions with regard to the primary standard, the final decision on the adequacy of the current standard is largely a public health policy judgment to be made by the Administrator. The Administrator's final decision draws upon scientific information and analyses about health effects, population exposure and risks, as well as judgments about how to consider the range and magnitude of uncertainties that are inherent in the scientific evidence and exposure/risk analyses. The approach to informing these judgments, discussed more fully below, is based on the recognition that the available health effects evidence generally reflects a continuum, consisting of levels at which scientists generally agree that health effects are likely to occur, through lower levels at which the likelihood and magnitude of the response become increasingly uncertain. This approach is consistent with the requirements of the NAAQS provisions of the Clean Air Act and with how the EPA and the courts have historically interpreted the Act. These provisions require the Administrator to establish primary standards that, in his judgment, are requisite to protect public health with an adequate margin of safety. In so doing, the Administrator seeks to establish standards that are neither more nor less stringent than necessary for this purpose. The Act does not require that primary standards be set at a zero-risk level, but rather at a level that avoids unacceptable risks to public health including the health of sensitive groups.

The four basic elements of the NAAQS (indicator, averaging time, level, and form) are considered collectively in evaluating the health protection afforded by a standard.

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]).

In evaluating the appropriateness of retaining or revising the current primary SO

standard, the EPA has adopted an approach that builds upon the general approach used in the last review and reflects the body of evidence and information now available. As summarized in section II.A.1 below, the Administrator's decisions in the prior review were based on an integration of information on health effects associated with exposure to SO

with information on the public health significance of key health effects, as well as on policy judgments as to when the standard is requisite to protect public health with an adequate margin of safety and on consideration of advice from the CASAC and public comments. These decisions were also informed by air quality and related analyses and quantitative exposure and risk information.

Similarly, in this review, as described in the PA, the proposal, and elsewhere in this document, we draw on the current evidence and quantitative assessments of exposure and risk pertaining to the public health risk of SO

in ambient air. The past and current approaches are both based, most fundamentally, on the EPA's assessments of the current scientific evidence and associated quantitative analyses. The EPA's assessments are primarily documented in the ISA, REA and PA, all of which have received CASAC review and public comment (80 FR 73183, November 24, 2015; 80 FR 79330, December 21, 2015; 81 FR 89097, December 9, 2016; 82 FR 11356, February 22, 2017; 82 FR 11449, February 23, 2017; 82 FR 23563, May 23, 2017; 82 FR 37123, August 9, 2017; 82 FR 43756, September 19, 2017; 83 FR 14638, April 5, 2018). To bridge the gap between the scientific assessments of the ISA and REA and the judgments required of the Administrator in determining whether the current standard remains requisite to protect

public health with an adequate margin of safety, the PA evaluates the policy implications of the current evidence in the ISA and of the quantitative analyses in the REA.

In considering the scientific and technical information, we consider both the information available at the time of the last review and information newly available since the last review, including most particularly that which has been critically analyzed and characterized in the current ISA. We additionally consider the quantitative exposure and risk information described in the REA that estimated SO

-related exposures and lung function decrements associated with air quality conditions just meeting the current standard in simulated at-risk populations in multiple case study areas (REA, chapter 5). The evidence-based discussions presented below (and summarized more fully in the proposal) draw upon evidence from studies evaluating health effects related to exposures to SO

, as discussed in the ISA. The exposure/risk-based discussions also presented below (and summarized more fully in the proposal) have been drawn from the quantitative analyses for SO

, as discussed in the REA. Sections II.A.2 and II.A.3 below provide an overview of the current health effects and quantitative exposure and risk information with a focus on the specific policy-relevant questions identified for these categories of information in the PA (PA, chapter 3).

1. Background on the Current Standard

The current primary standard was established in the last review of the primary NAAQS for SO

, which was completed in 2010 (75 FR 35520, June 22, 2010). The decision in that review to revise the primary standards (establishing a 1-hour standard and providing for revocation of the 24-hour and annual standards) reflected the extensive body of evidence of respiratory effects in people with asthma, which has expanded over the four decades since the first SO

standards were established in 1971 (U.S. EPA, 1982, 1986, 1994, 2008a). This evidence was assessed in the 2008 ISA.

A key element of the expanded evidence base was a series of controlled human exposure studies documenting effects on lung function associated with bronchoconstriction in people with asthma exposed while breathing at elevated rates

for periods as short as minutes (U.S. EPA, 1982, 1986, 1994, 2008a). Another aspect of the information available in the 2010 review was the air quality database, which had expanded since the previous review (completed in 1996), and which provided data on the pattern of peak 5-minute SO

concentrations occurring at that time. The EPA used these data in the 2009 quantitative exposure and risk assessments to provide an up-to-date ambient air quality context for interpreting the health effects evidence. In addition to providing support for decisions in the 2010 review, these aspects of that review provided support to the EPA in addressing the issues raised in the court remand of the Agency's 1996 decision not to revise the standards to specifically address 5-minute exposures with that decision (75 FR 35523, June 22, 2010). Together, the evidence characterized in the 2008 ISA, which included epidemiologic and animal toxicologic studies as well as the extensive set of controlled human exposure studies, and the quantitative assessments in the 2009 REA, as well as advice from the CASAC and public comment, formed the basis for the EPA's 2010 action to strengthen the primary NAAQS for SO

to provide the requisite protection of public health with an adequate margin of safety, and to provide increased protection for at-risk populations, such as people with asthma (75 FR 35550, June 22, 2010).

The phrase “elevated ventilation” (or “moderate or greater exertion”) was used in the 2009 REA and

Federal Register

notifications in the last review to refer to activity levels in adults that would be associated with ventilation rates at or above 40 liters per minute; an equivalent ventilation rate was derived in order to identify corresponding rates for the range of ages and sizes of the simulated populations (U.S. EPA, 2009, section 4.1.4.4). Accordingly, these phrases are used in the current review when referring to REA analyses from the last review. Otherwise, however, the documents for this review generally use the phrase “elevated breathing rates” in place of those phrases.

Thus, the 2010 decision focused on the effects most pertinent to SO

in ambient air and recognized the long-standing evidence regarding the sensitivity of some people with asthma to brief SO

exposures experienced while breathing at elevated rates. The robust evidence base, comprised of findings from controlled human exposure, epidemiologic, and animal toxicological studies, was judged “sufficient to infer a causal relationship” between short-term SO

exposures ranging from 5 minutes to 24 hours and respiratory morbidity (75 FR 35535, June 22, 2010). The “definitive evidence” for this conclusion came from studies of 5- to 10-minute controlled exposures that reported respiratory symptoms and decreased lung function in exercising individuals with asthma (2008 ISA, section 5.3). Supporting evidence was provided by epidemiologic studies of associations of a broader range of health outcomes with ambient air concentrations of SO

, with uncertainty noted about the magnitude of the study effect estimates, quantification of the concentration-response relationship, potential confounding by copollutants, and other aspects (75 FR 35535-36, June 22, 2010; 2008 ISA, section 5.3).

Accordingly, conclusions reached in the last review were based primarily on consideration of the health effects evidence for short-term exposures, and particularly on interpretation of the evidence from controlled human exposure studies within the context of the quantitative exposure and risk analyses. The epidemiologic evidence also provided support for various aspects of the decision. In making judgments on the public health significance of health effects related to short-term ambient air-related SO

exposures, the Administrator considered statements from the American Thoracic Society (ATS) regarding adverse effects of air pollution,

the CASAC's written advice and comments,

and judgments made by the EPA in considering similar effects in previous NAAQS reviews (75 FR 35526 and 35536, June 22, 2010; ATS, 1985, 2000a). Based on these considerations, the Administrator, in 2010, gave weight to the findings of respiratory effects in exercising people with asthma after 5- to 10-minute exposures as low as 200 ppb, and further recognized that higher exposures (at or above 400 ppb) were associated with respiratory symptoms and with a greater number of study subjects experiencing lung function decrements. Moreover, she took note of the greater severity of the response at and above 400 ppb, recognizing effects associated

with exposures as low as 200 ppb to be less severe (75 FR 35547, June 22, 2010).

The 1999 statement of the ATS (published in 2000) on “What Constitutes an Adverse Health Effect of Air Pollution?” is “intended to provide guidance to policy makers and others who interpret the scientific evidence on the health effects of air pollution for the purpose of risk management” and describes “principles to be used in weighing the evidence” when considering what may be adverse and nonadverse effects on health (ATS, 2000a). For example, the ATS statements recognized a distinction between reversible and irreversible effects, recommending that reversible loss of lung function in combination with the presence of symptoms be considered adverse (ATS 1985, 2000a; 75 FR 35526, June 22, 2010).

For example, the CASAC letter on the first draft SO

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 SO

” (Henderson, 2008).

As a result and based on consideration of the entire body of evidence and information available in the review, with particular attention to the exposure and risk estimates from the 2009 REA, as well as the advice from the CASAC and public comments, the Administrator concluded that the then-existing 24-hour standard did not adequately protect public health (75 FR 35536, June 22, 2010). The 2009 REA estimated that substantial percentages of children with asthma might be expected to experience exposures at least once annually that had been associated with moderate or greater lung function decrements

in the controlled human exposure studies (75 FR 35536, June 22, 2010). The Administrator judged that such exposures can result in adverse health effects in people with asthma and found that the estimated population frequencies for such exposures (24% of the at-risk population with at least one occurrence per year at or above 400 ppb and 73% with at least one occurrence per year at or above 200 ppb) were significant from a public health perspective and that the then-existing primary standards did not adequately protect public health (75 FR 35536, June 22, 2010).

In order to provide the requisite protection to people with asthma from the adverse health effects of 5-minute to 24-hour SO

exposures, she replaced the 24-hour standard with a new, 1-hour standard (75 FR 35536, June 22, 2010). Further, upon reviewing the evidence with regard to the potential for effects from long-term exposures,

the Administrator revoked the annual standard based on her recognition of the lack of sufficient health evidence to support a long-term standard and on air quality information indicating that the new short-term standard would have the effect of generally maintaining annual SO

concentrations well below the level of the revoked annual standard (75 FR 35550, June 22, 2010).

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 (FEV

) 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 FEV

was also consistent with the relationship observed between sRaw and FEV

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 FEV

” (U.S. EPA, 1994, p. 20). Thus, in the 2008 review, moderate or greater SO

-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 FEV

(2008 ISA, p. 3-5).

In giving particular attention to the exposure and risk estimates from the 2009 REA for air quality just meeting the then-existing standards, the Administrator also noted epidemiologic study findings of associations with respiratory-related health outcomes in studies of locations where maximum 24-hour average SO

concentrations were below the level of the then-existing 24-hour standard, while also recognizing uncertainties associated with the epidemiologic evidence (75 FR 35535-36, June 22, 2010).

