Policy Assessment for the Review of 

the Primary National Ambient Air 

Quality Standard for Sulfur Oxides,

External Review Draft
[This page intentionally left blank.]
EPA-452/P-17-003

August 2017

Policy Assessment for the Review of 

the Primary National Ambient Air 

Quality Standard for Sulfur Oxides,

External Review Draft

U. S. Environmental Protection Agency

Office of Air Quality Planning and Standards

Health and Environmental Impacts Division

Research Triangle Park, North Carolina
August 24, 2017 i Draft – Do Not Quote or Cite

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. This document is being circulated to facilitated discussion with the Clean 

Air Scientific Advisory Committee and for public comment to inform the EPA’s consideration of 

the primary national ambient air quality standard for sulfur oxides. This information is 

distributed for purposes of pre-dissemination peer review under applicable information quality 

guidelines. It does not represent and should not be construed to represent any Agency 

determination or policy.

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......................................................................................................... 1-3

1.2.1 Legislative Requirements....................................................................................... 1-3

1.2.2 History of the Reviews of the Primary NAAQS for SOX ...................................... 1-5

1.2.3 Current SO2 NAAQS Review................................................................................ 1-8

1.3 General Approach and Organization of this Document ........................................ 1-10

REFERENCES .......................................................................................................................... 1-11

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.......................................................................................... 2-7

REFERENCES .......................................................................................................................... 2-12

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................................................................... 3-35

3.2.3 Preliminary Staff Conclusions on the Current Standard...................................... 3-51

3.3 Key Uncertainties and Areas for Future Research and Data Collection ..................... 3-58

REFERENCES .......................................................................................................................... 3-60
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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 (2013-2015)

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 with 5-minute data. ................................... 2-4

Figure 2-4. National temporal trend in SO2 concentrations: 1980-2015 (45 sites).................... 2-5

Figure 2-5. Temporal trend in SO2 concentrations: 2000-2015 (227 sites).. ............................. 2-6

Figure 2-6. Temporal trend in daily maximum 5-minute SO2 concentrations: 2011-2015. ...... 2-6

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

99thpercentile daily maximum 1-hour concentrations) at sites with datasets meeting 

completeness requirements for 2013-2015.............................................................. 2-7

Figure 2-8. Distributions of daily maximum 5-minute concentrations during 2013-2015. ..... 2-11

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 

(adapted from Table 5-2 in the second draft ISA)................................................. 3-24

Table 3-2. 2015 National Asthma Prevalence. ....................................................................... 3-34

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 at elevated ventilation.................................................................................. 3-42

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..................... 3-43
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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 1 INTRODUCTION 

2 1.1 PURPOSE 

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

4 Quality Standard for Sulfur Oxides, External Review Draft (hereafter referred to as Draft PA), 

5 presents the draft policy assessment for the U.S. Environmental Protection Agency’s (EPA’s) 

current review of the primary (health-based)1 6 national ambient air quality standard (NAAQS) for 

sulfur oxides (SOX).2 7 The overall plan and schedule for this review were presented in the 

8 Integrated Review Plan for the Primary National Ambient Air Quality Standard for Sulfur 

9 Dioxide (IRP; U.S. EPA, 2014). The IRP also identified key policy-relevant issues to be 

10 addressed in this review and discussed the key documents that generally inform NAAQS 

11 reviews, including an Integrated Science Assessment (ISA), a Risk and Exposure Assessment 

12 (REA), and a Policy Assessment (PA). 

13 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 Administrator.3 14 Ultimately, a 

15 final decision on the primary standard for SOX will reflect the judgments of the Administrator. 

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

17 presented in the ISA and REA, and the judgments required of the EPA Administrator in 

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

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

20 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.4 21 These elements, 

                                                            

1

 The EPA is separately reviewing the welfare effects associated with sulfur oxides and the public welfare protection 

provided by the secondary SO2 standard, in conjunction with a review of the secondary standards for nitrogen 

oxides and particulate matter with respect to their protection of the public welfare from adverse effects related to 

ecological effects (U.S. EPA, 2017a). 

