Policy Assessment for the Review of the 

Primary National Ambient Air Quality Standard 

for Sulfur Oxides

EPA-452/R-18-002

May 2018

Policy Assessment for the Review of the Primary National Ambient Air Quality Standard for 

Sulfur Oxides

U.S. Environmental Protection Agency

Office of Air Quality Planning and Standards

Health and Environmental Impacts Division

Research Triangle Park, NC
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DISCLAIMER

This document has been prepared by staff in the Health and Environmental Impacts 

Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency 

(EPA). Any findings and conclusions are those of the authors and do not necessarily reflect the 

views of the Agency. Mention of trade names or commercial products is not intended to 

constitute endorsement or recommendation for use. Questions or comments related to this 

document should be addressed to Dr. Nicole Hagan, U.S. Environmental Protection Agency, 

Office of Air Quality Planning and Standards, C504-06, Research Triangle Park, North Carolina 

27711 (email: hagan.nicole@epa.gov).
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TABLE OF CONTENTS

LIST OF APPENDICES................................................................................................................iii

LIST OF FIGURES ....................................................................................................................... iv

LIST OF TABLES.......................................................................................................................... v

LIST OF ACRONYMS AND ABBREVIATIONS ...................................................................... vi

1 INTRODUCTION .............................................................................................................. 1-1

1.1 Purpose.......................................................................................................................... 1-1

1.2 Background ................................................................................................................... 1-2

1.2.1 Legislative Requirements....................................................................................... 1-2

1.2.2 History of the Reviews of the Primary NAAQS for SOX ...................................... 1-4

1.2.3 Current SO2 NAAQS Review................................................................................ 1-7

1.3 General Approach and Organization of this Document.............................................. 1-19

REFERENCES .......................................................................................................................... 1-10

2 CURRENT AIR QUALITY .............................................................................................. 2-1

2.1 Sources to Ambient Air................................................................................................. 2-1

2.2 Ambient Air Monitoring Methods and Network........................................................... 2-3

2.3 Ambient Air Monitoring Concentrations...................................................................... 2-5

2.3.1 Trends .................................................................................................................... 2-5

2.3.2 Current Concentrations.......................................................................................... 2-8

REFERENCES .......................................................................................................................... 2-13

3 REVIEW OF THE PRIMARY STANDARD FOR SULFUR OXIDES ....................... 3-1

3.1 Approach ....................................................................................................................... 3-1

3.1.1 Approach in the Previous Review.......................................................................... 3-2

3.1.2 Approach for the Current Review........................................................................ 3-11

3.2 Adequacy of the Current Standard.............................................................................. 3-14

3.2.1 Evidence-based Considerations........................................................................... 3-14

3.2.2 Exposure/Risk-based Considerations................................................................... 3-37

3.2.3 CASAC Advice.................................................................................................... 3-56

3.2.4 Staff Conclusions on the Current Standard.......................................................... 3-58

3.3 Key Uncertainties and Areas for Future Research and Data Collection ..................... 3-67

REFERENCES .......................................................................................................................... 3-69
iii

LIST OF APPENDICES

A. Preparation of data files for generation of figures in Chapter 2

B. Additional information on datasets presented in Figure 2-8

C. Occurrences of 5-minute SO2 concentrations of interest in the recent ambient air 

monitoring data (2014-2016)

D. Air quality information for geographical areas of three selected U.S. 

epidemiological studies

E. Derivation of design values presented in Appendix D

F. Geographic distribution of continental U.S. facilities emitting more than 1,000 tpy 

SO2 and population density based on U.S. census tracts
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LIST OF FIGURES

Figure 2-1. Percent contribution of SO2 emissions by sector................................................... 2-2

Figure 2-2. National SO2 emission trends by sector................................................................. 2-3

Figure 2-3. Temporal trend in number of monitors reporting 5-minute concentrations. ......... 2-5

Figure 2-4. National temporal trend in SO2 concentrations: 1980-2016 (24 sites). ................. 2-6

Figure 2-5. Temporal trend in SO2 concentrations: 2000-2016 (193 sites).............................. 2-7

Figure 2-6. Temporal trend in daily maximum 5-minute SO2 concentrations: 2011-2016...... 2-7

Figure 2-7. Concentrations of SO2 in terms of the current standard (3-year average of annual 

99th percentile daily maximum 1-hour concentrations) at sites with datasets 

meeting completeness requirements for 2014-2016. ............................................. 2-9

Figure 2-8. Distributions of daily maximum 5-minute concentrations during 2014-2016..... 2-12

Figure 3-1. Overview of the approach for review of the current primary standard................... 3-13
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LIST OF TABLES

Table 1-1. History of the primary national ambient air quality standard(s) for sulfur oxides 

since 1971................................................................................................................ 1-7

Table 3-1. Percentage of adults with asthma in controlled human exposure studies 

experiencing sulfur dioxide-induced decrements in lung function and respiratory 

symptoms.............................................................................................................. 3-24

Table 3-2. 2015 National Asthma Prevalence....................................................................... 3-36

Table 3-3. Air quality conditions adjusted to just meet the current standard: Percent of 

simulated populations of children with asthma estimated to experience at least one 

daily maximum 5-minute exposure per year at or above indicated concentrations 

while breathing at an elevated rate....................................................................... 3-45

Table 3-4. Air quality conditions adjusted to just meet the current standard: Percent of 

simulated population of children with asthma estimated to experience at least one 

day per year with a SO2-related increase in sRaw of 100% or more................... 3-46

Table 3-5. Population size near larger sources of SO2 emissions. ........................................ 3-55
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LIST OF ACRONYMS AND ABBREVIATIONS

AHR airway hyperresponsiveness

APEX Air Pollutants Exposure model

AQCD Air Quality Criteria Document

AQS Air Quality System

CAA Clean Air Act

CASAC Clean Air Scientific Advisory Committee

CHAD Consolidated Human Activity Database

DV design value

ED emergency department

EGU Electricity generating unit

EPA Environmental Protection Agency

FEM federal equivalent method

FEV1 forced expiratory volume in one minute

FRM federal reference method

IRP Integrated Review Plan

ISA Integrated Science Assessment

ME microenvironment

NAAQS National Ambient Air Quality Standard

NCEA National Center for Environmental Assessment

NEI National Emissions Inventory

NO2 nitrogen dioxide

O3 ozone

OAQPS Office of Air Quality Planning and Standards

ppb parts per billion

ppm parts per million

PA Policy Assessment

PM particulate matter

REA Risk and Exposure Assessment

SLAMS State and Local Air Monitoring Stations

SO2 sulfur dioxide

SO3 sulfur trioxide

SOX oxides of sulfur

sRaw specific airway resistance

USB United States background

UVF ultraviolet fluorescence
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1 INTRODUCTION

1.1 PURPOSE

This document, Policy Assessment for the Review of the Primary National Ambient Air 

Quality Standard for Sulfur Oxides (hereafter referred to as PA), presents the policy assessment 

for the U.S. Environmental Protection Agency’s (EPA’s) current review of the primary (healthbased) national ambient air quality standard (NAAQS) for sulfur oxides (SOX).1 The overall 

plan for this review was presented in the Integrated Review Plan for the Primary National 

Ambient Air Quality Standard for Sulfur Dioxide, Final (IRP; U.S. EPA, 2014a). The IRP also 

identified key policy-relevant issues to be addressed in this review and discussed the key 

documents that generally inform NAAQS reviews, including an Integrated Science Assessment 

(ISA), a Risk and Exposure Assessment (REA), and a Policy Assessment (PA). 

The PA presents a staff evaluation of the policy implications of the key scientific and 

technical information in the ISA and REA for consideration by the EPA Administrator.

2

Ultimately, a final decision on the primary standard for SOX will reflect the judgments of the 

Administrator. The role of the PA is to help “bridge the gap” between the Agency’s scientific 

assessments presented in the ISA and REA, and the judgments required of the Administrator in 

determining whether it is appropriate to retain or revise the NAAQS.

In evaluating the adequacy of the current standard and whether it is appropriate to 

consider alternative standards, the PA focuses on information that is most pertinent to evaluating 

the basic elements of the NAAQS: indicator, averaging time, form, and level.3 These elements, 

 1 This review focuses on the presence in ambient air of sulfur oxides, a group of closely related gaseous compounds 

that include sulfur dioxide and sulfur trioxide and of which sulfur dioxide (the indicator for the current standard) 

is the most prevalent in the atmosphere and the one for which there is a large body of scientific evidence on 

health effects. The health effects of particulate atmospheric transformation products of SOX, such as sulfates, are 

addressed in the review of the NAAQS for particulate matter. Additionally, the ecological welfare effects of 

sulfur oxides and particulate atmospheric transformation products are being considered in the review of the 

secondary NAAQS for Oxides of Nitrogen, Oxides of Sulfur, and Particulate Matter (U.S. EPA, 2017a), 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 particulate matter (U.S. EPA, 2016a).

2 The terms “staff,” “we,” and “our” throughout this document refer to the staff in the EPA’s Office of Air Quality 

Planning and Standards (OAQPS). 

3 The indicator defines the chemical species or mixture to be measured in the ambient air for the purpose of 

determining whether an area attains the standard. The averaging time defines the period over which air quality 

measurements are to be averaged or otherwise analyzed. The form of a standard defines the air quality statistic 

that is to be compared to the level of the standard in determining whether an area attains the standard. For 

example, the form of the annual NAAQS for fine particulate matter is the average of annual mean concentrations 

for three consecutive years, while the form of the 8-hour NAAQS for carbon monoxide is the second-highest 8-

hour average in a year. The level of the standard defines the air quality concentration used for that purpose.
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which together serve to define each standard, must be considered collectively in evaluating the 

health protection afforded by the primary standard for SOX.

The development of the PA is also intended to facilitate advice to the Agency and 

recommendations to the Administrator from an independent scientific review committee, the 

Clean Air Scientific Advisory Committee (CASAC), as provided for in the Clean Air Act 

(CAA). As discussed below in section 1.2.1, the CASAC is to advise on subjects including the 

Agency’s assessment of the relevant scientific information and on the adequacy of the current

standards, and to make recommendations as to any revisions of the standards that may be 

appropriate. The EPA makes available to the CASAC and the public one or more drafts of the 

PA for CASAC review and public comment.

4

In this PA, we take into account the available scientific and technical information, as 

assessed in the Integrated Science Assessment for Sulfur Oxides – Health Criteria (2017 ISA

[U.S. EPA, 2017b]) and Risk and Exposure Assessment for the Review of the Primary National 

Ambient Air Quality Standard for Sulfur Oxides (REA [U.S. EPA, 2018]). The evaluation and 

staff conclusions in this PA have been informed by the advice received from the CASAC based 

on its review of the draft PA (U.S. EPA, 2017c) and other draft Agency documents prepared thus 

far in this review, and also by public comment received thus far. 

Beyond informing the Administrator and facilitating the advice and recommendations of 

the CASAC, the PA is also intended to be a useful reference to all parties interested in the review 

of the primary NAAQS for SOX. In these roles, it is intended to serve as a source of policyrelevant information that informs the Agency’s review of the primary NAAQS for SOX, and it is 

written to be understandable to a broad audience.

1.2 BACKGROUND

1.2.1 Legislative Requirements

Two sections of the CAA 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 pollutants 

“emissions of which, 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 

 4 The decision whether to prepare one or more drafts of the PA is influenced by preliminary staff conclusions, taking 

into consideration CASAC advice and public comments, among other factors. Typically, a second draft PA has 

been prepared in cases where the available information calls into question the adequacy of the current standard 

and where analyses of potential alternative standards are developed. In such cases, a second draft PA includes 

preliminary staff conclusions regarding potential alternative standards and undergoes CASAC review and public 

comment prior to preparation of the final PA. When such analyses are not undertaken, a second draft PA may not 

be warranted, as is the case in this review of the primary NAAQS for SOX.
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results from numerous or diverse mobile or stationary sources”; and for which he “plans to issue 

air quality criteria...” 42 U.S.C. § 7408(a)(1). 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 [42 

U.S.C. § 7409(a)]. Section 109(b)(1) defines primary standards as ones “the attainment and 

maintenance of which in the judgment of the Administrator, based on such criteria and allowing 

an adequate margin of safety, are requisite to protect the public health.”5 Under 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.”6

The requirement that primary standards provide an adequate margin of safety was

intended to address uncertainties associated with inconclusive scientific and technical 

information available at the time of standard setting. It was also intended to provide a reasonable 

degree of protection against hazards that research has not yet identified. See Lead Industries 

Association v. EPA, 647 F.2d 1130, 1154 (D.C. Cir 1980), cert. denied. 449 U.S. 1042 (1980); 

American Petroleum Institute v. Costle, 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert. denied, 455 

U.S. 1034 (1982); Coalition of Battery Recyclers Ass'n v. EPA, 604 F.3d 613, 617-18 (D.C. Cir. 

2010); Mississippi v. EPA, 744 F. 3d 1334, 1353 (D.C. Cir. 2013). Both kinds of uncertainties 

are components of the risk associated with pollution at levels below those at which human health 

effects can be said to occur with reasonable scientific certainty. Thus, in selecting primary 

standards that include an adequate margin of safety, the Administrator is seeking not only to 

prevent pollution levels that have been demonstrated to be harmful but also to prevent lower 

pollutant levels that may pose an unacceptable risk of harm, even if the risk is not precisely 

identified as to nature or degree. The CAA does not require the Administrator to establish a 

primary NAAQS at a zero-risk level or at background concentration levels, see Lead Industries 

 5 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).

6 Under CAA section 302(h) (42 U.S.C. § 7602(h)), effects on welfare include, but are not limited to, “effects on 

soils, water, crops, vegetation, man-made materials, animals, wildlife, weather, visibility, and climate, damage to 

and deterioration of property, and hazards to transportation, as well as effects on economic values and on personal 

comfort and well-being.”
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v. EPA, 647 F.2d at 1156 n.51, Mississippi v. EPA, 744 F.3d at 1351, 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 the sensitive 

population(s), and the kind and degree of uncertainties. The selection of any particular approach 

to providing an adequate margin of safety is a policy choice left specifically to the 

Administrator’s judgment. See Lead Industries Association v. EPA, 647 F.2d at 1161-62;

Mississippi v. EPA, 744 F.3d at 1353.

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. In so doing, the EPA may not consider the 

costs of implementing the standards. See generally, Whitman v. American Trucking Associations, 

531 U.S. 457, 465-472, 475-76 (2001). Likewise, “[a]ttainability and technological feasibility are 

not relevant considerations in the promulgation of national ambient air quality standards” 

(American Petroleum Institute v. Costle, 665 F.2d at 1185).

Section 109(d)(1) requires that “[n]ot later than December 31, 1980, and at five-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 of the EPA’s Science Advisory 

Board.7

1.2.2 History of the Reviews of the Primary NAAQS for SOX

The initial air quality criteria for SOX were issued in 1969 (34 FR 1988, February 11, 

1969). Based on these criteria, the EPA, in initially promulgating NAAQS for SOX in 1971, 

established the indicator as SO2. The 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.

 7 Lists of the CASAC members and of members of the CASAC Sulfur Oxides Panel are available at: 

https://yosemite.epa.gov/sab/sabpeople.nsf/WebCommitteesSubcommittees/CASAC%20Sulfur%20Oxides%20P

anel
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The first review of the air quality criteria and standards for SOX was completed in several 

stages. In the first stage, the EPA released the Air Quality Criteria Document (AQCD) for PM 

and SOX in December 1981, and an addendum presenting information from subsequently 

available controlled human exposure studies in 1982 (U.S. EPA, 1982a, 1982b). The policy 

aspects of the air quality criteria, and preliminary exposure analyses were evaluated by OAQPS 

staff in the 1982 Staff Paper (U.S. EPA, 1982c). 

In 1986, the EPA published a second addendum to the 1982 AQCD, presenting newly 

available evidence from epidemiologic and controlled human exposure studies (U.S. EPA, 

1986a). Policy-relevant aspects of the new evidence and staff findings from a companion 

population exposure assessment were evaluated in a 1986 Addendum to the 1982 Staff Paper 

(U.S. EPA, 1986b, 1986c). The CASAC reviewed all of these documents and provided advice 

and recommendations with regard to decisions for the review of the standards. Based on the 

evidence in the 1982 and 1986 documents, staff evaluations and CASAC recommendations, in 

1988, the EPA proposed to retain the existing standards and solicited comment on the alternative 

of retaining the existing standards while additionally establishing a 1-hour standard of 0.4 ppm to 

protect against short-term exposures (53 FR 14926, April 26, 1988). In 1992, the American Lung 

association brought a lawsuit to compel the EPA to review and, if appropriate, revise the primary 

standards for SOX, and the remainder of the review was then completed under court order (59 FR 

58962, November 15, 1994; 61 FR 25566, May 22, 1996).

In 1994, the EPA prepared a supplement to the second addendum to the 1982 AQCD in 

response to publication of additional relevant controlled human studies on health effects of shortterm SO2 concentrations (1994 AQCD supplement [U.S. EPA, 1994a]). Policy-relevant aspects 

of the full body of evidence, including that newly available, along with the 1986 exposure 

analysis were evaluated in the 1994 Supplement to the 1982 Staff Paper (U.S. EPA, 1994b). Also 

in 1994, based on the available evidence, staff evaluations, CASAC advice, and public comment 

on the 1988 proposal, the EPA re-proposed to retain the existing standards and also solicited 

comment on retaining the existing standards in combination with one of three policy options to 

further reduce the health risk posed by exposure to high 5-minute peaks of SO2 if additional 

protection were judged to be necessary (59 FR 58958, November 15, 1994). The three 

alternatives were: (1) Revising the existing primary SO2 NAAQS by adding a new 5-minute 

standard of 0.60 ppm SO2, not to be exceeded more than once per calendar year; (2) establishing 

a new regulatory program under section 303 of the CAA to supplement protection provided by 

the existing NAAQS, with a trigger level of 0.60 ppm SO2, not to be exceeded more than once 

per calendar year; and (3) augmenting implementation of existing standards by focusing on those 

sources or source types likely to produce high 5-minute peak concentrations of SO2.
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This review was completed in 1996 with the EPA’s decision to retain without revision the 

existing standards (61 FR 25566, May 22, 1996). In reaching this decision, the Administrator

concluded, based on the staff exposure analysis, that exposure of individuals with asthma to SO2

levels that can reliably elicit adverse health effects was likely a rare event when viewed in the 

context of the entire population of people with asthma. As a result, the Administrator judged that 

5-minute peaks of SO2 did not pose a broad public health problem when viewed from a national 

perspective, and a 5-minute standard was not promulgated (61 FR 25566, May 22, 1996).

In 1996, the American Lung Association and the Environmental Defense Fund 

challenged the EPA’s decision not to establish a 5-minute standard. On January 30, 1998, the 

Court of Appeals for the District of Columbia (“D.C. Circuit”) found that the EPA had failed to 

adequately explain its determination that no revision to the SO2 NAAQS was appropriate and 

remanded the decision back to EPA for further explanation. Specifically, the court determined 

that the EPA had not provided adequate rationale to support the judgment that 5-minute peaks of 

SO2 do not pose a public health problem from a national perspective, given that the record for 

the rule indicated that these peaks would likely significantly affect a subset of individuals with 

asthma (American Lung Ass’n v. EPA, 134 F. 3d 388, 392-393 [D.C. Cir. 1998]). Following the 

remand, the EPA requested that states voluntarily submit 5-minute SO2 monitoring data for the

EPA to use to gain a better understanding of the magnitude and frequency of high, 5-minute peak 

SO2 concentrations. 

The next and most recent review of the air quality criteria and primary standards for SOX

was completed in 2010 (75 FR 35520, June 22, 2010; 74 FR 64810, December 8, 2009). The 

scientific evidence for this review was assessed in the 2008 ISA (U.S. EPA, 2008) and the 

exposure/risk analyses were presented in the 2009 REA (U.S. EPA, 2009). As a result of this 

review, the EPA promulgated a new 1-hour standard to provide the requisite protection for atrisk populations such as people with asthma against respiratory health effects related to shortterm SO2 exposures. The 1-hour standard was set with SO2 as the indicator based on its common 

occurrence in the atmosphere and the predominance of SO2 studies in the health effects 

information for SOX. The standard was set at a level of 75 parts per billion (ppb), based on the 3-

year average of the annual 99th percentile of 1-hour daily maximum SO2 concentrations. The 

EPA also revoked the then-existing 24-hour and annual primary standards based largely on the 

conclusion that the 1-hour standard would also control longer-term average concentrations, 

maintaining 24-hour and annual concentrations generally well below the levels of those 

standards, and on the lack of evidence indicating the need for such longer-term standards. The 

2010 action also addressed the remand by the D.C. Circuit in 1998. The 2010 and prior standards 

are summarized in Table 1-1.
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Table 1-1. History of the primary national ambient air quality standard(s) for sulfur 

oxides since 1971.

Final 

Rule/Decision Indicator Averaging Time Level Form

April 30, 1971

(36 FR 8186) SO2

24 hours 140 ppba one allowable exceedance per year

1 year 30 ppba arithmetic average

May 22, 1996

(61 FR 25566) Both the 24-hour and annual average standards retained without revision

June 22, 2010

(75 FR 35520) SO2

1 hour 75 ppb 99th percentile of yearly distribution of 1-hour 

daily maximums, averaged over 3 years

24-hour and annual standards revoked

a Although the levels were set in terms of ppm (0.14 ppm for the 24-hour standard and 0.03 ppm for the annual standard), 

they are shown here in ppb for consistency with units of current standard.

In conjunction with the 2010 revisions to the standards, the EPA revised the SO2 ambient 

air monitoring regulations to require that monitoring agencies using continuous SO2 methods 

report the highest 5-minute concentration for each hour of the day (along with the hourly 

average); many agencies additionally report all twelve 5-minute concentrations for each hour of 

the day (75 FR 35554, June 22, 2010; 40 CFR 58.16). The rationale for this requirement was to 

provide additional monitoring data for use in subsequent reviews of the primary standard, 

particularly in considering the extent of protection provided by the 1-hour standard against 5-

minute peak SO2 concentrations of concern (75 FR 35554, June 22, 2010).

After publication of the final rule, a number of industry groups and states filed petitions 

for review arguing (1) that the EPA failed to follow notice-and-comment rulemaking procedures

because the proposal did not indicate that EPA was considering changing its method of 

determining attainment from an air-monitoring approach to a hybrid approach using computer 

modeling in combination with air monitoring, and (2) that the decision to establish a 1-hour SO2

NAAQS at 75 ppb was arbitrary and capricious because it was lower than statutorily authorized. 

The D.C. Circuit rejected these challenges, dismissing the first argument for lack of jurisdiction 

and denying the petitions with respect to the second argument, explaining that the EPA did not 

act arbitrarily in setting the 2010 standard (National Environmental Developmental Association’s 

Clean Air Project v. EPA, 686 F. 3d 803[D.C. Cir. 2012]). Accordingly, the 2010 standard was 

upheld (Id.)

1.2.3 Current SO2 NAAQS Review

In May 2013, the EPA announced the initiation of the current periodic review of the air 

quality criteria for SOX and the primary NAAQS for sulfur oxides and issued a call for 
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information in the Federal Register (78 FR 27387, May 10, 2013). 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) 

participated in a workshop, held by the EPA on June 12-13, 2013 in Research Triangle Park, NC. 

The workshop provided for a public discussion of the key policy-relevant issues around which 

the EPA has structured the review and of the most meaningful new scientific information that 

would be available in this review to inform our understanding of these issues.

Building from the workshop discussions, the EPA developed the draft Integrated Review 

Plan for the Primary National Ambient Air Quality Standards for Sulfur Dioxide, External 

Review Draft (draft IRP, U.S. EPA, 2014b; 79 FR 14035, March 12, 2014) outlining the 

schedule, process, and key policy-relevant questions that would guide the evaluation of the air 

quality criteria for SO2 and the review of the primary NAAQS for SOX. The draft IRP was 

released in March 2014 (79 FR 14035, March 12, 2014) and was the subject of a consultation 

with the CASAC on April 22, 2014 (79 FR 16325, March 25, 2014). Comments received from 

the CASAC and the public were considered in the preparation of the final IRP, which was 

released in October 2014 (U.S. EPA, 2014a; 79 FR 66721, November 10, 2014).

The process for development of the first draft ISA included review of preliminary drafts 

of key ISA chapters by subject matter experts at a public workshop hosted by the EPA’s National 

Center for Environmental Assessment (NCEA) on June 23-24, 2014 (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 Integrated Science Assessment 

for Sulfur Oxides – Health Criteria (External Review Draft – November 2015, 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 Integrated Assessment for Sulfur Oxides – Health Criteria (Second 

External Review Draft – December 2016, U.S. EPA, 2016b) in December 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). The final ISA was 

released in December 2017 (U.S. EPA, 2017b; 82 FR 58600, December 13, 2017). 

As part of the planning process for development of the REA, the EPA completed the 

Review of the Primary National Ambient Air Quality Standard for Sulfur Oxides: Risk and 

Exposure Assessment Planning Document (REA Planning Document, U.S. EPA, 2017d) in

February 2017 (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). In consideration of CASAC 
1-9

comments at that consultation, as well as public comments, the EPA developed the draft REA 

(U.S. EPA, 2017e) and the draft PA (U.S. EPA 2017c), which were released on August 24, 2017 

(82 FR 43756, September 19, 2017). The draft REA and draft PA were reviewed by the CASAC

at a a public meeting on September 18-19, 2017 (82 FR 37213, August 9, 2017), with CASAC 

advice and comments provided in letters to the Administrator dated April 30, 2018 (Cox and 

Diez Roux, 2018a,b). Staff considered CASAC advice and public comments in completing these 

documents.

The schedule for completion of this review is governed by a consent decree, which, in 

relevant part, specifies signature on the notice setting forth the EPA’s proposed decision 

concerning its review of the primary NAAQS for SOX no later than May 25, 2018; and sign a 

notice setting forth EPA’s final decision concerning its review of the primary NAAQS for SOX

no later than January 28, 2019 (Consent Decree at 4, Center for Biological Diversity et al. v. 

Pruitt, Case No. 3:16-cv-03796-VC (N.D. Cal. April 28, 2017), Document No. 37 entered by the 

court on April 28, 2017).

1.3 GENERAL APPROACH AND ORGANIZATION OF THIS 

DOCUMENT

This PA draws on the policy-relevant aspects of the scientific evidence and quantitative 

air quality, exposure and risk analyses. With regard to the health effects evidence, we consider 

the nature of the key effects associated with SO2 in ambient air, the types and magnitudes of 

exposures associated with effects, and populations at greatest risk, as well as the uncertainties. 

Based on this information, we summarize associated potential public health impacts of SO2 in 

ambient air. We additionally consider the magnitude of exposures and risks estimated in the 

REA, along with the associated uncertainties. This evaluation supports staff conclusions with 

regard to the key policy-relevant questions for the review, including whether the currently 

available information appears to call into question the adequacy of public health protection 

afforded by the current standard.

Following this introductory chapter, chapter 2 focuses on current air quality, including 

sources of SO2 to ambient air, the ambient monitoring network for SO2, and trends and current 

conditions. Chapter 3 has three areas of focus. Section 3.1 focuses on the review of the primary 

NAAQS for SOX presenting background information on the rationale for previous reviews and 

the approach followed in the current review. Section 3.2 considers the evidence and exposure

and risk information for the current standard, as well as CASAC advice, and presents staff 

conclusions regarding these considerations in this review. Section 3.3 identifies key uncertainties 

and areas for future research.
1-10

REFERENCES

Cox, LA; Diez Roux, A. (2018a). Letter from Louis Anthony Cox, Chair, Clean Air Scientific 

Advisory Committee, and Ana Diez Roux, Immediate Past Chair, Clean Air Scientific 

Advisory Committee, to Administrator E. Scott Pruitt. Re: CASAC Review of the EPA’s 

Risk and Exposure Assessment for the Review of the Primary National Ambient Air 

Quality Standard for Sulfur Oxides (External Review Draft - August 2017). April 30, 

2018.

Cox, LA; Diez Roux, A. (2018b). Letter from Louis Anthony Cox, Chair, Clean Air Scientific 

Advisory Committee, and Ana Diez Roux, Immediate Past Chair, Clean Air Scientific 

Advisory Committee, to Administrator E. Scott Pruitt. Re: CASAC Review of the EPA’s 

Policy Assessment for the Review of the Primary National Ambient Air Quality Standard 

for Sulfur Oxides (External Review Draft - August 2017). April 30, 2018.

Diez Roux, A. (2016). Letter from Ana Diez Roux, Chair, Clean Air Scientific Advisory 

Committee, to Administrator Gina McCarthy. Re: CASAC Review of the EPA’s 

Integrated Science Assessment for Sulfur Oxides – Health Criteria (External Review 

Draft – November 2015). April 15, 2016.

U.S. EPA. (1982a). Air quality criteria for particulate matter and sulfur oxides (final, 1982). 

Environmental Criteria and Assessment Office, Washington, DC, EPA 600/8-82/029. 

Available at: https://www3.epa.gov/ttn/naaqs/standards/so2/s_so2_pr.html

U.S. EPA. (1982b). Air quality criteria for particulate matter and sulfur oxides, volume I 

addendum. Environmental Criteria and Assessment Office, Research Triangle Park, NC, 

EPA-600/8-82-029a. Available at: 

https://www3.epa.gov/ttn/naaqs/standards/so2/s_so2_pr.html

U.S. EPA. (1982c). Review of the National Ambient Air Quality Standards for Sulfur Oxides: 

Assessment of Scientific and Technical Information, OAQPS Staff Paper. Office of Air 

Quality Planning and Standards, Research Triangle Park, NC, EPA-450-5-82-007. 

Available at: https://www3.epa.gov/ttn/naaqs/standards/so2/s_so2_pr.html

U.S. EPA. (1986a). Air quality criteria for particulate matter and sulfur oxides (1982): 

assessment of newly available health effects information, 2nd addendum. Environmental 

Criteria and Assessment Office, Office of Health and Environmental Assessment, Office 

of Research and Development, Research Triangle Park, NC, EPA/600/8- 86/020F. 

Available at: https://www3.epa.gov/ttn/naaqs/standards/so2/s_so2_pr.html

U.S. EPA. (1986b). Review of the national ambient air quality standard for sulfur oxides: 

updated assessment of scientific and technical information. Addendum to the 1982 

OAQPS Staff Paper. Environmental Criteria and Assessment Office, Office of Health and 

Environmental Assessment, Office of Research and Development, Research Triangle 

Park, NC, EPA-452/05 86-013. Available at: 

https://www3.epa.gov/ttn/naaqs/standards/so2/s_so2_pr.html
1-11

U.S. EPA. (1986c). An Analysis of Short-Term Sulfur Dioxide Population Exposures in the 

Vicinity of Utility Power Plants. Office of Air Quality Planning and Standards, Research 

Triangle Park, NC. Available at: 

https://www3.epa.gov/ttn/naaqs/standards/so2/s_so2_pr.html

U.S. EPA. (1994a). Supplement to the second addendum (1986) to air quality criteria for 

particulate matter and sulfur oxides (1982): Assessment of new findings on sulfur dioxide 

acute exposure health effects in asthmatic individuals. Environmental Criteria and 

Assessment Office, Office of Health and Environmental Assessment, Office of Research 

and Development, Research Triangle Park, NC, EPA/600/FP-93/002, August 1994. 