In evaluating the health effects studies in the ISA, the EPA has generally categorized exposures of durations longer than a month to be “long-term” (ISA, p. 1-2; 2008 ISA, p. 3-1).

The Administrator selected a 1-hour averaging time for the new standard based on available air quality analyses in the REA that indicated that a 1-hour averaging time would be effective in addressing 5-minute peak SO

concentrations such that the requisite protection from 5- to 10-minute exposure events could be provided without having a standard with a 5-minute averaging time (75 FR 35539, June 22, 2010).

The analyses suggested that, compared to a 24-hour averaging time, a 1-hour averaging time would more efficiently and effectively limit 5-minute peak concentrations of SO

that had been shown in controlled human exposure studies to result in increased prevalence of respiratory symptoms and/or decrements in lung function in exercising people with asthma (2009 REA, section 10.5.2.2; 75 FR 35539, June 22, 2010). The analyses found that a 1-hour standard could substantially reduce the upper end of the distribution of SO

concentrations in ambient air that were more likely to be associated with respiratory effects, while the longer averaging time was shown to lack effectiveness and efficiency in addressing 5-minute peak SO

concentrations, likely over-controlling in some areas while under-controlling in others (75 FR 35539, June 22, 2010; 2009 REA, section 10.5.2.2). The CASAC additionally advised that “a one-hour standard is the preferred averaging time” (Samet, 2009, pp. 15, 16), finding the REA to provide a “convincing rationale” that supported “a one-hour standard as protective of public health” (Samet, 2009, pp. 1, 15 and 16). Thus, in consideration of the available information summarized here and CASAC advice, the Administrator judged that a 1-hour standard (given the appropriate level and form) was the appropriate means for controlling short-term exposures to SO

ranging from 5 minutes to 24 hours (75 FR 35539, June 22, 2010).

The Administrator judged that a standard with a 5-minute averaging time would result in significant and unnecessary instability in public health protection (75 FR 35539, June 22, 2010). Such instability could reduce public health protection by disrupting an area's ongoing implementation plans and associated control programs (75 FR 35537, June 22, 2010).

The statistical form for the 1-hour standard, the 99th percentile daily maximum 1-hour average concentrations averaged over 3 years, is based on consideration of the health effects evidence, stability in the public health protection provided by the programs implementing the standard, and advice from the CASAC, as well as results of the 2009 REA for alternative standard forms (75 FR 35541, June 22, 2010). With regard to stability, the concentration-based form averaged over 3 years was concluded to be appreciably more stable than a no-exceedance based form, which had been the form of the then-existing 24-hour standard (75 FR 35541, June 22, 2010). The Administrator's objective in selecting the specific concentration-based form was for the form of the new standard to be especially focused on limiting the upper end of the distribution of ambient SO

concentrations (

i.e.,

above 90th percentile SO

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 SO

concentrations in epidemiologic studies (75 FR 35541, June 22, 2010). Based on results of air quality and exposure analyses in the REA which indicated the 99th percentile form likely to be appreciably more effective at achieving the desired control of 5-minute peak exposures than a 98th percentile form, the Administrator decided the form should be the 99th percentile of daily maximum 1-hour concentrations averaged over 3 years (75 FR 35541, June 22, 2010).

The level for the new standard was set primarily based on consideration of the findings of the 2009 REA exposure analyses with regard to the varying degrees of protection that different levels of a 1-hour daily maximum SO

standard might be expected to provide against 5-minute exposures to concentrations of 200 ppb and 400 ppb.

For example, the single-year

exposure assessment for St. Louis

estimated that a 1-hour standard at 100 ppb would likely protect more than 99% of children with asthma in that city from experiencing any days in a year with at least one 5-minute exposure at or above 400 ppb while at moderate or greater exertion, and approximately 97% of those children with asthma from experiencing any days in a year with at least one exposure at or above 200 ppb while at moderate or greater exertion (75 FR 35546-47, June 22, 2010). The St. Louis study area results for the air quality scenario representing a 1-hour standard level of 50 ppb suggested that such a standard would further limit exposures, such that more than 99% of children at moderate or greater exertion would likely be protected from experiencing any days in a year with a 5-minute exposure at or above the 200 ppb benchmark concentration (75 FR 35542, June 22, 2010). In considering the implications of these estimates, and the substantial reduction in 5-minute exposures at or above 200 ppb, the Administrator did not judge that a standard level as low as 50 ppb

was warranted (75 FR 35547, June 22, 2010). Before reaching her conclusion with regard to level for the 1-hour standard, the Administrator additionally considered the epidemiologic evidence, placing relatively more weight on those U.S. epidemiologic studies (some conducted in multiple locations) reporting mostly positive and sometimes statistically significant associations between ambient SO

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 SO

effect estimate remained positive and statistically significant in copollutant models with PM (75 FR 35547-48, June 22, 2010).

The Administrator additionally noted the results of the analysis of the limited available air quality data for 5-minute SO

concentrations with regard to prevalence of higher 5-minute concentrations at monitor sites when data were adjusted to just meet a standard level of 100 ppb. This 40-county analysis, which compared 5-minute concentrations estimated to occur in these air quality scenarios to benchmark levels, indicated for a 1-hour standard level of 100 ppb, there would be a maximum annual average of 2 days per year with 5-minute concentrations above 400 ppb and 13 days with 5-minute concentrations above 200 ppb (75 FR 35546, June 22, 2010).

Of the two study areas assessed in the 2009 REA (St. Louis and Greene County, Missouri), the EPA considered the St. Louis results to be more informative to consideration of the adequacy of protection associated with the then-current and alternative standards (75 FR 35528, June 22, 2010; 74 FR 64840, December 8, 2009). The St. Louis study area included several counties and had population size and magnitudes of emissions density (on a spatial scale) similar to other urban areas in the U.S., while the second study area (Greene County, Missouri) was a rural county with much lower population and emissions density.

In the 2009 REA results for the St. Louis single year scenario with a level of 50 ppb (the only level below 100 ppb that was analyzed), 99.9% of children with asthma would be expected to be protected from a day with a 5-minute exposure at or above 200 ppb, and 100% from a day with a 5-minute exposure at or above 400 ppb (2009 REA, Appendix, p. B-62).

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 SO

concentrations occurring across these areas (75 FR 35547, June 22, 2010).

Based on the above considerations and the comments received on the proposal, advice from the CASAC, the entire body of evidence and information available in that review, and the related uncertainties,

the Administrator selected a standard level of 75 ppb. She concluded that such a standard, with a 1-hour averaging time and 99th percentile form, would provide an increase in public health protection compared to the then-existing standards and would be expected to provide the desired degree of protection against the respiratory effects elicited by SO

exposures in controlled human exposure studies and associated with ambient air concentrations in epidemiologic studies (75 FR 35548, June 22, 2010).

The Administrator emphasized the latter in judging that the level of 75 ppb provided an adequate margin of safety (75 FR 35548, June 22, 2010). Thus, she concluded that a NAAQS for SO

of 75 ppb, as the 99th percentile of daily maximum 1-hour average SO

concentrations averaged over 3 years, would provide the requisite protection of public health with an adequate margin of safety (75 FR 35547-35548, June 22, 2010).

Such uncertainties included both those with regard to the epidemiologic evidence, including potential confounding and exposure measurement error, and also those with regard to the information from controlled human exposure studies for at-risk groups, including the extent to which the results would be expected to be similar for individuals with more severe asthma than that in study subjects (75 FR 35546, June 22, 2010).

For example, such a standard was considered likely “to maintain SO

concentrations below those in locations where key U.S. epidemiologic studies have reported that ambient SO

is associated with clearly adverse respiratory health effects, as indicated by increased hospital admissions and emergency department visits” and also was “expected to substantially limit asthmatics' exposure to 5-10 minute SO

concentrations ≥200 ppb, thereby substantially limiting the adverse health effects associated with such exposures” (75 FR 35548, June 22, 2010).

2. Overview of Health Effects Evidence

In this section, we provide an overview of the policy-relevant aspects of the health effects evidence available for consideration in this review. Section II.B of the proposal provides a detailed summary of key information contained in the ISA and in the PA on the health effects associated with SO

exposures, and the related public health implications, focusing particularly on the information most relevant to consideration of effects associated with the presence of SO

in ambient air (83 FR 26761, June 8, 2018). The subsections below briefly outline this information in the four topic areas addressed in section II.B of the proposal.

a. Nature of Effects

Sulfur dioxide is a highly reactive and water-soluble gas that once inhaled is absorbed almost entirely in the upper respiratory tract

(ISA, sections 4.2 and 4.3). Brief exposures to SO

can elicit respiratory effects, particularly in individuals with asthma when breathing at elevated rates (ISA, p. 1-17). Under conditions of elevated breathing rates (

e.g.,

while exercising), SO

penetrates the upper respiratory tract, entering the tracheobronchial region,

where, in sufficient concentration, it results in responses linked to asthma exacerbation in individuals with asthma (ISA, sections 4.2, 4.3, and 5.2). People with asthma have an increased propensity for the airways to narrow in response to certain inhaled stimuli, as compared to people without asthma or allergies (ISA, section 5.2.1.2).

This narrowing or constriction of the airways in the respiratory tract, termed bronchoconstriction, is characteristic of an asthma attack and is the most sensitive indicator of SO

-induced lung function effects (ISA, p. 5-8). Bronchoconstriction causes an increase in airway resistance, often assessed by measurement of specific airway resistance (sRaw). Exercising individuals without asthma have also been found to exhibit increased sRaw or related responses, such as reduced forced expiratory volume in 1 second (FEV

), but at much higher SO

exposure concentrations than exercising individuals with asthma (ISA, section 5.2.1.7). For example, the ISA finds that “healthy adults are relatively insensitive to the respiratory effects of SO

below 1 ppm” (ISA, p. 5-9).

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).

The term “tracheobronchial region” refers to the region of the respiratory tract subsequent to the larynx and preceding the deep lung (or alveoli). This region includes the trachea, bronchi, and bronchioles.

The propensity for airways to narrow following inhalation of some stimuli is termed bronchial or airway responsiveness (ISA, section 5.2.1.2, p. 5-8). In clinical situations where airway responsiveness to methacholine or histamine is assessed and the concentration resulting in a specific reduction in lung function (the provocative concentration) meets the ATS criteria for classification of the subject as hyperresponsive, the terms airway hyperresponsiveness (AHR) or bronchial hyperresponsiveness (BHR) are used (ATS, 2000b). Along with symptoms, variable airway obstruction, and airway inflammation, AHR (or BHR) is a primary feature in the clinical definition and characterization of asthma severity (ISA, section 5.2.1.2; Reddel et al., 2009).