2

 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 is the most prevalent. Particulate 

atmospheric transformation products of SOX, such as sulfates, are addressed in the review of the NAAQS for 

particulate matter. 

3

 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). 

4

 The basic elements of a standard include the indicator, averaging time, form, and level. 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 

obtained and averaged or cumulated. 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. The level of the standard defines 

the air quality concentration used for that purpose (i.e., an ambient air concentration of the indicator). 
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1 which together serve to define each standard, must be considered collectively in evaluating the 

2 health protection afforded by the primary standard for SOX. 

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

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

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

6 (CAA). As discussed below in section 1.2.1, the CASAC is to advise not only on the Agency’s 

7 assessment of the relevant scientific information, but also on the adequacy of the current 

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

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

10 PA for CASAC review and public comment. 

11 The decision whether to prepare one or more drafts of the PA is influenced by 

12 preliminary staff conclusions and associated CASAC advice and public comments, among other 

13 factors. Typically, a second draft PA has been prepared in cases where the available information 

14 calls into question the adequacy of the current standard and analyses of potential alternative 

15 standards are developed taking into consideration CASAC advice and public comment. In such 

16 cases, a second draft PA includes preliminary staff conclusions regarding potential alternative 

17 standards and undergoes CASAC review and public comment prior to preparation of the final 

18 PA. When such analyses are not undertaken, a second draft PA may not be warranted. 

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

20 as assessed in the second draft Integrated Science Assessment for Sulfur Oxides – Health Criteria

21 (second draft ISA [U.S. EPA, 2016]) and the draft Risk and Exposure Assessment for the Review 

22 of the Primary National Ambient Air Quality Standard for Sulfur Oxides, External Review Draft

23 (draft REA [U.S. EPA, 2017b]). The evaluation and preliminary staff conclusions presented in 

24 this draft PA for the primary NAAQS for SOX have been informed by comments and advice 

25 received from the CASAC in their reviews of the other draft Agency documents prepared thus 

26 far in this NAAQS review. Review and comments from the CASAC, and public comment, on 

27 this draft of the PA will inform the final evaluation and staff conclusions in the final PA. The 

28 final PA will inform the Administrator’s decision in this review of the primary SO2 NAAQS. 

29 Beyond informing the EPA Administrator and facilitating the advice and 

30 recommendations of the CASAC, the PA is also intended to be a useful reference to all parties 

31 interested in the review of the primary NAAQS for SOX. In these roles, it is intended to serve as 

32 a source of policy-relevant information that is informing the Agency’s review of the primary 

33 NAAQS for SOX, and it is written to be understandable to a broad audience. 
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1 1.2 BACKGROUND 

2 1.2.1 Legislative Requirements 

3 Two sections of the CAA govern the establishment and revision of the NAAQS. Section 

4 108 [42 U.S.C. 7408] directs the Administrator to identify and list certain air pollutants and then 

5 to issue air quality criteria for those pollutants. The Administrator is to list those pollutants that 

6 in his “judgment, cause or contribute to air pollution which may reasonably be anticipated to 

7 endanger public health or welfare,” “the presence of which in the ambient air results from 

8 numerous or diverse mobile or stationary sources”; and for which he “plans to issue air quality 

9 criteria....” Air quality criteria are intended to “accurately reflect the latest scientific knowledge 

10 useful in indicating the kind and extent of all identifiable effects on public health or welfare 

11 which may be expected from the presence of [a] pollutant in the ambient air....” 42 U.S.C. § 

12 7408(a)(2). 

13 Section 109 [42 U.S.C. 7409] directs the Administrator to propose and promulgate 

14 “primary” and “secondary” NAAQS for pollutants for which air quality criteria are issued [42 

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

16 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 17 Under section 

18 109(b)(2), a secondary standard must “specify a level of air quality the attainment and 

19 maintenance of which, in the judgment of the Administrator, based on such criteria, is requisite 

20 to protect the public welfare from any known or anticipated adverse effects associated with the 

presence of [the] pollutant in the ambient air.”6 21 

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

23 intended to address uncertainties associated with inconclusive scientific and technical 

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

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

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

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

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

29 2010); Mississippi v. EPA, 744 F. 3d 1334, 1353 (D.C. Cir. 2013). Both kinds of uncertainties 

                                                            

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

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

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

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

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

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

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

8 v. EPA, 647 F.2d at 1156 n.51, Mississippi v. EPA, 744 F. 3d at 1351, but rather at a level that 

9 reduces risk sufficiently so as to protect public health with an adequate margin of safety. 