Available at: https://www3.epa.gov/ttn/naaqs/standards/so2/s_so2_pr.html

U.S. EPA (1994b). Review of the national ambient air quality standards for sulfur oxides: 

assessment of scientific and technical information. Supplement to the 1986 OAQPS Staff 

Paper Addendum. Environmental Criteria and Assessment Office, Office of Health and 

Environmental Assessment, Office of Research and Development, Research Triangle 

Park, NC, EPA/600/FP-93/002, EPA-452/R-94-013. Available at: 

https://www3.epa.gov/ttn/naaqs/standards/so2/s_so2_pr.html

U.S. EPA. (2008). Integrated Science Assessment (ISA) for Sulfur Oxides – Health Criteria 

(Final Report). National Center for Environmental Assessment-RTP Division, Office of 

Research and Development, Research Triangle Park, NC, EPA-600/R-08/047F, 

September 2008. Available at: 

http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=198843

U.S. EPA. (2009). Risk and Exposure Assessment to Support the Review of the SO2 Primary 

National Ambient Air Quality Standard. Office of Air Quality Planning and Standards, 

Research Triangle Park, NC, EPA-452/R-09-007, July 2009. Available at: 

https://www3.epa.gov/ttn/naaqs/standards/so2/data/200908SO2REAFinalReport.pdf

U.S. EPA. (2014a). Integrated Review Plan for the Primary National Ambient Air Quality 

Standard for Sulfur Dioxide, Final. Office of Air Quality Planning and Standards, 

Research Triangle Park, NC, EPA-452/P-14-007, October 2014. Available at: 

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

U.S. EPA. (2014b). Integrated Review Plan for the Primary National Ambient Air Quality 

Standard for Sulfur Dioxide, External Review Draft. Office of Air Quality Planning and 

Standards, Research Triangle Park, NC, EPA-452/P-14-005, March 2014. Available at: 

https://www3.epa.gov/ttn/naaqs/standards/so2/data/20140318so2reviewplan.pdf

U.S. EPA. (2015). Integrated Science Assessment (ISA) for Sulfur Oxides – Health Criteria 

(External Review Draft, Nov 2015). National Center for Environmental Assessment-RTP 

Division, Office of Research and Development, Research Triangle Park, NC, 

EPA/600/R-15/066, November 2015. Available at: 

https://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=310044

U.S. EPA. (2016a). Integrated Review Plan for the Secondary National Ambient Air Quality 

Standards for Particulate Matter. Office of Air Quality Planning and Standards, Research 
1-12

Triangle Park, NC, EPA-452/R-16-005, December 2016. Available at: 

https://www.epa.gov/naaqs/particulate-matter-pm-standards-planning-documents-currentreview

U.S. EPA. (2016b). Integrated Science Assessment (ISA) for Sulfur Oxides – Health Criteria 

(Second External Review Draft). National Center for Environmental Assessment-RTP 

Division, Office of Research and Development, Research Triangle Park, NC, 

EPA/600/R-16/351, December 2016. Available at: 

https://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=326450

U.S. EPA. (2017a). Integrated Review Plan for the Secondary National Ambient Air Quality 

Standard for Ecological Effects of Oxides of Nitrogen, Oxides of Sulfur and Particulate 

Matter. Office of Air Quality Planning and Standards, Research Triangle Park, NC, EPA452/R-17-002, January 2017. Available at: https://www.epa.gov/naaqs/nitrogen-dioxideno2-and-sulfur-dioxide-so2-secondarystandards-planning-documents-current

U.S. EPA. (2017b). Integrated Science Assessment (ISA) for Sulfur Oxides – Health Criteria 

(Final). National Center for Environmental Assessment-RTP Division, Office of 

Research and Development, Research Triangle Park, NC, EPA/600/R-17/451, December 

2017. Available at: https://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=338596

U.S. EPA. (2017c). Policy Assessment for the Review of the Primary National Ambient Air 

Quality Standard for Sulfur Oxides, External Review Draft. Office of Air Quality 

Planning and Standards, Research Triangle Park, NC, EPA-452/P-17-003, August 2017. 

Available at: https://www.epa.gov/naaqs/sulfur-dioxide-so2-primary-air-qualitystandards

U.S. EPA. (2017d). Review of the Primary National Ambient Air Quality Standard for Sulfur 

Oxides: Risk and Exposure Assessment Planning Document. Office of Air Quality 

Planning and Standards, Research Triangle Park, NC, EPA-452/P-17-001, February 

2017. Available at: 

https://www3.epa.gov/ttn/naaqs/standards/so2/data/20170216so2rea.pdf

U.S. EPA. (2017e). Risk and Exposure Assessment for the Review of the Primary National 

Ambient Air Quality Standard for Sulfur Oxides, External Review Draft. Office of Air 

Quality Planning and Standards, Research Triangle Park, NC, EPA-452/P-17-002, 

August 2017. Available at: https://www.epa.gov/naaqs/sulfur-dioxide-so2-primary-airquality-standards

U.S. EPA. (2018). Risk and Exposure Assessment for the Review of the Primary National 

Ambient Air Quality Standard for Sulfur Oxides, Final. Office of Air Quality Planning 

and Standards, Research Triangle Park, NC, EPA-452/R-18-003, May 2018. Available at: 

https://www.epa.gov/naaqs/sulfur-dioxide-so2-primary-air-quality-standards
2-1

2 CURRENT AIR QUALITY

This chapter presents a summary of our current understanding of SOX in ambient air 

largely drawn from the more detailed discussion provided in the ISA (ISA, chapter 2). Section 

2.1 summarizes the current information on sources and emissions and section 2.2 summarizes 

current ambient air monitoring methods and networks. Recent concentrations of SO2 in ambient 

air are summarized in section 2.3.

2.1 SOURCES TO AMBIENT AIR

In this section, we describe the most recently available information on sources and 

emissions of SOX into the ambient air. The section does not provide a comprehensive list of all 

sources, nor does it provide estimates of emission rates or emission factors for all source 

categories. Rather, the discussion here is intended to identify the larger source categories, either 

on a national or local scale, and generally describe their emissions and distribution within the 

U.S. based on the U.S. EPA 2014 National Emissions Inventory (NEI).

Sulfur oxides are emitted into air from specific sources (e.g., fuel combustion processes) 

and 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 SO2 and sulfur trioxide (SO3) (ISA, section 2.3). As a result of rapid 

atmospheric chemical reactions involving SO3, the most prevalent sulfur oxide in the atmosphere 

is SO2 (ISA, section 2.3).

Fossil fuel combustion is the main anthropogenic source of SO2 emissions, while 

volcanoes and landscape fires (wildfires as well as controlled burns) are the main natural sources

(ISA, section 2.1).

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 SO2 in the atmosphere (ISA, section 2.1). Anthropogenic SO2 emissions originate 

primarily from point sources, including coal-fired electricity generating units (EGUs) and other 

industrial facilities (ISA, section 2.2.1). The largest SO2-emitting sector within the U.S. is 

 1 The 2008 ISA (U.S. EPA, 2008) described a modeling analysis that estimated SO2 concentrations for 2001 in the 

absence of any U.S. anthropogenic emissions of SO2 (2008 ISA, section 2.5.3). Such concentrations are referred 

to as United States background or USB. The 2008 ISA analysis estimated USB concentrations of SO2 to be below 

0.01 ppb over much of the U.S., ranging up to a maximum of 0.03 ppb. In the U.S. Northwest, geothermal 

sources (e.g., volcanoes) were estimated to be responsible for up to 80% of the ambient air concentrations 

resulting solely from natural sources and sources outside of the U.S. (ISA, section 2.5.5).
2-2

electricity generation, as shown in Figure 2-1, of which 97% of SO2 from electricity generation 

is from coal combustion. 

Figure 2-1. Percent contribution of SO2 emissions by sector (Source: 2014 NEI).

2

Other anthropogenic sources of SO2 emissions include industrial fuel combustion and 

process emissions, industrial processing, commercial marine activity, and fire used in landscape 

management and agriculture (ISA, section 2.2.1). While electricity generation is the dominant 

industry sector contributing to SO2 emissions on a national scale, other sectors can also have a 

significant influence on local air quality. Large emissions facilities other than EGUs that may 

substantially impact local air quality include copper smelters, kraft pulp mills, Portland Cement 

plants, iron and steel mill plants, sulfuric acid plants, petroleum refineries, and chemical 

processing plants (ISA, p. 2-5). For example, ambient air monitoring sites that have recorded 

some of the highest 1-hour daily maximum SO2 concentrations in the U.S. are located near 

copper smelters in Arizona (ISA, sections 2.5.2 and 2.5.4; Figure 2-11). The two smelters in this 

area had estimated annual emissions of approximately 17,000 and 5,000 tpy in the 2014 NEI 

(ISA, p. 2-50).

 2 Total SO2 emissions from the 2014 NEI were 4,942,063 tons.

Electricity Generaton, 

65.9

Industrial 

Processes, 12.3

Industrial Fuel 

Combustion, 11.2

Commercial Marine 

Vessels, 3.5

Fires (Wildfires, 

Prescribed, 

Agricultural), 3.0

Commercial and 

Residential Fuel 

Combustion, 2.9

Mobile Sources 

(except CMV), 1.2
2-3

Figure 2-2 illustrates the national emissions trends from 1990 to 2016. Declines in SO2

emissions are likely related to the implementation of national control programs developed under 

the Clean Air Act Amendments of 1990, including Phase I and II of the Acid Rain Program, the 

Clean Air Interstate Rule, and the Cross-State Air Pollution Rule. An additional factor is changes 

in market conditions, e.g., reduction in energy generation by coal (U.S. EIA, 2017).3 Declines 

between 1971, when SOX NAAQS were first established, and 1990, when the Amendments were 

adopted, were on the order of 5,000 tpy deriving primarily from reductions in emissions from the 

metals processing sector (ISA, Figure 2-5).

Figure 2-2. National SO2 emission trends by sector.

2.2 AMBIENT AIR MONITORING METHODS AND NETWORK

To promote uniform enforcement of the air quality standards set forth under the CAA, the 

EPA has established federal reference methods (FRMs) and federal equivalent methods (FEMs) 

for ambient air sample collection and analysis. Measurements for determinations of NAAQS 

compliance must be made with FRMs or FEMs. The current SO2 monitoring network relies on 

 3 The reduction in energy generation by coal resulted in the use of fuels that emit less SO2 in energy generation (U.S. 

EIA, 2016).
2-4

the automated pulsed ultraviolet fluorescence (UVF) FRM (40 CFR Appendix A-1 to Part 50; 40 

CFR Appendix A-2 to Part 50). The UVF method is a continuous automated method that 

quantifies SO2 concentrations, providing averages across desired time periods, such as 5-minute 

and 1-hour averages.

Measurements of SO2 concentrations in ambient air are collected by networks of FRM 

monitors, primarily operated by state and local monitoring agencies in the U.S. The main 

network providing ambient data for NAAQS surveillance monitoring purposes is the State and 

Local Air Monitoring Stations (SLAMS) network. In 2016, there were 363 SLAMS sites

reporting SO2 concentrations to the Air Quality System (AQS), the EPA’s repository for detailed 

air pollution data. For each SO2 monitoring site, the SLAMS monitoring agencies report hourly 

concentrations and either the maximum 5-minute concentration in the hour (one of twelve 5-

minute periods within an hour) or all twelve 5-minute average SO2 concentrations within the 

hour. 

Five minute SO2 data have become much more widely available due to regulatory 

requirements promulgated in 2010 (Figure 2-3).4 Although 5-minute concentration 

measurements were available for fewer than 10% of monitoring sites at the time of the last 

review, such data (either all 12 values in each hour or just the maximum 5-minute 

concentrations) are currently available for nearly all of the SO2 sites operating nationwide, 

providing a more robust foundation for characterization of 5-minute ambient air concentrations 

in this review. Further, the newly available monitoring data also include more monitors reporting 

the 12 consecutive 5-minute concentrations for each hour than were available in the last review

(Figure 2-3). Of the monitors reporting 5-minute data in 2016, almost 40% are reporting all 

twelve 5-minute SO2 measurements in each hour while about 60% are reporting the maximum 5-

minute SO2 concentration in each hour.5

 4 At SO2 NAAQS compliance monitoring sites, air monitoring agencies are now required to report, for every hour of 

the day, the hourly average and either the maximum 5-minute value (one of twelve 5-minute periods) in the hour 

or all twelve 5-minute averages within the hour (75 FR 35554, June 22, 2010).

5 In 2016, three sites reported both the continuous 5-minute data and the maximum 5-minute data separately. 

Therefore, these monitors are included in the count for each of the categories of 5-minute measurements.
2-5

Figure 2-3. Temporal trend in number of monitors reporting 5-minute 

concentrations.

2.3 AMBIENT AIR MONITORING CONCENTRATIONS

This section briefly summarizes trends in ambient air SO2 concentrations and current 

conditions based on recent ambient air monitoring data.

2.3.1 Trends

Ambient air concentrations of SO2 in the U.S. have declined substantially from 1980 to 

2016. Figure 2-4 illustrates this decline in terms of the distribution of 3-year averages of annual 

99th percentile daily maximum 1-hour concentrations6 at 24 monitoring sites that have been 

operating across this period. The average of this dataset has declined by more than 82% over the 

36-year period (the white line in Figures 2-4 and 2-5). Over the past 16 years, a larger dataset of 

193 sites operating from 2000-2016 also indicates a decline, which is on the order of 69% for the 

 6 The form of the current 1-hour SO2 NAAQS is the 99th percentile of the yearly distribution of 1-hour daily 

maximums, averaged over 3 years.
2-6

average of that dataset (Figure 2-5).7 Daily maximum 5-minute SO2 concentrations have also 

consistently declined over time from 2011 to 2016 (Figure 2-6).8

Figure 2-4. National temporal trend in SO2 concentrations: 1980-2016 (24 sites).

Three-year average of annual 99th percentile of daily maximum 1-hour 

concentrations. (Note: Dashed line indicates the current standard [75 ppb].)

 7 In Figures 2-4 and 2-5, the year on the x-axis represents the last year of the 3-year average (e.g., 2015 represents 

the average of 2013-2015). Additionally, the lower and upper bounds of the shaded area are the 10th and 90th

percentiles, respectively.

8 In Figure 2-6, the number of sites with monitors for 2011, 2012, 2013, 2014, 2015, and 2016 were 301, 321, 366, 

359, 352, and 366, respectively.
2-7

Figure 2-5. Temporal trend in SO2 concentrations: 2000-2016 (193 sites). Three-year 

average of annual 99th percentile of daily maximum 1-hour concentrations.

(Note: Dashed line indicates the current standard [75 ppb]).

Figure 2-6. Temporal trend in daily maximum 5-minute SO2 concentrations: 2011-

2016. (N = number of measurements)
2-8

2.3.2 Current Concentrations

2.3.2.1 Geographic Variation in Concentrations

Concentrations of SO2 vary across the U.S. and tend to be higher in areas with sources 

having relatively higher SO2 emissions (e.g., EGUs).9 Consistent with the locations of larger 

anthropogenic SO2 sources, higher concentrations are primarily located in the eastern half of the 

continental U.S., especially in the Ohio River valley, upper Midwest, and along the Atlantic 

coast (Figure 2-7). The point source nature of SO2 emissions contribute to the relatively high 

spatial variability of SO2 concentrations compared with pollutants such as ozone (O3) and PM 

(ISA, section 3.2.3). Another contributing factor to the spatial variability is the dispersion and 

oxidation of SO2 in the atmosphere, resulting in decreasing SO2 concentrations with increasing 

distance from the source. Sulfur oxides emitted from point sources tends to travel away from the

emissions source as a plume, which may or may not impact large portions of surrounding 

populated areas depending on meteorological conditions and terrain (ISA, section 3.2.3). 

 9 Volcano emissions contribute to the elevated concentrations observed on the island of Hawaii.
2-9

Figure 2-7. Concentrations of SO2 in terms of the current standard (3-year average of annual 99th percentile daily 

maximum 1-hour concentrations) at sites with datasets meeting completeness requirements for 2014-2016.
2-10

2.3.2.2 Seasonal and Diel Variability in Concentrations

Recent (2013-2015) data indicate that 1-hour daily maximum SO2 concentrations vary 

across seasons, with the greatest variations seen in the upper percentile concentrations (versus 

average or lower percentiles) for each season (ISA, section 2.5.3.2). This is seen in the data

presented for six areas in the draft ISA10 (ISA, section 2.5.3.2). This variation, along with 

month-to-month variations in 1-hour daily maximum SO2 concentrations also presented in the 

ISA, were generally consistent with month-to-month emissions patterns and the expected 

atmospheric chemistry of SO2 for a given season. For example, “summertime minima, observed 

in the New York City, NY and Houston, TX, sites may correspond to enhanced oxidation of SO2

to SO4

2- by photochemically derived atmospheric oxidants that are more prevalent during the 

humid summer (Khoder, 2002)” (ISA, p. 2-63). The differences in seasonal pattern (as well as 

magnitude) of concentrations among areas studied indicate the variability of SO2 concentrations 

across local and regional scales (ISA, section 2.5.3.2).

Consistent with the nationwide diel patterns reported in the last review, 1-hour average 

and 5-minute hourly maximum SO2 concentrations for 2013-2015 in the six areas evaluated in 

the ISA 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 areas evaluated were likely related to a combination of source emissions and 

meteorological parameters (ISA, section 2.5.3.3; U.S. EPA 2008, section 2.5.1). For example, 

SO2 emitted from elevated point sources (e.g., power plants and industrial sources) may be 

entrained into the mixed boundary layer, which expands during the day with rising surface 

temperatures (U.S. EPA 2008, section 2.5.1, Figures 2-23 and 2-24).

2.3.2.3 Relationship Between 1-hour and 5-minute Concentrations

Peak concentrations within a plume of SO2 downwind from, but relatively nearby to, a 

source can greatly exceed mean concentrations across the plume (ISA, section 2.5.4). Further, 

measured 5-minute concentrations at a particular location can be much higher than the average 

concentration at the same location for the associated hour. However, as emissions travel further 

downwind and experience ever increasing dispersion, these differences lessen both spatially and 

temporally. This can contribute to greater spatial and temporal variability in 5-minute than in 1-

hour concentrations, as is seen in the six locations evaluated in the ISA (second draft ISA, p. 2-

56). 

 10 The six locations evaluated are: Cleveland, OH, Pittsburgh, PA, New York City, NY, St. Louis, MO-IL, Houston, 

TX, and Gila County, AZ (ISA, section 2.5.2.2). These six locations were chosen for the ISA “focus area” 

analysis based on (1) their relevance to current health studies (i.e., areas with peer-reviewed, epidemiologic 

analysis), (2) the existence of four or more monitoring sites located within the area boundaries, and (3) the 

presence of several diverse SO2 sources within a given focus area boundary (ISA, section 2.5.2.2).
2-11

Using monitoring data from 2014-2016, Figure 2-8 illustrates the general pattern of lower 

5-minute concentrations with lower 1-hour concentrations. The left panel of Figure 2-8 shows 

that across the monitors meeting data completeness criteria, on days when the maximum 1-hour 

concentrations are relatively low, the daily maximum 5-minute concentrations are also relatively

low. Similarly, as shown in the right panel of Figure 2-8, at sites with relatively lower design 

values,11 the distribution of maximum 5-minute concentrations is also lower. This is documented

by the distinct reduction in 99th percentile daily maximum 5-minute concentrations at lower

design values. For example, in areas with design values at or below the current standard (75 

ppb), 99.9 percent of daily maximum 5-minute concentrations are at or below approximately 131

ppb.12 This contrasts with the much higher distribution of daily maximum 5-minute 

concentrations at sites with design values exceeding the current standard. The 99th percentile of 

these daily maximum 5-minute concentrations is 359 ppb, meaning that one percent of the days 

at these sites has a maximum 5-minute concentration above 359 ppb (i.e., 186 occurrences).

 11 The design value (DV) is a statistic that describes the air quality status of a given area relative to a particular

NAAQS. A design value summarizes the concentrations of a criteria pollutant in terms of the statistical form of 

the standard for that pollutant, thus indicating whether the area meets or exceeds the standard. Consistent with the 

form of the SO2 standard, SO2 design values are calculated as the 3-year average of the annual 99th percentile of 

the daily maximum 1-hour average concentrations (see 40 CFR 50.17). By regulation, design values calculated 

from monitoring data are considered to be valid if they meet specified completeness criteria, which for SO2 are 

data for at least 75 percent of the sampling days in all four quarters of all three years of the period (see Appendix 

T to Part 50).

12 Additional information related to data in Figure 2-8 is presented in Appendix B, Tables B-1 and B-2.
2-12

Figure 2-8. Distributions of daily maximum 5-minute concentrations during 2014-

2016. Left panel presents varying distributions with varying daily maximum 

1-hour concentrations. Right panel presents varying distributions with varying 

design values; the last bin (>75 ppb) presents data for sites not meeting the 

current standard. (Note: The values represented in the boxplots are the 25th

percentile, the median, and the 75th percentile. The asterisk represents the 99th

percentile.)

Analyses of the current monitoring dataset, expanded since the last review, provide 

information on the occurrence of daily maximum 5-minute concentrations of interest at monitors 

having differing design values. For example, analysis of these data for the years 2014 to 2016

indicates that among monitors with design values meeting the current standard (i.e., at or below 

75 ppb), the vast majority have zero days with a daily maximum 5-minute concentration above 

400 ppb or even 100 ppb (Appendix C). Among the few monitors with any days recording a 5-

minute concentration above 400 ppb, the maximum number of such days in a year was seven; for 

monitors with any days recording 5-minute concentrations above 200 ppb, the maximum number 

of such days/year was 32 (Appendix C, Figures C-2 and C-4, lower panel).
2-13

REFERENCES

Khoder, MI. (2002). Atmospheric conversion of sulfur dioxide to particulate sulfate and nitrogen 

dioxide to particulate nitrate and gaseous nitric acid in an urban area. Chemosphere 49: 

675-684. http://dx.doi.org/10.1016/S0045-6535(02)00391-0

U.S. EIA (U.S. Energy Information Administration). (2016). Electric Power Annual 2015. U.S. 

Department of Energy, Washington, DC, November 2016. Available at: 

https://www.eia.gov/electricity/annual/pdf/epa.pdf

U.S. EIA (U.S. Energy Information Administration). (2017). Monthly Energy Review July 2017. 

U.S. Department of Energy, Washington, DC, DOE/EIA-0035(2017-07), July 2017. 

Available at: https://www.eia.gov/totalenergy/data/monthly/pdf/mer.pdf

U.S. EPA. (2008). Integrated Science Assessment (ISA) for Sulfur Oxides – Health Criteria 

(Final Report). National Center for Environmental Assessment-RTP Division, Office of 

Research and Development, Research Triangle Park, NC, EPA-600/R-08/047F, 

September 2008. Available at: 

http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=198843

U.S. EPA. (2017). Integrated Science Assessment (ISA) for Sulfur Oxides – Health Criteria 

(Final). National Center for Environmental Assessment-RTP Division, Office of 

Research and Development, Research Triangle Park, NC, EPA/600/R-17/451, December 

2017. Available at: https://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=338596
3-1

3 REVIEW OF THE PRIMARY STANDARD FOR 

SULFUR OXIDES

This chapter evaluates the policy implications of the key scientific and technical 

information in the ISA and REA. This evaluation is based on consideration of the available body 

of evidence assessed in the ISA and of quantitative analyses of SO2 air quality, exposures and 

risks presented in the REA and in this document. Based on this information, the staff offer 

conclusions regarding each of the critical elements of the standard, including indicator, averaging 

time, form, and level. This final PA is also informed by the advice and recommendations 

received from the CASAC during its review of the draft PA, and by public comments received 

on the draft document. The final PA is designed to help the Administrator in considering the 

currently available scientific and risk information and formulating judgments regarding the 

adequacy of the current primary standard.

3.1 APPROACH

Staff’s approach in this review of the primary standard for SOX takes into consideration 

the approaches used in the previous review. The past and current approaches described below are 

both based, most fundamentally, on using the EPA’s assessment of the current scientific 

evidence and associated quantitative analyses to inform the Administrator’s judgment regarding 

a primary standard for SOX that is requisite to protect public health with an adequate margin of 

safety. In reaching conclusions on options for the Administrator’s consideration, we note that the 

final decision to retain or revise the current SO2 primary standard is a public health policy 

judgment to be made by the Administrator. 

The final decision by the Administrator will draw upon the available scientific evidence 

for SO2-attributable health effects, and on quantitative analyses of population exposures and 

health risks, including judgments about the appropriate weight to assign the various uncertainties 

inherent in the evidence and analyses. Therefore, in developing conclusions in this PA, we are 

mindful that the Administrator’s judgments on the standard will reflect an interpretation of the 

available scientific evidence and exposure/risk information in consideration of the strengths and 

limitations of that evidence and information. Our general approach to informing these judgments, 

discussed more fully below, recognizes that the available health effects evidence reflects a 

continuum from relatively higher SO2 concentrations, at which scientists generally agree that 

health effects are likely to occur, through lower concentrations at which the likelihood and 

magnitude of a response become increasingly uncertain. This approach is consistent with the 

requirements of sections 108 and 109 of the CAA, as well as with how the EPA and the courts 
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have historically interpreted the Act. These provisions require the Administrator to establish 

primary standards that in the Administrator’s 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 reduces risk sufficiently so 

as to protect public health with an adequate margin of safety.

1

Section 3.1.1 below summarizes the approach used in the last review of the primary 

NAAQS for SOX and section 3.1.2 summarizes the general approach for the current review.

3.1.1 Approach in the Previous Review

The last review of the primary NAAQS for SOX was completed in 2010 and resulted in

substantial revisions to the standards (75 FR 35520, June 22, 2010). In consideration of the 

evidence of respiratory effects in people with asthma in response to exposures as short as five 

minutes, the EPA established a new short-term standard to provide increased protection for this 

at-risk group and other potentially at-risk populations2against an array of adverse respiratory 

effects that have been linked to short-term SO2 exposures in both controlled human exposure and 

epidemiologic studies (75 FR 35525-35526, June 22, 2010; 2008 ISA, section 5.5). Specifically, 

the EPA replaced the then-existing 24-hour standard with a 1-hour standard of 75 ppb in terms of 

the 3-year average of the 99th percentile of the yearly distribution of 1-hour daily maximum SO2

concentrations. In addition to replacing the 24-hour standard with a new 1-hour standard, the 

EPA revoked the then-existing annual standard, based largely on the lack of sufficient health 

evidence to support a long-term standard and a recognition that a 1-hour standard set at 75 ppb 

would have the effect of generally maintaining annual SO2 concentrations well below the level of 

the revoked annual standard (75 FR 35550, June 22, 2010).

The emphasis on short-term exposures of people with asthma reflected the health effects 

evidence that has expanded in this area over the four decades since the then-existing 24-hour and 

annual standards were set in 1971 (2008 ISA; U.S. EPA, 1982, 1986, 1994). A key element of 

the expanded evidence base was a series of controlled human exposure studies which 

 

1 The four basic elements of the NAAQS (indicator, averaging time, level and form) are considered collectively in 

evaluating the health protection afforded by the current standard.

2 As used here and similarly throughout the document, the term population refers to persons having a quality or 

characteristic in common, such as a specific pre-existing illness or a specific age or lifestage. A lifestage refers to 

a distinguishable time frame in an individual’s life characterized by unique and relatively stable behavioral and/or 

physiological characteristics that are associated with development and growth. Identifying at-risk populations 

includes consideration of intrinsic (e.g., genetic or developmental aspects) or acquired (e.g., disease or smoking 

status) factors that increase the risk of health effects occurring with exposure to sulfur oxides as well as extrinsic, 

nonbiological factors, such as those related to socioeconomic status, reduced access to health care, or exposure.
3-3

documented bronchoconstriction-related effects on lung function in people with asthma exposed 

while breathing at elevated rates3for periods as short as five minutes. In the 2010 review, the 

EPA also conducted quantitative analyses of air quality data, including 5-minute ambient air 

measurements, and of potential exposures for people with asthma. Consideration of these key 

aspects of the evidence and quantitative analyses informed the decision in the 2010 review, 

which additionally addressed the court remand4to the EPA of the EPA’s 1996 decision to retain 

the 1971 standards without revision. 

The quantitative assessment for the review focused particularly on the issue of exposures 

to SO2 in ambient air for a duration as short as five minutes (2008 ISA; 2009 REA). The 

quantitative analyses documented in the REA included characterizations of the likelihood of 

people with asthma being exposed (while breathing at elevated rates, such as associated with 

many common outdoor activities) to concentrations of SO2 from ambient air of a magnitude 

documented to elicit decrements in lung function (2009 REA). These analyses were performed

both for air quality conditions associated with just meeting the then-existing standards and for 

conditions associated with just meeting potential alternative standards. The REA additionally 

included air quality analyses that explored the extent to which potential alternative standards 

with 1-hour, 24-hour, and annual averaging times might be expected to control 5-minute ambient 

air concentrations (2009 REA, section 7.3). The quantitative assessments together with the health 

effects evidence informed the policy options considered by the Administrator. Considerations, 

conclusions and judgments by the Administrator that provided the basis for her decisions in the 

2010 review are summarized below. 

3.1.1.1 Considering the Need for Revision

The conclusions reached by the Administrator in the last review were based on the 

extensive body of scientific evidence on SO2-related health effects and quantitative analyses of 

air quality, exposure and risk. In her conclusion on the adequacy of the then-existing standards, 

which were set in 1971, the Administrator emphasized the evidence and quantitative analyses 

concerning 5-minute exposures. The Administrator gave particular attention to the robust 

evidence base, comprised of findings from controlled human exposure, epidemiologic, and 

animal toxicological studies that collectively were judged “sufficient to infer a causal 

 

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

Register notices in the last review to refer to activity levels that in adults would be associated with ventilation 

rates at or above 40 liters per minute; an equivalent ventilation rate was derived in order to identify corresponding 

rates for the range of ages and sizes of the simulated populations (2009 REA, section 4.1.4.4). Accordingly, these 

phrases are used in this draft PA when referring to the REA from the last review. Otherwise, however, the REA 

and PA for this review generally use the phrase “elevated breathing rates” to refer to the same occurrence.

4 See Am. Lung Ass’n v. EPA, 134 F.3d 388 (D.C. Cir. 1998) (remanding the 1996 decision to EPA).
3-4

relationship” between short-term SO2 exposures ranging from 5 minutes to 24 hours and 

respiratory morbidity (75 FR 35535, June 22, 2010). The “definitive evidence” for this 

conclusion came from studies of 5- to 10-minute controlled exposures that reported respiratory 

symptoms and decreased lung function in exercising individuals with asthma (2008 ISA, section 

5.2). Supporting evidence was provided by epidemiologic studies of a broader range of 

respiratory outcomes, with uncertainty noted about the magnitude of the study effect estimates, 

quantification of the exposure concentration-response relationship, potential confounding by copollutants, and other areas (75 FR 35535-35536, June 22, 2010; 2008 ISA, section 5.3).

In the controlled human exposure studies of exercising individuals with asthma, a doseresponse relationship was documented for bronchoconstriction-related effects, with both the 

percentage of individuals affected and the severity of the response increasing with increasing 

SO2 concentrations (75 FR 35525, June 22, 2010). The evidence from these studies documents 

the occurrence of SO2-related decrements in lung function based on reductions in forced 

expiratory volume in one second (FEV1) and increases in specific resistance of the airways 

(sRaw). Moderate5or greater decrements in lung function were reported in response to short (5-

to 10-minute) exposures to concentrations as low as 200 to 300 ppb in approximately 5-30% of 

exercising individuals with asthma. In response to exposures at or above 400 ppb, approximately 

20-60% experienced such decrements, frequently accompanied by respiratory symptoms; in 

many studies, responses at these concentrations were often statistically significant at the group 

mean level6(75 FR 35525-35526, June 22, 2010).