Based on assessment of the currently available evidence, as in the last review, the ISA concludes that there is a causal relationship between short-term SO

exposures (as short as a few minutes) and respiratory effects (ISA, section 5.2.1). The clearest evidence comes from the long-standing evidence base of controlled human exposure studies demonstrating effects related to asthma exacerbation including lung function decrements

and respiratory symptoms (

e.g.,

cough, shortness of breath, chest tightness and wheeze) in people with asthma exposed to SO

for 5 to 10 minutes at elevated breathing rates (U.S. EPA, 1994; 2008 ISA; ISA, section 5.2.1). Bronchoconstriction, evidenced by decrements in lung function, that are sometimes accompanied by respiratory symptoms, occurs in these studies at SO

concentrations as low as 200 ppb in some people with asthma exposed while breathing at elevated rates, such as during exercise (ISA, section 5.2.1.2). In contrast, respiratory effects are not generally observed in other people with asthma (nonresponders

) and healthy adults exposed to SO

concentrations below 1000 ppb while exercising (ISA, sections 5.2.1.2 and 5.2.1.7). Across studies, bronchoconstriction in response to SO

exposure is seen during respiratory conditions of elevated breathing rates, such as exercise, or with mouthpiece exposures that involve laboratory-facilitated rapid, deep breathing.

With these breathing conditions, breathing shifts from nasal breathing to oral (with mouthpiece) or oronasal breathing, which increases the concentrations of SO

reaching the tracheobronchial airways, where, depending on dose and the exposed individual's susceptibility, it may cause bronchoconstriction (ISA, sections 4.1.2.2, 4.2.2, and 5.2.1.2).

The specific responses reported in the evidence base that are described in the ISA as lung function decrements are increased sRaw and FEV

(ISA, section 5.2.1.2).

The data from controlled human exposure studies of people with asthma indicate that there are two subpopulations that differ in their airway responsiveness to SO

, with the second subpopulation (non-responders) being insensitive to SO

bronchoconstrictive effects at concentrations as high as 1000 ppb (ISA, pp. 5-14 to 5-21; Johns et al., 2010).

Laboratory-facilitated rapid deep breathing involves rapid, deep breathing through a mouthpiece that provides a mixture of oxygen with enough carbon dioxide to prevent an imbalance of gases in the blood usually resulting from hyperventilation. Breathing in the laboratory with this technique is referred to as eucapnic hypernea (ISA, p. 5-6).

The current evidence base of controlled human exposure studies of individuals with asthma,

is consistent with the evidence base from the last review, and is summarized in the ISA (ISA, section 5.2.1.2, Tables 5-1 and 5-2). With regard to effects related to asthma exacerbation, the main responses observed include increases in specific airway resistance (sRaw) and reductions in forced expiratory volume in one second (FEV

) after 5- to 10-minute exposures. As recognized in the last review, the results of these studies indicate that among individuals with asthma, some individuals (

e.g.,

responders) have a greater response to SO

than others, or a measurable response at lower exposure concentrations (ISA, p. 5-14). The SO

-induced bronchoconstriction in these studies occurs rapidly (in just a few minutes) when individuals are exposed while breathing at an elevated rate, and is transient, with recovery occurring with a return to resting breathing rate or cessation of exposure, generally within an hour (ISA, p. 5-14, Table 5-2; Linn et al., 1984; Johns et al., 2010).

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 3.2.1.3 and 3.2.1.4).

The currently available epidemiologic evidence includes studies reporting positive associations with short-term SO

exposures for asthma-related hospital admissions of children or emergency department visits by children (ISA, section 5.2.1). These findings provide supporting evidence of the EPA's conclusion of a causal relationship between short-term SO

exposures and respiratory effects, for which the controlled human exposure studies are the primary basis (ISA, section 5.2.1.9). Among the epidemiologic studies newly available in this review, there are a limited number that have investigated SO

effects related to asthma exacerbation, with the most supportive evidence coming from studies of asthma-related hospital admissions of children or emergency department visits by children (ISA, section 5.2.1.2). As in the last review, areas of uncertainty in the epidemiologic evidence are related to the characterization of exposure based on the use of ambient air concentrations at fixed site monitors as surrogates for population exposure (often over a substantially sized area and for durations greater than an hour) and the potential for confounding by PM

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).

The potential for confounding by PM is of particular interest given that SO

is a precursor to PM (ISA, p. 1-7).

For long-term SO

exposure and respiratory effects, the evidence base is somewhat augmented since the last review such that the current ISA concludes it to be suggestive of, but not sufficient to infer, a causal relationship (ISA, section 5.2.2). The support for this conclusion comes mainly from the limited epidemiologic findings of associations between long-term SO

concentrations and increases in asthma incidence combined with findings of laboratory animal studies involving newborn rodents that indicate a potential for SO

exposure to contribute to the development of asthma, especially allergic asthma, in children (ISA, section 1.6.1.2). The evidence showing increases in asthma incidence is coherent with results of animal toxicological studies that provide a pathophysiologic basis for the development of asthma. The overall body of evidence, however, lacks consistency (ISA, sections 1.6.1.2 and 5.2.2.7). Further, there are uncertainties associated with the epidemiologic evidence across the respiratory effects examined for long-term exposure (ISA, section 5.2.2.7).

For effects other than those involving the respiratory system, the current evidence is generally similar to the evidence available in the last review and leads to similar conclusions about the totality of adverse health effects. With regard to a relationship between short-term SO

exposure and total mortality, the ISA reaches the same conclusion as the previous review that the evidence is suggestive of, but not sufficient to infer, a causal relationship (ISA, section 5.5.1). This conclusion is based on the findings of previously and newly available multicity epidemiologic studies that report positive associations, accompanied by uncertainty with respect to the potential for SO

to have an independent effect on mortality. While recent studies have analyzed some key uncertainties and addressed data gaps from the previous review, uncertainties still exist. These uncertainties include that: The number of studies that examined copollutant confounding is limited; there is evidence of a reduction in the SO

-mortality effect estimates (

i.e.,

relative risks) in copollutant models with

nitrogen dioxide and PM with mass median aerodynamic diameter nominally below 10 microns (PM

); and a potential biological mechanism for mortality following short-term SO

exposures is lacking (ISA, section 1.6.2.4).

For other categories of health effects,

the currently available evidence is inadequate to infer the presence or absence of a causal relationship, mainly due to inconsistent evidence across specific outcomes and uncertainties regarding exposure measurement error, the potential for copollutant confounding, and potential modes of action (ISA, sections 5.3.1, 5.3.2, 5.4, 5.5.2, 5.6). These conclusions are consistent with those made in the previous review (ISA, p. xlviii).

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

Thus, given the strength of the evidence supporting the conclusion of a causal relationship between short-term exposure to SO

in ambient air and respiratory effects, in particular, asthma exacerbation in individuals with asthma, the focus in this review, as in prior reviews, is on such effects.

b. At-Risk Populations

In this review, we use the term “at-risk populations” to recognize populations with a quality or characteristic in common (

e.g.,

a specific pre-existing illness or specific age or lifestage) that contributes to them having a greater likelihood of experiencing SO

-related health effects. People with asthma are at increased risk for SO

-related health effects, specifically for respiratory effects, and specifically asthma exacerbation elicited by short-term exposures while breathing at elevated rates (ISA, sections 5.2.1.2 and 6.3.1). This conclusion of the at-risk status of people with asthma, as was the case in 2010, is based on the well-established and well-characterized evidence from controlled human exposure studies, supported by the evidence related to mode of action for SO

and evidence from epidemiologic studies (ISA, sections 5.2.1.2 and 6.3.1). Further, some individuals with asthma have a greater response to SO

than others with similar disease status (ISA, section 5.2.1.2; Horstman et al., 1986; Johns et al., 2010). The ISA also finds the evidence to be suggestive of increased risk for children and older adults, while noting some limitations and inconsistencies (ISA, sections 6.5.1.1 and 6.5.1.2).

Children with asthma, however, may be particularly at risk compared to adults with asthma (ISA, section 6.3.1). This conclusion reflects several characteristics of children as compared to adults, as summarized in section II.B of the proposal, that may put children with asthma at greater risk of SO

-related bronchoconstrictive effects than adults with asthma.

The current evidence for risk to older adults relative to other lifestages comes from epidemiologic studies, for which the findings are somewhat inconsistent, and studies with which there are uncertainties in the association with the health outcome (ISA, section 6.5.1.2).

There are few controlled human exposure studies to inform our understanding of any differences in exposure concentrations associated with bronchoconstrictive effects in young children as compared to adults or adolescents as those studies have not included subjects younger than 12 years (ISA, p. 5-22). The ISA does not find the evidence to be adequate to conclude differential risk status for subgroups of children with asthma (ISA, sections 6.5.1.1 and 6.6). In consideration of the limited information regarding factors related to breathing habit, however, the ISA suggests that children with asthma approximately 5 to 11 years of age, and “particularly boys and perhaps obese children, might be expected to experience greater responsiveness (

i.e.,

larger decrements in lung function) following exposure to SO

than normal-weight adolescents and adults” (ISA, pp. 5-36 and 4-7).

The finding that some individuals with asthma have a greater response to SO

than others with similar disease status is quantitatively analyzed in a study, newly available in this review, that examined differences in lung function response using individual subject data available from five studies of individuals with asthma exposed to multiple concentrations of SO

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 SO

in individuals with asthma, with one subpopulation that is insensitive to the bronchoconstrictive effects of SO

even at concentrations as high as 1.0 ppm, and another subpopulation that has an increased risk for bronchoconstriction at low concentrations of SO

” (ISA, p. 5-20). In analyses focused on the more sensitive subpopulation, the study demonstrated statistically significant increases in bronchoconstriction with exposures as low as 0.3 ppm (Johns et al., 2010). While such information provides documentation that some individuals with asthma have a greater response to SO

than others, the factors contributing to this greater susceptibility are not yet known (ISA, pp. 5-14 to 5-21).

c. Exposure Concentrations Associated With Health Effects

Our understanding of exposure duration and concentrations associated with SO

-related health effects is largely based, as it was in the last review, on the longstanding evidence base of controlled human exposure studies. These studies in individuals with asthma exposed to SO

for 5 to 10 minutes while breathing at elevated rates demonstrate clear and consistent increases in magnitude and occurrence of decrements in lung function (

e.g.,

increased sRaw and reduced FEV

) and in occurrence of respiratory symptoms with increasing SO

exposure (ISA, section 1.6.1.1, Table 5-2 and pp. 5-35, 5-39). Further, the evidence base demonstrates the occurrence of SO

-related effects resulting from peak exposures on the order of minutes

and other short-term exposures have been found to elicit a similar bronchoconstrictive response for somewhat longer (

e.g.,

30-minute) exposure durations (ISA, p. 5-14; Kehrl et al., 1987).