10 In addressing the requirement for an adequate margin of safety, the EPA considers such 

11 factors as the nature and severity of the health effects involved, the size of the sensitive 

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

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

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

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

16 In setting primary and secondary standards that are “requisite” to protect public health 

17 and welfare, respectively, as provided in section 109(b), the EPA’s task is to establish standards 

18 that are neither more nor less stringent than necessary. In so doing, the EPA may not consider the 

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

20 531 U.S. 457, 465-472, 475-76 (2001). Likewise, “[a]ttainability and technological feasibility are 

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

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

23 Section 109(d)(1) requires that “[n]ot later than December 31, 1980, and at five-year 

24 intervals thereafter, the Administrator shall complete a thorough review of the criteria published 

25 under section [108] and the national ambient air quality standards...and shall make such 

26 revisions in such criteria and standards and promulgate such new standards as may be 

27 appropriate....” Section 109(d)(2) requires that an independent scientific review committee 

28 “shall complete a review of the criteria...and the national primary and secondary ambient air 

29 quality standards...and shall recommend to the Administrator any new...standards and revisions 

30 of existing criteria and standards as may be appropriate....” Since the early 1980s, this 

31 independent review function has been performed by the CASAC of the EPA’s Science Advisory 

Board.7 32 

                                                            

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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1 1.2.2 History of the Reviews of the Primary NAAQS for SOX

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

3 1969). Based on these criteria, the EPA, in initially promulgating NAAQS for SOX in 1971, 

4 established the indicator as SO2. The two primary standards set in 1971 were 0.14 parts per 

5 million (ppm) averaged over a 24-hour period, not to be exceeded more than once per year, and 

6 0.03 ppm, as an annual arithmetic mean. 

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

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

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

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

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

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

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

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

15 1986a). Policy-relevant aspects of the new evidence and staff findings from a companion 

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

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

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

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

20 1988, the EPA proposed to retain the existing standards and solicited comment on the alternative 

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

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

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

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

25 58962, November 15, 1994; 61 FR 25566, May 22, 1996). 

26 In response to publication of additional relevant controlled human studies on health 

27 effects of short-term SO2 concentrations, the EPA prepared a supplement to the second 

28 addendum to the 1982 AQCD (1994 AQCD supplement [U.S. EPA, 1994a]). Policy-relevant 

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

30 exposure analysis were evaluated in the 1994 Supplement to the 1982 Staff Paper (U.S. EPA, 

31 1994b). In 1994, based on the available evidence, staff evaluations, CASAC advice, and public 

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

33 solicited comment on retaining the existing standards in combination with one of three policy 

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

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

36 alternatives were: (1) Revising the existing primary SO2 NAAQS by adding a new 5-minute 
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1 standard of 0.60 ppm SO2, not to be exceeded more than once per calendar year; (2) establishing 

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

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

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

5 sources or source types likely to produce high 5-minute peak concentrations of SO2. 

6 This review was completed in 1996 with the EPA’s decision to retain without revision the 

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

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

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

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

11 5-minute peaks of SO2 did not pose a broad public health problem when viewed from a national 

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

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

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

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

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

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

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

19 SO2 do not pose a public health problem from a national perspective even though these peaks 

20 will likely cause adverse health impacts in a subset of individuals with asthma. American Lung 

21 Ass’n v. EPA, 134 F. 3d 388, 392-393 (D.C. Cir. 1998). Following the remand, the EPA 

22 requested that states voluntarily submit 5-minute SO2 monitoring data for the EPA to use to gain 

23 a better understanding of the magnitude and frequency of high, 5-minute peak SO2

24 concentrations. 