In reaching conclusions regarding the significance of the reported responses to the 5- to 

10-minute controlled exposures, the Administrator considered guidelines from the American 

Thoracic Society (ATS), the CASAC’s written advice and recommendations, and judgments 

made by the EPA in considering similar effects in previous NAAQS reviews (75 FR 35526 and 

35536, June 22, 2010). Based on these considerations, the Administrator judged that the effects 

reported in exercising people with asthma following 5- to 10-minute SO2 exposures at or above

 

5

In assessments for NAAQS reviews, the lung function responses described as indicative of a moderate functional 

response include increases in 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 FEV1 of 10 to 20% (e.g., U.S. EPA, 

1996, Table 8). For the 2008 ISA, the midpoint of that range (15%) was used to indicate a moderate response. A 

focus on 15% reduction in FEV1 is also consistent with the relationship observed between sRaw and FEV1

responses in the Linn et al. studies for which “a 100% increase in sRaw roughly corresponds to a 12 to 15% 

decrease in FEV1” (U.S. EPA, 1994, p. 20). Thus, in the 2008 review, moderate or greater SO2-related 

bronchoconstriction or decrements in lung function referred to the occurrence of at least a doubling in sRaw or at 

least a 15% reduction in FEV1 (2008 ISA, p. 3-5).

6 At concentrations of 400 to 500 ppb, the 2008 ISA notes that the evidence shows “stronger evidence with some 

statistically significant increases in respiratory symptoms,” and at 600 ppb to 1 ppm, the 2008 ISA notes the 

evidence to show “clear and consistent increases in SO2 induced respiratory symptoms” (2008 ISA, Table 3-1). 
3-5

200 ppb, especially at or above 400 ppb, can result in adverse health effects (75 FR 35536, June 

22, 2010).7In so doing, she recognized that effects reported for exposures below 400 ppb are 

appreciably less severe than those at and above 400 ppb (75 FR 35547, June 22, 2010).

In applying the health effects evidence to her consideration of the adequacy of the thenexisting standards, the Administrator gave particular attention to the quantitative analyses that 

evaluated the potential for exercising individuals with asthma to experience exposures of a 

magnitude associated with adverse effects under air quality conditions that just met the thenexisting standards. In addition to comparison of 5-minute air concentrations in 40 U.S. counties 

to 5-minute concentrations of potential concern (benchmark concentrations ranging from 100-

400 ppb), the analyses included a population exposure-based assessment in two study areas, St. 

Louis, MO and Greene County, MO. Five-minute exposure concentrations were estimated for 

people with asthma while breathing at elevated rates. The 5-minute exposure concentrations 

were compared to benchmark concentrations, and also used to estimate the risk of lung function 

decrements in simulated at-risk populations. Among these analyses, the Administrator 

emphasized those that utilized the 5-minute benchmark concentrations that were derived from 

the controlled human exposure evidence and ranged from 100 ppb to 400 ppb. Based on her 

judgments regarding the significance of effects associated with 5-minute concentrations at or 

above 200 ppb and 400 ppb, the Administrator considered results of comparisons of exposure 

estimates to those benchmark concentrations to be particularly important, giving greater 

emphasis to those at or above 400 ppb (75 FR 35547, June 22, 2010). 

The exposure-based assessment estimated the portion of the population with asthma in 

these two areas that would be expected to experience 5-minute exposures at or above 400 ppb 

and 200 ppb while engaged in activities causing them to be breathing at elevated rates. The 

Administrator particularly noted the exposure analysis results for the St. Louis case study. This 

analysis estimated that for air quality simulated to just meet the then-existing standards, 

substantial percentages of children with asthma would be exposed at least once annually, while 

engaged in activities associated with moderate or greater exertion,

8

to air quality exceeding the 

200 ppb and 400 ppb 5-minute benchmarks (75 FR 35536, June 22, 2010). The Administrator 

judged these 5-minute exposures to be significant from a public health perspective due to their 

 

7 The 2010 decision notice additionally stated that “[t]he Administrator notes that although these decrements in lung 

function have not been shown to be statistically significant at the group mean level, or to be frequently 

accompanied by respiratory symptoms, she considers effects associated with exposures as low as 200 ppb to be 

adverse in light of CASAC advice, similar conclusions in prior NAAQS reviews, and the ATS guidelines” (75 FR 

35546, June 22, 2010).

8

In the 2009 REA, an equivalent ventilation rate of 22 L/min-m2 was identified as the minimum value to reflect 

“moderate” or greater exertion that would correspond to the elevated ventilation rate for the exercising subjects in 

the controlled human exposure studies, which was 40-50 L/min (2009 REA, p. 236).
3-6

estimated frequency: approximately 24% of children with asthma in St. Louis were estimated to 

be exposed while at moderate or greater exertion at least once per year to air quality exceeding 

the 5-minute 400 ppb benchmark. Additionally, approximately 73% of children with asthma in 

St. Louis at moderate or greater exertion were estimated to be exposed at least once per year to 

air quality exceeding the 5-minute 200 ppb benchmark (75 FR 35536, June 22, 2010).

The Administrator also took note of the CASAC conclusion that the then-existing 

standards did not adequately protect public health. Specifically, the CASAC advised that: “the 

current 24-hour and annual standards are not adequate to protect public health, especially in 

relation to short-term exposures to SO2 (5-10 minutes) by exercising asthmatics” (Samet, 2009, 

p. 15). Based on all of the considerations summarized above, the Administrator concluded that 

the then-existing 24-hour and annual primary standards were not providing the requisite 

protection of public health with an adequate margin of safety. In considering approaches to 

revising the standards, the Administrator concluded it to be appropriate to set a new standard that 

would provide requisite protection with an adequate margin of safety to people with asthma at 

elevated ventilation and that would afford protection from the adverse health effects of 5-minute 

to 24-hour SO2 exposures (75 FR 35536, June 22, 2010).

3.1.1.2 Approach for Considering Revisions to the Standards

With regard to revisions to provide requisite public health protection, the Administrator 

concluded it was appropriate to set a 1-hour SO2 standard at a level of 75 ppb based on the 3-

year average of the 99th percentile of the yearly distribution of 1-hour daily maximum 

concentrations. The rationale and approach for selecting the 1-hour standard is presented below 

in terms of the individual elements of a NAAQS: indicator, averaging time, form, and level. 

3.1.1.2.1 Indicator

In reaching her decision on the indicator for the new standard, the Administrator

considered the conclusions of the ISA and REA, as well as advice from the CASAC and public 

comments (75 FR 35536, June 22, 2010). The EPA continued to focus on SO2 as the most 

appropriate indicator for sulfur oxides because the available scientific information regarding 

health effects was overwhelmingly indexed by SO2. Although the presence of SOX species other 

than SO2 in ambient air had been recognized, no alternative to SO2 had been advanced as a more 

appropriate surrogate for SOX (75 FR 35536, June 22, 2010). Controlled human exposure studies 

and animal toxicological studies provided specific evidence for health effects following 

exposures to SO2, and epidemiologic studies typically analyzed associations of health outcomes

with concentrations of SO2. Based on the information available in the last review and consistent 

with the views of the CASAC that “for indicator, SO2 is clearly the preferred choice” (Samet,

2009, p. 14), the Administrator concluded it was appropriate to continue to use SO2 as the 
3-7

indicator for a standard that was intended to address effects associated with exposure to SO2, 

alone or in combination with other sulfur oxides (75 FR 35536, June 22, 2010). In so doing, the 

EPA recognized that measures leading to reductions in population exposures to SO2 will also 

likely reduce exposures to other sulfur oxides (75 FR 35536, June 22, 2010).

3.1.1.2.2 Averaging Time

With regard to the setting of the new standard, the Administrator agreed with the staff 

conclusion, based on conclusions in the ISA, advice from the CASAC, and quantitative analyses, 

that the standard should be set to provide protection from short-term exposures of 5 minutes to 

24 hours (75 FR 35539, June 22, 2010). Based on air quality analyses presented in the REA, the 

Administrator judged that the requisite protection from 5- to 10-minute exposure events could be 

provided without having a standard with a 5-minute averaging time (75 FR 35539, June 22, 

2010). She 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).9 Accordingly, 

she considered other averaging times.

Results of air quality analyses in the REA suggested that a standard based on 24-hour 

average SO2 concentrations would not likely be an effective or efficient approach for addressing 

5-minute peak SO2 concentrations, likely over-controlling in some areas, while under-controlling 

in others (2009 REA, section 10.5.2.2). In contrast, these analyses suggested that a 1-hour 

averaging time would be more efficient and effective at limiting 5-minute peaks of SO2 (2009 

REA, section 10.5.2.2.). Drawing on this information, the Administrator concluded that a 1-hour 

standard, with the appropriate form and level, would be likely to substantially reduce 5- to 10-

minute peaks of SO2 that had been shown in controlled human exposure studies to result in 

increased prevalence of respiratory symptoms and/or decrements in lung function in exercising 

people with asthma (75 FR 35539, June 22, 2010). Further she found that a 1-hour standard 

could substantially reduce the upper end of the distribution of SO2 concentrations in ambient air 

that were more likely to be associated with respiratory outcomes (75 FR 35539, June 22, 2010). 

The Administrator additionally took note of advice from the CASAC. The CASAC stated 

that the REA had presented a “convincing rationale” for a 1-hour standard, and that “a one-hour 

standard is the preferred averaging time” (Samet, 2009, pp. 15, 16). The CASAC further stated 

that it was “in agreement with having a short-term standard and finds that the REA supports a 

one-hour standard as protective of public health” (Samet, 2009, p. 1). Thus, in consideration of 

the available information summarized here and the CASAC’s advice, the Administrator 

concluded that a 1-hour standard (given the appropriate level and form) was an appropriate 

 

9 Such instability could reduce public health protection by disrupting an area’s ongoing implementation plans and 

associated control programs (75 FR 35537, June 22, 2010). 
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means of controlling short-term exposures to SO2 ranging from 5 minutes to 24 hours (75 FR 

35539, June 22, 2010).

3.1.1.2.3 Form

In considering the statistical form for the new short-term standard, the Administrator 

judged that the form of the standard should reflect the health effects evidence presented in the 

ISA that indicated that the percentage of people with asthma affected and the severity of the 

response increased with increasing SO2 concentrations (75 FR 35541, June 22, 2010). She 

additionally found it reasonable to consider stability (e.g., to avoid disruption of programs 

implementing the standard and the related public health protections from those programs) as part 

of her consideration of the form for the standard (75 FR 35541, June 22, 2010). In so doing, she 

noted that a concentration-based form averaged over three years would likely be appreciably 

more stable than a no-exceedance based form, which had been the form of the then-existing 24-

hour standard (75 FR 35541, June 22, 2010). The CASAC additionally stated that “[t]here is 

adequate information to justify the use of a concentration-based form averaged over 3 years” 

(Samet, 2009, p. 16). In consideration of this information, the Administrator judged a 

concentration-based form averaged over three years to be most appropriate (75 FR 35541, June 

22, 2010). 

In selecting a specific concentration-based form, the Administrator considered health 

evidence from the ISA as well as air quality and exposure information from the REA. In so 

doing, the Administrator concluded that the form of a new 1-hour standard should be especially 

focused on limiting the upper end of the distribution of ambient SO2 concentrations (i.e., above 

90th percentile SO2 concentrations) in order to provide protection with an adequate margin of 

safety against effects reported in epidemiologic and controlled human exposure studies (75 FR 

35541, June 22, 2010). The Administrator further noted, based on results of air quality and 

exposure analyses in the REA, that a 99th percentile form was likely to be appreciably more 

effective at limiting 5-minute peak exposures of concern than a 98th percentile form (75 FR 

35541, June 22, 2010). Thus, the Administrator selected a 99th percentile form averaged over 

three years (75 FR 35541, June 22, 2010).

3.1.1.2.4 Level

In selecting the level of a new 1-hour standard, the Administrator gave primary emphasis 

to the body of health effects evidence assessed in the ISA. In so doing, she noted that the 

controlled human exposure studies provided the most direct evidence of respiratory effects from 

exposure to SO2. The Administrator drew on evidence from these studies in reaching judgments 

on the magnitude of adverse respiratory effects and associated potential public health 
3-9

significance for the air quality exposure and risk analysis results of air quality scenarios 

representing just meeting alternative levels for a new 1-hour standard.

In particular, the Administrator considered effects in exercising people with asthma after 

5- to 10-minute exposures as low as 200 ppb to be adverse in light of the CASAC advice on 

relevance of these effects, conclusions on similar effects in prior NAAQS reviews, and ATS 

guidelines (75 FR 35546, June 22, 2010; ATS, 1985, 2000). This judgment was based on several 

findings from the controlled human exposures studies. Five- to 10-minute exposures to 400 ppb 

or greater resulted in moderate or greater decrements in lung function in 20-60% of exercising 

individuals with asthma. These decrements are often statistically significant at the group mean 

level and frequently accompanied by respiratory symptoms. Thus, exposures to SO2

concentrations at or above 400 ppb were concluded to clearly result in adverse respiratory effects 

based on the ATS guidelines (ATS, 1985). Further, 5- to 10-minute exposures to 200 to 300 ppb 

resulted in moderate or greater decrements in lung function in 5-30% of exercising individuals 

with asthma (75 FR 35546, June 22, 2010). Although such effects have not been shown to be 

statistically significant at the full study group mean level,10 or to be frequently accompanied by 

respiratory symptoms, the Administrator considered effects associated with exposures as low as 

200 ppb to be adverse in light of the CASAC’s advice11 and similar conclusions in prior reviews 

as well as the ATS guidelines (ATS, 1985, 2000). 

The Administrator then considered what the findings of the REA exposure analyses 

indicated with regard to varying degrees of protection that different 1-hour standard levels might 

be expected to provide against 5-minute exposures to concentrations of 200 ppb and 400 ppb.12

For example, the exposure assessment for St. Louis13 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 

 

10 As summarized in section 3.2.1.1 below and described more fully in the ISA for the current review, study subjects 

have since been described as falling into two subpopulations that differ in susceptibility to SO2. Thus, the extent 

to which the more susceptible subpopulation is represented among the full study group may influence study mean 

responses.

11 The CASAC letter on the first draft SO2 REA to the Administrator stated: “CASAC believes strongly that the 

weight of clinical and epidemiology evidence indicates there are detectable clinically relevant health effects in 

sensitive subpopulations down to a level at least as low as 0.2 ppm SO2” (Henderson, 2008).

12 The Administrator additionally noted the results of the 40-county analysis of limited available 5-minute 

concentration data that indicated for a 1-hour standard level of 100 ppb a maximum annual average of two days 

per year with 5-minute concentrations above 400 ppb and 13 days with 5-minute concentrations above 200 ppb

(76 FR 35546, June 22, 2010).

13 St. Louis was one of two study areas assessed in the REA (2009 REA).
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exertion (75 FR 35547, June 22, 2010). Results for the air quality scenario for a 1-hour standard 

level of 50 ppb suggested that such a standard would somewhat 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 35542-47, June 22, 2010). 

In considering the implications of the exposure assessment results the Administrator 

noted that although she considered the health effects resulting from 5-minute SO2 exposures as 

low as 200 ppb to be adverse, she also recognized that such effects are appreciably less severe 

than those at SO2 concentrations at or above 400 ppb and found little difference between the 

results for standard levels of 50 and 100 ppb with regard to 5-minute exposures at or above 400 

ppb (75 FR 35547, June 22, 2010). She recognized that a standard level below 100 ppb may 

somewhat further limit 5-minute SO2 ambient air concentrations and exposures above 200 ppb, 

although she did not judge that a standard level of 50 ppb was warranted. 

Before reaching her conclusion with regard to level for the 1-hour standard, the 

Administrator additionally considered the epidemiological evidence among the U.S. 

epidemiologic studies (some conducted in multiple locations) reporting mostly positive and 

sometimes statistically significant associations between ambient SO2 concentrations and 

emergency department visits and hospital admissions. She noted there was a cluster of three 

studies for which 99th percentile 1-hour daily maximum concentrations were estimated to be 

between 78 and 150 ppb and for which the SO2 effect estimate remained positive and statistically 

significant in copollutant models with particulate matter (PM) (75 FR 35547, June 22, 2010).14

Given the above considerations and the comments received on the proposal, the 

Administrator determined that the appropriate judgment, based on the entire body of evidence 

and information available in this review, and the related uncertainties,15 was a standard level of 

75 ppb. She concluded that such a standard, with a 1-hour averaging time and 99th percentile 

form, would provide a significant increase in public health protection compared to the thenexisting standards and would be expected to provide protection, with an adequate margin of 

safety, against the respiratory effects that have been linked with SO2 exposures in both controlled 

human exposure and epidemiologic studies. Specifically, she concluded that such a standard 

would limit 1-hour exposures at and above 75 ppb. (75 FR 35548, June 22, 2010). Such a 

 

14 Regarding the monitor concentrations in these studies, the EPA noted that although they may be a reasonable 

approximation of concentrations occurring in the areas, the monitored concentrations were likely somewhat lower 

than the absolute highest 99th percentile 1-hour daily maximum SO2 concentrations occurring across these areas 

(75 FR 35547, June 22, 2010). 

15 Such uncertainties included both those with regard to the epidemiologic evidence and also those with regard to the 

information from controlled human exposure studies for at-risk groups, including representation of individuals 

with more severe asthma than that in study subjects (75 FR 35546, June 22, 2010).
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standard was also considered likely “to maintain SO2 concentrations below those in locations 

where key U.S. epidemiologic studies have reported that ambient SO2 is associated with clearly 

adverse respiratory health effects, as indicated by increased hospital admissions and emergency 

department visits.” The Administrator also found that “a 1-hour standard at a level of 75 ppb is 

expected to substantially limit asthmatics’ exposure to 5–10 minute SO2 concentrations ≥ 200 

ppb, thereby substantially limiting the adverse health effects associated with such exposures.” 

Lastly, the Administrator noted “that a standard level of 75 ppb is consistent with the consensus 

recommendation of CASAC.” The Administrator also considered the likelihood of public health 

benefits at lower standard levels, and judged a 1-hour standard at 75 ppb to be sufficient to 

protect public health with an adequate margin of safety (75 FR 35547-35548, June 22, 2010). 

This judgment included consideration of the appropriate degree of protection with an 

adequate margin of safety for populations at increased risk for adverse respiratory effects from 

short-term exposures to SO2 for which the evidence supports a causal relationship with SO2

exposures. In reaching these conclusions, the Administrator considered the requirement for a 

standard that is neither more nor less stringent than necessary for this purpose and recognized 

that the CAA does not require that primary NAAQS be set at a zero-risk level or to protect the 

most susceptible individual, but rather at a level that reduces risk sufficiently so as to protect 

public health with an adequate margin of safety (75 FR 35548, June 22, 2010).

3.1.1.2.5 Revoking the Then-Existing 24-Hour and Annual Standards

In addition to setting a new 1-hour standard at 75 ppb, the then-existing 24-hour and 

annual standards were revoked based largely on the recognition that a 1-hour standard set at 75 

ppb would have the effect of generally maintaining 24-hour and annual SO2 concentrations well 

below the levels of those standards (75 FR 35550, June 22, 2010). In addition, with regard to the 

annual standard, there was a lack of evidence supporting a relationship between long-term SO2

exposures and adverse health effects. That is, the 2008 ISA judged the health evidence linking 

long-term SO2 exposure to adverse health effects to be “inadequate” to infer the presence or 

absence of a causal relationship (75 FR 35550, June 22, 2010; 2008 ISA, section 5.5).

3.1.2 Approach for the Current Review

For evaluation in the current review of whether it is appropriate to consider retaining the 

current SO2 primary standard, or whether consideration of revision is appropriate, we have 

adopted an approach that builds on the general approach used in the last review and reflects the 

body of evidence and information now available. As summarized above, the Administrator’s 

decisions in the prior review were based on an integration of information on health effects 

associated with exposure to SO2, expert judgments on the adversity and public health 

significance of key health effects, air quality and related analyses and quantitative exposure and 
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risk assessments, and policy judgments as to when the standard is requisite to protect public

health with an adequate margin of safety.

In conducting this assessment, we draw on the current evidence and quantitative 

assessments of exposure pertaining to the public health risk of SO2 in ambient air. In considering 

the scientific and technical information, we consider both the information available at the time of 

the last review and information newly available since the last review, including the ISA and REA

for this review. Figure 3-1 below illustrates the basic construct of our two-part approach in 

developing conclusions regarding options to consider with regard to the adequacy of the current 

primary standard. In the boxes of Figure 3-1, the range of questions that we consider in sections 

3.2.1 and 3.2.2 below are represented by a summary of policy-relevant questions that frame our 

consideration of the scientific evidence and quantitative analyses.
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Figure 3-1. Overview of the approach for review of the current primary standard.
3-14

3.2 ADEQUACY OF THE CURRENT STANDARD

In considering the adequacy of the current SO2 primary standard, the overarching 

question we consider is:

• Does the currently available scientific evidence- and exposure/risk-based 

information, as reflected in the ISA and REA, support or call into question the 

adequacy of the protection afforded by the current SO2 primary standard?

To assist us in interpreting the currently available scientific evidence and the results of 

recent quantitative exposure/risk analyses to address this question, we have focused on a series 

of more specific questions, as detailed in sections 3.2.1 and 3.2.2 below. 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 which have been critically 

analyzed and characterized in the 2008 ISA for the last review and the ISA for the current

review. In so doing, a primary consideration is whether the information newly available in this 

review alters our overall conclusions from the last review regarding health effects associated 

with SOX in ambient air.

3.2.1 Evidence-based Considerations

In considering the evidence with regard to the overarching question posed above 

regarding the adequacy of the current standard, we address a series of more specific questions 

that focus on policy-relevant aspects of the evidence. These questions begin with consideration 

of the available evidence on health effects associated with exposure to SOX, and particularly SO2

(section 3.2.1.1). The subsequent questions consider identification of populations at-risk of SO2-

related health effects (section 3.2.1.2), and the exposure durations and levels of SO2 associated 

with health effects (section 3.2.1.3). Important uncertainties associated with the evidence are 

considered in section 3.2.1.4 and public health implications are discussed in section 3.2.1.5. 

3.2.1.1 Health Effects Associated with Exposure to SOX

Among the species of SOX (a group of closely related gaseous compounds including SO2

and SO3), SO2 is the most commonly occurring in the atmosphere and the one most clearly 

associated with human health effects. Accordingly, the large body of scientific evidence has over 

the past reviews been predominantly focused on exposures to SO2. 

• Is there newly available evidence that indicates the importance of SOX other than 

SO2 with regard to abundance in ambient air, and potential for human exposures 

and health effects? 

As in the last review, the health effects evidence evaluated in the ISA for SOX is focused 

on SO2 (ISA, p. 5-1). This is consistent with the conclusion that “[o]f the sulfur oxides, SO2 is 

the most abundant in the atmosphere, the most important in atmospheric chemistry, and the one 
3-15

most clearly linked to human health effects” (ISA, p. 2-1). With regard to SO3, it “is known to be 

present in the emissions of coal-fired power plants, factories, and refineries, but it reacts with 

water vapor in the stacks or immediately after release into the atmosphere to form H2SO4” and 

“gas-phase H2SO4...quickly condenses onto existing atmospheric particles or participates in new

particle formation” (ISA, section 2.3). Thus, the ISA states that “only SO2 is present at 

concentrations in the gas phase that are relevant for chemistry in the atmospheric boundary layer 

and troposphere, and for human exposures” (ISA, p. 2-18), and also that the available health 

evidence for SOX is focused on SO2 (ISA, p. 5-1). Thus, we conclude that the current evidence, 

including that newly available in this review, continues to support a focus on SO2 in considering 

the adequacy of public health protection provided by the primary NAAQS for SOX.

• Does the current evidence alter our conclusions from the previous review regarding 

the health effects associated with exposure to SO2?

Rather than altering our conclusions from the last review, the current evidence continues 

to support our prior conclusions regarding the key health effects associated with SO2 exposure. 

Specifically, the full body of evidence continues to support the conclusion that short-term SO2

exposures of durations as short as a few minutes are causally related to respiratory effects in atrisk individuals (ISA, section 5.2.1.9). With regard to respiratory effects and long-term 

exposures,16 as well as total mortality and short-term exposures, the evidence available in this 

review is “suggestive of, but not sufficient to infer,” a causal relationship (ISA, sections 5.2.2.7 

and 5.5.1.6). The evidence is inadequate for reaching conclusions regarding causality for other 

categories of effects (ISA, section 1.6.2).17

Respiratory Effects

As in the last review, the currently available evidence in this review supports the 

conclusion that there is a causal relationship between short-term SO2 exposure and respiratory 

effects, particularly in individuals with asthma (ISA, p. l-17).18 The clearest evidence for this 

conclusion comes from controlled human exposure studies available at the time of the previous 

 

16 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).

17 Based on the currently available evidence, the ISA concluded that the evidence was inadequate to infer the 

presence or absence of a causal relationship between SO2 exposures and reproductive and developmental effects; 

between long-term SO2 exposures and mortality or cancer; and, between short- or long-term SO2 exposures and 

cardiovascular effects (ISA, section 1.6.2).

18 While effects have been documented for short (5- to 10- minute) exposures lower than 1.0 ppm in controlled 

exposure studies of individuals with asthma, the exposure concentrations consistently eliciting effects in study 

subjects without asthma are higher. Such exposures are generally above 1.0, with most studies reporting no 

respiratory symptoms at concentrations up to 2.0 ppm (ISA, section 5.2.1.7, pp. 116-117, 132-133).
3-16

review and included in the 2008 ISA. These studies demonstrate asthma exacerbation-related 

lung function decrements19 and respiratory symptoms in people with asthma exposed to SO2 for 

5 to 10 minutes at elevated breathing rates (ISA, section 5.2.1). The epidemiologic evidence, 

including recent evidence not available at the time of the previous review, includes studies 

reporting positive associations for asthma-related hospital admissions and emergency department 

visits with short-term SO2 exposures (ISA, section 5.2.1). These findings are generally 

supportive of the causal relationship conclusion for which the controlled exposure studies are the 

primary basis (ISA, section 5.2.1.9). 

Sulfur dioxide is a highly reactive and water-soluble gas that once inhaled is absorbed 

almost entirely in the upper respiratory tract20 (ISA, sections 4.2 and 4.3). Under conditions of 

elevated breathing rates (e.g., while exercising), SO2 penetrates into the tracheobronchial 

region,21 where it may contribute to responses linked to asthma exacerbation in individuals with 

asthma (ISA, sections 4.2, 4.3 and 5.2). More specifically, bronchoconstriction, which is 

characteristic of an asthma attack, is the most sensitive indicator of SO2-induced lung function 

effects. Associated with this bronchoconstriction response is an increase in airway resistance 

which is an index of airway hyperresponsiveness (AHR).

22 Exercising individuals without 

asthma have also been found to exhibit such responses, but at much higher SO2 exposure 

concentrations, above 1000 ppb (ISA, section 1.5.2). 

Bronchoconstriction, evidenced by decrements in lung function, is observed in controlled 

human exposure studies in response to exposures as short as 5- to 10-minutes and can occur at 

SO2 concentrations as low as 200 ppb in some people with asthma exposed while breathing at 

elevated rates, such as during exercise (ISA, section 5.2.1.2).23 More consistent decrements in 

lung function are seen in such individuals with asthma following exposures to 400 ppb and 

greater (ISA, section 5.2.1.2). In contrast, respiratory effects are not observed in other people 

with asthma (nonresponders) and healthy adults exposed while exercising to SO2 concentrations 

 

19 The specific responses reported in the evidence base that are described in the ISA as lung function decrements are 

increased specific airway resistance (sRaw) and reduced forced expiratory volume in 1 second (FEV1) (ISA, 

section 5.2.1.2). 

20 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).

21 The term “tracheobronchial region” refers to the region of the respiratory tract subsequent to the larynx and 

preceding the deep lung (or alveoli). This region includes the trachea and bronchii.

22 Airway hyperresponsiveness, which is an increased propensity of the airways to narrow in response to 

bronchoconstrictive stimuli, is a characteristic feature of people with asthma (ISA, section 5.2.1.2).

23 The data from controlled human exposure studies of people with asthma indicate there to be two subpopulations 

that differ in their airway responsiveness to SO2, with the second subpopulation being insensitive to SO2

bronchoconstrictive effects at concentrations as high as 1.0 ppm (ISA, pp. 5-14 to 5-21; Johns et al., 2010). 
3-17

below 1000 ppb (ISA, sections 5.2.1.2 and 5.2.1.7). Across studies, bronchoconstriction in 

response to SO2 exposure is mainly seen during conditions of elevated breathing rates, such as 

exercise or laboratory-facilitated rapid, deep breathing.24 These conditions lead to a shift from 

nasal breathing to oral/nasal breathing, which increases the concentration of SO2 reaching the 

tracheobronchial region of lower airways, where depending on dose and the exposed individual’s 

susceptibility, it may cause bronchoconstriction (ISA, sections 4.1.2.2, 4.2.2 and 5.2.1.2). 

The evidence base of controlled human exposure studies for people with asthma is the 

same in this review as in the last review. Such studies reporting asthma exacerbation-related 

effects for individuals with asthma are summarized in Tables 5-1 and 5-2, and section 5.2.1.2 of 

the ISA. The main responses observed include increases in specific airway resistance (sRaw) and 

reductions in forced expiratory volume in one second (FEV1) after 5- to 10-minute exposures. As 

in the last review, the ISA in this review quantifies the percentage of exposed study subjects with 

at least 100%, 200% or 300% increases in sRaw (i.e., a doubling, tripling or greater increase) and 

also those with at least 15%, 20% or 30% reduction in FEV1. As recognized in the last review, 

the results of these studies indicate that among individuals with asthma, some individuals have a 

greater response to SO2 than others or a measurable response at lower exposure concentrations 

(ISA, p. 5-14). The SO2-induced bronchoconstriction in these studies occurs rapidly, in as little 

as two minutes from exposure start, and is transient, with recovery following cessation of 

exposure (ISA, p. 5-14).

The studies of subjects with asthma breathing at elevated rates have found effects to 

become more pronounced with increased exposure concentrations. Among individuals with 

asthma, both the percentage of individuals affected and the severity of the response increases 

with increasing SO2 concentrations. For example, at concentrations ranging from 200 to 300 ppb, 

as many as 5 to 30% of exercising study subjects with asthma experienced moderate25 or greater 

decrements in lung function (ISA, Table 5-2). At concentrations at or above 400 ppb, moderate 

or greater decrements in lung function occurred in 20 to 60% of exercising study subjects with 

asthma, and compared to exposures at 200 to 300 ppb, a larger percentage of subjects 

experienced severe decrements in lung function (i.e., an increase in sRaw of at least 200%, 

and/or a reduction in FEV1 of at least 20%) (ISA, Table 5-2). Moreover, at the higher SO2

concentrations, moderate or greater decrements in lung function were frequently accompanied by 

 

24 In the laboratory, study subjects perform this rapid, deep breathing through a mouthpiece that provides a mixture 

of oxygen with enough carbon dioxide to prevent the imbalance of gases in the blood usually resulting from 

hyperventilation. Breathing in the laboratory with this technique is referred to as eucapnic hyperpnea.