While the air quality metrics in the epidemiologic studies are for time periods longer than the 5- to 10-minute exposures eliciting effects in the controlled human exposure studies, these studies may not adequately capture the spatial and temporal variation in SO

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 SO

concentration (ISA, pp. 5-49, 5-59, 5-25).

The controlled human exposure studies of people with asthma further demonstrate

that SO

concentrations as low as 200 to 300 ppb for 5 to 10 minutes elicited moderate or greater lung function decrements (a decrease in FEV

of at least 15% or an increase in sRaw of at least 100%) in a subset of the study subjects (ISA, sections 1.6.1.1 and 5.2.1). The percent of individuals affected, the severity of response, and the accompanying occurrence of respiratory symptoms increased with increasing SO

exposure concentrations (ISA, section 5.2.1). At concentrations ranging from 200 to 300 ppb, the lowest levels for which the ISA describes the occurrence of moderate or greater SO

-related lung function decrements, as many as 33% of exercising study subjects with asthma experienced such decrements in lung function (ISA,

section 5.2.1, Table 5-2).

At concentrations at or above 400 ppb, moderate or greater decrements in lung function occurred in as many as approximately 30 to 60% of exercising individuals with asthma, and compared to the results for exposures at 200 to 300 ppb, a larger percentage of individuals with asthma experienced the more severe decrements in lung function (

i.e.,

an increase in sRaw of at least 200%, and/or a 20% or more decrease in FEV

) at these higher concentrations (ISA, section 5.2.1.2, 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).

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 SO

-specific effect.

Additionally, analyses of data from the full set of these studies that focused only on the results for the study subjects that are responsive to SO

at exposure concentrations below 1000 ppb found there to be statistically significant increases in lung function decrements occurring at 300 ppb (ISA, p. 153; Johns et al., 2010).

Two hundred ppb is the lowest exposure concentration for which individual study subject data for percent changes in sRaw and FEV

are available from studies that have assessed the SO

effect

versus

the effect of exercise in clean air (ISA, Table 5-2 and Figure 5-1). In nearly all of these studies (and all of these studies with such data for concentrations from 200 to 400 ppb), study subjects breathed freely (

e.g.,

without using a mouthpiece).

In studies that tested 200 ppb exposures, a portion of the exercising study subjects with asthma (approximately 8 to 9%) responded with at least a doubling in sRaw or an increase in FEV

of at least 15% (ISA, Table 5-2 and Figure 5-2; PA, Table 3-1; Linn et al., 1983a; Linn et al., 1987).

Studies of free-breathing subjects generally make use of small rooms in which the atmosphere is experimentally controlled such that study subjects are exposed by freely breathing the surrounding air (

e.g.,

Linn et al., 1987).

With regard to exposure concentrations below 200 ppb, very limited evidence is available for concentrations as low as 100 ppb. Some differences in methodology and the reporting of results complicate comparison of the studies with 100 ppb exposure to studies using higher exposures. In the studies evaluating the 100 ppb concentration level, subjects were exposed by mouthpiece rather than freely breathing in an exposure chamber (Sheppard et al., 1981; Sheppard et al., 1984; Koenig et al., 1989; Koenig et al., 1990; Trenga et al., 2001; ISA, section 5.2.1.2; PA, section 3.2.1.3). Additionally, only a few of these studies included an exposure to clean air while exercising that would have allowed for distinguishing the effect of SO

from the effect of exercise in causing bronchoconstriction (Sheppard et al., 1981; Sheppard et al., 1984; Koenig et al., 1989). In those few cases, a limited number of adult and adolescent study subjects were reported to experience small changes in sRaw, with the magnitudes of change appearing to be smaller than responses reported from studies at exposures of 200 ppb or more.

50 51

Thus, while the studies evaluating 100 ppb exposures are limited and their interpretation is complicated by the use of different reporting of results and exposure methods that differ from those used in studies of higher concentrations, the 100 ppb studies do not indicate that exposure at 100 ppb results in as much as a doubling in sRaw, based on the extremely few adults and adolescents tested (Sheppard et al., 1981; Sheppard et al., 1984; Koenig et al., 1989).

For example, although individual study subject data for SO

-attributable changes in sRaw in these studies are not available in the terms needed to summarize the responses consistent with the study result summaries in the ISA, Table 5-2 (

e.g.,

percent change), the increase in sRaw reported for two young adult subjects exposed to 100 ppb in the study by Sheppard et al. (1981) was slightly less than half the response of these subjects at 250 ppb, and the results for the study by Sheppard et al. (1984) indicate that none of the eight study subjects experienced as much as a doubling in sRaw in response to the mouthpiece exposure to 125 ppb while exercising (in Table 2 of Sheppard et al., 1984, concentrations calculated to cause a doubling of sRaw in all subjects are higher than 125 ppb, the lowest exposure concentration). In the study of adolescents (aged 12 to 18 years), among the three individual study subjects for which total respiratory resistance appears to have increased with SO

exposure, the magnitude of increase in that metric after consideration of the response to exercise appears to be less than 100% in each subject (Koenig et al., 1989).

In a mouthpiece exposure system, the inhaled breath completely bypasses the nasal passages where SO

is efficiently removed, thus allowing more of the inhaled SO

to penetrate the tracheobronchial airways (2008 ISA, p. 3-4; ISA, section 4.1.2.2). This allowance of deeper penetration of SO

into the tracheobronchial airways, as well as limited evidence comparing responses by mouthpiece and chamber exposures, leads to the expectation that SO

-responsive people with asthma breathing SO

using a mouthpiece, particularly while breathing at elevated rates, would experience greater lung function responses than if exposed to the same test concentration while freely breathing in an exposure chamber (ISA, p.5-23; Linn et al., 1983b).

Specific exposure concentrations that may be eliciting respiratory responses are not available from the epidemiologic evidence base, which includes studies that find associations with outcomes such as asthma-related emergency department visits and hospital admissions. For example, in noting limitations of epidemiologic studies with regard to uncertainties in SO

exposure estimates, the ISA recognized that “[it] is unclear whether SO

concentrations at the available fixed site monitors adequately represent variation in personal exposures especially if peak exposures are as important as indicated by the controlled human exposure studies” (ISA, p. 5-37). This extends the observation of the 2008 ISA that “it is possible that these epidemiologic associations are determined in large part by peak exposures within a 24-h[our] period” (2008 ISA, p. 5-5). Another key uncertainty in the epidemiologic evidence available in this review, as in the last review, is potential confounding by copollutants, particularly PM, given the important role of SO

as a precursor to PM in ambient air (ISA, p. 5-5). Among the U.S. epidemiologic studies reporting mostly positive and sometimes statistically significant associations between ambient SO

concentrations and emergency department visits or hospital admissions (some conducted in multiple locations), few studies have attempted to address the uncertainty of potential copollutant confounding. For example, as in the last review, there are three U.S. studies for which the SO

effect estimate remained positive and statistically significant in copollutant models with PM. No additional such studies have been newly identified in this review that might inform this issue (83 FR 26765, June 8, 2018). Thus, such uncertainties regarding copollutant confounding, as well as exposure measurement error, remain in the currently available epidemiologic evidence base (ISA, p. 5-6).

d. Potential Impacts on Public Health

In general, the magnitude and implications of potential impacts on public health are dependent upon the type and severity of the effect, as well as the size and other features of the population affected (ISA, section 1.7.4; PA, 3.2.1.5). The information discussed in this section indicates the potential for exposures to SO

in ambient air to be of public health importance. Such considerations contributed to the basis for the 2010 decision to appreciably strengthen the primary SO

NAAQS and to establish a 1-hour standard to provide the requisite public health protection for at-risk populations from short-term exposures of concern.

The potential public health impacts of SO

concentrations in ambient air relate to respiratory effects of short-term exposures and particularly those effects

associated with asthma exacerbation in people with asthma. As summarized above in section II.A.2.a, these effects include bronchoconstriction resulting in decrements in lung function and elicited by short-term exposures during periods of elevated breathing rate. Consistent with these SO

-related effects, asthma-related health outcomes such as emergency department visits and hospital admissions have been positively associated with ambient air concentrations of SO

in epidemiologic studies (ISA, section 5.2.1.9).

As summarized in section II.A.2.b above, people with asthma are the population at risk for SO

-related effects and children with asthma are considered to be at relatively greater risk than other age groups (ISA, section 6.3.1). The evidence supporting this conclusion comes primarily from studies of individuals with mild to moderate asthma,

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 SO

exposures) across individuals with asthma of differing severity.

However, the two available studies “suggest that adults with moderate/severe asthma may have more limited reserve to deal with an insult compared with individuals with mild asthma” (ISA, p. 5-22; Linn et al., 1987; Trenga et al., 1999). Consideration of such baseline differences among members of at-risk populations and of the relative transience or persistence of these responses (

e.g.,

as noted in section II.A.2.a above), as well as other factors, is important to characterizing implications for public health, as recognized by the ATS in their recent statement on evaluating adverse health effects of air pollution (Thurston et al., 2017).

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).

The ISA identifies two studies that have investigated the influence of asthma severity on responsiveness to SO

, with one finding that a larger change in lung function observed in the moderate/severe asthma group was attributable to the exercise component of the study protocol while the other did not assess the role of exercise in differences across individuals with asthma of differing severity (Linn et al., 1987; Trenga et al., 1999). Based on the criteria used in the study by Linn et al. (1987) for placing individuals in the “moderate/severe” group, however, the asthma of these individuals “would likely be classified as moderate by today's classification standards” (ISA, p. 5-22; Johns et al., 2010; Reddel, 2009).

Multiple statements by the ATS on what constitutes an adverse health effect of air pollution inform the Administrator's judgment on the public health significance of SO

-related effects, particularly those with the potential to occur under air quality conditions allowed by the current standard. Building on the earlier statement by the ATS that was considered in the last review (ATS, 2000a), the recent policy statement by the ATS provides a general framework for interpreting evidence that proposes a “set of considerations that can be applied in forming judgments” for this context (Thurston et al., 2017). The earlier ATS statement, in addition to emphasizing clinically relevant effects (

e.g.,

the adversity of small transient changes in lung function metrics in combination with respiratory symptoms), also emphasized both the need to consider changes in “the risk profile of the exposed population” and effects on the portion of the population that may have a diminished reserve that could put its members at potentially increased risk of effects from another agent (ATS, 2000a). The consideration of effects on individuals with preexisting diminished lung function continues to be recognized as important in the more recent ATS statement (Thurston et al., 2017). All of these concepts, including the consideration of the magnitude or severity of effects occurring in just a subset of study subjects, as well as the consideration of persistence or transience of effects,

are recognized as important considerations in the more recent ATS statement (Thurston et al., 2017) and continue to be relevant to consideration of the evidence base for SO

In speaking of transient effects, the recent statement refers to effects lasting on the order of hours (Thurston et al., 2017).