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

26 was completed in 2010 (75 FR 35520, June 22, 2010). As a result of this review, the EPA 

27 promulgated a new 1-hour standard to provide the requisite protection for at-risk populations 

28 such as people with asthma against an array of adverse respiratory health effects related to short29 term SO2 exposures. The 1-hour standard was set with SO2 as the indicator based on its common 

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

31 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 32 percentile of 1-hour daily maximum SO2 concentrations. The 

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

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

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

36 standards, and on the lack of evidence indicating the need for such longer-term standards. The 
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1 2010 action also addressed the remand by the D.C. Circuit in 1998. The 2010 and prior standards 

2 are summarized in Table 1-1. 

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

4 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 

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. 

5 

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

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

8 report the highest 5-minute concentration for each hour of the day; many agencies additionally 

9 report all twelve 5-minute concentrations for each hour of the day (75 FR 35554, June 22, 2010; 

10 40 CFR 58.16). The rationale for this requirement was to provide additional monitoring data for 

11 use in subsequent reviews of the primary standard, particularly in considering the extent of 

12 protection provided by the 1-hour standard against 5-minute peak SO2 concentrations of concern 

13 (75 FR 35554, June 22, 2010). 

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

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

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

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

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

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

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

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

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

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

24 upheld. Id. 
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1 1.2.3 Current SO2 NAAQS Review 

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

3 quality criteria for sulfur oxides and the primary NAAQS for sulfur oxides and issued a call for 

4 information in the Federal Register (78 FR 27387, May 10, 2013). A wide range of external 

5 experts as well as EPA staff representing a variety of areas of expertise (e.g., epidemiology, 

6 human and animal toxicology, statistics, risk/exposure analysis, atmospheric science) 

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

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

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

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

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

12 Plan for the Primary National Ambient Air Quality Standards for Sulfur Dioxide (IRP, U.S. 

13 EPA, 2014) outlining the schedule, process, and key policy-relevant questions that would guide 

14 the evaluation of the air quality criteria for SO2 and the review of the primary NAAQS for SOX. 

15 The draft IRP was released in March 2014 (79 FR 14035, March 12, 2014) and was the subject 

16 of a consultation with the CASAC on April 22, 2014 (79 FR 16325, March 25, 2014). Comments 

17 received from the CASAC and the public were considered in the preparation of the final IRP, 

18 which was released in October 2014 (U.S. EPA, 2014). 

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

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

21 Center for Environmental Assessment (NCEA) on June 23-24, 2014 (79 FR 33750, June 12, 

22 2014). Comments received from this review as well as comments from the public and the 

23 CASAC on the draft IRP were considered in preparation of the Integrated Science Assessment 

24 for Sulfur Oxides – Health Criteria (External Review Draft – November 2015), released in 

25 November 2015 (80 FR 73183, November 24, 2015). The first draft ISA was reviewed by the 

26 CASAC at a public meeting in January 2016 and a public teleconference in April 2016 (80 FR 

27 79330, December 21, 2015; 80 FR 79330, December 21, 2015; Diez Roux, 2016). 

28 The EPA released the Integrated Assessment for Sulfur Oxides – Health Criteria (Second 

29 External Review Draft – December 2016) in December 2016 (81 FR 89097), which was 

30 reviewed by the CASAC at a public meeting in March 2017 and a public teleconference in June 

31 2017 (82 FR 11449, February 23, 2017; 82 FR 23563, May 23, 2017). Completion of the final 

32 ISA is expected in December 2017. 

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

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

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

36 February 2017 (82 FR 11356), and held a consultation with the CASAC at a public meeting in 
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1 March 2017 (82 FR 11449). In consideration of CASAC comments at that consultation and 

2 public comments, the EPA developed the draft REA (U.S. EPA, 2017b). The draft REA and this 

3 draft PA are being provided to the CASAC for their review and released to the public for 

4 comment. The CASAC advice and public comments will be considered in completing these 

5 documents. 