25 As in the last review (described in section 3.1.1.1 above), the ISA describes moderate or greater lung function 

decrements as the occurrence of at least a doubling in sRaw or at least a 15% reduction in FEV1 (ISA, section 

1.6.1.1).
3-18

respiratory symptoms, such as cough, wheeze, chest tightness, or shortness of breath (ISA, Table 

5-2).

With regard to newly available epidemiological studies, there are a limited number of 

such studies that have investigated SO2 effects related to asthma exacerbation, with the most 

cohesive evidence coming from studies on asthma-related emergency department (ED) visits 

(ISA, section 5.2.1.2). As in the last review, areas of uncertainty in the epidemiologic evidence 

relate to the characterization of exposure through the use of fixed site monitor concentrations as 

surrogates for population exposure (often over a substantially sized area and for durations greater 

than an hour) and the potential for confounding by PM26 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).

As in the last review, the evidence base for short-term SO2 exposures and respiratory 

effects other than asthma exacerbation is limited and inconsistent (ISA, sections 5.2.1.3-5.2.1.8, 

p. 5-155). The ISA finds the evidence for an effect of SO2 exposure on allergy exacerbation, 

COPD exacerbation, respiratory infection, respiratory effects in healthy populations, and 

respiratory mortality to be inconsistent within and across disciplines and outcomes and/or 

lacking in biological plausibility (ISA, p. 5-155). Additional uncertainty associated with the 

epidemiological evidence for these endpoints is related to potential confounding by copollutants 

(ISA, section 5.2.1.9, p. 5-155).

The evidence base for long-term SO2 exposure and respiratory effects is somewhat 

augmented since the last review such that the ISA in the current review concludes it to be 

suggestive of, but not sufficient to infer, a causal relationship (ISA, section 5.2.2). The support 

for this conclusion comes mainly from the limited epidemiological study findings of associations 

between long-term SO2 concentrations and increases in asthma incidence combined with 

findings of laboratory animal studies involving newborn rodents that indicate a potential for SO2

exposure to contribute to the development of asthma, especially allergic asthma, in children 

(ISA, section 1.6.1.2). For example, the evidence showing increases in asthma incidence is 

coherent with results of animal toxicological studies that provide a pathophysiologic basis for the 

development of asthma. The overall body of evidence, however, lacks consistency (ISA, section 

1.6.1.2). Further there are uncertainties, discussed in section 3.2.1.4 below, that apply to the 

epidemiologic evidence, including that newly available, across the respiratory effects examined 

for long-term SO2 exposure (ISA, section 5.2.2.7).

 

26 The potential for confounding by PM is of particular interest given that SO2 is a precursor to PM (ISA, p. 1-7).
3-19

Other Health Effects

For effects other than respiratory effects, the current evidence is generally similar to the 

evidence available in the last review, and leads to similar conclusions. With regard to a 

relationship between short-term SO2 exposure and total mortality, the ISA reaches the same 

conclusion as in 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 previously available and 

recent multicity epidemiologic studies providing consistent evidence of positive associations 

coupled with uncertainty regarding the potential for SO2 to have an independent effect on 

mortality. While recent studies have analyzed some key uncertainties and data gaps from the 

previous review, uncertainties still exist, given the limited number of studies that examined 

copollutant confounding, the evidence for a decrease in the size of SO2-mortality associations in 

copollutant models with NO2 and PM10, and the lack of a potential biological mechanism for 

mortality following short-term SO2 exposures (ISA, section 1.6.2.4).

For other categories of health effects,

27 the evidence is inadequate to infer the presence or 

absence of a causal relationship, mainly due to inconsistent evidence across specific outcomes 

and uncertainties regarding exposure measurement error, copollutant confounding, and potential 

modes of action (ISA, sections 5.3.1, 5.3.2, 5.4, 5.5.2, 5.6). These conclusions are consistent with 

those made in the previous review.

In summary, rather than altering our conclusions from the previous review, the current 

evidence provides continued support for our previous conclusions regarding the health effects 

associated with exposure to SO2 and most particularly respiratory effects following short-term 

SO2 exposure, particularly in individuals with asthma. Accordingly, as in prior reviews, this 

review gives primary focus to those effects most pertinent to exposures related to current 

concentrations in ambient air, in particular, asthma exacerbation in individuals with asthma.

3.2.1.2 Populations At-Risk of SO2-Related Health Effects

Populations or lifestages can be at increased risk of an air pollutant-related health effect 

due to one or more of a number of factors. These factors can be intrinsic, such as physiological 

factors that may influence the internal dose or toxicity of a pollutant, or extrinsic, such as 

sociodemographic, or behavioral factors (ISA, p. 6-1). The questions considered in this section 

address what the currently available evidence indicates regarding which populations are 

particularly at risk of health effects related to exposure to SO2 in ambient air. 

 

27 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 exposure (ISA, Table 1-1). 
3-20

• Does the current evidence alter our understanding of populations that are 

particularly at-risk from SO2 exposures? Is there new evidence that suggests 

additional at-risk populations that should be given increased focus in this review?

The currently available evidence continues to support our primary conclusions from the 

previous review that people with asthma are at increased risk for SO2-related health effects, 

specifically for respiratory effects, and specifically asthma exacerbation, associated with shortterm 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 is based on the well-established and wellcharacterized evidence from controlled human exposure studies, supported by the evidence on 

mode of action for SO2 and with limited additional support from epidemiologic studies (ISA, 

sections 5.2.1.2 and 6.3.1). Somewhat similar to the conclusion in the last review that children 

and older adults are potentially susceptible populations, the ISA (relying on a framework that is 

new in this review for evaluating the evidence for risk factors) indicates the evidence to be 

suggestive of increased risk for these groups, with some limitations and inconsistencies (ISA, 

sections 6.5.1.1 and 6.5.1.2).28

Further, the ISA finds that children with asthma may be particularly at risk compared to 

adults with asthma (ISA, section 6.3.1). This conclusion reflects several characteristics of 

children as compared to adults, which include their greater responsiveness to methacholine,

29 a 

chemical that can elicit bronchoconstriction in people with asthma, as well as their greater use of 

oral breathing, particularly by boys (ISA, sections 5.2.1.2 and 4.1.2). Oral breathing (vs. nasal 

breathing) and increased breathing rate are factors that allow for greater SO2 penetration into the 

tracheobronchial region of the lower airways, and reflect conditions of individuals with asthma 

in which bronchoconstriction-related responses have been observed in the controlled exposure 

studies (ISA, sections 4.2.2, 5.2.1.2 and 6.3.1). 

We additionally recognize the well-documented finding that some individuals with 

asthma have a greater response to SO2 than others with similar disease status (ISA, section 

 

28 The current evidence for risk to older adults relative to other lifestages comes from epidemiological studies, for 

which the findings are somewhat inconsistent, and studies for which there are uncertainties in the association with 

the health outcome (ISA, section 6.5.1.2).

29 The ISA concluded that potential differences in airway responsiveness of children to SO2 relative to adolescents 

and adults may be inferred by the responses to methacholine (ISA, section 5.2.1.2). Methacholine is a chemical 

that can elicit bronchoconstriction through its action on airway smooth muscle receptors. It is commonly used to 

identify people with asthma and accordingly has been used to screen subjects for studies of SO2 effects. However, 

results of studies of the extent to which airway response to methacholine is predictive of SO2 responsiveness have 

varied somewhat. For example, an analysis of the extent to which airway responsiveness to methacholine, a 

history of respiratory symptoms, and atopy were significant predictors of airway responsiveness to SO2, found 

that about 20 to 25% of subjects ranging in age from 20 to 44 years that were hyperresponsive to methacholine 

were also hyperresponsive to SO2 (ISA, section 5.2.1.2; Nowak et al., 1997). Another study focused on 

individuals with airway responsiveness to methacholine found only a weak correlation between airway 

responsiveness to SO2 and methacholine (ISA, section 5.2.1.2; Horstman et al., 1986).
3-21

5.2.1.2; Horstman et al., 1986; Johns et al., 2010). This occurrence is quantitatively analyzed in a 

study newly available in this review. This study uses the available individual subject data from 

five studies involving exposure of individuals with asthma to multiple concentrations of SO2 for 

5 to 10 minutes while breathing at elevated rates to examine the differences in lung function 

response (Johns et al., 2010). As noted in the ISA, “these data demonstrate a bimodal distribution 

of airway responsiveness to SO2 in individuals with asthma, with one subpopulation that is 

insensitive to the bronchoconstrictive effects of SO2 even at concentrations as high as 1.0 ppm, 

and another subpopulation that has an increased risk for bronchoconstriction at low 

concentrations of SO2” (ISA, p. 5-20). To date, the characteristics that may define the 

subpopulation of responders have not been identified. The current evidence for factors other than 

those discussed above (asthma status and lifestage) is inadequate to determine whether they 

might contribute to an increased risk of SO2-related effects (ISA, section 6.6).

3.2.1.3 Exposure Concentrations Associated with Health Effects

At the time of the last review, the EPA’s conclusions regarding concentrations of SO2

associated with respiratory effects were based primarily on the strong evidence base of 

controlled human exposure studies of individuals with asthma. These studies have documented 

bronchoconstriction-related moderate or greater decrements in lung function following 5- to 10-

minute exposures during exercise. The severity of observed responses, the percentage of 

individuals responding, statistical significance at the study group level and the accompanying 

occurrence of respiratory symptoms have been found to increase with increasing exposure 

concentration (75 FR 35526, June 22, 2010). This information was critical in the REA analyses 

in the last review, the results of which were a primary consideration in reaching a conclusion on 

the level for the 2010 standard.

• Does the current evidence alter our conclusions from the previous review regarding 

the exposure duration and concentrations associated with health effects?

Our understanding of exposure duration and concentrations associated with SO2-related 

health effects is largely based, as it was in the last review, on the longstanding evidence base of 

controlled human exposure studies that demonstrates a dose-response relationship between 5-

and 10-minute SO2 exposure concentrations and decrements in lung function (e.g., increased 

sRaw and reduced FEV1) in individuals with asthma exposed while breathing at elevated rates

(ISA, section 1.6.1.1). At the higher concentrations, there are clear and consistent increases in 

SO2-induced respiratory symptoms (ISA, Table 5-2 and pp. 5-35, 5-39). 

The available and well characterized evidence documents an effect of short-term 

exposures on the respiratory system. As summarized in section 3.2.1.1, SO2-induced 

bronchoconstriction occurs rapidly in responding study subjects with asthma exposed for just a 
3-22

few minutes while breathing at elevated rates (ISA, section 5.2.1.2). Additionally, exposures as 

short as 5 minutes have been found to elicit a similar bronchoconstrictive response at somewhat 

longer exposures. For example, during exposure to SO2 over a 30-minute period with continuous 

exercise, the response to SO2 has been found to develop rapidly and is maintained throughout the 

30-minute exposure (ISA, p. 5-14). In a study involving short exercise periods within a 6-hour 

exposure period, the effects observed following exercise were documented to return to baseline 

levels within one hour after the cessation of exercise, even with continued exposure (Linn et al., 

1984). In considering the epidemiological evidence with regard to the question of exposure 

duration, while we note the associations of asthma-related emergency room visits and hospital 

admissions with 1-hour to 24-hour ambient air concentration metrics, we recognize that current 

methods are not able to address whether these associations are indicative of a potential response

to exposure on the order of hours or much shorter-term exposure to peaks in SO2 concentration.

As noted in the ISA, the air quality metrics in the epidemiological studies are for time periods 

longer than the 5- to 10-minute exposures eliciting effects in the controlled human exposure 

studies and also may not adequately capture the spatial and temporal variation in SO2

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

With regard to the evidence for exposure concentrations eliciting effects, we focus 

primarily on the controlled human exposure study findings for which data are available to the 

EPA for individual subjects with asthma that were exposed while breathing at elevated rates, 

summarized in Table 3-1 (ISA, Table 5-2).30 These data demonstrate that SO2 concentrations as 

low as 200 to 300 ppb for 5 to 10 minutes elicited moderate or greater bronchoconstriction, 

measured as a decrease in FEV1 of at least 15% or an increase in sRaw of at least 100%, in a 

subset of the subjects (ISA, section 5.2.1). Both the percent of individuals affected and the 

severity of response increased with increasing SO2 concentrations. At concentrations ranging 

from 200 to 300 ppb, the lowest levels for which there are study results that provide for 

assessment of the SO2-related effect independent of any effect of exercise in clean air, 5 to 30% 

of exercising individuals with asthma experienced moderate or greater decrements in lung 

function (ISA, section 5.2.1). At concentrations at or above 400 ppb, moderate or greater 

decrements in lung function occurred in 20 to 60% of exercising individuals with asthma and a 

larger percentage of individuals with asthma experienced more severe decrements in lung 

function (i.e., an increase in sRaw of at least 200%, and/or a 20% or more decrease in FEV1), 

compared to exposures at 200 to 300 ppb (ISA, section 5.2.1). Additionally, at concentrations at 

or above 400 ppb, moderate or greater decrements in lung function were frequently accompanied 

 

30 The findings summarized in Table 5-2 of the ISA and in Table 3-1 of this PA are based on results that have been 

adjusted for effects at exercise in clean air so that they have separated out any effect of exercise in causing 

bronchoconstriction and reflect the SO2-specific effect.
3-23

by respiratory symptoms, with some of these findings reaching statistical significance (ISA, 

section 5.2.1).
3-24

Table 3-1. Percentage of adults with asthma in controlled human exposure studies experiencing sulfur dioxide-induced 

decrements in lung function and respiratory symptoms.

SO2

Conc 

(ppm)

Exposure 

Duration 

(min) N

Ventilation 

(L/min)

Percentage of Responders

(Number of Subjects)a

Study

Respiratory Symptoms: 

Supporting Studies

sRaw ≥100%  ≥200%  ≥300% 

FEV1 ≥15%  ≥20%  ≥30% 

0.2 5 23 ~48 sRaw 9% (2)b 0 0 Linn et al. (1983b) Limited evidence of SO2-induced 

increases in respiratory 

symptoms in some people with 

asthma: Linn et al., 1983b; Linn 

et al., 1987; Linn et al., 1988; 

Linn et al. 1990; Schachter et al., 

1984

10 40 ~40 sRaw 7.5% (3)c 2.5% (1)c 0

c Linn et al. (1987)c

10 40 ~40 FEV1 9% (3.5)c 2.5% (1)c 1% (0.5)c Linn et al. (1987)c

0.25 5 19 ~50−60 sRaw 32% (6) 16% (3) 0 Bethel et al. (1985)

5 9 ~80−90 sRaw 22% (2) 0 0

10 27 ~42 sRaw 0 0 0 Horstman et al. (1986)

10 28 ~40 sRaw 4% (1) 0 0 Roger et al. (1985)

0.3 10 20 ~50 sRaw 10% (2) 5% (1) 5% (1) Linn et al. (1988)d

10 21 ~50 sRaw 33% (7) 10% (2) 0 Linn et al. (1990)d

10 20 ~50 FEV1 15% (3) 0 0 Linn et al. (1988)

10 21 ~50 FEV1 24% (5) 14% (3) 10% (2) Linn et al. (1990)

0.4 5 23 ~48 sRaw 13% (3) 4% (1) 0 Linn et al. (1983b) Stronger evidence with some 

statistically significant increases 

in respiratory symptoms: Balmes 

et al., 1987;f Gong et al., 1995 ; 

Linn et al., 1983b; Linn et al., 

1987 ; Roger et al., 1985

10 40 ~40 sRaw 24% (9.5)c 9% (3.5)c 4% (1.5)c Linn et al. (1987)c

10 40 ~40 FEV1 27.5% (11)c 17.5% (7)c 10% (4)c Linn et al. (1987)c

0.5 5 10 ~50−60 sRaw 60% (6) 40% (4) 20% (2) Bethel et al. (1983)

10 27 ~42 sRaw 22.2% (6) 3.7% (1) 11% (3) Horstman et al. (1986)

10 28 ~40 sRaw 18% (5) 4% (1) 4% (1) Roger et al. (1985)
3-25

SO2

Conc 

(ppm)

Exposure 

Duration 

(min) N

Ventilation 

(L/min)

Percentage of Responders

(Number of Subjects)a

Study

Respiratory Symptoms: 

Supporting Studies

sRaw ≥100%  ≥200%  ≥300% 

FEV1 ≥15%  ≥20%  ≥30% 

10 45 ~30 sRaw 36% (16) 16% (7) 13% (6) Magnussen et al. (1990)f

0.6 5 23 ~48 sRaw 39% (9) 26% (6) 17% (4) Linn et al. (1983b) Clear and consistent increases in 

SO2-induced respiratory 

symptoms: Gong et al., 1995; 

Horstman et al., 1988; Linn et al., 

1983b; Linn et al., 1987; Linn et 

al., 1988; Linn et al., 1990

10 40 ~40 sRaw 34% (13.5)c 24% (9.5)c 19% (7.5)c Linn et al. (1987)c

10 20 ~50 sRaw 60% (12) 35% (7) 10% (2) Linn et al. (1988)

10 21 ~50 sRaw 62% (13) 29% (6) 14% (3) Linn et al. (1990)

10 40 ~40 FEV1 47.5% (19)c 39% (15.5)c 17.5% (7)c Linn et al. (1987)c

10 20 ~50 FEV1 55% (11) 55% (11) 5% (1) Linn et al. (1988)

10 21 ~50 FEV1 43% (9) 38% (8) 14% (3) Linn et al. (1990)

1.0 10 28 ~40 sRaw 50% (14) 25% (7) 14% (4) Roger et al. (1985)e

10 10 ~40 sRaw 60% (6) 20% (2) 0 Kehrl et al. (1987)

10 27 ~42 sRaw 55.6% (15) 25.9% (7) 11% (1) Horstman et al. (1986)

Conc = concentration; FEV1 = forced expiratory volume in 1 sec; sRaw = specific airway resistance; SO2 = sulfur dioxide.

This table is adapted from ISA Table 5-2. Information in Horstman et al (1986) is an addition (ISA, pp. 5-14 and 5-19).

aData presented from all references from which individual data were available in the published paper or were provided to EPA (Johns, 2009; Johns and Simmons, 2009; Smith, 

1993). Percentage of individuals who experienced greater than or equal to a 100, 200, or 300% increase in specific airway resistance, or a 15, 20, or 30% decrease in FEV1. Lung 

function decrements are adjusted for the effects of exercise in clean air (calculated as the difference between the percent change relative to baseline with exercise/SO2 and the 

percent change relative to baseline with exercise/clean air).

bNumbers in parenthesis represent the number of subjects experiencing the indicated effect.

cResponses of people with mild and moderate asthma reported in Linn et al. (1987) have been combined. Data are the average of the first and second round exposure responses 

following the first 10 min period of exercise. In some cases, the average had a first decimal place value of 5, which is reported in the table to avoid a high bias in values due to 

rounding. In all other cases, the calculated percentages were rounded to the nearest integer. 

dAnalysis includes data from only people with mild (Linn et al., 1988) and moderate (Linn et al., 1990) asthma who were not receiving supplemental medication.

eOne subject was not exposed to 1 ppm due to excessive wheezing and chest tightness experienced at 0.5 ppm. For this subject, the values used for 0.5 ppm were also used for 

1.0 ppm under the assumption that the response at 1.0 ppm would be equal to or greater than the response at 0.5 ppm.

f

Indicates studies in which exposures were conducted using a mouthpiece rather than a chamber.
3-26

The lowest exposure concentration in Table 3-1 is 200 ppb. This is the lowest exposure 

concentration for which individual study subject data are available in terms of the sRaw and 

FEV1 metrics presented in Table 3-1 that have been calculated with assessment of the SO2 effect 

versus that of exercise in clean air. In nearly all of the studies in this table (and all of the studies 

for concentrations below 500 ppb), study subjects breathed freely (e.g., without using a 

mouthpiece).31 In studies that tested 200 ppb, a portion of the exercising study subjects with 

asthma (approximately 8 to 9%) responded with at least a doubling in sRaw or an increase in 

FEV1 of at least 15% (Table 3-1; Linn et al., 1983b; Linn et al., 1987). 

With regard to exposure concentrations below 200 ppb, the available evidence is very 

limited. In the studies testing this concentration, subjects were exposed by mouthpiece rather 

than freely breathing in an exposure chamber (Sheppard et al., 1981; Sheppard et al., 1984; 

Koenig et al., 1989; Koenig et al., 1990; Trenga et al., 2001).32 Additionally, only a few of these 

studies included an exposure to clean air while exercising that would have allowed for 

determining the effect of SO2 versus that of exercise in causing bronchoconstriction (Sheppard et 

al., 1981, 1984; Koenig et al., 1989). In those cases, a limited number of adult and adolescent

study subjects were reported to experience small changes in sRaw, with the magnitudes of 

change appearing to be smaller than responses reported from studies at exposure concentrations

of 200 ppb or more. For example, the increase in sRaw reported for two young adult subjects 

exposed to 100 ppb in the study by Sheppard et al. (1981) was slightly less than half the response 

of these subjects at 250 ppb and the results for the study by Sheppard et al. (1984) indicate that 

none of the 8 study subjects experienced as much as a doubling in sRaw in response to the 

mouthpiece exposure to 100 ppb, while exercising. In the study of adolescents (aged 12 to 18 

years), among the three individual study subjects for which respiratory resistance appears to have 

increased with SO2 exposure, the magnitude of any increase after consideration of the response 

to exercise appears to be less than 100% in each subject (Koenig et al., 1989).

In considering what may be indicated by these mouthpiece studies of 100 ppb, we note 

that in a mouthpiece exposure system, the inhaled breath completely bypasses the nasal passages 

where SO2 is efficiently removed, thus allowing more of the inhaled SO2 to penetrate into the 

 

31 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).

32 A subset of these studies is cited in the ISA; additionally, three of them (Sheppard et al., 1981; Koenig et al., 

1990; Trenga et al., 2001) are cited in the 2008 ISA and a fourth (Sheppard et al., 1984) is cited in the 1986 

Addendum and 1994 Supplement to the 1982 AQCD. The fifth study (Koenig et al., 1989) is not cited in the prior 

AQCDs, the 2008 ISA, or the ISA for the current review. This study is an investigation involving nine adolescent 

subjects with allergic asthma (positive response to a methacholine challenge test at or below 20 mg/mL) exposed 

by mouthpiece to 0.1 ppm during exercise. Measurements of FEV1 and RT were taken at baseline and subsequent 

to SO2 and air only exposures during exercise (Koenig et al., 1989). 
3-27

tracheobronchial airways (2008 ISA, p. 3-4; ISA, section 4.1.2.2). This occurrence, as well as 

limited evidence comparing responses by mouthpiece and chamber exposures, leads to the 

expectation that SO2-responsive people with asthma breathing SO2 using a mouthpiece, 

particularly while breathing at elevated rates, would experience greater lung function responses 

than if exposed to the same test concentration while freely breathing in an exposure chamber 

(ISA, p. 5-23; Linn et al., 1983a). Thus, we conclude that the set of studies for the 100 ppb 

exposure concentration, while quite limited, does not indicate as much as a doubling in sRaw in 

the extremely few adults and adolescents tested (Sheppard et al., 1981, 1984; Koenig et al., 

1989).

We have also considered what may be indicated by the epidemiological studies regarding 

exposure concentrations associated with health effects. Although exposure concentrations 

eliciting respiratory responses are not available from such studies, studies that find associations 

with outcomes such as asthma-related ED visits and hospitalizations have the potential to 

indicate ambient air concentrations that may contribute to exposures that may be eliciting effects. 

For example, in recognizing the general coherence of epidemiological study findings for 24-hour 

ambient air concentrations with the findings of the controlled human exposure studies for 

exercising study subjects with asthma exposed for 5 to 10 minutes, the 2008 ISA recognized that 

“it is possible that these epidemiologic associations are determined in large part by peak 

exposures within a 24-h period” (2008 ISA, p. 5-5). In considering the epidemiological studies in 

this light, we additionally note that given the important role of SO2 as a precursor to PM in 

ambient air, a key uncertainty in the epidemiological evidence available in the last review was 

potential confounding by copollutants, particularly PM (ISA, p. 5-5). Among the U.S. 

epidemiologic studies reporting mostly positive and sometimes statistically significant 

associations between ambient SO2 concentrations and ED visits and hospital admissions (some 

conducted in multiple locations), few studies have attempted to address this uncertainty, e.g., 

through the use of copollutant models. For example, as in the last review, there are three U.S. 

studies for which the SO2 effect estimate remained positive and statistically significant in 

copollutant models with PM (Appendix D).33 No additional such studies have been newly 

identified in this review. Such uncertainty regarding copollutant confounding, as well as 

exposure measurement error, remain in the currently available epidemiologic evidence base 

(ISA, p. 5-6).

 

33 Based on data available for specific time periods at some monitors in the areas of these studies, the 99th percentile 

1-hour daily maximum concentrations were estimated in the last review to be between 78-150 ppb (Thompson 

and Stewart, 2009).
3-28

3.2.1.4 Uncertainties in the Health Effects Evidence

A number of key uncertainties and limitations were identified in the previous review with 

respect to the health effects evidence, as described in the 2009 REA. This section considers the 

currently available information, including that newly available in this review, with regard to such 

areas of uncertainty.

• To what extent have important uncertainties identified in the last review been 

reduced and/or have new uncertainties emerged?

We have not identified any new uncertainties since the last review. However, we 

continue to recognize important uncertainties that also existed in the last review. These important 

areas of uncertainty relate to the current health evidence, including that newly available in this 

review, are summarized below.

Although the evidence clearly demonstrates that short-term SO2 exposures cause 

respiratory effects, particularly asthma exacerbation in exercising individuals with asthma, as in 

the previous review, we continue to recognize uncertainties that remain in several aspects of our 

understanding of these effects. Such uncertainties include those associated with the severity and 

prevalence of responses to very short (5- to 10-minute) SO2 exposures below 200 ppb and with 

the potential extent of such responses in individuals of some population groups not included in 

the controlled exposure studies (e.g., those with more severe asthma and children). There are also 

uncertainties concerning the potential influence of exposure history and co-exposure to other 

pollutants on the relationship between short-term SO2 exposures and respiratory effects. With 

regard to the evidence base, we also recognize a complication associated with interpreting the 

epidemiologic evidence related to uncertainty in the exposure estimates. The following 

discussion touches on each of these types of uncertainty.

With regard to the potential for and magnitude of these effects in at-risk populations 

exposed to 5- to 10-minute concentrations below 200 ppb, there is very limited evidence from a 

small set of studies of exposure concentrations as low as 100 ppb, as discussed in section 3.2.1.3 

above. Although only a few of these studies included an exposure to clean air while exercising 

that would have allowed for determining the effect of SO2 versus that of exercise, these studies 

indicate the likelihood of an appreciable reduction in SO2-induced response in exercising people 

with asthma from that observed for exposures at 200 ppb, with no evidence provided for as much 

as a doubling in sRaw at an exposure concentration of 100 ppb. Given the limited number of 

subjects in these studies and study design differences from free breathing chamber studies, 

however, uncertainties remain with regard to a complete characterization of the extent of 

response in exercising individuals with asthma exposed through natural or free breathing to 

exposure concentrations below 200 ppb. The extent to which the epidemiological evidence, 
3-29

including that newly available, can inform this area of uncertainty is limited, at best.

34

Accordingly, this remains an area of uncertainty in this review.

Some uncertainty also remains with regard to the extent to which the controlled human 

exposure study evidence describes the responses of the populations most at risk of SO2-related 

respiratory effects (e.g., those with the greatest likelihood of the most severe response or of 

responding at the lowest exposure concentration). For example, the available studies have 

generally involved subjects with mild or moderate asthma, such that the response of individuals 

with more severe asthma is unknown.35 Further, while it is well documented that some 

individuals have a greater response to SO2 than others with the same disease status, the factors 

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

Uncertainty also remains related to the responses for children with asthma. Although the 

epidemiological evidence includes a number of studies focused on health outcomes in children 

that are supportive of the qualitative conclusions of causality (ISA, section 5.2.1.2), there are few 

controlled human exposure studies to inform our understanding of exposure concentrations 

associated with effects in this population group. Those studies have not included subjects 

younger than 12 years (ISA, p. 5-22). Some characteristics particular to school age children 

younger than 12 years, such as increased propensity for mouth breathing (ISA, p. 4-5), however, 

suggest that this age group of children with asthma might be expected to experience larger lung 

function decrements than adults with asthma (ISA, p. 5-25).

Other areas of uncertainty concerning the potential influence of SO2 exposure history and 

co-exposure to other pollutants on the relationship between short-term SO2 exposures and 

respiratory effects also remain from the last review. There is some limited evidence regarding the 

potential for an increased response to SO2 exposures occurring in the presence of other common 

pollutants such as PM (potentially including particulate sulfur compounds), nitrogen dioxide and 

 

34 As associations reported in the epidemiologic analyses are associated with air quality concentration metrics as 

surrogates for the actual pattern of exposures experienced by study population individuals over the period of a 

particular study, the studies are limited in what they can convey regarding the specific patterns of exposure 

circumstances (e.g., magnitude of concentrations over specific durations and frequency) that might be eliciting 

reported health outcomes. 

35 The ISA identifies two studies that have investigated the influence of asthma severity on responsiveness to SO2, 

with one finding that a larger change in lung function observed in the moderate/severe asthma group was 

attributable to the exercise component of the study protocol while the other did not assess the role of exercise in 

differences across individuals with asthma of differing severity (Linn et al., 1987; Trenga et al., 1999). The ISA 

states, “[h]owever, both studies suggest that adults with moderate/severe asthma may have more limited reserve 

to deal with an insult compared with individuals with mild asthma” (ISA, p. 5-22). Based on the criteria used in 

the study by Linn et al (1987) for placing individuals in the “moderate/severe” group, the ISA concluded that the 

asthma of these individuals “would likely be classified as moderate by today’s classification standards” (ISA, p. 

5-22; Johns et al., 2010; Reddel, 2009).
3-30

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).36 There is also some evidence 

suggestive of a potential for SO2 exposure to contribute to an increased sensitivity to allergens;

however, the studies are very few and are limited to experimental animal models (ISA, section 

5.2.1.9).

There are additional complications associated with interpretation of epidemiologic 

studies of SO2 in ambient air that pertain to exposure measurement error and copollutant 

confounding (ISA, sections 3.4, 5.2.1.1 and 5.2.1.2). With regard to the former, a key uncertainty 

in the epidemiologic evidence is whether study findings reflect an independent association for 

SO2 given that the studies assigned exposure from fixed site monitors while SO2 concentrations 

in ambient air tend to show high spatiotemporal variability within a city, and correlations with 

personal exposure are poorly characterized. Accordingly, there is uncertainty regarding the 

extent to which measurements at the study monitors, and the associated air quality concentration 

metric for the study, adequately represent the spatiotemporal variability in ambient SO2

concentrations in the study area (ISA, sections 5.2.1.2 and 3.4.1.3).

With regard to copollutant confounding, not only is SO2 but one component of a complex 

mixture of pollutants present in the ambient air, an issue not unique to SO2 epidemiological 

studies, but SO2 is also a precursor to sulfate, which can be a principal component of PM, an air 

pollutant commonly occurring across the U.S. (ISA, section 2.3; U.S. EPA, 2009, Table 3-2 and 

section 3.3.2). This uncertainty affects the extent to which effect estimates from epidemiologic 

studies reflect the independent contribution of SO2 to the adverse respiratory outcomes assessed 

in these studies. This area of uncertainty was recognized in the last review and remains in the 

current review. In first summarizing the epidemiological evidence from the last review, the ISA 

 

36 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/m3and 

higher) and SO2 (1 ppm and higher) utilized in these studies are much higher than ambient levels” (2008 ISA, p. 