Such concepts are routinely considered by the Agency in weighing public health implications for decisions on primary NAAQS, as summarized in section I.A above. For example, in deliberations on a standard that provides the requisite public health protection under the Act, the EPA traditionally recognizes the nature and severity of the health effects involved, recognizing the greater public health significance of more severe health effects, including, for example, responses that have been documented to be accompanied by respiratory symptoms, and of the risk of repeated occurrences of effects (76 FR 54308, August 31, 2011; 80 FR 65292, October 26, 2015). Another area of consideration is characterization of the population at risk, including its size and, as pertinent, the exposure/risk estimates in this regard. Such factors related to public health significance, and the kind and degree of associated uncertainties, are considered by the EPA in addressing the CAA requirement that the primary NAAQS be requisite to protect public health, including an adequate margin of safety, as summarized in section I.A above.

Ambient air concentrations of SO

vary considerably in areas near sources, but concentrations in the vast majority of the U.S. are well below the current standard (PA, Figure 2-7). Thus, while the population counts discussed below may convey information and context regarding the size of populations living near sizeable sources of SO

emissions in some areas, the concentrations in most areas of the U.S. are well below the conditions assessed in the REA.

With regard to the size of the U.S. population at risk of SO

-related effects, the National Center for Health Statistics data from the 2015 National Health Interview Survey (NHIS)

indicate that approximately 8% of the U.S. population has asthma (PA, Table 3-2; CDC, 2017). The estimated prevalence is greater in children (8.4% for children less than 18 years of age) than adults (7.6%) (PA, Table 3-2; CDC, 2017). Asthma was the leading chronic illness affecting children in 2012, the most recent year for which such an evaluation is available (Bloom et al., 2013). As noted in the PA, there are more than 24 million people with asthma currently in the U.S., including more than 6 million children (PA, sections 3.2.2.4 and 3.2.4). Among populations of different races or ethnicities, black non-Hispanic and Puerto Rican Hispanic children are estimated to have the highest

prevalence, at 13.4% and 13.9%, respectively. Asthma prevalence is also increased among populations in poverty, with the prevalence estimated to be 11.1% among people living in households below the poverty level compared to 7.2% of those living above it (CDC, 2017).

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

With regard to the potential for exposure of the populations at risk from exposures to SO

in ambient air, while SO

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 SO

concentrations still contribute to air quality that is near or above the standard. For example, the PA noted that the air quality monitoring data for the 2014-2016 period indicated there to be 15 core-based statistical areas

with air quality exceeding the primary SO

standard (design values

were above the existing standard level of 75 ppb), of which a number have sizeable populations (PA, section 3.2.2.4). In addition to this evidence of elevated ambient air SO

concentrations, there are limitations in the monitoring network with regard to the extent that it might be expected to capture all areas with the potential to exceed the standard (

e.g.,

75 FR 35551; June 22, 2010). In recognition of these limitations, we also examined the proximity of populations to sizeable SO

point sources using the recently available emissions inventory information (2014 NEI), which is also characterized in the ISA (PA, section 3.2.2.4, Appendix F; ISA, section 2.2.2). This information indicates that there are more than 300,000 and 60,000 children living within 1 km of facilities emitting at least 1000 and 2000 tpy of SO

, respectively (PA, section 3.2.2.4). Within 5 km of such sources, the numbers are approximately 1.4 million and 700,000, respectively (PA, Table 3-5). While information on SO

concentrations in locations of maximum impact of such sources is not available for all these areas, and SO

concentrations vary appreciably near sources, simply considering the 2015 national estimate of asthma prevalence of approximately 8% (noted above), this information would suggest there may be as many as 24,000 to more than 100,000 children with asthma that live in areas near substantially sized sources of SO

emissions to ambient air (PA, section 3.2.1.5; Table 3-5).

Core-based statistical area (CBSA) is a geographic area defined by the U.S. Office of Management and Budget to consist of an urban area of at least 10,000 people in combination with its surrounding or adjacent counties (or equivalents) with which there are socioeconomic ties through commuting (

https://www.census.gov/geo/reference/gtc/gtc_cbsa.html

). Populations in the 15 CBSAs referred to in the body of the text range from approximately 30,000 to more than a million (based on 2016 U.S. Census Bureau estimates).

A design value is a statistic that describes the air quality status of a given area relative to the level of the standard, taking into account the averaging time and form (as well as indicator). Thus, design values for the SO

NAAQS are in terms of 3-year averages of annual 99th percentile 1-hour daily maximum concentrations of SO

. Design values are typically used to assess whether the NAAQS is violated, to classify nonattainment areas, to track air quality trends and progress toward meeting the NAAQS and to develop control strategies.

3. Overview of Risk and Exposure Information

Our consideration of the scientific evidence available in the current review (summarized in section II.A.2 above), as at the time of the last review, is informed by results from a quantitative analysis of estimated population exposure and associated risk of respiratory effects that the evidence indicates to be elicited in some portion of exercising people with asthma by short-term exposures to elevated SO

concentrations,

e.g.,

such as exposures lasting 5 or 10 minutes. This analysis, for the air quality scenario of just meeting the current standard, estimates two types of risk metrics in terms of percentages of the simulated at-risk populations of adults with asthma and children with asthma (REA, section 4.6). The first of the two risk metrics is based on comparison of the estimated 5-minute exposure concentrations for individuals breathing at elevated rates to 5-minute exposure concentrations of potential concern (benchmark concentrations). The second risk metric utilizes exposure-response (E-R) information from studies in which subjects experienced moderate or greater lung function decrements (specifically a doubling or more in sRaw) to estimate the portion of the simulated at-risk population likely to experience one or more days with a SO

-related increase in sRaw of at least 100% (REA, sections 4.6.1 and 4.6.2). Both metrics are used in the REA to characterize health risk associated with 5-minute peak SO

exposures among simulated at-risk populations during periods of elevated breathing rates. These risk metrics were also derived in the REA for the last review and the associated estimates informed the 2010 decision that established the current standard (75 FR 35546-35547, June 22, 2010).

The following subsections provide brief overviews of the key aspects of the design and methods of the quantitative assessment in this review (section II.A.3.a) and the important uncertainties associated with these analyses (section II.A.3.b). The results of the analyses are summarized in section II.A.3.c. These overviews are drawn from the summary presented in section II.C of the proposal (83 FR 26767, June 8, 2018).

a. Key Design Aspects

In this section, we provide a brief overview of key aspects of the quantitative exposure and risk assessment conducted for this review and summarized in more detail in section II.C.1 of the proposal (83 FR 26767, June 8, 2018), including the study areas, air quality adjustment approach, modeling tools, at-risk populations simulated, and benchmark concentrations assessed. The assessment is described in detail in the REA and summarized in section 3.2.2 of the PA.

The REA focuses on air quality conditions that just meet the current standard, and the analyses estimate exposure and risk for at-risk populations in three urban study areas in: (1) Fall River, MA; (2) Indianapolis, IN; and (3) Tulsa, OK. The three study areas present a variety of circumstances related to population exposure to short-term peak concentrations of SO

in ambient air, including a range in total population size, different mixtures of SO

emissions sources, and three different climate regions of the U.S.: The Northeast, Ohio River Valley (Central), and South (REA, section 3.1; Karl and Koss, 1984).

The latter two regions comprise the part of the U.S. with generally the greatest prevalence of elevated SO

concentrations and large emissions sources (PA, Figure 2-7 and Appendix F). Accordingly, the three study areas illustrate three different patterns of exposure to SO

concentrations in a populated area in the U.S. (REA, section 5.1). While the same air quality scenario is simulated in all three study areas (conditions that just meet the current standard), study-area-specific characteristics related to sources, meteorology, topography and population contribute to variation in the estimated magnitude of exposure and associated risk across study areas.

Additionally, continuous 5-minute ambient air monitoring data (

i.e.,

all 5-minute values for each hour) are available in all three study areas (REA, section 3.2).

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

exposures and risks that may be associated with the air quality conditions occurring under the current SO

standard. The REA analyses are not designed to provide a comprehensive national assessment of such conditions (REA, section 2.2). The objective of the REA is not to present an exhaustive analysis of exposure and risk in areas of the U.S. that currently just meet the standard or an analysis of exposure and risk associated with air quality adjusted down to just meet the standard in areas that currently do not meet the standard.

Rather, the purpose is to assess, based on current tools and information, the potential for exposures and risks beyond those indicated by the information available at the time the current standard was established. Accordingly, capturing an appropriate level of diversity in study areas and air quality conditions (that reflect the current standard scenario) is important to the role of the REA in informing the EPA's understanding of, and conclusions on, the public health protection afforded by the current standard (PA, section 3.2.2.2).

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

A broad variety of spatial and temporal patterns of SO

concentrations can exist when ambient air concentrations just meet the current standard. These patterns will vary due to many factors including the types of emissions sources in a study area and several characteristics of those sources, such as magnitude of emissions and facility age, use of various control technologies, patterns of operation, and local factors, as well as local meteorology. Estimates derived using the particular analytical approaches and methodologies for characterizing the study area-specific air quality provide an indication of this variability in the spatial and temporal patterns of SO

concentrations occurring under air quality conditions just meeting the current standard. In light of the uncertainty associated with these concentration estimates, the REA presents results from two different approaches to adjusting air quality to just meet the current standard (described in more detail in sections 3.4 and 6.2.2.2 of the REA).

The first approach uses the highest design value across all modeled air quality receptors to estimate the amount of SO

concentration reduction needed to adjust the air quality concentrations in each area to just meet the standard (REA, section 3.4). In recognition of potential uncertainty in the first approach, the second approach uses the air quality receptor having the 99th percentile of the distribution of design values (instead of the receptor with the maximum design value) to estimate the SO

concentration reductions needed to adjust the air quality to just meet the standard, setting all receptors at or above the 99th percentile to just meet the standard (REA, section 6.2.2.2).