6 The schedule for completion of this review is governed by a consent decree entered by 

7 the court, which, in relevant part, specifies that the appropriate EPA official issue a final 

8 Integrated Science Assessment addressing human health effects of SOX no later than December 

9 14, 2017; sign a notice setting forth its proposed decision concerning its review of the primary 

10 NAAQS for SOX no later than May 25, 2018; and sign a notice setting forth its final decision 

11 concerning its review of the primary NAAQS for SOX no later than January 28, 2019 (Consent 

12 Decree at 4, Center for Biological Diversity et al. v. Pruitt, Case No. 3:16-cv-03796-VC (N.D. 

13 Cal. April 28, 2017), Document No. 37). 

14 1.3 GENERAL APPROACH AND ORGANIZATION OF THIS 

15 DOCUMENT 

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

17 quantitative air quality, exposure and risk analyses. With regard to the health effects evidence, 

18 we consider the nature of the key effects associated with SO2 in ambient air, the types and 

19 magnitudes of exposures associated with effects, and populations at greatest risk, as well as the 

20 uncertainties. Based on this information, we summarize associated potential public health 

21 impacts of SO2 in ambient air. We additionally consider the magnitude of exposures and risks 

22 estimated in the REA, along with the associated uncertainties. This evaluation supports 

23 preliminary staff conclusions with regard to the key policy-relevant questions for the review, 

24 including whether the currently available information appears to call into question the adequacy 

25 of public health protection afforded by the current standard. 

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

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

28 conditions. Chapter 3 focuses on the review of the primary NAAQS for SOX presenting 

29 background information on the rationale for previous reviews and the approach followed in the 

30 current review. Chapter 3 further discusses the adequacy of the current standards, taking into 

31 account evidence- and exposure-/risk-based considerations, and includes preliminary staff 

32 conclusions. Chapter 3 also identifies key uncertainties and areas for future research. 
August 24, 2017 1-10 External Review Draft – Do Not Quote or Cite

1 REFERENCES 

2 Diez Roux. (2016). Letter to EPA Administrator Gina McCarthy: CASAC Review of the EPA’s 

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

4 Draft – November 2015). Available at: 

5 https://yosemite.epa.gov/sab/sabproduct.nsf/264cb1227d55e02c85257402007446a4/8DE

6 C36A7E2A54BA485257F9600667D81/$File/EPA-CASAC+2016-002+Unsigned.pdf

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

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

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

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

11 addendum. (EPA-600/8-82-029a). Research Triangle Park. NC: Environmental Criteria 

12 and Assessment Office. Available at: 

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

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

15 Assessment of Scientific and Technical Information, OAQPS Staff Paper. (EPA-450-5-

16 82-007). Research Triangle Park, NC: Office of Air Quality Planning and Standards. 

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

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

19 assessment of newly available health effects information, 2nd addendum. (EPA/600/8- 

20 86/020F). Washington, DC: Office of Health and Environmental Assessment. Available 

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

22 U.S. EPA. (1986b). Second addendum to air quality criteria for particulate matter and sulfur 

23 oxides (1982): Assessment of newly available health effects information. (EPA/600/8-

24 86/020F). Research Triangle Park, NC: Environmental Criteria and Assessment Office. 

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

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

27 Vicinity of Utility Power Plants. Research Triangle Park, NC: Office of Air Quality 

28 Planning and Standards. Available at: 

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

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

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

32 acute exposure health effects in asthmatic individuals. (EPA/600/FP-93/002). Research 

33 Triangle Park, NC: Environmental Criteria and Assessment Office. Available at: 

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

35 U.S. EPA (1994b). Supplement to the Second Addendum (1986) to Air Quality Criteria for 

36 Particulate Matter and Sulfur Oxides (1982): Assessment of New Findings on Sulfur 

37 Dioxide and Acute Exposure Health Effects in Asthmatic Individuals. (EPA/600/FP-
August 24, 2017 1-11 External Review Draft – Do Not Quote or Cite

1 93/002). Research Triangle Park, NC: Environmental Criteria and Assessment Office. 