3-30). The 2008 ISA further stated that “the SO2-adsorbed PM utilized in some of these studies is not 

representative of ambient PM,” providing the example that “some of the laboratory-generated aerosols contained 

sulfite but atmospheric chemistry studies do not indicate significant amounts of sulfite ion in atmospheric PM” 

(2008 ISA, p. 3-30). Thus, the 2008 ISA concluded that “animal toxicological studies conducted since the [prior] 

review suggest that SO2 effects may be potentiated by coexposure to PM but the relevance of these results to 

ambient exposures is not clear” (2008 ISA, p. 3-30).
3-31

indicated that it was strongest for increased respiratory symptoms and respiratory-related 

hospital admissions and ED visits, especially in children, while noting that “a key uncertainty 

was potential confounding by copollutants, particularly PM” (ISA, p. 5-5). With regard to the 

newly available evidence, “uncertainties related to exposure measurement error and copollutant 

confounding remain” (ISA, p. 5-6).37

There remains uncertainty in the evidence with regard to the potential role of long-term 

exposure to SO2 in eliciting SO2-related respiratory effects. As noted in section 3.2.1.1 above, 

the ISA has determined the evidence to be suggestive of this being a causal relationship. The 

strongest evidence supporting this conclusion is provided by epidemiological study findings of 

associations between long-term SO2 concentrations and increases in asthma incidence combined 

with findings of laboratory animal studies involving newborn rodents that indicate a potential for 

SO2 exposure to contribute to the development of asthma, especially allergic asthma, in children. 

However, “some uncertainty remains regarding an independent effect of long-term SO2 exposure 

on the development of asthma” and “potential confounding by other pollutants is unexamined, 

and largely unavailable, for epidemiologic studies of asthma among children” (ISA, p. 5-182). 

Another area of uncertainty recognized by the ISA relates to conclusions regarding the 

potential for SO2 in ambient air to contribute to health effects other than respiratory effects. As 

noted in section 3.2.1.1 above, the ISA has determined the evidence to be suggestive of, but 

insufficient to infer, a causal relationship between short-term SO2 exposure and mortality and to 

be inadequate to infer the presence or absence of a causal relationship for other types of 

exposures and health effects for which there are studies available (ISA, section 1.6.2). 

In summary, a variety of uncertainties from the last review remain, including those 

related to the extent of effects at concentrations below those evaluated in controlled human 

exposure studies of exercising individuals with asthma, and the potential for greater impacts in 

individuals with more severe asthma and in children with asthma, as well as exposure 

measurement error and potential copollutant confounding in the epidemiologic studies (ISA, 

section 5.2.1.9). 

3.2.1.5 Public Health Implications

In general, implications and the magnitude of potential impacts on public health are 

dependent upon the type and severity of the effect, as well as the size of population affected. 

 

37 With regard to asthma-related outcomes, “a small number of epidemiologic studies examined copollutant models” 

and while “[s]ome associations were relatively unchanged in magnitude after adjustment for a copollutant; others 

did not persist” (ISA, p. 5-154). The ISA concludes that “inference from copollutant models is limited given 

potential differences in exposure measurement error for SO2 compared to NO2, CO, PM, and O3 and in many 

cases, high copollutant correlations” (ISA, p. 5-154). The evidence for nonasthma-related outcomes is described 

as “limited and inconsistent” (ISA, pp. 5-155 to 5-156).
3-32

With regard to SO2 concentrations in ambient air, the public health implications and potential 

public health impacts relate to the effects causally related to SO2 exposures of interest in this 

review. These are respiratory effects of short-term exposures, and particularly those effects 

associated with asthma exacerbation in people with asthma. As summarized in section 3.2.1.1, 

the most strongly demonstrated effects are bronchoconstriction-related effects resulting in 

decrements in lung function elicited by short term exposures during periods of elevated breathing 

rate, while asthma-related health outcomes such as ED visits and hospital admissions have also 

been statistically associated with ambient air SO2 concentration metrics in epidemiological 

studies (ISA, section 5.2.1.9).

In considering public health implications, in addition to the difference in severity of 

different effects, it is important to consider aspects of the same effect with regard to its impact on 

population groups of differing susceptibility. For example, with regard to bronchoconstrictionrelated effects, the same percentage increase in sRaw or reduction in FEV1 for two groups of 

individuals that differ in their baseline sRaw or FEV1 may result in the two groups being affected 

differently with regard to increased susceptibility to other physiological threats or challenges. 

Accordingly, consideration of such baseline differences and also the relative transience or 

persistence of these responses, as well as other factors, is important to characterizing 

implications for public health, as recognized by the ATS in their statements on evaluating 

adverse health effects of air pollution (ATS, 2000; Thurston et al., 2017).

Building on the earlier policy statement by the ATS that was considered in the last review 

(ATS, 2000), the recent policy statement by the ATS on what constitutes an adverse health effect 

of air pollution provides a general framework for interpreting evidence that proposes a 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 

puts its members at potentially increased risk if affected by another agent (ATS, 2000). The 

consideration of effects on individuals with pre-existing diminished lung function continues to be 

recognized as important in the more recent ATS statement (Thurston et al., 2017). For example, 

in adding emphasis in this area, this statement conveys the view that “small lung function 

changes” in individuals with compromised function, such as that resulting from asthma, should 

be considered adverse, even without accompanying respiratory symptoms (Thurston et al., 

2017). All of these concepts, including the consideration of the magnitude of effects occurring in 
3-33

just a subset of study subjects, continue to be recognized as important in the more recent ATS 

statement (Thurston et al., 2017) and continue to be relevant to the evidence base for SO2.

38

As summarized in section 3.2.1.3 above, people with asthma are the key population at 

risk for SO2-related effects and children with asthma are considered to be at relatively greater 

risk than other age groups within this at-risk population (ISA, section 6.3.1). In recognizing that 

asthma as a disease can vary in its severity, we take note of the relative lack of evidence for 

individuals with the most severe asthma. The evidence base of controlled exposure studies of 

exercising people with asthma provides limited information that indicates there to be similar 

relative responses of individuals with differences in severity of their asthma,

39 although the 

evidence from one study indicates that the absolute changes in lung function are larger for 

individuals with more severe asthma compared to those characterized as having mild asthma. In 

that study, the larger absolute change in lung function was attributable to a larger response to the 

exercise component of the exposure protocol in the moderate/severe asthma group compared to 

the mild asthma group (ISA, p. 5-22; Linn et al., 1987). Because the role of exercise was not 

determined in the second study, it is unclear whether a greater response to the exercise itself (vs 

the SO2 exposure) played a role in its findings (ISA, p. 5-22; Trenga et al., 1999). 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).

The information below characterizes the size and other features of the populations in the 

U.S. concluded to be at risk of SO2-related effects (when breathing at elevated rates). As a 

whole, the discussion in this section indicates the potential for exposures to SO2 in ambient air to 

be of appreciable public health importance. Such considerations contributed to the basis for the 

2010 decision to appreciably strengthen the primary SO2 NAAQS and to establish a 1-hour 

standard to protect the at-risk populations from short term exposures of concern. Such 

considerations remain relevant in the current review. 

 

38 In the Administrator’s judgments on the then-existing standard in the last review, as well as on the appropriate 

level for the new 1-hour standard, the Administrator considered the 2000 ATS policy statement, as well as advice 

from CASAC and recommendations and judgments made by EPA in previous NAAQS reviews (section 3.1.1 

above).

39 These studies categorized with regard to 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 ability to engage in moderate to heavy levels of exercise (ISA, p. 5-22; 

Johns et al., 2010; Reddel, 2009). 
3-34

• What does the information available in this review indicate with regard to the size of 

at-risk populations and their distribution in the U.S.?

The magnitude and characterization of a public health impact is dependent upon the size 

and characterization of the populations affected, as well as the type or severity of the effect. As 

summarized above, the population group most at risk of health effects associated with exposure 

to SO2 in ambient air is people with asthma.40 The National Center for Health Statistics data 

from the National Health Information Survey (NHIS)41 for 2015 indicate that approximately 8% 

of the U.S. population has asthma (Table 3-2; CDC, 2017). These data indicate the size of the 

key at-risk population for SO2 in ambient air. It is this population that the primary NAAQS for 

SO2 is intended to protect. Table 3-2 below considers the currently available information that 

helps to characterize key features of this population.

Population groups with relatively greater asthma prevalence might be expected to have a 

potential for relatively greater population-level SO2 impacts. Among all U.S. adults, asthma

prevalence is estimated to be 7.6%, with women having a higher estimate (9.7%) than men

(5.4%). The estimated prevalence is greater in children (less than 18 years of age) than adults 

(Table 3-2). 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). 

Among all U.S. children, the asthma prevalence estimate is greater for boys (9.9%) than 

girls (6.9%), and, with regard to age, is generally greatest in young teenagers (Table 3-2). 

Among populations of different races or ethnicities, black non-Hispanic and Puerto Rican 

Hispanic children are estimated to have the highest estimated prevalences, at 13.4% and 13.9%, 

respectively. For the age group 5-14 years, the estimates are 16.3% and 14.7% for black non-

 

40 We additionally note, that some individuals with asthma have a greater response to SO2 than others with asthma 

(ISA, p. 5-14). Analyses of publicly available primary data from five studies demonstrated a bimodal distribution 

of SO2 responses in study subjects with asthma, “with one subpopulation that is insensitive to the 

bronchoconstrictive effects of SO2 even at concentrations as high as 1.0 ppm, and another subpopulation that has 

an increased risk of bronchoconstriction ... at low concentrations” (ISA, p. 5-19 to 5-20; Johns et al., 2010).

41 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) and current asthma prevalence table 

(https://www.cdc.gov/asthma/most_recent_data.htm).
3-35

Hispanic and Puerto Rican children, respectively (Table 3-2).42 Asthma prevalence is also 

increased among populations in poverty (e.g., 11.1% among people living in households below 

the poverty level compared to 7.2% of those living above it).43

The information on which to base estimates of asthma prevalence in other subgroups of 

children is much more limited (e.g., as discussed in the REA, section 4.1.2). For example, the 

more limited information from the National Health Information Survey (NHIS) for 2011-2015 

indicates there to be a greater prevalence of asthma in children that are obese compared to those 

that are not (REA, section 4.1.2, Figure 4-2).44

 

42 Interestingly, in black, non-Hispanic children aged 5 to 14 years, the estimated asthma prevalence is greater in 

boys (19.0%) than girls (13.5%). While in Puerto Rican children aged 5 to 14 years, the estimated prevalence is 

greater in girls (18.5%) than boys (11.6%) (https://www.cdc.gov/asthma/nhis/2015/table4-1.htm).

43 There is also a correlation between asthma prevalence and obesity (REA, section 4.1.2).

44 In consideration of the limited information regarding factors related to breathing habit (whether one is breathing 

through their nose or mouth) and recognizing the lack of evidence from controlled human exposure studies of 

SO2-induced lung function decrements in children, approximately 5 to 11 years of age, with asthma, the ISA 

suggests that this age group of children and “particularly boys and perhaps obese children, might be expected to 

experience greater responsiveness (i.e., larger decrements in lung function) following exposure to SO2 than 

normal-weight adolescents and adults” (ISA, p. 4-7 and 5-36). However, the ISA does not find the evidence to be 

adequate to conclude differential risk status for subgroups of children with asthma (ISA, Chapter 6).
3-36

Table 3-2. 2015 National Asthma Prevalence.

Characteristic 1

Number with Current 

Asthma (in thousands) 2

Percent with Current 

Asthma

Total 24,633 7.8

Child (Age <18) 6,188 8.4

Adult (Age 18+) 18,445 7.6

All Age Groups

0-4 years 935 4.7

5-14 years 4,033 9.8

15-19 years 2,107 10.2

20-24 years 1,655 7.6

25-34 years 2,916 6.8

35-64 years 9,907 8.0

65+ years 3,079 6.6

Child Age Group

0-4 years 935 4.7

5-11 years 2,761 9.6

12-17 years

 12-14 years

 15-17 years

2,492

1,272

1,219

10.0

10.3

9.8

Sex

Males 9,998 6.5

 Boys (Age <18)

 Boys (Age 5-14)

3,705

2,428

9.9

11.6

 Men (Age 18+) 6,293 5.4

Females 14,634 9.1

 Girls (Age <18)

 Girls (Age 5-14)

2,483

1,605

6.9

8.0

 Women (Age 18+) 12,151 9.7

Race/Ethnicity

White NH3 15,244 7.8

 Child (Age <18)

 Child (Age 5-14)

2,810

1,750

7.4

8.2

 Adult (Age 18+) 12,435 7.9

Black NH 3,931 10.3

 Child (Age <18)

 Child (Age 5-14)

1,336

911

13.4

16.3

 Adult (Age 18+) 2,595 9.1

Other NH 1,793 6.9

 Child (Age <18)

 Child (Age 5-14)

605

389

8.4

9.4

 Adult (Age 18+) 1,188 6.3

Hispanic, all 3,665 6.6

 Child (Age <18)

 Child (Age 5-14)

1,438

983

8.0

9.7

 Adult (Age 18+)

Hispanic, Puerto Rican

 Child (Age<18)

 Child (Age 5-14)

 Adult (Age 18+)

2,227

715

198

117

516

5.9

13.7

13.9

14.7

13.6
3-37

Characteristic 1 Number with Current 

Asthma (in thousands) 2

Percent with Current 

Asthma

Hispanic, Mexican/Mexican-American

 Child (Age<18)

 Child (Age 5-14)

 Adult (Age 18+)

2,126

899

646

1,226

6.0

7.3

9.2

5.3

Federal Poverty Threshold

 Below 100% of poverty level 5,086 11.1

 100% to less than 250% of poverty level 7,664 8.4

 250% to less than 450% of poverty level 4,989 6.3

 450% of poverty level or higher 6,894 6.9

1 Numbers within selected characteristics may not sum to total due to rounding

2 Includes persons who answered “yes” to the questions “Have you EVER been told by a doctor or other health 

professional that you had asthma” and “Do you still have asthma?”

3 NH = non-Hispanic

Adapted from https://www.cdc.gov/asthma/most_recent_data.htm and

https://www.cdc.gov/asthma/nhis/2015/table4-1.htm (CDC, 2017).

3.2.2 Exposure/Risk-based Considerations

Our consideration of the scientific evidence available in the current review, as at the time 

of the last review (summarized in section 3.1 above), is informed by results from a quantitative 

analysis of estimated population exposure and associated risk. The overarching consideration is 

whether the current exposure/risk information alters our overall conclusions from the previous 

review regarding health risk associated with exposure to SO2 in ambient air. As in our 

consideration of the evidence in section 3.2.1 above, we have organized the discussion regarding 

the exposure/risk information around a set of key questions to assist us in considering the 

exposure/risk analyses of at-risk populations living in three urban areas under air quality 

conditions simulated to just meet the existing SO2 primary standard. 

Prior to addressing the individual exposure/risk questions, we provide a summary of key 

aspects of the assessment, including the study areas, populations simulated, modeling tools and 

exposure and risk metrics derived (section 3.2.2.1). We then consider aspects of the questions 

beginning with the magnitude of exposure and risk estimated for the simulated at-risk 

populations (section 3.2.2.2), followed by the key uncertainties associated with the quantitative 

analyses with regard to drawing conclusions as to the adequacy of protection afforded by the 

current SO2 standard (section 3.2.2.3). Lastly, we consider the exposure and risk estimates from 

the quantitative assessment with regard to the extent to which such estimates may be judged to 

be important from a public health perspective (section 3.2.2.4).

3.2.2.1 Exposure/Risk Analyses

In the assessment conducted for this review, described in detail in the REA, we have 

estimated SO2 exposure and risk associated with air quality conditions that just meet the current 
3-38

standard. These analyses inform our understanding of the protection provided by the current SO2

standard from effects that the health effects evidence indicates to be elicited in some portion of 

exercising people with asthma by short (e.g., 5- to 10-minute) elevations in SO2 exposure 

concentrations. 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 with regard to population exposure to short-term peak 

concentrations of SO2 in ambient air. This set of study areas and the associated exposed 

populations are intended to be informative to the EPA’s consideration of potential exposures and 

risks that may be associated with the air quality conditions that meet the current SO2 standard. 

The three study areas range in total population size from approximately 180,000 to 

540,000 and reflect different mixtures of SO2 emissions sources, including utilities using fossil 

fuel and non-utility sources, such as petroleum refineries and secondary lead smelting (REA, 

section 3.1). The three study areas – in Massachusetts, Indiana and Oklahoma –are in three 

different climate regions of the U.S.: the Northeast, Ohio River Valley (Central), and South (Karl 

and Koss, 1984). The latter two regions comprise the part of the U.S. with generally the greatest 

prevalence of elevated SO2 concentrations and large emissions sources (Figure 2-7, Appendix F). 

Additionally, continuous 5-minute ambient air monitoring data (i.e., all 12 5-minute values for 

each hour) are available in all three study areas (REA, section 3.2). 

Consistent with the health effects evidence in this review (summarized in section 3.2.1 

above), the focus of the REA is on short-term exposures of individuals in the population with 

asthma during times when they are breathing at an elevated rate. Exposure and risk is 

characterized for two population groups: adults (individuals older than 18 years) with asthma and 

school-aged children (aged 5 to 18 years)45 with asthma. The focus on these populations is 

consistent with the ISA’s identification of individuals with asthma as the population at risk of 

SO2-related effects, and its conclusion that within this population, children with asthma may be 

at greater risk than adults with asthma (ISA, section 6.6). Asthma prevalence estimates for the 

populations simulated in the three study areas ranges from 8.0 to 8.7% (REA, section 5.1). For 

children, the study area prevalence rates range from 9.7 to 11.2% (REA, section 5.1). Variation 

within each study area related to age, sex and family income was also accounted for (section 

4.1.2 and Appendix E of REA).46 For children, this variation is greatest in the Fall River study 

 

45 The child population group focuses on ages 5 to 18 in recognition of data limitations and uncertainties, including 

those related to accurately simulating activities performed, estimating physiological attributes, as well as 

challenges in asthma diagnoses for very young children.

46 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 family income from the NHIS.
3-39

area, with census block level, age-specific prevalence estimates ranging from 7.9 to 18.6% for 

girls and from 10.7 to 21.5% for boys (REA, Table 4-2).

In the REA, 1-hour SO2 concentrations were estimated across a 3-year period (consistent 

with the period represented by the form of the standard) using air quality modeling of SO2

emissions sources in each area,47 and were adjusted, as described in the REA, such that the air 

quality modeling receptor location with the highest concentrations just met the current 

standard.48 In addition, sensitivity analyses were performed using an alternative adjustment 

approach and are summarized in section 3.2.2.2. 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 receptor locations in each 

area (REA, section 3.5).

The exposure modeling, presented in detail in the REA, relied on the EPA’s Air Pollutant 

Exposure model (APEX), which estimates human exposure using a stochastic, event-based 

microenvironmental approach. This model has a history of application, evaluation, and 

progressive model development in estimating human exposure and dose for reviews of NAAQS 

for gaseous pollutants (U.S. EPA, 2008; 2010; 2014). This general exposure modeling approach 

was also used in the 2009 REA for the last review of the primary standard for SOX, although a 

number of updates have been made to the model and various datasets used with it (2009 REA; 

U.S. EPA, 2017b, section 3.4). For example, exposure modeling for the REA includes reliance 

on updates to several key inputs to the model including (1) a significantly expanded 

Consolidated Human Activity Database (CHAD), that now has over 55,000 diaries, with over 

25,000 for school-aged children; (2) the updated NHANES data (2009-2014), which are the basis 

for the age- and sex-specific body mass distributions from which APEX samples to specify the 

individuals in the modeled population; (3) the algorithms used to estimate age- and sex-specific 

resting metabolic rate, a key input to estimating a simulated individual’s activity-specific 

ventilation (or breathing) rate; and (4) the ventilation rate algorithm itself. Further, the current 

model uses updated population demographic data based on the most recent Census. 

The APEX model probabilistically generates a sample of hypothetical individuals from 

an actual population database and simulates each individual’s movements through time and 

space (e.g., indoors at home, inside vehicles) to estimate his or her exposure to a pollutant. 

 

47 As described in chapter 3 of the REA, the air quality modeling utilized emissions estimates and meteorological 

data for the years 2011 through 2013 as conditions in this time period are close to those just meeting the current 

standard, thus requiring a smaller adjustment to create the current standard scenario.

48 As described in more detail in section 3.4 of the REA, the adjustments were implemented with a focus on 

reducing emissions from the source contributing to the standard exceedances until the areas just met the standard.
3-40

Population characteristics are taken into account to represent the demographic profile of the 

population in each study area. Age and gender demographics for the simulated at-risk population 

(adults and children with asthma) were drawn from the prevalence estimates provided by the 

2011-2015 National Health Interview Survey.49 The APEX model generates each simulated 

person or profile by probabilistically selecting values for a set of profile variables, including 

demographic variables, status and physical attributes (e.g., residence with air conditioning, 

height, weight, body surface area) and ventilation rate.

Based on minute-by-minute activity levels, and physiological characteristics of the 

simulated person (see REA, section 4.1), APEX estimates an equivalent ventilation rate (EVR), 

based on normalizing the simulated individuals’ activity-specific ventilation rate to their body 

surface area; the EVR is used to identify exposure periods during which an individual is at or 

above a specified ventilation level (REA, section 4.1.3.3). The level specified is based on the 

ventilation rates of subjects in the controlled human exposure studies of exercising people with 

asthma (Table 3-1). The APEX simulations performed for this review have focused on exposures 

to SO2 emitted into ambient air that occurs in microenvironments,50 without additional 

contribution from indoor SO2 emissions sources.51

As in the last review, the REA for this 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 based on information from the controlled 

human exposure studies on the occurrence of bronchoconstriction-related effects in some study 

subjects with asthma who are exposed during exercise (REA, section 4.6). In drawing on this 

evidence base for this purpose, the REA has given primary focus to the well-documented studies 

summarized in Table 5-2 and Figure 5-1 of the ISA for 5- to 10-minute exposure concentrations 

ranging from 200 ppb to 600 ppb (Table 3-1 of this document). The first risk metric is based on 

comparison of the estimated 5-minute exposure concentrations for individuals breathing at 

elevated rates to 5-minute concentrations of potential concern (benchmark concentrations), and 

the second utilizes exposure-response information for study subjects experiencing 

 

49 Information about the National Health Interview Survey is available at http://www.cdc.gov/nchs/nhis.htm.

50 Five microenvironments (MEs) are modeled in the REA as representative of a larger number of 

microenvironments. The 2009 REA results indicated that the majority of peak SO2 exposures occurred while 

individuals were within outdoor microenvironments (2009 REA, Figure 8-21). Based on that finding and the 

objective (i.e., understanding how often and where short-term peak SO2 exposures occur), the approach 

implemented in the REA recognizes the added efficiency of minimizing the number of MEs, particularly indoor 

MEs, that are parameterized and included in the modeling. Accordingly, the number of MEs was aggregated to 

address exposures of ambient origin that occur within a core group of indoor, outdoor, and vehicle MEs (REA,

section 4.4).

51 Indoor sources are generally minor in comparison to SO2 from ambient air (ISA, p. 3-6; REA, sections 2.1.1 and 

2.1.2).
3-41

bronchoconstriction-related effects on lung function (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 an SO2-related increase in sRaw of at least 100%. Both of these metrics are used in the REA 

to characterize health risk associated with 5-minute peak SO2 exposures among the simulated atrisk population 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 Administrator’s 2010 

decision on the new standard (75 FR 35546-35547, June 22, 2010).

For the benchmarks metric, the REA for this review, like the 2009 REA in the last 

review, uses benchmark concentrations that range from 400 ppb down to 100 ppb (REA, section 

4.6.1). At the upper end of this range, 400 ppb represents the lowest concentration in freebreathing 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, including statistically 

significant increased occurrences (ISA, section 5.2.1.2). At 300 ppb, statistically significant 

increases in lung function decrements (specifically reduced FEV1) have been documented in 

analyses of the subset of controlled human exposure study subjects with asthma that are 

responsive to SO2 at concentrations below 600 or 1000 ppb (ISA, p. 153 and Table 5-21; Johns 

et al., 2010). The 200 ppb benchmark concentration represents the lowest level tested in studies 

where subjects were freely breathing in exposure chambers, and where comparisons with 

exposures to clean air while exercising were conducted, thus providing for conclusions regarding 

SO2-attributable responses. At this concentration, moderate or greater lung function decrements

occurred in a percentage of exercising study subjects and there was also limited evidence of SO2-

related respiratory symptoms (ISA, section 5.2.1.2). For exposure concentrations below 200 ppb, 

limited data are available that while not completely comparable to the data at higher 

concentrations do not indicate responses on the order of a doubling in sRaw (section 3.2.1.3

above). However, in consideration of the nonzero percentage of subjects with asthma 

experiencing moderate transient decrements in lung function at the 200 ppb exposure 

concentration (approximately 8 to 9%) and the scarcity or lack of specific controlled human 

exposure study data for some groups of individuals with asthma, such as primary-school-age 

children and those with more severe asthma,

52 a benchmark concentration of 100 ppb (one half 

 

52 Recognizing that even the study subjects described as “moderate/severe” group (had well-controlled asthma, were 

generally able to withhold medication, were not dependent on corticosteroids, and were able to engage in 

moderate to heavy levels of exercise) would likely be classified as moderate by today’s classification standards 

(ISA, pp. 5-22; Johns et al., 2010; Reddel, 2009), we have considered the evidence with regard to the response of 

individuals with severe asthma that are not generally represented in the full set of controlled human exposure 

studies. There is no evidence to indicate such individuals would experience moderate or greater lung function 

decrements at lower SO2 exposure concentrations than individuals with moderate asthma. With regard to the 
3-42

the lowest exposure concentration for which the ISA provides quantified SO2-attributable 

responses resulting from free breathing exposure studies), has been included.

The exposure-response (E-R) function for the 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 SO2 concentrations from 1000 ppb 

down as low as 200 ppb (REA, Table 4-12). Beyond the assessment of these studies and their 

results in past reviews, there has been extensive evaluation of the individual subject results, 

including a data quality review in the last SO2 NAAQS review (Johns and Simmons, 2009), and 

detailed analysis in two subsequent publications (Johns et al., 2010; Johns and Linn, 2011). The 

sRaw responses reported in these studies have been summarized in the ISA, as in the last review, 

in terms of percent of study subjects experiencing responses of a magnitude equal to a doubling 

or tripling or more. 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). The E-R function used in the main analysis of the REA was derived from these data 

using a probit function (REA, section 4.6.2). 

In summary, while the general approach and methodology for the exposure-based 

assessment in this review is similar to that in the last review, there are a number of ways in 

which these analyses differ (see 2009 REA and REA for this review). In addition to the 

expansion in the number and type of study areas assessed, we note the number of improvements 

to input data and modeling approaches, including the availability of continuous 5-minute air 

monitoring data at monitors within the three study areas. 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.

3.2.2.2 At-Risk Population Exposures and Risk

In this section, we summarize the exposure and risk estimates from the REA and consider 

the following question.

 

severity of the response, the limited data that are available indicate a similar magnitude SO2-specific response (in 

sRaw) as that for individuals with less severe asthma, although the individuals with more severe asthma are 

indicated to have a greater response to exercise prior to SO2 exposure, indicating that those individuals “may have 

more limited reserve to deal with an insult compared with individuals with mild asthma” (ISA, p. 5-22). As noted 

in sections 3.2.1.3 and 3.2.1.4 above, evidence from controlled human exposure studies are not available for 

children younger than 12 years old, and the ISA indicates that the information regarding behavior and 

methacholine responsiveness for the subset of this age group that is of school age (e.g., 5-12 years) indicates a 

potential for greater response (ISA, pp. 5-22 to 5-25).
3-43

• What is the magnitude of population exposure and risk in at-risk populations in 

areas simulated to just meet the current SO2 standard? What portion of the at-risk 

populations are estimated to experience exposures of concern or lung function 

decrements at levels of potential health concern?

Given these overarching questions, the air quality scenario analyzed in the REA focuses 

on air quality conditions that just meet the current standard. In addressing these questions, we 

consider the population estimates provided by the REA simulations (REA, Chapters 5 and 6) and 

in considering these REA estimates, we particularly focus on the extent of protection provided 

by the standard from SO2 exposures of potential concern. As described in the prior section, the 

REA presents two sets of 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 SO2-related lung function decrement in a 

year and the number and percent of people estimated to experience multiple lung function 

decrements associated with SO2 exposures.

As an initial matter, we note that, as indicated by the use of a case study approach 

(summarized in section 3.2.2.1 above), the REA analyses are not intended to provide a 

comprehensive national assessment. The REA objective is not to present an exhaustive analysis 

of exposure and risk in the areas that currently just meet the current standard and/or of exposure 

and risk associated with air quality adjusted to just meet the current standard in areas that 

currently do not meet the standard. Rather, the analyses 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. 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 standard was established. Accordingly, capturing an appropriate 

diversity in study areas and air quality conditions (that reflect the current standard scenario)53 is 

important to the role of the REA in informing the EPA’s conclusions on the public health 

protection afforded by the current standard.

In this light, we present the REA results from two different approaches to adjusting air 

quality. The first approach uses the highest design value across all modeled air quality receptors

to adjust the air quality concentrations in each area to just meet the standard (REA, section 3.4). 

 

53 A broad variety of spatial and temporal patterns of SO2 concentrations can exist when ambient air concentrations 

just meet the current standard. These patterns will vary due to many factors including the types of emissions 

sources in a study area and several characteristics of those sources, such as magnitude of emissions and facility 

age, use of various control technologies, patterns of operation, and local factors, as well local meteorology. 

Variability and uncertainty in these patterns is indicated by the estimates derived by the particular analytical 

approaches and methodologies used to describe the study area-specific air quality.
3-44

This is done by estimating the amount of SO2 concentration reduction needed for concentrations 

at this highest receptor to be adjusted to just meet the current standard, and based on this amount, 

all other receptors impacted by the highest source(s) are adjusted accordingly. The second 

approach is included in the REA as a sensitivity analysis in recognition of the potential 

uncertainty associated with the estimated concentrations across the modeling domain, 

particularly the very highest concentrations. Accordingly, the second approach uses the air 

quality receptor having the 99th percentile of the distribution of design values (instead of the 

receptor having the maximum design value) to estimate the SO2 concentration reductions needed 

to adjust the air quality to just meet the standard (REA, section 6.2.2.1). In study areas in which 

estimated concentrations at a very small number of receptors are substantially higher than those 

at all other air quality receptors, these two different approaches can result in very different SO2

concentrations across an area. In such study areas in particular, the first approach generally 

results in much more significant reductions being applied to reduce SO2 concentrations at the 

small group of highest receptor locations such that concentrations at those receptors are just at or 

just below the standard and concentrations at the other receptors across the area are appreciably 

lower. We have represented both sets of results in the tables below in recognition of the 

uncertainty and variability inherent in representing air quality conditions just meeting the current 

standard.

54

Of the two types of risk metrics derived in the REA, we turn first to the results for the 

benchmark-based risk metric with regard to 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 (Table 3-3). The estimates for adults are 

lower, generally due to the lesser amount and frequency of time spent outdoors (REA, section 

5.2). As an initial matter, we note that the estimates for the Tulsa study area are much lower than 

those for the other two areas. For Tulsa, the fraction of the simulated child population with 

asthma was less than 0.5% for the 100 ppb benchmark and zero for the other benchmarks. 