Consistent with the health effects evidence summarized in section II.A.2 above, the focus of the REA is on short-term (5-minute) exposures of individuals with asthma in the simulated populations during times when they are breathing at an elevated rate. Five-minute concentrations in ambient air were estimated for the current standard scenario using a combination of 1-hour concentrations from the EPA's preferred near-field dispersion model, the American Meteorological Society/EPA regulatory model (AERMOD), with adjustment such that they just meet the current standard, and relationships between 1-hour and 5-minute concentrations occurring in the local ambient air monitoring data. The air quality modeling step was taken to capture the spatial variation in ambient SO

concentrations across each urban study area. Such variation can be relatively high in areas affected by large point sources and is unlikely to be captured by the limited number of monitoring locations in each area. The modeling step yields 1-hour concentrations at model receptor sites across the modeling domain across the 3-year modeling period (consistent with the 3-year form of the standard). These concentrations were adjusted such that the air quality modeling receptor location(s) with the highest concentrations just met the current standard. Rather than applying the same adjustment to concentrations at all receptors in a study area, the adjustment was derived by focusing on reducing emissions from the source(s) contributing the most to the standard exceedances (REA, section 3.4 and 6.2.2.1). Relationships between 1-hour and 5-minute concentrations at local monitors were then used to estimate 5-minute concentrations associated with the adjusted 1-hour concentrations across the 3-year period at all model receptor locations in each of the three study areas (REA, section 3.5). In this way, available continuous 5-minute ambient air monitoring data (datasets with all twelve 5-minute concentrations in each hour) were used to reflect the fine-scale temporal variation in SO

concentrations documented by these data. This approach was used in recognition of the limitations associated with air quality modeling at this fine temporal scale,

e.g.,

limitations in the time steps of currently available model input data such as for emissions estimates.

The estimated 5-minute concentrations in ambient air across each study area were then used together with the Air Pollutants Exposure (APEX) model, a probabilistic human exposure model that simulates the activity of individuals in the population, including their exertion levels and movement through time and space, to estimate concentrations of 5-minute SO

exposure events in indoor, outdoor, and in-vehicle microenvironments. The use of APEX for estimating exposures allows for consideration of factors that affect exposures that are not addressed by consideration of ambient air concentrations alone. These factors include: (1) Attenuation in SO

concentrations expected to occur in some indoor microenvironments; (2) the influence of human activity patterns on the time series of exposure concentrations; and (3) accounting for human physiology and the occurrence of elevated breathing rates concurrent with SO

exposures (REA, section 2.2). These factors are all key to appropriately characterizing exposure and associated health risk for SO

The exposure modeling performed for this review, including ways in which it has been updated since the 2009 REA are summarized in section II.C of the proposal and described in detail in the REA (

e.g.,

REA, Chapter 4 and Appendices E through I).

The at-risk populations for which exposure and risk are estimated (children and adults with asthma) ranges from 8.0 to 8.7% of the total populations (ages 5-95) in the exposure modeling domains for the three study areas (REA, section 5.1). The percent of children with asthma in the simulated populations ranges from 9.7 to 11.2% across the three study areas (REA, section 5.1). Within each study area the percent varies with age, sex and whether family income is above or below the poverty level (REA, section 4.1.2, Appendix E).

This variation is greatest in the Fall River study area, with census block level, age-specific asthma prevalence estimates ranging from 7.9 to 18.6% for girls and from 10.7 to 21.5% for boys (REA, Table 4-1).

As described in section 4.1.2 and Appendix E of the REA, asthma prevalence in the exposure modeling domain is estimated based on national prevalence information and study area demographic information related to age, sex and poverty status.

The REA for this review, consistent with the analyses in the last review, uses the APEX model estimates of 5-minute exposure concentrations for simulated individuals with asthma while breathing at elevated rates to

characterize health risk in two ways (REA, section 4.5). The first is the percentage of the simulated at-risk populations expected to experience days with 5-minute exposures, while breathing at elevated rates, that are at or above a range of benchmark levels. The second is the percentage of these populations expected to experience days with an occurrence of a doubling or tripling of sRaw.

The benchmark concentrations used in the comparison-to-benchmarks analysis (400, 300, 200 and 100 ppb) were identified based on consideration of the evidence discussed in section II.A.2 above. In particular, benchmark concentrations of 400 ppb, 300 ppb, and 200 ppb were based on concentrations included in the well-documented controlled human exposure studies summarized in section II.A.2 above, and the 100 ppb benchmark was selected in consideration of uncertainties with regard to lower concentrations and population groups with more limited data (REA, section 4.5.1). At the upper end of this range, 400 ppb represents the lowest concentration in free-breathing controlled human exposure studies of exercising people with asthma where moderate or greater lung function decrements occurred that were often statistically significant at the group mean level and were frequently accompanied by respiratory symptoms, with some increases in these symptoms also being statistically significant at the group level (ISA, Section 5.2.1.2 and Table 5-2). At 300 ppb, statistically significant increases in lung function decrements (specifically reductions in FEV

) have been documented in analyses of the subset of controlled human exposure study subjects with asthma that are responsive to SO

at concentrations below 600 or 1000 ppb (ISA, pp. 5-85 and 5-153 and Table 5-21; Johns et al., 2010). The 200 ppb benchmark concentration represents the lowest level for which studies are available that have assessed the SO

effect

versus

the effect of exercise in clean air and for which individual study subject data are available to summarize percent changes in sRaw and FEV

; moderate or greater lung function decrements were documented in some of these study subjects (ISA, Table 5-2 and Figure 5-1; PA, Table 3-1; REA, section 4.6.1). With regard to exposure concentrations below 200 ppb, limited data are available for exposures at 100 ppb that, while not directly comparable to the data at higher concentrations because of differences in methodology and metrics reported,

do not indicate that study subjects experienced responses of a magnitude as high as a doubling in sRaw. However, in consideration of some study subjects with asthma experiencing moderate or greater decrements in lung function at the 200 ppb exposure concentration (approximately 8 to 9% of the study group) and of the paucity or lack of any specific study data for some groups of individuals with asthma, such as primary-school-age children and those with more severe asthma (described in sections II.B.3 and II.C.1 of the proposal), a benchmark concentration of 100 ppb (one half the 200 ppb exposure concentration) was also included in the analyses.

As explained in section II.B.3 of the proposal, these studies involved exposures via mouthpiece, and only a few of these studies included an exposure to clean air while exercising that would have allowed for determining the effect of SO

versus

that of exercise in causing bronchoconstriction and associated lung function decrements (ISA, section 5.2.1.2; PA, section 3.2.1.3).

The E-R function for estimating risk of lung function decrements was developed from the individual subject results for sRaw from the controlled exposure studies of exercising, freely breathing people with asthma exposed to SO

concentrations from 1000 ppb down to as low as 200 ppb (REA, Table 4-11). In addition to the assessment of these studies and their results in past NAAQS reviews, there has been extensive evaluation of the individual subject results, including a data quality review in the 2010 review of the primary SO

standard (Johns and Simmons, 2009) and detailed analysis in two subsequent publications (Johns et al., 2010; Johns and Linn, 2011). The E-R function was derived from the sRaw responses reported in the controlled exposure studies as summarized in the ISA in terms of percent of study subjects experiencing responses of a magnitude equal to a doubling or tripling or more (

e.g.,

ISA, Table 5-2; Long and Brown, 2018; REA, section 4.6.2). Across the exposure range from 200 to 1000 ppb, the percentage of exercising study subjects with asthma having at least a doubling of sRaw increases from about 8-9% (at exposures of 200 ppb) up to approximately 50-60% (at exposures of 1000 ppb) (REA, Table 4-11).

b. Key Limitations and Uncertainties

While the general approach and methodology for the exposure-based assessment in this review is similar to that used in the last review, there are a number of ways in which the current analyses are different; some differences reflect improvements and, in some cases, reflect improvements that may address limitations of the 2009 assessment. For example, the number and type of study areas assessed has been expanded since the last review, and input data and modeling approaches have improved in a number of ways, including the availability of continuous 5-minute air monitoring data at monitors within the three study areas. In addition, the REA for the current review extends the time period of simulation to a 3-year simulation period, consistent with the form established for the now-current standard. Further, the years simulated reflect more recent emissions and circumstances subsequent to the 2010 decision.

In characterizing uncertainty associated with the risk and exposure estimates in this review, the REA used a qualitative uncertainty characterization approach adapted from the World Health Organization (WHO) approach for characterizing uncertainty in exposure assessment (WHO, 2008) accompanied by quantitative sensitivity analyses of key aspects of the assessment approach (REA, chapter 6).

The approach used in the REA places a greater focus on evaluating the direction and the magnitude of the uncertainty (

i.e.,

qualitatively rating how the source of uncertainty, in the presence of alternative information, may affect the estimates of exposure and risk). The evaluation considers the limitations and uncertainties underlying the analysis inputs and approaches and the relative impact that these uncertainties may have on the resultant exposure/risk estimates. Consistent with the WHO (2008) approach, the overall impact of the uncertainty is then characterized by the extent or magnitude of the impact of the uncertainty (

e.g.,

high, moderate, low) as implied by the relationship between the source of the uncertainty and the exposure/risk output. The REA also evaluated the direction of influence, indicating how the source of uncertainty was judged to affect the exposure and risk estimates (

e.g.,

likely to produce over- or under-estimates).

The approach used has been applied in REAs for past NAAQS review for nitrogen oxides, carbon monoxide, and ozone (U.S. EPA, 2008b; 2010; 2014d), as well as SO

(U.S. EPA, 2009).

Several areas of uncertainty are identified as particularly important, with some similarities to those recognized in the last review. Generally, these areas of uncertainty include estimation of the spatial distribution of SO

concentrations across each study

area under air quality conditions just meeting the current standard, including the fine-scale temporal pattern of 5-minute concentrations. They also include uncertainty with regard to population groups and exposure concentrations for which the health effects evidence base is limited or lacking (PA, section 3.2.2.3).

With regard to the spatial distribution of SO

concentrations, there is some uncertainty associated with the ambient air concentration estimates in the air quality scenarios assessed. A more detailed characterization of contributors to this uncertainty is presented in section 6.2 of the REA, with a brief overview provided here. Some aspects of the assessment approach contributing to this uncertainty include estimation of the 1-hour concentrations and the approach employed to adjust the air quality surface to concentrations just meeting the current standard (REA, section 6.2.2.2; PA, section 3.2.2.2), as well as the estimation of 1-hour ambient air concentrations resulting from emissions sources not explicitly modeled. All of these assessment approaches influence the resultant temporal and spatial pattern of concentrations and associated exposure circumstances represented in the study areas (REA, sections 6.2.1 and 6.2.2). There is also uncertainty in the estimates of 5-minute concentrations in ambient air across the modeling receptors in each study area. The ambient air monitoring dataset available to inform the 5-minute estimates, much expanded in this review over the dataset available in the last review, is used to draw on relationships occurring at one location and over one range of concentrations to estimate the fine-scale temporal pattern in concentrations at the other locations. While this is an important area of uncertainty in the REA results, because the ambient air 5-minute concentrations are integral to the 5-minute estimates of exposure, the approach used to represent fine-scale temporal variability in the three study areas is strongly based in the available information and has been evaluated in the REA (REA, Table 6-3; sections 3.5.2 and 3.5.3).