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

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

4 Standard for Sulfur Dioxide. EPA-452/P-14-005, October 2014. Available at: 

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

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

7 (Second External Review Draft). EPA/600/R-16/351, December 2016. Available at: 

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

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

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

11 Matter. EPA-452/R-17-002, January 2017. Available at: 

12 https://www.epa.gov/naaqs/nitrogen-dioxide-no2-and-sulfur-dioxide-so2-

13 secondarystandards-planning-documents-current 

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

15 Ambient Air Quality Standard for Sulfur Oxides, External Review Draft. EPA-452/P-17-

16 002, August 2017. Available at: https://www.epa.gov/naaqs/sulfur-dioxide-so2-primary17 air-quality-standards

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

19 Oxides: Risk and Exposure Assessment Planning Document. EPA-452/P-17-001, 

20 February 2017. Available at: 

21 https://www3.epa.gov/ttn/naaqs/standards/so2/data/20170216so2rea.pdf
August 24, 2017 2-1 Draft – Do Not Quote or Cite

1 2 CURRENT AIR QUALITY

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

3 largely drawn from the more detailed discussion provided in the second draft ISA (second draft 

4 ISA, chapter 2). Section 2.1 summarizes the current information on sources and emissions and 

5 section 2.2 summarizes current ambient air monitoring methods and networks. Recent 

6 concentrations of SO2 in ambient air are summarized in section 2.3.

7 2.1 SOURCES TO AMBIENT AIR

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

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

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

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

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

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

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

15 and also formed in the atmosphere from other atmospheric compounds (e.g., as an oxidation 

16 product of reduced sulfur compounds, such as sulfides). Sulfur oxides are also transformed in the 

17 atmosphere to particulate sulfur compounds, such as sulfates. Sulfur oxides known to occur in 

18 the troposphere include SO2 and sulfur trioxide (SO3) (second draft ISA, section 2.3). As a result 

19 of rapid atmospheric chemical reactions involving SO3, the most prevalent sulfur oxide in the 

20 atmosphere is SO2 (second draft ISA, section 2.3).

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

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

(second draft ISA, section 2.1).

1

23 Industrial chemical production, pulp and paper production, 

24 natural biological activity (plants, fungi, and prokaryotes), and volcanoes are among many 

25 sources of reduced sulfur compounds that contribute, through various oxidation reactions in the 

26 atmosphere, to the formation of SO2 in the atmosphere (second draft ISA, section 2.1).

27 Anthropogenic SO2 emissions originate primarily from point sources, including coal-fired 

28 electricity generating units (EGUs) and other industrial facilities (second draft ISA, section 

 

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. (second draft ISA, section 2.5.5).
August 24, 2017 2-2 Draft – Do Not Quote or Cite

1 2.2.1). The largest SO2-emitting sector within the U.S. is electricity generation, of which 97% of 

2 SO2 from electricity generation is from coal combustion, as shown in Figure 2-1. Other 

3 anthropogenic sources of SO2 emissions include industrial fuel combustion and process 

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

5 management and agriculture (second draft ISA, section 2.2.1).

6

7

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

2 8

9

10 Figure 2-2 illustrates the emissions trends from 1990 to 2015. Declines in SO2 emissions 

11 are likely related to the implementation of Clean Air Act national control programs including 

12 Phase I and II of the Acid Rain Program, the Clean Air Interstate Rule, and the Cross-State Air 

13 Pollution Rule. An additional factor is changes in market conditions, e.g., reduction in energy

generation by coal (U.S. EIA, 2017).314

 

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

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).

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
August 24, 2017 2-3 Draft – Do Not Quote or Cite

1

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

3

4 2.2 AMBIENT AIR MONITORING METHODS AND NETWORK

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

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

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

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

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

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

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

12 and 1-hour averages.

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

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

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

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

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

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

19 concentrations and either the maximum 5-minute concentration in the hour (one of twelve 5-
August 24, 2017 2-4 Draft – Do Not Quote or Cite

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

2 hour. 