Under air quality conditions just meeting the current standard in the other two study areas

(Indianapolis and Fall River), 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 (Table 3-3). With regard to the 200 ppb benchmark, the two study areas’ estimates are as 

 

54 Details regarding the sensitivity analyses focused on the impact of the adjustment approach are presented in the 

REA, section 6.2.2.1.
3-45

high as 0.7 percent,55 on average across the 3-year period, and range up to as high as 2.2%56 in a 

single year (Table 3-3). Less than 0.1% of either area’s children with asthma were estimated to 

experience multiple days with such an exposure at or above 200 ppb (REA, Table 6-9). 

Additionally, in the study area with the highest estimates (Indianapolis), approximately a quarter 

of a percent of simulated children with asthma were estimated to experience a day with a 5-

minute exposure at or above 300, on average across the 3-year period; the percentage was 0.1% 

for the 400 ppb benchmark (Table 3-3). 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).

Table 3-3. Air quality conditions adjusted to just meet the current standard: Percent of 

simulated populations of children with asthma estimated to experience at least 

one daily maximum 5-minute exposure per year at or above indicated 

concentrations while breathing at an elevated rate. 

5-minute 

Exposure 

Concentration

(ppb)

Percent (%) of Population of Children (5-18 years) with Asthma

Average per year A 

Fall River, MA Indianapolis, IN Tulsa, OK

> 100 19.4 – 26.7 22.4 – 23.0 0.1 – 0.4

> 200 <0.1 B – 0.7 0.6 – 0.7 C 0

> 300 0 0.2 – 0.3 D 0

> 400 0 <0.1 – 0.1 D 0

A The values presented in each cell are the average of the results for the three years simulated based on the two 

approaches to air quality adjustment (drawn from Table 6-8 of the REA). 

B <0.1 is used to represent nonzero estimates below 0.1%. A value of zero (0) indicates there were no individuals 

estimated to have the selected exposure in any year.

C The highest single year result for 200 ppb was for Fall River where the estimate ranged up to 2.2% (for the 

second air quality adjustment approach in REA, Table 6-8).

D The highest single year results for 300 and 400 ppb were for Indianapolis where the estimates ranged up to 

0.8% and 0.3%, respectively (REA, Table 6-8).

We next consider the estimates for risk of lung function decrements in terms of a 

doubling or more in sRaw, focusing on results for children with asthma (Table 3-4). The 

estimates for the Tulsa study area are lower than for the other two areas (Table 3-4), the results 

for which are summarized next.

 

55 This percentage in the Fall River study area corresponds to 28 children with asthma, while in the larger 

Indianapolis study area, it corresponds to 71 such children (REA, section 5.2 and Appendix J).

56 This percentage, estimated for the Fall River study area, corresponds to 88 children with asthma (REA, Appendix 

J).
3-46

Under air quality conditions just meeting the current standard in the Indianapolis and Fall 

River study areas, as many as 1.3% and 1.1%, respectively,57 of children with asthma, on 

average across the 3-year period, were estimated to experience at least one day per year with a 

SO2-related doubling in sRaw (Table 3-4). 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, and 1% in a single year (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 SO2-related tripling in sRaw (Table 3-4), with 0.2% or less estimated to experience multiple 

such days (REA, Table 6-11).

Table 3-4. Air quality conditions adjusted to just meet the current standard: Percent of 

simulated population of children with asthma estimated to experience at least 

one day per year with a SO2-related increase in sRaw of 100% or more. 

Lung function 

decrement 

(increase in sRaw)

Percent (%) of Population of Children (5-18 years) with AsthmaA

Average per year 

Fall River, MA Indianapolis, IN Tulsa, OK

> 100% 0.9 – 1.1 C 1.3 – 1.3 <0.1 B- <0.1

> 200% 0.1 – 0.2 D 0.3 – 0.3 D 0

A The values presented in each cell are the average of the results for the three years simulated based on two 

approaches to air quality adjustment (drawn from Table 6-7 of the REA). 

B <0.1 is used to represent nonzero estimates below 0.1%. A value of zero (0) indicates there were no individuals 

estimated to have the selected decrement in any year.

C The highest single year result for at least 100% increase in sRaw was for Fall River where the estimate ranged 

up to 1.9% (for the second air quality adjustment approach in REA, Table 6-10).

D The highest single year results for at least 200% increase in sRaw were for Indianapolis and Fall River where 

the estimates ranged up to 0.4%,(REA, Table 6-10).

In understanding these results, we note that the three study areas provide a variety of 

circumstances with regard to population exposure to short-term peak concentrations of SO2 in 

ambient air. These three study areas reflect different combinations of different types of SO2

emissions sources, including utilities using fossil fuels and non-utility sources (REA, section 

3.1), and illustrate three different patterns of exposure to SO2 concentrations in a populated area 

in the U.S. (REA, section 5.1). In this way, the three areas provide a variety of examples of 

exposure patterns that can be informative to the EPA’s consideration of potential exposures and 

risks that may be associated with air quality conditions occurring under the current SO2 standard. 

 

57 The 1.3% estimate in the Indianapolis study area corresponds to approximately 140 children with asthma, and the 

1.1% estimate for Fall River corresponds to 55 such children (REA, section 5.3 and Appendix J).
3-47

While the same conceptual air quality scenario is simulated in all three study areas (i.e., 

conditions that just meet the existing standard), source and population characteristics in the study 

areas contribute to variability in the estimated magnitude of exposure and associated risk across 

study areas.

Where the higher SO2 concentrations that result from the sizeable SO2 sources in a study 

area do not strongly coincide with parts of the area in which people reside and/or frequent, the 

exposure and risk estimates for the 3-year period are relatively lower. The Tulsa study area 

provides an example of such an area (REA, section 5.4). The relationship between SO2

concentrations and population in this area is illustrated in Figure 5-7 of the REA, which 

illustrates the relationships between population distribution and locations with relatively lower 

design values that contribute to this study area having exposure and risk estimates that are lower 

than those estimated for the other two study areas (REA, section 5.1). These differences occur

even though total study area population size is similar to that for the Fall River study area (REA, 

sections 5.1 and 5.4).

Where the simulated air quality conditions for a study area includes relatively large 

spatial extents of higher concentrations – i.e., areas with design values in proximity to the level 

of the standard – that overlap with the more populated parts of the study area, exposure and risk 

results are relatively higher (REA, section 5.4). Among the three study areas, this best describes 

the Fall River and Indianapolis study areas, which are areas where source characteristics 

contribute to a sizeable spread of source-influenced relatively higher concentrations that coincide 

or overlap with locations where people reside and/or frequent. This association between 

concentrations and population in these two areas is illustrated in Figures 5-5 and 5-6 of the REA. 

Inclusion of areas with these characteristics in the REA provides some insight into the potential 

exposure and risk associated with other areas across the U.S. with similar characteristics and is 

therefore particularly informative to evaluation of the level of protection provided by the 

standard. 

The REA provides exposure and risk estimates associated with air quality that might 

occur in an area under conditions that just meet the current standard and, in so doing, it illustrates 

the differences likely to occur across various locations with such air quality as a result of areaspecific differences in emissions and population characteristics. In the context of the overarching 

question for the review regarding whether the currently available information calls into question 

the adequacy of the current standard (see section 3.1.2 above), our discussions here and in the 

sections below, accordingly, focus particularly on results for the areas with combinations of 

emissions and population characteristics that contribute to relatively higher exposures and risk

(Indianapolis and Fall River).
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For these areas, the REA indicates that the percent of children with asthma that might be 

expected to experience 5-minute SO2 concentrations at or above the 200 ppb benchmark 

concentration, in an urban area that just meets the current standard, may be as high as 0.7%, on 

average across the three years, and 2.2% in a single-year period (Table 3-3). With regard to the 

300 ppb and 400 ppb benchmarks, these percentages may be as high, respectively, as 0.3 and 

0.1% on average across the three years and 0.8% and 0.3% in a single-year period (Table 3-3). 

With regard to the lung function risk, the REA indicates the percent of children that might be 

expected to experience at least a doubling of specific airway resistance, under conditions just 

meeting the current standard, may be as high as 1.3%, on average across the 3-year period, and 

1.9% in a single year (Table 3-4). 

In framing these same exposure estimates from the perspective of estimated protection 

indicated to be provided by the current standard, these results for the Fall River and Indianapolis 

study areas indicate that, in the single year with the highest concentrations across the 3-year 

period, nearly 98% to just over 99% of the population of children with asthma would not be 

expected to experience such a day with an exposure at or above the 200 ppb; between 99.7% and 

just over 99.9% would not be expected to experience such a day with exposure at or above the 

400 ppb benchmark. These and the similar estimates for a doubling or more in sRaw are of a 

magnitude roughly consistent with the level of protection that was described in establishing the 

now-current standard in 2010 (as summarized in section 3.1.1.2.4 above).58 As noted in section 

3.2.2.1 above, the current REA additionally provides estimates for a 3-year simulation period, 

consistent with the form established for the now-current standard. Such estimates for the 

Indianapolis study area, on average across the 3-year period, indicate that 99.9% and 99.3% of 

the population of children with asthma would not be expected to experience a day with an 

exposure at or above 400 ppb and 200 ppb, respectively (Table 3-3 above).

3.2.2.3 Uncertainties

In this section, we consider the uncertainties associated with the quantitative estimates of 

exposure and risk, including those recognized by the characterization of uncertainty in the REA

 

58 Although the 2009 REA did not include an air quality scenario representing the now-current standard, among the 

scenarios it did include were single-year air quality scenarios representing standard levels of 100 and 50 ppb. For 

the single-year scenario representing a standard level of 100 ppb in the study area with the highest population 

exposure and risk (St. Louis), the 2009 REA estimated 2.7% of children with asthma to experience at least one 

day with exposure at or above 200 ppb, while at elevated ventilation (2.1-2.9% to experience one or more SO2-

attributable increases in sRaw of at least 100%); this estimate was 0.09% for the scenario representing a standard 

level of 50 ppb (0.4-0.9% to experience one or more SO2-attributable increases in sRaw of at least 100%) (2009 

REA, Table 9-8 and Appendix B). While we recognize a number of differences between the 2009 REA and the 

quantitative modeling and analyses performed in the current REA, we note that the single year estimates for the 

Indianapolis and Fall River study areas in the current REA fall between the estimates for the two most similar air 

quality scenarios assessed in the last review.
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(REA, section 6.2). The characterization in the REA is based on an approach intended to identify 

and compare the relative impact that important sources of uncertainty may have on the exposure 

and risk estimates. The approach used has been applied in REAs for past NAAQS reviews for 

ozone, nitrogen oxides, carbon monoxide (U.S. EPA, 2008; 2010; 2014) and SOX (U.S. EPA,

2009). In the characterization of uncertainty for the current analysis, the REA utilized a 

qualitative uncertainty characterization approach adapted from the WHO approach for 

characterizing uncertainty in exposure assessment (WHO, 2008) accompanied by quantitative 

sensitivity analyses of key aspects of the assessment approach. This characterization and 

analyses are described in detail in chapter 6 of the REA. The approach used in the REA varies 

from that of WHO (2008) in that the REA approach placed 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 estimated exposures and 

health risk results). 

The characterization and analyses in the REA involve consideration of the various types 

of inputs and approaches that together result in the exposure and risk estimates for the three 

study areas. In so doing, the REA considers the limitations and uncertainties underlying these 

inputs and approaches and the extent of their influence on the resultant exposure/risk estimates. 

Consistent with the WHO (2008) guidance, the overall impact of the uncertainty is scaled by 

considering the extent or magnitude of the impact of the uncertainty 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/risk estimates (e.g., likely to over- or under-estimation). 

• What are the key uncertainties associated with the exposure and risk estimates, 

including those of particular significance with regard to drawing conclusions as to 

the adequacy of the protection afforded by the current SO2 standard?

Based on the uncertainty characterization and associated analyses in the REA and 

consideration of associated policy implications, we recognize several areas of uncertainty as 

particularly important in our consideration of the exposure and risk estimates, as was also the 

case in the last review. Generally, these areas include estimation of the spatial distribution of SO2

concentrations across each study area under air quality conditions just meeting the existing 

standard, including the fine-scale temporal pattern of 5-minute concentrations. Among other 

areas, we additionally recognize the uncertainty with regard to population groups and exposure 

concentrations for which the health effects evidence base is limited or lacking.

With regard to the spatial distribution of SO2 concentrations, the REA recognizes some 

uncertainty associated with the model estimates of 1-hour concentrations and the approach used 

to adjust the air quality surface to concentrations just meeting the current standard. The REA 
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analyzed the potential quantitative impact of this uncertainty on the exposure and risk estimates 

by deriving estimates based on an alternative adjustment approach (described in section 6.2.2.1

of the REA). As discussed in section 3.2.2.2 above, we have considered estimates from both 

approaches in summarizing the REA estimates. Additionally, we recognize uncertainty in the 

estimation of concentrations associated with SO2 emissions sources not explicitly modeled (e.g., 

REA, Table 6-3) and in the estimates of 5-minute concentrations in ambient air across the 

modeling receptors in each study area. While the ambient air monitoring dataset available to 

inform these estimates is much expanded in this review over the dataset available in the last 

review, we are still drawing on relationships occurring at one location and over one range of 

concentrations to estimate the fine-scale temporal pattern in concentrations at other locations. 

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. While we recognize this as an 

important area of uncertainty, the approach used has taken into account the currently available 

information and is considered to provide a reasonable representation of fine-scale temporal 

variability in the three study areas. 

We also recognize an important area of uncertainty that is particular to our interpretation 

of the lung function risk estimates. This area concerns estimates of lung function risk derived for 

exposure concentrations below those represented in the evidence base. The exposure-response 

function on which the primary risk estimates are based generates non-zero predictions of a 

percent of the at-risk population exposure expected to experience a day with at least a doubling 

of sRaw for all exposures experienced while breathing at an elevated rate. In considering these 

estimates, we recognize that the uncertainty in the response estimates increases substantially with 

decreasing exposure concentration below those supported by study data. In so doing, we note the 

appreciable contribution to the risk estimates of exposure concentrations below 200 ppb; the 

large majority of 5-minute exposure concentrations contributing to estimated occurrences of a 

doubling or more in sRaw were between 50 and 150 ppb, while none were below 40 ppb (REA, 

section 5.3). 

Other areas of uncertainty concern the potential influence of SO2 exposure history and 

co-exposure to other pollutants on the relationship between short-term SO2 exposures and 

respiratory effects. With regard to the former, we note that 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 increased sRaw. While the health effects evidence indicates the 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 
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repeated exercising exposure events over an hour (Kehrl et al., 1987),59 information is somewhat 

limited with regard to the length of time after recovery from one exposure by which a repeat 

exposure would elicit a similar effect as that of the initial event. With regard to the potential 

influence of copollutants on SO2-related health risk, we note the very limited information 

regarding the potential for the presence of other commonly occurring pollutants to affect 

individual response to SO2, as summarized in section 3.2.1.4 above.

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 SO2 in ambient air. As 

recognized in sections 3.2.1.1 and 3.2.1.4, the controlled human exposure study evidence base 

does not include studies of children younger than 12 years old, and is extremely limited with 

regard to studies of people with more severe asthma.

60 The limited evidence that informs our 

understanding of potential risk to these groups is uncertain but indicates the potential for them to 

experience greater effects or have lesser reserve to protect against such effects than other 

population groups with asthma under similar exposure circumstances, as summarized in section 

3.2.1.4 above. Further we note the lack of information on the factors contributing to increased 

susceptibility to SO2-induced bronchoconstriction among some people with asthma. Thus, there 

is uncertainty associated with our interpretation of the exposure/risk estimates with regard to the 

extent to which they represent the populations at greatest risk of SO2-related respiratory effects

that is important to consideration of the exposure and risk results with regard to the adequacy of 

protection provided by the current standard.

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, we recognize several here as particularly important, noting that 

they are generally similar to uncertainties recognized in the last review. These include 

uncertainty related to estimation of the spatial and temporal pattern of 5-minute concentrations in 

ambient air for the current standard scenario; the prevalence of different exposure circumstances 

represented by the three study areas; the lack of information from controlled human exposure 

studies for the lower, more prevalent, concentrations of SO2; and, characterization of risk for 

particular subgroups of people with asthma that may be at greater risk.

 

59 This study exposed mild asthmatic males to 1.0 ppm SO2 during three 10-minute exercise periods separated by 

15-minute rest periods within the chamber. The sRaw response to SO2 decreased linearly from the first to the 

second and the third SO2 exposures with the response following the third exposure being statistically less than 

after the first (Kehrl et al., 1987).

60 We additionally recognize that limitations in the activity pattern information for children younger than five years 

old precluded their inclusion in the populations of children simulated in the REA.
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3.2.2.4 Potential Public Health Implications

In considering public health implications of the quantitative exposure and risk estimates 

that may inform the Administrator’s judgments in this area, this section discusses the information 

pertaining to the following question. 

• To what extent are the estimates of exposures and risks to at-risk populations that 

remain under conditions just meeting the current SO2 standard important from a 

public health perspective?

Several factors are important to consideration of public health implications. These 

include the magnitude or severity of the effects associated with the exposures estimated in the 

REA, as well as their adversity at the individual and population scale. Other important 

considerations include the size of the population estimated to experience such effects or to 

experience exposures associated with such effects. These considerations are discussed below.

Based on the currently available evidence which is largely consistent with that available 

in the last review (as summarized in section 3.2.1 above), the quantitative exposure and risk 

analyses focus on the potential for lung function decrements in people with asthma exposed to 

SO2 while breathing at an elevated rate. Additionally, we have again focused on estimates for 

two types of risk metrics, one involving comparison to benchmark concentrations and the second 

involving estimates of lung function risk with regard to moderate or greater increases in sRaw. In 

considering these estimates, we recognize that although the lung function decrements, which are 

related to bronchoconstriction, are expected to be transient, we additionally recognize that such 

decrements, while occurring, may contribute to a diminished reserve in lung function (ISA, p. 1-

17, section 5.2.1.2). For population groups already at diminished reserve, such as those with 

more severe asthma, this may be particularly important. Thus, the discussion here reflects 

consideration of the health evidence, and exposure and risk estimates, as well as the 

consideration of potential public health implications in previous NAAQS decisions and ATS 

policy statements (as also discussed in section 3.2.1.5).

In light of the conclusion that among all people with asthma, children may be particularly 

at risk (summarized in section 3.2.1.2 above) and the REA findings of higher exposures and risks

for children (in terms of percent of that population), we have focused the discussion here on 

children. We recognize that the REA estimates indicate that in some areas of the U.S. where SO2

concentrations just meet the current standard, on average across the 3-year period simulated 

(consistent with the form of the current standard), less than 1%, 0.3% and 0.1% of the simulated 

population of children with asthma might be expected to experience a single day per year with a 

5-minute exposure at or above 200 ppb, 300 ppb and 400 ppb, respectively, while breathing at an 

elevated rate. With regard to the lowest benchmark considered (100 ppb), the corresponding 

percentage is approximately 20 to 25%, with higher percentages in some individual years. 
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With regard to estimates of lung function decrements, the REA indicates that in some 

such areas, approximately 1% of children with asthma, on average across a 3-year period, might 

be expected to experience at least one day per year with a SO2-related increase in sRaw of 100% 

or more; the estimate for two or more days is lower, at 0.4% (REA, Table 6-8). Additionally, 

under such conditions (just meeting the current standard), the estimated percent of children with 

asthma that might be expected to experience a single day per year with a SO2-related increase in 

sRaw of 200% or more, on average across the 3-year period, is 0.2 to 0.3% (Table 3-4).

In considering the severity of responses associated with the REA estimates, we take note 

of the health effects evidence for the different benchmark concentrations and judgments made 

with regard to the severity of these effects in the last review. As in the last review, we recognize 

that the responses documented for exposures of 400 ppb are frequently accompanied by 

respiratory symptoms and thus are appropriately considered to be adverse respiratory effects 

consistent with past and recent ATS position statements. At 300 ppb, statistically significant 

increases in lung function decrements (specifically reduced FEV1) have been documented in 

analyses of the subset of controlled human exposure study subjects with asthma that are 

responsive to SO2 at concentrations below 600 or 1000 ppb (ISA, p. 153 and Table 5-21; Johns 

et al., 2010). With regard to the lower benchmark concentration of 200 ppb, we recognize that, 

while the responses documented in studies of exercising subjects with asthma are not 

consistently accompanied by respiratory symptoms, conclusions in past NAAQS reviews 

recognized that moderate decrements in lung function can be clinically significant in some 

individuals with asthma (75 FR 35526, June 22, 2010). Accordingly, the Administrator in the last 

review considered effects associated with exposures as low as 200 ppb to be adverse in light of 

CASAC advice, 61 ATS statements and conclusions in past NAAQS reviews (75 FR 35546, June 

22, 2010). While noting the very limited or lack of such information for some population groups 

with asthma, including primary-school-age children and people with more severe asthma, we 

additionally recognize the uncertainty with regard to effects that might be associated with 

exposures as low as 100 ppb (as discussed in section 3.2.1.3 and 3.2.1.4 above).

The size of the at-risk population (people with asthma, particularly children) in the U.S. 

is substantial. As summarized in section 3.2.1.5, nearly eight percent of the total U.S. population 

(more than 24 million people) and 8.4% of U.S. children have asthma. The asthma prevalence in 

U.S. child populations of different races or ethnicities ranges from 7.4% to 13.4% (Table 3-2 

above). This is well reflected in the REA study areas in which the asthma prevalence ranged 

from 8% to 8.7% of the total populations and 9.7% to 11.2% of the children, with the highest 

 

61 In the last review, the CASAC letter on the first draft SO2 REA to the Administrator stated: “CASAC believes 

strongly that the weight of clinical and epidemiology evidence indicates there are detectable clinically relevant 

health effects in sensitive subpopulations down to a level at least as low as 0.2 ppm SO2” (Henderson, 2008).
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prevalence represented in the Fall River study area. In each study area, the prevalence varies 

among census tracts, with the highest tract in Fall River having a prevalence in boys of 21.5%

and the highest tract in Indianapolis having a prevalence in girls of 19.4% (REA, Table 4-1). 

In considering the public health implications of the REA estimates, we recognize that 

current SO2 concentrations measured in ambient air in all three of the REA study areas are lower 

than those simulated in the air quality assessed. In so doing, we note the purpose for the study 

areas is to provide examples of exposure circumstances that may occur in areas that just meet the 

current standard, and not to estimate exposure and risk associated with conditions occurring in 

those specific locations today. However, concentrations in numerous areas across the U.S. 

contribute to air quality that is near or above the existing standard. For example, 15 core-based 

statistical areas62 were identified with 2014-2016 design values above the existing standard level 

of 75 ppb, including areas with sizeable populations.63 Accordingly, we recognize that, while 

concentrations in the specific areas simulated in the REA may be lower today than the three year 

period simulated in the assessment, the exposure and risk estimates for these areas are 

informative to consideration of exposures and risks in areas still existing across the U.S. that 

have source and population characteristics similar to the study areas assessed, and with ambient 

concentrations of SO2 that just meet the current standard today or that will be reduced to do so at 

some period in the future. Thus, such air quality and exposure circumstances are of particular 

importance in considering whether the currently available information calls into question the 

adequacy of public health protection afforded by the current standard. 

In considering the potential extent of similar areas is in the U.S. today, we recognize that 

the monitoring network information on SO2 concentrations in populated areas across the U.S. 

provides evidence of the occurrence of such exposure circumstances of interest in multiple 

regions of the U.S. (as indicated by the 2014-2016 design values referenced above). There are, 

however, limitations with regard to the extent that it might be expected to capture all areas with 

the potential to exceed the standard and uncertainty related to the extent to which monitors in the 

SO2 monitoring network are located in populated areas with air quality impacted by large sources 

of SO2 emissions. In recognition of this limitation, we also examined the proximity of 

populations to sizeable SO2 point sources using the most recently available emissions inventory 

 

62 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. Populations in the 15 CBSAs referred 

to here range from approximately 30,000 to more than a million (based on 2016 U.S. Census Bureau estimates).

63 Table 5c. Monitoring Site Listing for Sulfur Dioxide 1-Hour NAAQS in the Excel file labeled 

So2_designvalues_20142016_final_07_19_16.xlsx downloaded from https://www.epa.gov/air-trends/air-qualitydesign-values on January 26, 2018.
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information (2014). For example, this information indicates there to be many densely-populated 

areas in the U.S. in which there are facilities with sizeable SO2 emissions (e.g., Appendix F).64

Information is not currently available to estimate numbers of children with asthma in such areas,

making it difficult to estimate the numbers of people potentially at risk. However, the available 

information indicates that there are more than 300,000 children living within 1 km of facilities 

emitting at least 1,000 tpy of SO2 and more than a million within 5 km (Table 3-5). Simply 

considering the asthma prevalence at the national scale of approximately 8%, this information 

indicates on the order of 24,000 to more than 100,000 children with asthma living in areas with 

sources such as those assessed in the REA. It is important to clarify, however, that ambient air 

concentrations of SO2 in the vast majority of the U.S. are well below the current standard, as 

indicated by Figure 2-7 above.65 Thus, while the population counts in Table 3-5 may convey 

information regarding the size of populations living near sources, the concentrations in most 

areas are currently well below the conditions assessed in the REA.

Table 3-5. Population size near larger sources of SO2 emissions.

Sources emitting at least 1,000 tpy (N = 527 facilities)

Population within:

1 km 2 km 3 km 5 km 10 km

All Ages 1,309,212 1,529,478 2,625,196 6,067,574 23,161,915 

Younger Than 18 Years 300,966 341,817 603,261 1,440,466 5,436,439 

Sources emitting at least 2,000 tpy (N = 372 facilities)

Population within:

1 km 2 km 3 km 5 km 10 km

All Ages 248,007 438,760 1,281,473 2,969,007 14,280,740 

Younger Than 18 Years 61,823 103,169 308,289 713,235 3,401,327 

Sources: SO2 Facilities – NEI 2014 v2, Population – U.S. Census 2010

tpy = tons per year

 

64 Although source characteristics and meteorological conditions - in addition to magnitude of emissions - influence 

the distribution of concentrations in ambient air, Appendix F focuses on the distribution of large sources, rather 

than ambient concentrations, due to limitations in the available information with regard to spatial (and temporal) 

patterns of SO2 concentrations in the proximity of such sources in urban areas (ISA, section 2.5.2.2).

65 As discussed in the ISA, “the point source nature of these emissions contributes to the relatively high spatial 

variability of SO2 concentrations (both ambient and exposure)” and “[a]nother contributing factor to spatial 

variability is the dispersion and oxidation of SO2 in the atmosphere” which results in “decreasing ambient SO2

concentrations with increasing distance from sources” (ISA, section 3.2.3). The ISA additionally notes that “SO2

from point sources travels as a plume, which may or may not impact portions of an urban area depending on 

meteorological conditions” (ISA, section 3.2.3).
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Although exposure and risk estimates were not available in the last review for air quality 

conditions just meeting the now-current standard, the findings and considerations summarized 

here are generally similar to those considered in the last review, and indicate a level of protection 

consistent with that described in the 2010 decision. The exposure and risk estimates for the three 

study areas assessed in the REA for this review reflect differences in exposure circumstances

among those areas and illustrate the exposures and risk that might be expected to occur in other 

areas with such circumstances under air quality conditions that just meet the current standard. 

Thus, the REA estimates indicate the magnitude of exposure and risk that might be expected in 

some areas and illustrate the importance to consideration of the public health protection afforded 

by the current standard of those areas where locations of relatively higher SO2 concentrations in 

ambient air across the area coincide with the locations of higher population density.

In summary, the considerations raised here are important to conclusions regarding the 

public health significance of the REA results. We recognize that such conclusions also depend in 

part on public health policy judgments that will weigh in the Administrator’s decision in this 

review with regard to the adequacy of protection afforded by the current standard. Such 

judgments that are common to NAAQS decisions include those related to public health 

implications of effects of differing severity (75 FR 355260 and 35536, June 22, 2010; 76 FR 

54308, August 31, 2011; 80 FR 65292, October 26, 2015). Such judgments also include those 

concerning the public health significance of effects at exposures for which evidence is limited or 

lacking, such as effects at the lower benchmark concentrations considered and lung function risk 

estimates associated with exposure concentrations lower than those tested in the controlled 

exposure studies. 

3.2.3 CASAC Advice

In our consideration of the adequacy of the current standard, in addition to the evidenceand risk/exposure-based information discussed above, we have also considered the advice and 

recommendations of the CASAC, based on their review of the ISA, the REA Planning 

Document, the draft REA, and the earlier draft of this document, as well as comments from the 

public on the earlier draft of this document.

A limited number of public comments have been received in this review to date, 

including comments focused on the draft IRP, the REA Planning Document, the draft REA or 

the draft PA. Of the five commenters that addressed adequacy of the current primary SO2

standard, two are in agreement with staff conclusions in the draft PA. One expressed the view 
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that the standard should be revised to be more restrictive and two others recommended 

consideration be given to a less restrictive standard.66

In their comments on the draft PA, the CASAC SOX Panel concurred with staff’s overall 

preliminary conclusions that it is appropriate to consider retaining the primary current standard 

without revision, stating that “the current scientific literature does not support revision of the

primary NAAQS for SO2” (Cox and Diez Roux, 2018, p. 1 of letter). The CASAC further noted

that “the new scientific information in the current review does not lead to different conclusions 

from the previous review” (Cox and Diez Roux, 2018, p. 3 of letter). Thus, the CASAC stated 

that “based on review of the current state of the science, the CASAC supports retaining the 

current standard, and specifically recommends that all four elements (indicator, averaging time, 

form, and level) should remain the same” (Cox and Diez Roux, 2018, p. 3 of letter). The CASAC 

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

With regard to indicator, SO2 is the most abundant of the gaseous SOX species. 

Because, as the PA states, “the available scientific information regarding health 

effects was overwhelmingly indexed by SO2”, 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 scientific evidence from the controlled human 

exposure studies used in the previous NAAQS review, which show a causal effect 

of SO2 exposure on asthma exacerbations. Specifically, controlled five-minute 

average exposures as low as 200 ppb lead to adverse health effects. Although 

there is no definitive experimental evidence below 200 ppb, the monotonic doseresponse suggests that susceptible individuals could be affected below 200 ppb. 

Furthermore, short-term epidemiology studies provide supporting evidence even 

though these studies cannot rule out the effects of co-exposures and are limited by 

the available monitoring sites, which do not adequately capture population 

exposures to SO2. Thus, the CASAC concludes that the 75 ppb average level, 

based on the three-year average of 99th percentile daily maximum one-hour 

concentrations, is protective and that levels above 75 ppb do not provide the same 

level of protection.

The comments from the CASAC also took note of the uncertainties that remain in this 

review, stating that the PA “clearly identifies most of the key uncertainties,” while additionally 

 

66 All written comments submitted to the Agency will be available in the docket for this rulemaking, as will be 

CASAC letters reflecting its review of the earlier draft of this document, of the REA Planning Document and 

draft REA and of drafts of the ISA.
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recognizing several additional uncertainties, including uncertainties in quantifying risk to some 

subpopulations of people with asthma for which there may be potential for increased SO2

sensitivity but for which the scientific evidence is limited or lacking. In so doing, it stated that 

the “CASAC notes that there are many susceptible subpopulations that have not been studied and 

which could plausibly be more affected by SO2 exposures than adults with mild to moderate 

asthma,” providing as examples people with severe asthma and obese children with asthma, and 

citing physiologic and clinical understanding (Cox and Diez Roux, 2018b, p. 3 of letter). The 

CASAC stated that “[i]t is plausible that the current 75 ppb level does not provide an adequate 

margin of safety in these groups[, h]owever because there is considerable uncertainty in 

quantifying the sizes of these higher risk subpopulations and the effect of SO2 on them, the 

CASAC does not recommend reconsideration of the level at this time” (Cox and Diez Roux, 

2018b, p. 3 of letter).