Another important area of uncertainty in the REA is particular to the lung function risk estimates derived for exposure concentrations below those represented in the evidence base (REA, Table 6-3). The E-R function on which the risk estimates are based generates non-zero predictions of the percentage of the at-risk population expected to experience a day with the occurrence of at least a doubling of sRaw for all 5-minute exposure concentrations each simulated individual encounters while breathing at an elevated rate. The uncertainty in the response estimates increases substantially with decreasing exposure concentrations below those well represented in the data from the controlled human exposure studies (

i.e.,

below 200 ppb).

Additionally, the assessment focuses on the daily maximum 5-minute exposure during a period of elevated breathing rate, summarizing results in terms of the days on which the magnitude of such exposure exceeds a benchmark or contributes to a doubling or tripling of sRaw. Although there is some uncertainty associated with the potential for additional, uncounted events in the same day, the health effects evidence indicates a lack of a cumulative effect of multiple exposures over several hours or a day (ISA, section 5.2.1.2) and a reduced response to repeated exercising exposure events over an hour (Kehrl et al., 1987). Further, information is somewhat limited with regard to the length of time after recovery from one exposure by which a repeat exposure would elicit an effect similar to that of the initial exposure event (REA, Table 6-3). In addition, there is uncertainty regarding the potential influence of co-occurring pollutants on the relationship between short-term SO

exposures and respiratory effects. For example, there is some limited evidence regarding the potential for an increased response to SO

exposures occurring in the presence of other common pollutants such as PM (potentially including particulate sulfur compounds), nitrogen dioxide and ozone, although the studies are limited (

e.g.,

with regard to their relevance to ambient exposures) and/or provide inconsistent results (ISA, pp. 5-23 to 5-26, pp. 5-143 to 5-144; 2008 ISA, section 3.1.4.7).

For example, “studies of mixtures of particles and sulfur oxides indicate some enhanced effects on lung function parameters, airway responsiveness, and host defense”; however, “some of these studies lack appropriate controls and others involve [sulfur-containing species] that may not be representative of ambient exposures” (ISA, p. 5-144). These toxicological studies in laboratory animals, which were newly available in the last review, were discussed in greater detail in the 2008 ISA. That ISA stated that “[r]espiratory responses observed in these experiments were in some cases attributed to the formation of particular sulfur-containing species” yet, “the relevance of these animal toxicological studies has been called into question because concentrations of both PM (1 mg/m

and higher) and SO

(1 ppm and higher) utilized in these studies are much higher than ambient levels” (2008 ISA, p. 3-30).

Another area of uncertainty, which remains from the last review and is important to our consideration of the REA results, concerns the extent to which the quantitative results represent the populations at greatest risk of effects associated with exposures to SO

in ambient air. As recognized in section II.A.2, the evidence base of controlled human exposure studies does not include studies of children younger than 12 years old and is limited with regard to studies of people with more severe asthma.

The limited evidence that informs our understanding of potential risk to these groups indicates the potential for them to experience greater impacts than other population groups with asthma under similar exposure circumstances or, in the case of people with severe asthma, to have a more limited reserve for addressing this risk (ISA, section 5.2.1.2). Further, we note the lack of information on the factors contributing to increased susceptibility to SO

-induced bronchoconstriction among some people with asthma compared to others (ISA, pp. 5-19 to 5-21). These data limitations contribute uncertainty to the exposure/risk estimates with regard to the extent to which they represent the populations at greatest risk of SO

-related respiratory effects.

We additionally recognize that limitations in the activity pattern information for children younger than 5 years old precluded their inclusion in the populations of children simulated in the REA (REA, section 4.1.2).

In summary, among the multiple uncertainties and limitations in data and tools that affect the quantitative estimates of exposure and risk and their interpretation in the context of considering the current standard, several are particularly important. These include uncertainties related to the following: Estimation of 5-minute concentrations in ambient air; the lack of information from controlled human exposure studies for the lower, more prevalent concentrations of SO

and limited information regarding multiple exposure episodes within a day; the prevalence of different exposure circumstances represented by the three study areas; and characterization of particular subgroups of people with asthma that may be at greater risk.

c. Summary of Exposure and Risk Estimates

The REA provides estimates for two simulated at-risk populations: Adults with asthma and school-aged children

with asthma (REA, section 2.2). This summary focuses on the population of children with asthma given that the ISA describes children as “particularly at risk” and the REA generally yields higher exposure and risk estimates for children than adults (in terms of percentage of the population group). Summarized here are two sets of exposure and risk estimates for the 3-year simulation in each study area: (1) The number (and percent) of simulated persons experiencing exposures at or above the particular benchmark concentrations of interest while breathing at elevated rates; and (2) the number and percent of people estimated to experience at least one SO

-related lung function decrement in a year and the number and percent of people experiencing multiple lung function decrements associated with SO

exposures (detailed results are presented in chapter 5 of the REA). Both types of estimates are lower for adults with asthma compared to children with asthma, generally due to the lesser amount and frequency of time spent outdoors while breathing at elevated rates (REA, section 5.2). As summarized in section II.A.3.b above, the REA provides results for two different approaches to adjusting air quality. The estimates summarized here are drawn from the results for both approaches, as presented in Tables 1 and 2 of the proposal (83 FR 26772, June 8, 2018).

The adult population group is comprised of individuals older than 18 years of age and school-aged children are individuals aged 5 to 18 years old. As in other NAAQS reviews, this REA does not estimate exposures and risk for children younger than 5 years old due to the more limited information contributing relatively greater uncertainty in modeling their activity patterns and physiological processes compared to children between the ages of 5 to 18 (REA, p. 2-8).

This summary focuses first on the results for the benchmark-based risk metric in terms of the percent of the simulated populations of children with asthma estimated to experience at least one daily maximum 5-minute exposure per year at or above the different benchmark concentrations while breathing at elevated rates under air quality conditions just meeting the current standard (REA, Tables 6-8 and 6-9). In two of the three study areas, approximately 20% to just over 25% of a study area's simulated children with asthma, on average across the 3-year period, are estimated to experience one or more days per year with a 5-minute exposure at or above 100 ppb while breathing at elevated rates (83 FR 26772 [Table 1], June 8, 2018).

With regard to the 200 ppb benchmark concentration, these two study areas' estimates are as high as 0.7%, on average across the 3-year period, and range up to as high as 2.2% in a single year. Less than 0.1% of either area's simulated children with asthma were estimated to experience multiple days with such an exposure at or above 200 ppb (REA, Tables 6-8 and 6-9). Additionally, in the study area with the highest estimates for exposures at or above 200 ppb, approximately a quarter of a percent of simulated children with asthma also were estimated to experience a day with a 5-minute exposure at or above 300 ppb across the 3-year period (the percentage for the 400 ppb benchmark was 0.1% or lower). Across all three areas, no children were estimated to experience multiple days with a daily maximum 5-minute exposure (while breathing at an elevated rate) at or above 300 ppb (REA, Table 6-9).

These estimates for the third area (Tulsa) are much lower than those for the other two areas. No individuals of the simulated at-risk population in the third study area were estimated to experience exposures at or above 200 ppb and less than 0.5% are estimated to experience an exposure at or above the 100 ppb benchmark.

With regard to lung function risk, in the two study areas for which the exposure estimates are highest, as many as 1.3% and 1.1%, respectively, of children with asthma, on average across the 3-year period (and as many as 1.9% in a single year), were estimated to experience at least 1 day per year with a SO

-related doubling in sRaw (83 FR 26772 [Table 2], June 8, 2018; REA, Tables 6-10 and 6-11).

The corresponding percentage estimates for experiencing two or more such days ranged as high as 0.7%, on average across the 3-year simulation period (REA, Table 6-11). Additionally, as much as 0.2% and 0.3%, in Fall River and Indianapolis, respectively, of the simulated populations of children with asthma, on average across the 3-year period, was estimated to experience a single day with a SO

-related tripling in sRaw (83 FR 26772 [Table 2], June 8, 2018).

As with the comparison-to-benchmark results, the estimates for risk of lung function decrements in terms of a doubling or more in sRaw are also lower in the Tulsa study area than the other two areas (83 FR 26772 [Table 2], June 8, 2018; REA, Tables 6-10 and 6-11).

B. Conclusions on Standard

In drawing conclusions on the adequacy of the current primary SO

standard, in view of the advances in scientific knowledge and additional information now available, the Administrator has considered the evidence base, information, and policy judgments that were the foundation of the last review and reflects upon the body of evidence and information newly available in this review. In so doing, the Administrator has taken into account both evidence-based and exposure- and risk-based considerations, as well as advice from the CASAC and public comments. Evidence-based considerations draw upon the EPA's assessment and integrated synthesis of the scientific evidence from controlled human exposure studies and epidemiologic studies evaluating health effects related to exposures of SO

as presented in the ISA, with a focus on policy-relevant considerations as discussed in the PA (summarized in sections II.B and II.D.1 of the proposal and section II.A.2 above). The exposure- and risk-based considerations draw from the results of the quantitative analyses presented in the REA (as summarized in section II.C of the proposal and section II.A.3 above) and consideration of these results in the PA.

Consideration of the evidence and exposure/risk information in the PA and by the Administrator is framed by consideration of a series of key policy-relevant questions. Section II.B.1 below summarizes the rationale for the Administrator's proposed decision, drawing from section II.D.3 of the proposal. The advice and recommendations of the CASAC and public comments on the proposed decision are addressed below in sections II.B.2 and II.B.3, respectively. The Administrator's conclusions in this review regarding the adequacy of the current primary standard and whether any revisions are appropriate are described in section II.B.4.

1. Basis for Proposed Decision

At the time of the proposal, the Administrator carefully considered the assessment of the current evidence and conclusions reached in the ISA; the currently available exposure and risk information, including associated limitations and uncertainties, described in detail in the REA and characterized in the PA; considerations and staff conclusions and associated rationales presented in the PA, including consideration of commonly accepted guidelines or criteria within the public health community, including the ATS, an organization of respiratory disease specialists; the advice and recommendations from the CASAC; and public comments that had been offered up to that point (83 FR 26778, June 8, 2018). In reaching his proposed decision on the primary SO

standard, the Administrator first recognized the long-standing evidence that has established the key aspects of the harmful effects of very short SO

exposures on people with asthma. This evidence, drawn largely from the controlled human exposure studies, demonstrates that very short exposures (for as short as a few minutes) to less than 1000 ppb SO

, while breathing at an elevated rate (such as while exercising), induces bronchoconstriction and related

respiratory effects in people with asthma and provides support for identification of this group as the population at risk from short-term peak concentrations in ambient air (ISA; 2008 ISA; U.S. EPA, 1994).

Within this evidence base, there is a relative lack of such information for some subgroups of this population, including young children and people with severe asthma. The evidence base additionally includes epidemiologic evidence that supports the conclusion of a causal relationship between short-term SO

exposures and respiratory effects, for which the controlled human exposure studies are the primary evidence.

For people without asthma, such effects have only been observed in studies of exposure concentrations at or above 1000 ppb (ISA, section 5.2.1.7).

With regard to the health effects evidence newly available in this review, in the proposal the Administrator noted that, while the health effects evidence, as assessed in the ISA, has been augmented with additional studies since the time of the last review, including more than 200 new health studies, it does not lead to different conclusions regarding the primary health effects of SO

in ambient air or regarding exposure concentrations associated with those effects. Nor does it identify different or additional populations at risk of SO

-related effects. Thus, the Administrator recognized that the health effects evidence available in this review and addressed in the ISA is consistent with evidence available in the last review when the current standard was established and that this strong evidence base continues to demonstrate a causal relationship between relevant short-term exposures to SO

and respiratory effects, particularly with regard to effects related to asthma exacerbation in people with asthma. He also recognized that the ISA conclusion on the respiratory effects caused by short-term exposures is based primarily on the evidence from controlled human exposure studies that reported effects in people with asthma exposed to SO

for 5 to 10 minutes while breathing at an elevated rate (ISA, section 5.2.1.9), and that the current 1-hour standard was established to provide protection from effects such as these (75 FR 35520, June 22, 2010; 83 FR 26778, June 8, 2018).

In considering exposure concentrations of interest in this review, the Administrator particularly noted the evidence from controlled human exposure studies, also available in the last review, that demonstrate the occurrence of moderate or greater lung function decrements in some people with asthma exposed to SO

concentrations as low as 200 ppb for very short periods of time while breathing at elevated rates (ISA, Table 5-2

and Figure 5-1, summarized in Table 3-1 of the PA).

He recognized that the data for the 200 ppb exposures include limited evidence of respiratory symptoms accompanying the lung function effects observed, and that the severity and number of individuals affected is found to increase with increasing exposure levels, as is the frequency of accompaniment by respiratory symptoms, such that, at concentrations at or above 400 ppb, the moderate or greater decrements in lung function were frequently accompanied by respiratory symptoms, with some of these findings reaching statistical significance at the study group level (ISA, Table 5-2 and section 5.2.1; PA, section 3.2.1.3; 83 FR 26779, June 8, 2018).

The availability of individual subject data from these studies allowed for the comparison of results in a consistent manner across studies (ISA, Table 5-2; Long and Brown, 2018).

The Administrator additionally considered the very limited evidence for exposure concentrations below 200 ppb, for which relatively less severe effects are indicated, while noting the limitations of this dataset (83 FR 26781, June 8, 2018).

In considering the potential public health significance of these effects associated with SO

exposures, the Administrator's proposed decision recognized both the greater significance of larger lung function decrements, which are more frequently documented at exposures above 200 ppb, and the potential for greater impacts of SO

-induced decrements in people with more severe asthma, as recognized in the ISA and by the CASAC (as summarized in section II.D.2 of the proposal).

Thus, the Administrator recognized that health effects resulting from exposures at and above 400 ppb are appreciably more severe than those elicited by exposure to SO

concentrations at 200 ppb, and that health impacts of short-term SO

exposures (including those occurring at concentrations below 400 ppb) have the potential to be more significant in the subgroup of people with asthma that have more severe disease and for which the study data are more limited (83 FR 26779, June 8, 2018).

The ISA notes that while extremely limited evidence for adults with moderate to severe asthma indicates such groups may have similar relative lung function decrements in response to SO

as adults with less severe asthma, individuals with severe asthma may have greater absolute decrements that may relate to the role of exercise (ISA, pp. 1-17 and 5-22). The ISA concluded that individuals with severe asthma may have “less reserve capacity to deal with an insult compared with individuals with mild asthma” (ISA, pp. 1-17 and 5-22).

As was the case for the 2010 decision, the Administrator's proposed decision in this review recognized the importance of considering the health effects evidence in the context of the exposure and risk modeling performed for this review. The Administrator recognized that such a context is critical for SO

, a chemical for which the associated health effects that occur in people with asthma are linked to exposures during periods of elevated breathing rates, such as while exercising. Accordingly, in considering the adequacy of public health protection provided by the current standard, the Administrator considered the evidence in this context. In so doing, he found the PA considerations regarding the REA results and the associated uncertainties, as well as the nature and magnitude of the uncertainties inherent in the scientific evidence upon which the REA is based, to be important to judgments such as the extent to which the exposure and risk estimates for air quality conditions that just meet the current standard in the three study areas indicate exposures and risks that are important from a public health perspective.

Thus, in considering whether the current standard provides the requisite protection of public health in the proposal, the Administrator took note of: (1) The PA consideration of a sizeable number of at-risk individuals living in locations near large SO

emissions sources that may contribute to increased concentrations in ambient air, and associated exposures and risk; (2) the REA estimates of children with asthma estimated to experience single or multiple days across the 3-year assessment period, as well as in a single year, with a 5-minute exposure at or above 200 ppb, while breathing at elevated rates; and (3) limitations and associated uncertainties with regard to population groups at potentially greater risk but for which the evidence is lacking, recognizing that the CAA requirement that primary standards provide an adequate margin of safety is intended to address uncertainties associated with inconclusive scientific and technical information, as well as to provide a reasonable degree of protection against hazards that research has not yet identified (83 FR 26780, June 8, 2018). Further, the proposed decision recognized advice received from the CASAC, including its conclusion that the current evidence and exposure/risk information supports retaining the current standard, as well as its statement that it did not

recommend reconsideration of the level of the standard to provide a greater margin of safety (83 FR 26780, June 8, 2018). Based on all of these considerations, the Administrator proposed to conclude that a less stringent standard would not provide the requisite protection of public health, including an adequate margin of safety (83 FR 26780, June 8, 2018).

The Administrator also considered the adequacy of protection provided by the current standard from effects associated with lower short-term exposures, including those at or below 200 ppb. In so doing, he considered the REA estimates for such effects, and the significance of estimates for single (

versus

multiple) occurrences of exposures at or above the lower benchmark concentrations and associated lung function decrements, and the nature and magnitude of the various uncertainties that are inherent in the underlying scientific evidence and REA analyses. Based on these, he placed little weight on the significance of estimates of occurrences of short-term exposures below 200 ppb and focused on the REA results for exposures at and above 200 ppb in light of his considerations, noted above, regarding the health significance of findings from the controlled human exposure studies. He further placed relatively less weight on the significance of infrequent or rare occurrences of exposures at or just above 200 ppb, and more weight on the significance of repeated such occurrences, as well as occurrences of higher exposures. With this weighing of the REA estimates and recognizing the uncertainties associated with such estimates for the scenarios of air quality developed to represent conditions just meeting the current standard, the Administrator considered the current standard to provide a high degree of protection to at-risk populations from SO

exposures associated with the more severe health effects, which are more clearly of public health concern, as indicated by the extremely low estimates of occurrences of exposures at or above 400 ppb (and at or above 300 ppb); and to additionally provide a slightly lower, but still high, degree of protection for the appreciably less severe effects associated with lower exposures (

i.e.,

at and below 200 ppb), for which public health implications are less clear. The Administrator further observed that although the CASAC stated that there is uncertainty in the adequacy of the margin of safety provided by the current standard for less well studied yet potentially susceptible population groups, it concluded that “the CASAC does not recommend reconsideration of the level in order to provide a greater margin of safety” (Cox and Diez Roux, 2018b, Consensus Responses, p. 5; 83 FR 26780, June 8, 2018). Based on these and all of the above considerations, the Administrator proposed to conclude that a more stringent standard is not needed to provide requisite protection and that the current standard provides the requisite protection of public health under the Act (83 FR 26781, June 8, 2018).

In summary, the Administrator considered the specific elements of the existing standard and proposed to retain the existing standard, in all of its elements. With regard to SO

as the indicator, he recognized the support for retaining this indicator in the current evidence base, noting the ISA conclusion that SO

is the most abundant of the SO

in the atmosphere and the one most clearly linked to human health effects. The Administrator additionally recognized the control exerted by the 1-hour averaging time on 5-minute ambient air concentrations of SO

and the associated exposures of particular importance for SO

-related health effects. Lastly, with regard to form and level of the standard, the Administrator noted the REA results and the level of protection that they indicate the elements of the current standard to collectively provide. The Administrator additionally noted CASAC support for retaining the current standard and the CASAC's specific recommendation that all four elements should remain the same.

Thus, based on consideration of the evidence and exposure/risk information available in this review, with its attendant uncertainties and limitations, and information that might inform public health policy judgments, as well as consideration of advice from the CASAC, including their concurrence with the PA conclusions that the current evidence does not support revision of the primary SO

standard, the Administrator proposed to conclude that it is appropriate to retain the current standard without revision based on his judgment that the current primary SO

standard provides an adequate margin of safety against adverse effects associated with short-term exposures to SO

in ambient air. For these reasons, and all of the reasons discussed above, and recognizing the CASAC conclusion that the current evidence and REA results provide support for retaining the current standard, the Administrator proposed to conclude that the current primary SO

standard is requisite to protect public health with an adequate margin of safety from effects of SO

in ambient air and should be retained, without revision.

2. CASAC Advice in This Review

In comments on the draft PA, the CASAC concurred with staff's overall preliminary conclusions that “the current scientific literature does not support revision of the primary NAAQS for SO

,” additionally stating the following (Cox and Diez Roux, 2018b, p. 3 of letter):

The CASAC notes that the new scientific information in the current review does not lead to different conclusions from the previous review. Thus, based on review of the current state of the science, the CASAC supports retaining the current standard, and specifically notes that all four elements (indicator, averaging time, form, and level) should remain the same.

The CASAC further stated the following (Cox and Diez Roux, 2018b, p. 3 of letter):

With regard to indicator, SO

is the most abundant of the gaseous SO

species. Because, as the PA states, “the available scientific information regarding health effects was overwhelmingly indexed by SO

,” it is the most appropriate indicator. The CASAC affirms that the one-hour averaging time will protect against high 5-minute exposures and reduce the number of instances where the 5-minute concentration poses risks to susceptible individuals. The CASAC concurs that the 99th percentile form is preferable to a 98th percentile form to limit the upper end of the distribution of 5-minute concentrations. Furthermore, the CASAC concurs that a three-year averaging time for the form is appropriate.

The choice of level is driven by s

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