The CASAC additionally recognized a number of areas for future research and data 

gathering that would inform the next primary SO2 NAAQS review (Cox and Diez Roux, 2018).

These are reflected in section 3.3 below.

3.2.4 Staff Conclusions on the Current Standard

This section describes staff conclusions regarding the adequacy of the current primary 

SO2 standard. These conclusions are based on considerations described in the sections above, 

and in the discussion below regarding the currently available scientific evidence (as summarized 

in the ISA, and the ISA and AQCDs from prior reviews), and the risk and exposure information 

drawn from the REA. Further, these staff conclusions have taken into account advice from the 

CASAC and public comment on the draft PA and the associated preliminary staff conclusions.

Taking into consideration the discussions responding to specific questions above in this 

and the prior chapter, this section addresses the following overarching policy question.

• Does the currently available scientific evidence- and exposure/risk-based 

information, as reflected in the ISA and REA, support or call into question the 

adequacy of the protection afforded by the current SO2 standard?

In considering this question, we recognize as an initial matter that, as is the case in 

NAAQS reviews in general, the extent to which the current primary SO2 standard is judged to be 

adequate will depend on a variety of factors, including science policy judgments and public 

health policy judgments. These factors include public health policy judgments concerning the 

appropriate benchmark concentrations on which to place weight, as well as judgments on the 

public health significance of the effects that have been observed at the exposures evaluated in the 

health effects evidence. The factors relevant to judging the adequacy of the standards also 

include the interpretation of, and decisions as to the weight to place on, different aspects of the 
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results of the exposure assessment for the three areas studied and the associated uncertainties. 

Thus, we recognize that the Administrator’s conclusions regarding the adequacy of the current 

standard will depend in part on public health policy judgments, science policy judgments 

regarding aspects of the evidence and exposure/risk estimates, and judgments about the level of 

public health protection with an adequate margin of safety that is requisite under the Clean Air 

Act.

Our response to the overarching question above takes into consideration the discussions 

that address the specific policy-relevant questions in prior sections of this document (see sections 

3.2.1-3.2.2) and the approach described in section 3.1 that builds on the approach from the last 

review. We focus first on consideration of the evidence, including that newly available in this 

review, and the extent to which it alters key conclusions supporting the current standard. We 

then turn to consideration of the quantitative exposure and risk estimates drawn from the REA, 

including associated limitations and uncertainties, and the extent to which they indicate differing 

conclusions regarding the magnitude of risk, as well as level of protection from adverse effects, 

associated with the current standard. We additionally consider the key aspects of the evidence 

and exposure/risk estimates emphasized in establishing the now-current standard, and the 

associated public health policy judgments and judgments about the uncertainties inherent in the 

scientific evidence and quantitative analyses that are integral to decisions on the adequacy of the 

current primary SO2 standard.

As an initial matter, we recognize the support in the current evidence for SO2 as the 

indicator for SOX. As recognized in section 3.2.1.1 above, “[o]f the sulfur oxides, SO2 is the 

most abundant in the atmosphere, the most important in atmospheric chemistry, and the one most 

clearly linked to human health effects” (ISA, p. 2-1). Controlled human exposure studies and 

animal toxicological studies provided specific evidence for health effects following exposures to 

SO2, and epidemiologic studies typically analyzed associations of health outcomes with 

concentrations of SO2. The advice received from the CASAC in this review concurs with the use 

of SO2 as the indicator for the standard. We additionally note that measures taken to meet the 

standard in terms of SO2 that may reduce population exposures to SO2 are also likely to reduce 

exposures to other sulfur oxides. Thus, we conclude that the current evidence, including that 

newly available in this review, continues to support a focus on SO2 for the primary NAAQS for 

SOX.

In considering the currently available evidence, staff gives great weight to the longstanding body of health effects evidence for SO2, augmented in some aspects since the last 

review, that provides the foundation of our understanding of the health effects of SO2 in ambient 

air. In so doing, we give particular attention to the evidence from controlled human exposure 

studies that demonstrates that very short exposures to less than 1000 ppb SO2, while breathing at 
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an elevated rate, induces bronchoconstriction in some people with asthma; and, supports the 

identification of people with asthma as the population at risk from short-term peak 

concentrations in ambient air (ISA; 2008 ISA; 1994 AQCD supplement). 

It is such effects associated with short-term exposures against which the current standard,

with its averaging time of one hour, was established to protect. As summarized in section 3.2.1

above and addressed in detail in the ISA, the evidence base in this review does not include new 

evidence of effects associated with other exposure durations. Thus, in considering the 

information available at this time, we continue to focus on short-term exposures as those of 

importance in this review. Air quality analyses summarized in chapter 2 above demonstrate the 

relationship between 1-hour and 5-minute SO2 concentrations in ambient air as did those 

available at the time the standard was set. Further, the chapter 2 analyses indicate the appreciably 

lower prevalence of elevated 5-minute concentrations in areas meeting the current standard 

compared to those that do not (e.g., Figure 2-8 above). As discussed below, protection is also 

provided against exposures associated with such ambient air concentrations.

Further, while the evidence base has been augmented since the time of the last review, we 

note that the newly available evidence does not lead to different conclusions regarding the 

primary health effects of SO2 in ambient air or regarding exposure concentrations associated 

with those effects; nor does it identify different populations at risk of SO2-related effects. In this 

way, the health effects evidence available in this review is consistent with evidence available in 

the last review when the current standard was established. This strong evidence base continues to 

demonstrate a causal relationship between short-term SO2 exposures and respiratory effects, 

particularly in people with asthma. This conclusion is primarily based on evidence from 

controlled human exposure studies available at the time of the last review that reported lung 

function decrements and respiratory symptoms in people with asthma exposed to SO2 for 5 to 10 

minutes while breathing at an elevated rate. Support is also provided by the epidemiological 

evidence that is coherent with the controlled exposure studies. The epidemiological evidence, 

including that recently available, includes studies reporting positive associations for asthmarelated hospital admissions and emergency department visits (of individuals of all ages, 

including adults and children) with short-term SO2 exposures (ISA, section 5.2.1.2).67

The health effects evidence newly available in this review also does not extend our 

understanding of the range of 5-minute exposure concentrations that elicit effects in people with 

asthma exposed while breathing at an elevated rate beyond what was understood in the last 

review. As in the last review, 200 ppb remains the lowest concentration tested in exposure 

 

67 While uncertainties remain related to the potential for confounding by PM or other co-pollutants and the 

representation of fine-scale temporal variation in personal exposures, the findings of the epidemiological studies

continue to provide supporting evidence for the conclusion on the causal relationship (ISA, section 5.2.1.2).
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studies where study subjects are freely breathing in exposure chambers. At that exposure 

concentration, approximately eight to nine percent of study subjects with asthma, breathing at an 

elevated rate, experienced moderate or greater lung function decrements following 5- to 10-

minute controlled exposures. The limited information available for exposure concentrations

below 200 ppb, while not amenable to direct quantitative comparisons with information from 

studies at higher concentrations, generally indicates somewhat lesser response. In considering 

what may be indicated by the epidemiological evidence with regard to exposure concentrations 

eliciting effects, we recognize complications associated with interpretation of epidemiologic 

studies of SO2 in ambient air that relate to whether measurements at the study monitors 

adequately represent the spatiotemporal variability in ambient SO2 concentrations in the study 

areas and associated population exposures (ISA, section 5.2.1.9). 

In this review, as in the last review, we recognize some uncertainty with regard to 

exposure levels eliciting effects in some population groups not included in the available 

controlled human exposure studies, such as individuals with severe asthma, as well as 

uncertainty in the extent of effects at exposure levels below those studied. Collectively, these 

aspects of the evidence and associated uncertainties contribute to a recognition that for SO2, as 

for other pollutants, the available evidence base in a NAAQS review generally reflects a 

continuum, consisting of ambient 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.

As at the time of the last review, the exposure and risk estimates developed from 

modeling exposures to SO2 emitted into ambient air are critically important to consideration of 

the potential for exposures and risks of concern under air quality conditions of interest, and 

consequently are critically important to judgments on the adequacy of public health protection 

provided by the current standard. In considering the public health implications of estimated 

occurrences of exposures of different magnitudes, we take note of guidance from the ATS, the 

CASAC’s written advice and recommendations in past reviews, and judgments made by the EPA 

in considering similar effects in previous NAAQS reviews (75 FR 35526 and 35536, June 22, 

2010). As recognized in section 3.2.1.5, an additional publication by the ATS that further 

addresses judgments on what constitutes an adverse health effect of air pollution is newly 

available in this review (Thurston et al., 2017). The more recent statement expands upon the 

2000 statement, that was considered in the last SO2 NAAQS review, and recognizes additional 

considerations with regard to such judgments that remain consistent with the EPA’s judgments in 

the 2010 review. In that review, the Administrator judged that the effects reported in exercising 

people with asthma following 5- to 10-minute SO2 exposures at or above 200 ppb, and especially 

at or above 400 ppb (often accompanied by respiratory symptoms and for which the evidence is 
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stronger), can result in adverse health effects (75 FR 35536, June 22, 2010). In so doing, she also 

recognized that effects reported for exposures below 400 ppb are less severe than those at and 

above 400 ppb (75 FR 35547, June 22, 2010). 

In considering the REA analyses available in this review, we are aware of a number of 

ways in which these analyses differ from and improve upon those available in the last review. In 

addition to the expansion in the number and type of study areas assessed, we note the number of 

improvements to input data and modeling approaches, including the availability of continuous 5-

minute air monitoring data at monitors within the three study areas. The current REA extends the 

time period of simulation by including 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 considering the REA results, 

we also take note of the array of emissions and exposure circumstances represented by the three 

study areas. As summarized in section 3.2.2 above, the areas fall into three different geographic 

regions of the U.S. They range in total population size from approximately 180,000 to 

approximately one half million, and vary in population demographic characteristics. 

Additionally, the types of large sources of SO2 emissions represented in the three study areas 

vary with regard to emissions characteristics and include EGUs, petroleum refineries, glassmaking facilities, secondary lead smelters (from battery recycling), and chemical manufacturing. 

As at the time of the last review, people with asthma are the population at risk of 

respiratory effects related to SO2 in ambient air. Children with asthma may be particularly at risk 

(section 3.2.1.2 above). While there are more adults in the U.S. with asthma than children with 

asthma, the REA results in terms of percent of the simulated at-risk populations, indicate higher 

exposures and risks for children with asthma as compared to adults. This finding relates to 

children’s greater frequency and duration of outdoor activity (section 3.2.2.2 above). In light of 

these conclusions and findings, we have focused our consideration of the REA results here on 

children.

As can be seen by the variation in exposure estimates, the three study areas in the REA 

represent an array of exposure circumstances, including those contributing to relatively higher 

and relatively lower exposures and associated risk. As recognized in the REA and in section 

3.2.2.2 above, the analyses in the REA are not intended to provide a comprehensive national 

assessment. Rather, the analyses for this array of study areas and air quality patterns are intended 

to indicate the magnitude of exposures and risks that may be expected in areas of the U.S. that 

just meet the current standard but that may differ in ways affecting population exposures of 

interest. In that way, the REA is intended to be informative to the EPA’s consideration of 

potential exposures and risks associated with the current standard and the Administrator’s 

decision on the adequacy of protection provided by the current standard. As discussed in sections 
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3.2.2.2 and 3.2.2.4 above, consideration of exposures occurring in those areas where locations of 

relatively higher SO2 concentrations in ambient air across an area that just meets the current 

standard coincide with the locations of higher population density are particularly important to 

consideration of the public health protection afforded by the current standard, particularly to the 

overarching question concerning the availability of information that calls into question the 

standard’s adequacy.

With regard to the REA representation of air quality conditions associated with just 

meeting the current standard, while we note reduced uncertainty in a few aspects of the approach 

for developing this air quality scenario, we recognize the uncertainty associated with the 

application of adjustments to the highest model receptor in the study area. As summarized in 

sections 3.2.2.2 and 3.2.2.3 above, sensitivity analyses described in section 6.2.2 of the REA 

indicate the quantitative impact potentially associated with this area of uncertainty, which 

appears to be generally small for the Indianapolis study area and somewhat higher for Fall River. 

Given the importance of this aspect of the REA to consideration of the level of protection 

provided by the current standard, we have considered the results for each study area in terms of a 

range bounded on the low end by the results for the main analysis and on the upper end by those 

based on the alternative adjustment approach used in the sensitivity analysis. 

In this context for the air quality scenario for the current standard, with its 1-hour 

averaging time and 99th percentile form, we note that across all three study areas, which provide 

an array of SO2 emissions and exposure situations, the percent of children with asthma estimated 

to experience at least one day with as much as a doubling in sRaw (attributable to SO2), on 

average across the 3-year period, ranges from <0.1 % to 1.3%; the highest study area estimate is 

just under 2% for the highest single year (Table 3-4). Accordingly, results for the three case 

study areas indicate 98.7% or more of at-risk populations to be protected from a SO2-related 

doubling in sRaw, as an average across the 3-year period, and approximately 98% or more 

protected from as much as a single occurrence in a single year. Greater protection (e.g., 99% or 

more) is indicated for multiple occurrences and more severe sRaw increases.

With regard to exposures compared to benchmark concentrations, less than 1% of 

children with asthma are estimated to experience, while breathing at an elevated rate, a daily 

maximum 5-minute exposure per year at or above 200 ppb, on average across the 3-year period, 

with a maximum for the study area with the highest estimates just over 2% in the highest single 

year (Table 3-3). Further, the percentage for at least one day with such an exposure above 400 

ppb is 0.1% or less, as an average across the 3-year period (and 0.3% or less in each of the three 

years simulated across the three study areas). No simulated at-risk individuals were estimated to 

experience multiple such days. Thus, in light of current ATS guidance and CASAC advice, as 

well as EPA conclusions in prior NAAQS reviews, the REA exposure and risk estimates for the 
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current review indicate that the current standard is likely to provide a high level of protection 

from SO2-related health effects to at-risk populations of children and adults with asthma.

As recognized above, the protection afforded by the current standard stems from its 

elements collectively, including the level of 75 ppb, the averaging time of one hour and the form 

of the 99th percentile of daily maximum concentrations averaged across three years. The current 

evidence as considered in the ISA, the current air quality information as analyzed in the REA 

and earlier in this document, and the current risk and exposure information presented in the REA 

and summarized here provide continued support to these elements, as well as to the current 

indicator, as discussed earlier in this section.

In summarizing the information discussed thus far, we reflect on the key aspects of the 

2010 decision that established the current standard. As an initial matter, effects associated with 

5- to 10-minute exposures as low as 200 ppb of people with asthma while breathing at an 

elevated rate were considered to be adverse; this judgment was based on consideration of the 

CASAC’s advice and EPA decisions in prior NAAQS reviews, as well as ATS guidance (75 FR 

35546, June 22, 2010). We note that the newly available information in this review includes an 

additional statement from ATS on adversity which is generally consistent with the earlier 

statement (available at the time of the 2010 decision). 

While recognizing the differences between the current and past analyses, including the 

lack of an air quality scenario specific to the now-current standard in the last review, as well as 

uncertainties associated with such analyses, we note a rough consistency of the associated 

estimates when considering the array of study areas in both reviews. Overall, the newly available 

quantitative analyses appear to comport with the conclusions reached in the last review regarding 

control expected to be exerted by the now-current 1-hour standard on 5-minute exposures of 

concern. With regard to the results for the REA in the last review (which were for a single-year 

simulation), the 2010 decision recognized those results for the area with the highest estimates 

and largest population (St. Louis) to indicate that a one-hour standard with a level between the 

two levels assessed (50 and 100 ppb) might be expected to protect more than 97% of children 

with asthma (and somewhat less than 100%) from experiencing exposures at or above a 200 ppb 

benchmark concentration, and more than 99% of that population group from experiencing 

exposures at or above a 400 ppb benchmark. Single-year results in the current REA for the two 

study areas with the highest estimates (including the area with the most sizeable population, 

Indianapolis) indicate protection of approximately 98 to 99% of the populations of children with 

asthma from experiencing exposures at or above a 200 ppb benchmark concentration and 99.7% 

or more of the study area at-risk populations from exposures at or above 400 ppb. Additionally, 

the 2010 decision also took note of the magnitude of the SO2 concentrations in ambient air in 

U.S. epidemiological studies of associations between ambient air concentrations and emergency 
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department visits and hospital admissions, for which the effect estimate remained positive and 

statistically significant in copollutant models with PM. In considering these studies, the 

Administrator judged that the level chosen for the new 1-hour standard provided an adequate 

margin of safety. No additional such studies are available in the current review (as noted in 

section 3.2.1.3 above). Thus, in considering the main aspects of the decision in the last review, 

we find the currently available information to be consistent with that on which the decision 

establishing the current standard was based. 

Based on all of the above, and taking into consideration related information, limitations 

and uncertainties, such as those recognized above, we draw conclusions regarding the extent to 

which the newly available information in this review supports or calls into question the adequacy 

of protection afforded by the current standard. In considering the conclusions that may be 

supported by the exposure and risk estimates, we take note of the more than 24 million people 

with asthma in the U.S., including more than 6 million children, with potentially 100,000 living 

within 5 km of large sources of SO2 emissions. We additionally note the uncertainties or 

limitations of the current evidence base with regard to the exposure levels at which effects may 

be elicited in some population groups (e.g., children with asthma and individuals with severe 

asthma), as well as the severity of the effects. In so doing, we recognize that the controlled 

human exposure studies, on which the depth of our understanding of SO2-related health effects is 

based, provide little or no information with regard to responses in people with more severe 

asthma or in children younger than 12 years. Additionally, some aspects of our understanding 

continue to be limited; among these aspects are the potential for effects in some people with 

asthma exposed to concentrations below 200 ppb, as well as the potential for other air pollutants 

to affect responses to SO2. In light of this we note the REA results for the lowest benchmark that 

indicate that in some areas of the U.S. with air quality conditions that just meet the current 

standard, approximately 20 to 25% of children with asthma may experience one or more 

exposures, on average across a 3-year period, to concentrations at or above 100 ppb while 

breathing at an elevated rate. Thus, the evidence and exposure/risk information related to the 

lowest exposures studied lead us to conclude that the combined consideration of the body of 

evidence and the quantitative exposure estimates continue to provide support for a standard as 

protective as the current one.

We additionally recognize that conclusions regarding the adequacy of the current 

standard depend in part on public health policy judgments identified above and judgments about 

the level of public health protection that is appropriate, allowing for an adequate margin of 

safety. In so doing, we take note of the long-standing health effects evidence that documents the 

effects of SO2 exposures as short as a few minutes on people with asthma that are exposed while 

breathing at elevated rates and recognize that such effects have been documented in the lowest 
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concentration studied in exposure chambers with appropriate clean-air controls (200 ppb). In so 

doing, we recognize the limitations, and associated uncertainty, in the evidence available for 

lower exposure concentrations (e.g., 100 ppb), as was the case in the last review, and we note the 

lower responses reported. Thus, in focusing on the potential for 5-minute exposures at and above 

200 ppb, and recognizing that it has been previously recognized that exposures to such 

concentrations can result in adverse health effects in people with asthma (June 22, 2010; 75 FR 

35547), we take note of the REA results that indicate the current standard may be expected to 

protect approximately 98% and nearly 99% of populations of children with asthma from

experiencing any days with such exposures, in a single- and 3-year period, respectively. We 

additionally note the REA results that indicate protection of at least 99.7% and 99.9% of children 

with asthma from experiencing any days with a 5-minute exposure of 400 ppb or higher in a 

single and 3-year period, respectively. In light of ATS guidance, CASAC advice and EPA 

conclusions in past NAAQS reviews, these results indicate a high level of protection of at-risk 

populations from SO2-related health effects that we note is consistent with the level of protection 

specified when the standard was set. Thus, we reach the conclusion that the currently available 

evidence and quantitative information, including the associated uncertainties, do not call into 

question the adequacy of protection provided by the current standard, and thus support 

consideration of retaining the current standard, without revision.

In summary, the newly available health effects evidence, critically assessed in the ISA as 

part of the full body of evidence, reaffirms conclusions on the respiratory effects recognized for 

SO2 in the last review. Further, we observe the general consistency of the current evidence with 

the evidence that was available in the last review with regard to key aspects on which the current 

standard is based. We additionally note the quantitative exposure and risk estimates for 

conditions just meeting the current standard that indicate a similar level of protection, for at-risk 

populations from respiratory effects considered to be adverse, as that described in the last review

for the now-current standard. We also recognize, as in the last review, the limitations and 

uncertainties associated with the available information. Collectively, these considerations 

(including those discussed above) provide the basis for the staff conclusion that consideration 

should be given to retaining the current standard of 75 ppb SO2, as the 99th percentile of daily 

maximum 1-hour concentrations averaged across three years, without revision. Accordingly, and 

in light of this conclusion that it is appropriate to consider the current standard to be adequate, 

we have not identified any potential alternative standards for consideration in this review.
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3.3 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH 

AND DATA COLLECTION

In this section, we highlight key uncertainties associated with reviewing and establishing 

the primary NAAQS for sulfur oxides. Such key uncertainties and areas for future research, 

model development, and data gathering are outlined below. In some cases, research in these 

areas can go beyond aiding standard setting to aiding in the development of more efficient and 

effective control strategies. We note, however, that a full set of research recommendations to 

meet standards implementation and strategy development needs is beyond the scope of this 

discussion. Rather, listed below are key uncertainties, research questions and data gaps that have 

been thus far highlighted in this review of the primary standard.

• A critical aspect of our consideration of the evidence and the quantitative dose estimates 

is our understanding of SO2 effects below the lowest concentrations studied in controlled 

human exposure studies. Additional information in several areas would reduce 

uncertainty in our interpretation of the available information for purposes of risk

characterization and, accordingly, reduce uncertainty in characterization of SO2-related 

health effects. 

 A key area of uncertainty relates to whether and to what extent some population 

groups, including young children or people with severe asthma, are more 

responsive to peak SO2 exposures (or responsive to lower concentrations), while 

breathing at elevated rates, than the groups that have been studied. 

 Additional information that might improve our understanding of the effects 

(severity and occurrence) and the shape of the exposure-response relationship 

expected at lower 5-minute exposure concentrations (i.e., below 200 ppb) would 

help to reduce uncertainty in the estimates of lung function effects and, 

accordingly, in characterizing SO2-related health effects.

 A better understanding of the demographic characteristics of people with asthma 

would facilitate greater detail in our characterization of SO2 exposure and risk for 

at-risk populations with asthma. For example, the CASAC has identified people

with asthma who are obese and/or African American, as well as young children 

and those with severe asthma as population groups for which such information is 

needed. 

 Little information is available on the factors contributing to the susceptibility to 

lower concentrations of SO2 of a subgroup of people with asthma, termed 

“responders” in the ISA (ISA, section 5.2.1.2, Table 5-21; Johns and Linn, 2011).

New and innovative studies focused on characterizing this subgroup would 

contribute to improved characterization of SO2-related risk. 

 There is also only very limited evidence regarding the potential influence of 

history of exposure and potential for enhanced effects associated with cooccurring exposure to other air pollutants, such as particulate matter, including

particulate sulfur compounds (as recognized in section 3.2.1.4 above). Further 

research is needed in this area to better inform our characterization of health risk 

related to SO2. 
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• Characterization of the fine-scale spatial and temporal gradients of ambient air SO2

concentrations in residential areas, as well as near sources of SO2 emissions in areas with 

air quality that just meets the current standard, is a key element in our assessment of 

exposure and risk. Additional information in this area is needed to address current 

limitations that contribute to uncertainty in characterization of ambient air SO2 levels in 

the risk assessment and the resulting exposure and risk estimates. 

 Ambient air monitoring data that provides more detailed characterization of the 

fine-scale spatial and temporal variation in ambient air SO2 concentrations in 

different environments and related to different sources would help reduce this 

uncertainty and might support further evaluation of air quality model performance 

in describing fine-scale spatial variation. 

 Additional fine-scale temporal monitoring data (e.g., reporting of all 12 5-minute 

concentrations for each hour at all ambient air monitors) would help to reduce 

uncertainty in our estimation of fine-scale temporal variation.

• Uncertainties with regard to other aspects of the health effects evidence include that 

regarding what may be indicated with regard to exposure concentrations eliciting effects 

by the epidemiologic studies that show an association between short-term SO2 exposures 

and asthma-related hospital admission and emergency department visits. Uncertainty 

remains regarding the extent of copollutant confounding in these studies, particularly by 

PM. Additionally, there is uncertainty related to the representation of exposure through 

fixed site monitors and capturing peak SO2 concentrations that limits the informativeness 

of the ambient air concentrations analyzed in the studies to standard reviews.

• National surveys provide information that supports national and regional estimates of 

asthma prevalence. Additional clarity in this survey information regarding asthma 

prevalence in additional population subgroups, such as those with obesity, as well as 

clarity with regard to the extent of the potential for underestimation related to people with 

undiagnosed asthma, would address some uncertainties noted in this review. 

• While the CHAD is much expanded over the last review, limited information and 

associated uncertainty remain in several aspects of the available human activity data. 

Additional information would reduce uncertainty in these aspects of our exposure and 

risk estimates.

 Collection and analysis of multiday activity patterns that consider the attributes 

most influential to determining long-term activity patterns, as well as related

research, would improve our ability to better evaluate and improve on existing 

approaches used to generate longitudinal activity profiles (as discussed in the 

REA, section 4.3.4). 

 Activity data for some population subgroups, such as people with severe asthma 

and very young children with asthma, as well as people with asthma of different 

ethnic backgrounds, including African Americans, and also people with asthma 

who are obese, would address limitations in the information needed to address

questions related to the potential for activity patterns and, accordingly, exposures 

to differ for such groups.
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Linn, WS; Shamoo, DA; Spier, CE; Valencia, LM; Anzar, UT; Venet, TG; Hackney, JD. 

(1983a). Respiratory effects of 0.75 ppm sulfur dioxide in exercising asthmatics: 

Influence of upper-respiratory defenses. Environ Res 30: 340-348. 

Linn, WS; Venet, TG; Shamoo, DA; Valencia, LM; Anzar, UT; Spier, CE; Hackney, JD. 

(1983b). Respiratory effects of sulfur dioxide in heavily exercising asthmatics: A doseresponse study. Am Rev Respir Dis 127: 278-283.

Linn, WS; Avol, EL; Shamoo, DA; Venet, TG; Anderson, KR; Whynot, JD; Hackney, JD. 

(1984). Asthmatics' responses to 6-hr sulfur dioxide exposures on two successive days. 

Arch Environ Health 39: 313-319. 

Linn, WS; Avol, EL; Peng, RC; Shamoo, DA; Hackney, JD. (1987). Replicated dose-response 

study of sulfur dioxide effects in normal, atopic, and asthmatic volunteers. Am Rev 

Respir Dis 136: 1127-1134. 

Linn, WS; Avol, EL; Shamoo, DA; Peng, RC; Spier, CE; Smith, MN; Hackney, JD. (1988). 

Effect of metaproterenol sulfate on mild asthmatics' response to sulfur dioxide exposure 

and exercise. Arch Environ Occup Health 43: 399-406. 
3-71

Linn, WS; Shamoo, DA; Peng, RC; Clark, KW; Avol, EL; Hackney, JD. (1990). Responses to 

sulfur dioxide and exercise by medication-dependent asthmatics: Effect of varying 

medication levels. Arch Environ Occup Health 45: 24-30.

Magnussen, H; Jorres, R; Wagner, HM; von Nieding, G. (1990). Relationship between the 

airway response to inhaled sulfur dioxide, isocapnic hyperventilation, and histamine in 

asthmatic subjects. Int Arch Occup Environ Health 62: 485-491.

Mazurek JM; Syamlal G. (2018). Prevalence of Asthma, Asthma Attacks, and Emergency 

Department Visits for Asthma Among Working Adults — National Health Interview 

Survey, 2011–2016. MMWR Morb Mortal Wkly Rep 67:377–386.

Nowak, D; Jorres, R; Berger, J; Claussen, M; Magnussen, H. (1997). Airway responsiveness to 

sulfur dioxide in an adult population sample. Am J Respir Crit Care Med 156: 1151-

1156.

Reddel, HK. (2009). Characterizing asthma phenotypes: Predictors and outcomes at the extremes 

of asthma severity [Editorial]. Respirology 14: 778-780. 

Roger, LJ; Kehrl, HR; Hazucha, M; Horstman, DH. (1985). Bronchoconstriction in asthmatics 

exposed to sulfur dioxide during repeated exercise. J Appl Physiol 59: 784-791.

Samet J. (2009). Letter from Johnathan M. Samet, Chair, Clean Air Scientific Advisory 

Committee, to Administrator Lisa P. Jackson. Re: Clean Air Scientific Advisory 

Committee’s (CASAC) Review of EPA's Risk and Exposure Assessment (REA) to 

Support the Review of the SO2 Primary National Ambient Air Quality Standards: Second 

Draft. May 18, 2009.

Sheppard, D; Saisho, A; Nadel, JA; Boushey, HA. (1981). Exercise increases sulfur dioxideinduced bronchoconstriction in asthmatic subjects. Am Rev Respir Dis 123: 486-491.

Sheppard, D; Eschenbacher, WL; Boushey, HA; Bethel, RA. (1984). Magnitude of the 

interaction between the bronchomotor effects of sulfur dioxide and those of dry (cold) air. 

Am Rev Respir Dis 130: 52-55. 

Smith, E. (1993). Subject Data Supplied by the Researchers for the Recent Controlled Human 

Studies Analyzed in the Staff Paper Supplement and Accompanying Memorandum. 

Memorandum to SO2 Doeket (A-84-25). August 11, 1993.

Strickland, MJ; Darrow, LA; Klein, M; Flanders, WD; Sarnat, JA; Waller, LA; Sarnat, SE; 

Mulholland, JA; Tolbert, PE. (2010). Short-term associations between ambient air 

pollutants and pediatric asthma emergency department visits. Am J Respir Crit Care Med 

182: 307-316. 

Thurston, GD; Kipen, H; Annesi-Maesano, I; Balmes, J; Brook, RD;, Cromar, K; De Matteis,

S; Forastiere, F; Forsberg, B; Frampton, MW; Grigg, J; Heederik, D; Kelly, FJ; Kuenzli,

N; Laumbach, R; Peters, A; Rajagopalan, ST; Rich, D; Ritz, B; Samet, JM; Sandstrom,

T; Sigsgaard, T; Sunyer, J; Brunekreef, B. (2017). A joint ERS/ATS policy statement: 
3-72

what constitutes an adverse health effect of air pollution? An analytical framework. Eur 

Respir J 11: 1600419.

Trenga, CA; Koenig, JQ; Williams, PV. (1999). Sulphur dioxide sensitivity and plasma 

antioxidants in adult subjects with asthma. Occup Environ Med 56: 544-547.

Trenga, CA; Koenig, JQ; Williams, PV. (2001). Dietary antioxidants and ozone-induced 

bronchial hyperresponsiveness in adults with asthma. Arch Environ Occup Health 56: 

242-249. 

U.S. EPA. (1994). Supplement to the second addendum (1986) to air quality criteria for 

particulate matter and sulfur oxides (1982): Assessment of new findings on sulfur dioxide 

acute exposure health effects in asthmatic individuals. Environmental Criteria and 

Assessment Office, Office of Health and Environmental Assessment, Office of Research 

and Development, Research Triangle Park, NC, EPA/600/FP-93/002, August 1994. 

Available at: https://www3.epa.gov/ttn/naaqs/standards/so2/s_so2_pr.html

U.S. EPA. (1996). Air Quality Criteria for Ozone and Related Photochemical Oxidants. National 

Center for Environmental Assessment, Office of Research and Development, Research 

Triangle Park, NC, EPA/600/P-93/004aF, July 1996. Available at: 

https://nepis.epa.gov/Exe/ZyPDF.cgi?Dockey=300026GN.PDF

U.S. EPA. (2008). Integrated Science Assessment (ISA) for Sulfur Oxides – Health Criteria 

(Final Report). National Center for Environmental Assessment-RTP Division, Office of 

Research and Development, Research Triangle Park, NC, EPA-600/R-08/047F, 

September 2008. Available at: 

http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=198843

U.S. EPA. (2009). Risk and Exposure Assessment to Support the Review of the SO2 Primary 

National Ambient Air Quality Standard. Office of Air Quality Planning and Standards, 

Research Triangle Park, NC, EPA-452/R-09-007, July 2009. Available at: 

https://www3.epa.gov/ttn/naaqs/standards/so2/data/200908SO2REAFinalReport.pdf

U.S. EPA. (2010). Quantitative Risk and Exposure Assessment for Carbon Monoxide -

Amended. Office of Air Quality Planning and Standards, Research Triangle Park, NC,

EPA-452/R-10-006, July 2010. Available at: https://www.epa.gov/naaqs/carbonmonoxide-co-standards-risk-and-exposure-assessments-current-review

U.S. EPA. (2014). Health Risk and Exposure Assessment for Ozone. Office of Air Quality 

Planning and Standards, Research Triangle Park, NC, EPA-452/R-14-004a, August 2014. 

Available at: https://www.epa.gov/naaqs/ozone-o3-standards-risk-and-exposureassessments-current-review

U.S. EPA. (2016). Integrated Science Assessment (ISA) for Sulfur Oxides – Health Criteria 

(Second External Review Draft). National Center for Environmental Assessment-RTP 

Division, Office of Research and Development, Research Triangle Park, NC, 

EPA/600/R-16/351, December 2016. Available at: 

https://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=326450
3-73

WHO. (2008). WHO/IPCS Harmonization Project Document No. 6. Part 1: Guidance Document 

on Characterizing and Communicating Uncertainty in Exposure Assessment. 

International Programme on Chemical Safety, World Health Organization, Geneva, 

Switzerland. Available at: 

http://www.who.int/ipcs/methods/harmonization/areas/exposure/en/
A-1

APPENDIX A

PREPARATION OF DATA FILES FOR GENERATION OF FIGURES IN CHAPTER 2

The raw data came from pre-generated AQS extract files. Files are located at 

https://aqs.epa.gov/aqsweb/airdata/download_files.html. Documentation of files is located at 

http://aqsdr1.epa.gov/aqsweb/aqstmp/airdata/FileFormats.html. Hourly Data Files were used. A 

separate Hourly Data File for each parameter and year combination was run. The type of SO2

data is determined by the parameter code and duration code and is coded as follows:

• 1-hour values data - parameter code = 42401 and duration code = 1

• 5-minute data (12 observations per hour) - parameter code = 42401 and duration code = H

• 5-minute data (hourly max) – parameter code = 42406 and duration code = 1

For the 1-hour data at a Site/POC to be used, it must have met the following 

completeness criteria:

• 75% or more of the hourly observations in a day (18 or more) must be present.

• 75% or more of the days in a quarter must be present and complete:

• 1st Quarter – 68 observations or 69 observations in leap year

− 2nd Quarter – 69 observations

− 3rd Quarter – 69 observations

− 4th Quarter – 69 observations

• 4 quarters for each of at least 3 of the 5 years (2011-2016) must be present and complete. 

For this analytical purpose, the three years do not have to be consecutive. This dataset 

was prepared in February 2018.

After completeness criteria were applied, the following data screens were also performed 

to account for some outliers in the 5-minute data:

• Only 5 minute data with a corresponding hourly value in AQS (parameter 42401 and 

duration code 1) were kept.

• Only 5 minute values with an hourly mean value under 120% of the hourly value in AQS 

(parameter 42401 and duration code 1) were kept.

• Only hours where a 5-minute max hourly value (AQS parameter 42406 and duration code 

1) was reported and fell between 1 and 12 times the AQS hourly value (parameter 42401 

and duration code 1) were kept.
B-1

APPENDIX B

ADDITIONAL INFORMATION ON DATASETS PRESENTED IN FIGURE 2-8

Table B-1. Summary statistics (in ppb) for distributions of daily maximum 5-minute 

SO2 concentrations on days with differing daily maximum 1-hour SO2

concentrations for 2014-2016.

Bin Daily Maximum 1-hour Concentration (ppb)

<=25 >25-50 >50-75 >75

N 339471 4732 1338 1272

25th percentile 0.8 47.2 95.8 170.1

Median 1.2 62.8 122.6 218.0

Mean 4.4 73.7 137.4 259.5

75th percentile 4.2 88.0 164.2 293.6

95th percentile 19.0 150.0 254.5 512.4

99th percentile 40.5 213.2 352.4 829.6

When the three data sets for sites with DVs at or below 75 ppb are combined, the 

99th percentile is 53.3 ppb and the 99.9th percentile is 131 ppb.

Table B-2. Summary statistics (in ppb) for distributions of daily maximum 5-minute 

SO2 concentrations at sites with differing design values for 2014-2016.

Bin Design Value (ppb)

<=25 >25-50 >50-75 >75

N 259617 48951 19634 18611

25th percentile 0.6 1.5 2.0 2.0

Median 1.5 4.0 6.0 6.0

Mean 3.1 9.8 18.5 38.3

75th percentile 3.1 11.3 23.0 35.7

95th percentile 11.0 36.3 75.0 192.0

99th percentile 26.0 72 130.3 359.3
B-2

Figure B-1. Monitoring data for sites meeting the current standard: Frequency of daily 

maximum 5-minute values on days with differing daily maximum 1-hour concentrations

(2014-2016).

Figure B-2. Monitoring data for sites not meeting the current standard: Frequency of daily 

maximum 5-minute values on days with differing daily maximum 1-hour concentrations 

(2014-2016).

0

50

100

150

200

250

<=25 >25-50 >50-75 >75

Number of Occurrences

Maximum Hourly Concentrations (ppb)

# >100 ppb # >200 ppb # >300 ppb # >400 ppb

0

200

400

600

800

1000

1200

<=25 >25-50 >50-75 >75

Number of Occurrences

Maximum Hourly Concentrations (ppb)

# >100 ppb # >200 ppb # >300 ppb # >400 ppb
C-1

APPENDIX C

OCCURRENCES OF 5-MINUTE SO2 CONCENTRATIONS OF INTEREST

IN THE RECENT AMBIENT AIR MONITORING DATA (2014-2016)

Figure C-1. As is (unadjusted) SO2 monitoring data (2014-2016). Mean number of days/year 

(top panel) and maximum number of days/year (bottom panel) with daily maximum 5-minute 

concentrations of SO2 at or above 100 ppb.

Observation: For DV < 75, 

are monitors in the dataset 

with as many as 80 days 

with a 5-minute

concentration ≥100 ppb.

Observation: For DV < 75, 

are monitors in the dataset 

with, on average, as many 

as 36 days with a 5-minute

concentration ≥100 ppb.
C-2

Figure C-2. As is (unadjusted) SO2 monitoring data (2014-2016). Mean number of days/year 

(top panel) and maximum number of days/year (bottom panel) with daily maximum 5-minute 

concentrations of SO2 at or above 200 ppb.

Observation: For DV < 75, 

are monitors in the dataset 

with, on average, as many 

as 18 days with a 5-minute

concentration ≥200 ppb.

Observation: For DV < 75, 

are monitors in the dataset 

with as many as 32 days 

with a 5-minute

concentration ≥200 ppb.
C-3

Figure C-3. As is (unadjusted) SO2 monitoring data (2014-2016). Mean number of days/year 

(top panel) and maximum number of days/year (bottom panel) with daily maximum 5-minute 

concentrations of SO2 at or above 300 ppb.

Observation: For DV < 75, 

are monitors in the dataset 

with, on average, as many 

as 17 days with a 5-minute

concentration ≥300 ppb.

Observation: For DV < 75, 

are monitors in the dataset 

with as many as 17 days 

with a 5-minute

concentration ≥200 ppb.
C-4

Figure C-4. As is (unadjusted) SO2 monitoring data (2014-2016). Mean number of days/year 

(top panel) and maximum number of days/year (bottom panel) with daily maximum 5-minute 

concentrations of SO2 at or above 400 ppb.

Observation: For DV < 75, 

are monitors in the dataset 

with, on average, as many 

as 7 days with a 5-minute

concentration ≥400 ppb.

Observation: For DV < 75, 

are monitors in the dataset 

with as many as 7 days 

with a 5-minute

concentration ≥400 ppb.
C-5

Figure C-5. Monitoring data (2014-2016), unadjusted. Total number of days across 3-year 

period with daily maximum 5-minute concentrations of SO2 above 100, 200, 300 and 400 ppb

across monitors grouped by design value.
C-6

Figure C-6. Monitoring data (2014-2016) adjusted1 to just meet the current standard (75 

ppb as a 3-year average of annual 99th percentile 1-hour daily maximum concentrations).

Mean number of days/year (top panel) and maximum number of days/year (bottom panel) with 

daily maximum 5-minute concentrations of SO2 at or above 100, 200, 300 and 400 ppb.

 1 Based on 2014-2016 design values, a single adjustment factor was derived for each monitor by dividing 75 by the 

DV. Ambient concentrations for each year in the averaging period were then multiplied by this adjustment factor 

to have the three-year averaging period of ambient concentrations just meet the current standard. The data were 

limited to those with DVs within a factor of 5 (15 ppb < DV < 325 ppb), to limit instances where uncertainties 

associated with the adjustment would be greatest.

10% of monitors in dataset:

 average 5 to 28 days per year 

when the maximum 5-minute 

concentration is above 200 ppb.

 average 2 to 22 days per year 

when the maximum 5-minute 

concentration is above 300 ppb.

 average 2 to 15 days per year 

when maximum 5-minute 

concentration is above 400 ppb. 

10% of monitors in dataset:

 there are as many as 10–32 days per 

year when the maximum 5-minute 

concentration is above 200 ppb.

 there are as many as 4–22 days per 

year when the maximum 5-minute 

concentration is above 300 ppb.

 there are as many as 2–15 days per 

year when the maximum 5-minute 

concentration is above 400 ppb. 
D-1

APPENDIX D

AIR QUALITY INFORMATION FOR GEOGRAPHICAL AREAS

OF THREE SELECTED U.S. EPIDEMIOLOGICAL STUDIES
D-2

Table D-1. Air quality information for geographical areas of the three U.S. epidemiological studies for which the SO2 effect 

estimates for hospital admissions or emergency department visits (for asthma or other respiratory disease) and 

areawide 24-hour average SO2 concentrations remained positive and statistically significant in copollutant models with 

particulate matter.

Study Information Ambient Air Quality A

Study Area Study Time 

Period

Study 

Reference

SO2

Concentration 

Metric

Associated 

with Health 

Outcome

Assignment of 

Monitors to 

Study Subjects 

for Study 

Analyses

Study-reported SO2

Concentrations, B

24-hour average

(ppm)

99th

percentile of 

daily 

maximum 

1-hour 

concentratio

ns across 

study period 

at highest 

monitor in 

study 

dataset (ppb)

Annual 99th

percentile of 

daily maximum 

1-hour 

concentrations 

at monitor 

yielding 

highest design 

value (ppb)

Design Value 

for Current NAAQS

(3-year average of annual 

99th percentile daily 

maximum 1-hour 

concentrations),

ppm

(monitor ID) Mean Upper 

Percentiles

Bronx County, 

NY Jan 1999-Dec 2000 ATSDR 2006 C 24-hr ave 2 monitors collecting 

data in series 12 - 78 D 1999 - E

2000

New York City, 

NY Jan 1999-Dec 2002 Ito et al 2007 24-hr ave Average across all 

(19) monitors

7.8 75th=10

95th=17 82 F

1999 78

1999-2001 73

(36-061-0056) 2000 71

2001 71 2000-2002 69

(36-061-0056) 2002 65

New Haven, CT Jan 1988-Dec 1990 Schwartz, 1995 24-hr ave Average across all 

(6) monitors 29.8 75th =38.2 

90th=60.7 150 G

1988 159

1988-1990 147

(09-009-1123) 1989 167

1990 116

A Air quality information provided here is drawn from monitors reporting to AQS, as documented in Appendix E). Design values are SO2 concentrations for the study area in the statistical form of 

the standard, derived in accordance with 40 CFR, Part 50, Appendix T. Presented is the highest valid design value at a monitor reporting to AQS for specified 3-year period.

B Ambient SO2 concentrations in terms of study metric that are reported in the second draft ISA Table 5-9 (for ATSDR, 2006 and Ito et al., 2007) and Table 5-14 (for Schwartz, 1995). Where 

multiple monitors contribute data, these are the arithmetic mean and percentiles of the dataset of daily multi-monitor average concentrations for the full study period. 

C This study was cited as NY DOH, 2006 in the 2008 ISA.

D This statistic is for combined dataset of 2 monitoring sites due to construction at the initial site (Thompson and Stewart, 2009). Data are from the first monitor (36-005-0073) for the period Jan 1 to 

July 14, 1999. Data are from the second monitor (36-005-0110), approximately 1⁄2 mile northeast of first, for the period Sept 2, 1999 to Nov 22, 2000.

E Due to incomplete quarters or years, there is not a valid design value for a monitor in the Bronx any of the 3-year periods that include the study period.

F This statistic is based on monitor 36-061-0080 (Thompson and Stewart, 2009), for which five quarters of data are available during the study period (from 1999 through first quarter of 2000).

G This statistic is based on monitor 09-009-1123 (Thompson and Stewart, 2009), for which 12 quarters of data are available during the study period (1988 through 1990).
D-3

REFERENCES

ATSDR (Agency for Toxic Substances and Disease Registry). (2006). A study of ambient air 

contaminants and asthma in New York City: Part A and B. Atlanta, GA: U.S. Department 

of Health and Human Services. 

http://permanent.access.gpo.gov/lps88357/ASTHMA_BRONX_FINAL_REPORT.pdf

Ito, K; Thurston, GD; Silverman, RA. (2007). Characterization of PM2.5, gaseous pollutants, 

and meteorological interactions in the context of time-series health effects models. J 

Expo Sci Environ Epidemiol 17: S45-S60. http://dx.doi.org/10.1038/sj.jes.7500627

Schwartz, J; Morris, R. (1995). Air pollution and hospital admissions for cardiovascular disease 

in Detroit, Michigan. Am J Epidemiol 142: 23-35.

Thompson, R; Stewart, MJ. (2009). Memorandum to Sulfur Dioxide Review Docket (EPA-HQOAR-2007-0352). Air Quality Statistics for Cities Referenced in Key U.S. and Canadian 

Hospital Admission and Emergency Department Visits for All Respiratory Causes and 

Asthma. Docket ID No. EPA-HQ-OAR-2007-352-0018.
E-1

APPENDIX E

DERIVATION OF DESIGN VALUES PRESENTED IN APPENDIX D
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

DESIGN VALUE REPORT

Report Request ID: 1565153 Report Code: AMP480 Jun. 20, 2017

Selection Criteria Page 1

User ID: DST

State County City Site Parameter POC AQCR UAR CBSA CSA

EPA

Region

09 009

GEOGRAPHIC SELECTIONS

PROTOCOL SELECTIONS

Parameter

Classification Parameter Method Duration

DESIGN VALUE 42401

SELECTED OPTIONS

SINGLE EVENT PROCESSING

WORKFILE DELIMITER

USER SITE METADATA

MERGE PDF FILES

QUARTERLY DATA IN WORKFILE

AGENCY ROLE

Option Type Option Value

EXCLUDE REGIONALLY CONCURRED EVENTS

,

STREET ADDRESS

YES

NO

PQAO

DATE CRITERIA

1990

Start Date End Date

1990

Tribal

Code

APPLICABLE STANDARDS

Standard Description

SO2 1-hour 2010
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

AIR QUALITY SYSTEM

PRELIMINARY DESIGN VALUE REPORT

Report Date: Jun. 20, 2017

Notes: 1. Computed design values are a snapshot of the data at the time the report was run (may not be all data for year). 

 2. Some PM2.5 24-hour DVs for incomplete data that are marked invalid here may be marked valid in the Official report due to additional analysis.

 3. Annual Values not meeting completeness criteria are marked with an asterisk ('*').

Page 1 of 3
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

AIR QUALITY SYSTEM

PRELIMINARY DESIGN VALUE REPORT

Report Date: Jun. 20, 2017

Notes: 1. Computed design values are a snapshot of the data at the time the report was run (may not be all data for year). 

 2. Some PM2.5 24-hour DVs for incomplete data that are marked invalid here may be marked valid in the Official report due to additional analysis.

 3. Annual Values not meeting completeness criteria are marked with an asterisk ('*').

Page 2 of 3

Pollutant:

Standard Units:

NAAQS Standard:

Statistic:

Sulfur dioxide(42401)

Parts per billion(008)

SO2 1-hour 2010

Annual 99th Percentile Level:

Design Value Year: 1990

REPORT EXCLUDES MEASUREMENTS WITH REGIONALLY CONCURRED EVENT FLAGS.

75 State Name: Connecticut

Site ID STREET ADDRESS

|

|

|

Comp.

Qrtrs

99th

Percentile

Cert&

Eval

|

|

|

Comp.

Qrtrs

99th

Percentile

Cert&

Eval

|

|

|

Comp.

Qrtrs

99th

Percentile

Cert&

Eval

|

|

|

Design

Value

Valid

Ind.

|

|

|

3-Year 1990 1989 1988

09-009-0010

09-009-0017

09-009-1003

09-009-1123

09-009-2123

09-009-3008

EGAN CENTER, MATHEW ST

LOMBARD STREET

ANIMAL SHELTER, COMMERCE ST

715 STATE STREET

Bank St at Meadow St (see c

LYDIA STREET EXTENTION

3

4

4

4

3

 114

 68

 116

 83

 93

*

*

Y

Y

Y

Y

Y

4

3

4

4

4

4

 113

 112

 99

 167

 97

 110

*

3

4

4

4

4

4

 118

 113

 95

 159

 85

 100

* 115

 113

 87

 147

 88

 101

N

N

Y

Y

Y

Y
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

AIR QUALITY SYSTEM

PRELIMINARY DESIGN VALUE REPORT

Report Date: Jun. 20, 2017

Notes: 1. Computed design values are a snapshot of the data at the time the report was run (may not be all data for year). 

 2. Some PM2.5 24-hour DVs for incomplete data that are marked invalid here may be marked valid in the Official report due to additional analysis.

 3. Annual Values not meeting completeness criteria are marked with an asterisk ('*').

Page 3 of 3

M

N

S

U

X

Y

The monitoring organization has revised data from this monitor since the


most recent certification letter received from the state.

The certifying agency has submitted the certification letter and required


summary reports, but the certifying agency and/or EPA has determined


that issues regarding the quality of the ambient concentration data cannot


be resolved due to data completeness, the lack of performed quality


assurance checks or the results of uncertainty statistics shown in the


AMP255 report or the certification and quality assurance report.

The certifying agency has submitted the certification letter and required


summary reports. A value of "S" conveys no Regional assessment regarding


data quality per se. This flag will remain until the Region provides an "N" or


"Y" concurrence flag.

Uncertified. The certifying agency did not submit a required certification


letter and summary reports for this monitor even though the due date has


passed, or the state's certification letter specifically did not apply the


certification to this monitor.

Certification is not required by 40 CFR 58.15 and no conditions apply to be


the basis for assigning another flag value

The certifying agency has submitted a certification letter, and EPA has no


unresolved reservations about data quality (after reviewing the letter, the


attached summary reports, the amount of quality assurance data


submitted to AQS, the quality statistics, and the highest reported


concentrations).

MEANING

CERTIFICATION EVALUATION AND CONCURRENCE FLAG MEANINGS

FLAG
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

DESIGN VALUE REPORT

Report Request ID: 1565370 Report Code: AMP480 Jun. 21, 2017

Selection Criteria Page 1

User ID: DST

State County City Site Parameter POC AQCR UAR CBSA CSA

EPA

Region

36

36

36

36

36

005

047

061

081

085

GEOGRAPHIC SELECTIONS

PROTOCOL SELECTIONS

Parameter

Classification Parameter Method Duration

DESIGN VALUE 42401

SELECTED OPTIONS

SINGLE EVENT PROCESSING

WORKFILE DELIMITER

USER SITE METADATA

MERGE PDF FILES

QUARTERLY DATA IN WORKFILE

AGENCY ROLE

Option Type Option Value

EXCLUDE REGIONALLY CONCURRED EVENTS

,

STREET ADDRESS

YES

NO

PQAO

DATE CRITERIA

2000

Start Date End Date

2002

Tribal

Code

APPLICABLE STANDARDS

Standard Description

SO2 1-hour 2010
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

AIR QUALITY SYSTEM

PRELIMINARY DESIGN VALUE REPORT

Report Date: Jun. 21, 2017

Notes: 1. Computed design values are a snapshot of the data at the time the report was run (may not be all data for year). 

 2. Some PM2.5 24-hour DVs for incomplete data that are marked invalid here may be marked valid in the Official report due to additional analysis.

 3. Annual Values not meeting completeness criteria are marked with an asterisk ('*').

Page 1 of 5
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

AIR QUALITY SYSTEM

PRELIMINARY DESIGN VALUE REPORT

Report Date: Jun. 21, 2017

Notes: 1. Computed design values are a snapshot of the data at the time the report was run (may not be all data for year). 

 2. Some PM2.5 24-hour DVs for incomplete data that are marked invalid here may be marked valid in the Official report due to additional analysis.

 3. Annual Values not meeting completeness criteria are marked with an asterisk ('*').

Page 2 of 5

Pollutant:

Standard Units:

NAAQS Standard:

Statistic:

Sulfur dioxide(42401)

Parts per billion(008)

SO2 1-hour 2010

Annual 99th Percentile Level:

Design Value Year: 2000

REPORT EXCLUDES MEASUREMENTS WITH REGIONALLY CONCURRED EVENT FLAGS.

75 State Name: New York

Site ID STREET ADDRESS

|

|

|

Comp.

Qrtrs

99th

Percentile

Cert&

Eval

|

|

|

Comp.

Qrtrs

99th

Percentile

Cert&

Eval

|

|

|

Comp.

Qrtrs

99th

Percentile

Cert&

Eval

|

|

|

Design

Value

Valid

Ind.

|

|

|

3-Year 2000 1999 1998

36-005-0073

36-005-0080

36-005-0083

36-005-0110

36-047-0011

36-047-0076

36-061-0010

36-061-0056

36-081-0097

36-085-0067

IS 155, 470 JACKSON AV.

MORRISANIA CENTER, 1225-57 

200TH STREET AND SOUTHERN B

IS 52 681 KELLY ST

301 GREENPOINT AVENUE

PS 321 180 7TH AV,

MABEL DEAN HIGH SCH.ANNEX, 

PS 59, 228 E. 57TH STREET, 

56TH AVE AT SPRINGFIELD BLV

SUSAN WAGNER HS, 1200 MAN

1

2

4

0

3

4

4

1

 94

 62

 86

 36

 72

 71

 50

 54

*

*

*

*

*

2

4

1

3

4

4

4

4

4

 68

 77

 98

 51

 54

 79

 78

 53

 46

*

*

*

Y

Y

Y

Y

Y

Y

Y

Y

Y

4

4

4

3

3

4

2

4

 70

 69

 42

 59

 64

 69

 52

 46

*

*

*

Y

Y

Y

Y

Y

Y

Y

Y

 69

 80

 62

 92

 47

 50

 72

 73

 52

 49

N

N

N

N

N

N

N

Y

N

N
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

AIR QUALITY SYSTEM

PRELIMINARY DESIGN VALUE REPORT

Report Date: Jun. 21, 2017

Notes: 1. Computed design values are a snapshot of the data at the time the report was run (may not be all data for year). 

 2. Some PM2.5 24-hour DVs for incomplete data that are marked invalid here may be marked valid in the Official report due to additional analysis.

 3. Annual Values not meeting completeness criteria are marked with an asterisk ('*').

Page 3 of 5

Pollutant:

Standard Units:

NAAQS Standard:

Statistic:

Sulfur dioxide(42401)

Parts per billion(008)

SO2 1-hour 2010

Annual 99th Percentile Level:

Design Value Year: 2001

REPORT EXCLUDES MEASUREMENTS WITH REGIONALLY CONCURRED EVENT FLAGS.

75 State Name: New York

Site ID STREET ADDRESS

|

|

|

Comp.

Qrtrs

99th

Percentile

Cert&

Eval

|

|

|

Comp.

Qrtrs

99th

Percentile

Cert&

Eval

|

|

|

Comp.

Qrtrs

99th

Percentile

Cert&

Eval

|

|

|

Design

Value

Valid

Ind.

|

|

|

3-Year 2001 2000 1999

36-005-0073

36-005-0080

36-005-0083

36-005-0110

36-047-0011

36-047-0076

36-061-0010

36-061-0056

36-081-0097

36-081-0124

36-085-0067

IS 155, 470 JACKSON AV.

MORRISANIA CENTER, 1225-57 

200TH STREET AND SOUTHERN B

IS 52 681 KELLY ST

301 GREENPOINT AVENUE

PS 321 180 7TH AV,

MABEL DEAN HIGH SCH.ANNEX, 

PS 59, 228 E. 57TH STREET, 

56TH AVE AT SPRINGFIELD BLV

Queens College 65-30 Kiss

SUSAN WAGNER HS, 1200 MAN

4

3

2

4

4

1

 71

 81

 69

 71

 50

 57

*

*

*

Y

Y

Y

Y

Y

Y

1

2

4

0

3

4

4

1

 94

 62

 86

 36

 72

 71

 50

 54

*

*

*

*

*

2

4

1

3

4

4

4

4

4

 68

 77

 98

 51

 54

 79

 78

 53

 46

*

*

*

Y

Y

Y

Y

Y

Y

Y

Y

Y

 68

 86

 67

 88

 51

 45

 73

 73

 51

 57

 50

N

N

N

N

N

N

N

Y

Y

N

N
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

AIR QUALITY SYSTEM

PRELIMINARY DESIGN VALUE REPORT

Report Date: Jun. 21, 2017

Notes: 1. Computed design values are a snapshot of the data at the time the report was run (may not be all data for year). 

 2. Some PM2.5 24-hour DVs for incomplete data that are marked invalid here may be marked valid in the Official report due to additional analysis.

 3. Annual Values not meeting completeness criteria are marked with an asterisk ('*').

Page 4 of 5

Pollutant:

Standard Units:

NAAQS Standard:

Statistic:

Sulfur dioxide(42401)

Parts per billion(008)

SO2 1-hour 2010

Annual 99th Percentile Level:

Design Value Year: 2002

REPORT EXCLUDES MEASUREMENTS WITH REGIONALLY CONCURRED EVENT FLAGS.

75 State Name: New York

Site ID STREET ADDRESS

|

|

|

Comp.

Qrtrs

99th

Percentile

Cert&

Eval

|

|

|

Comp.

Qrtrs

99th

Percentile

Cert&

Eval

|

|

|

Comp.

Qrtrs

99th

Percentile

Cert&

Eval

|

|

|

Design

Value

Valid

Ind.

|

|

|

3-Year 2002 2001 2000

36-005-0080

36-005-0083

36-005-0110

36-047-0076

36-061-0010

36-061-0056

36-081-0097

36-081-0124

36-085-0067

MORRISANIA CENTER, 1225-57 

200TH STREET AND SOUTHERN B

IS 52 681 KELLY ST

PS 321 180 7TH AV,

MABEL DEAN HIGH SCH.ANNEX, 

PS 59, 228 E. 57TH STREET, 

56TH AVE AT SPRINGFIELD BLV

Queens College 65-30 Kiss

SUSAN WAGNER HS, 1200 MAN

4

4

4

4

 62

 67

 65

 57

Y

Y

Y

Y

4

3

2

4

4

1

 71

 81

 69

 71

 50

 57

*

*

*

Y

Y

Y

Y

Y

Y

1

2

4

0

3

4

4

1

 94

 62

 86

 36

 72

 71

 50

 54

*

*

*

*

*

 94

 65

 78

 36

 71

 69

 50

 57

 54

N

N

N

N

N

Y

N

N

N
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

AIR QUALITY SYSTEM

PRELIMINARY DESIGN VALUE REPORT

Report Date: Jun. 21, 2017

Notes: 1. Computed design values are a snapshot of the data at the time the report was run (may not be all data for year). 

 2. Some PM2.5 24-hour DVs for incomplete data that are marked invalid here may be marked valid in the Official report due to additional analysis.

 3. Annual Values not meeting completeness criteria are marked with an asterisk ('*').

Page 5 of 5

M

N

S

U

X

Y

The monitoring organization has revised data from this monitor since the


most recent certification letter received from the state.

The certifying agency has submitted the certification letter and required


summary reports, but the certifying agency and/or EPA has determined


that issues regarding the quality of the ambient concentration data cannot


be resolved due to data completeness, the lack of performed quality


assurance checks or the results of uncertainty statistics shown in the


AMP255 report or the certification and quality assurance report.

The certifying agency has submitted the certification letter and required


summary reports. A value of "S" conveys no Regional assessment regarding


data quality per se. This flag will remain until the Region provides an "N" or


"Y" concurrence flag.

Uncertified. The certifying agency did not submit a required certification


letter and summary reports for this monitor even though the due date has


passed, or the state's certification letter specifically did not apply the


certification to this monitor.

Certification is not required by 40 CFR 58.15 and no conditions apply to be


the basis for assigning another flag value

The certifying agency has submitted a certification letter, and EPA has no


unresolved reservations about data quality (after reviewing the letter, the


attached summary reports, the amount of quality assurance data


submitted to AQS, the quality statistics, and the highest reported


concentrations).

MEANING

CERTIFICATION EVALUATION AND CONCURRENCE FLAG MEANINGS

FLAG
F-1

APPENDIX F

GEOGRAPHIC DISTRIBUTION OF CONTINENTAL

U.S. FACILITIES EMITTING MORE THAN 1,000 TPY SO2

AND POPULATION DENSITY BASED ON U.S. CENSUS TRACTS
F-2

Figure F-1. Continental U.S.: Facilities emitting more than 1,000 tpy SO2 (n=619 in 2011 NEI) and population density.
F-3

Figure F-2. Northeast U.S.: Facilities emitting more than 1,000 tpy SO2 and population density.
F-4

Figure F-3. Southeast U.S.: Facilities emitting more than 1,000 tpy SO2 and population density.
F-5

Figure F-4. Northwest U.S.: Facilities emitting more than 1,000 tpy SO2 and population density.
F-6

Figure F-5. Southwest U.S.: Facilities emitting more than 1,000 tpy SO2 and population density.
United States

Environmental Protection

Agency

Office of Air Quality Planning and Standards

Health and Environmental Impacts Division

Research Triangle Park, NC

Publication No. EPA-452/R-18-002

May 2018