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

requirements promulgated in 2010 (Figure 2-3).44 Although 5-minute data were available for 

5 fewer than 10% of monitoring sites at the time of the last review, such data (either all 12 values 

6 in each hour or just the maximum 5-minute concentrations) are currently available for nearly all

7 of the operating SO2 sites nationwide, providing a more robust foundation for characterization of 

8 5-minute ambient air concentrations in this review. Further, the newly available monitoring data 

9 also include more monitors reporting the 12 consecutive 5-minute concentrations for each hour

10 than were available in the last review (Figure 2-3). Of the monitors reporting 5-minute data in 

11 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.512

13

14

15 Figure 2-3. Temporal trend in number of monitors with 5-minute data.

 

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 of the 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 types of 5-minute monitors.
August 24, 2017 2-5 Draft – Do Not Quote or Cite

1 2.3 AMBIENT AIR MONITORING CONCENTRATIONS

2 This section briefly summarizes trends and current conditions based on recent ambient air 

3 monitoring data.

4 2.3.1 Trends

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

6 2015. Figure 2-4 illustrates this decline in terms of the distribution of 3-year average of annual 

99th percentile daily maximum 1-hour concentrations67 at 45 monitoring sites that have been 

8 operating across this period. The average of this dataset has declined by more than 83% over the 

9 35-year period. Over the past 15 years, a larger dataset of 227 sites operating from 2000-2015 

10 also indicates a decline, which is on the order of 67% for the average of that dataset (Figure 2-

5).711 Daily maximum 5-minute SO2 concentrations have also consistently declined over time from 

2011 to 2015 (Figure 2-6).812

13

14

15 Figure 2-4. National temporal trend in SO2 concentrations: 1980-2015 (45 sites).

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

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

 

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

averaged over 3 years.

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).

8

In Figure 2-6, the number of sites with monitors for 2011, 2012, 2013, 2014, and 2015 were 301, 321, 366, 359, 

and 352, respectively.
August 24, 2017 2-6 Draft – Do Not Quote or Cite

1

2 Figure 2-5. Temporal trend in SO2 concentrations: 2000-2015 (227 sites). Three-year 

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

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

5

6

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

8 2015. (N = number of measurements)
August 24, 2017 2-7 Draft – Do Not Quote or Cite

1 2.3.2 Current Concentrations

2 2.3.2.1 Geographic Variation in Concentrations

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

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

5 sources, higher concentrations are primarily located in the eastern half of the continental U.S., 

6 especially in the Ohio River valley, upper Midwest, and along the Atlantic coast (Figure 2-7).

7 The point source nature of SO2 emissions contribute to the relatively high spatial variability of 

8 SO2 concentrations compared with pollutants such as ozone (O3) (second draft ISA, section 

9 3.2.3). Another contributing factor to the spatial variability is the dispersion and oxidation of SO2

10 in the atmosphere, resulting in decreasing SO2 concentrations with increasing distance from the 

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

12 as a plume, which may or may not impact large portions of surrounding populated areas 

13 depending on meteorological conditions and terrain. 
August 24, 2017 2-8 Draft – Do Not Quote or Cite

1

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

3 maximum 1-hour concentrations) at sites with datasets meeting completeness requirements for 2013-2015.
August 24, 2017 2-9 Draft – Do Not Quote or Cite

1 2.3.2.2 Seasonal and Diel Variability in Concentrations

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

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

4 average or lower percentiles) for each season (second draft ISA, section 2.5.3.2). This is seen in 

the data presented for six urban areas in the draft ISA95 (second draft ISA, section 2.5.3.2). This 

6 variation, along with month-to-month variations in 1-hour daily maximum SO2 concentrations

7 also presented in the ISA, were generally consistent with month-to-month emissions patterns and 

8 the expected atmospheric chemistry of SO2 for a given season. For example, “summertime 

9 minima, observed in the New York City, NY and Houston, TX, sites may correspond to 

enhanced oxidation of SO2 to SO4

2-

10 by photochemically derived atmospheric oxidants that are 

11 more prevalent during the humid summer (Khoder, 2002)” (second draft ISA, p. 2-55). The 

12 differences in seasonal pattern (as well as magnitude) of concentrations among areas studied 

13 indicate the variability of SO2 concentrations across local and regional scales (second draft ISA, 

14 section 2.5.3.2).

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

16 and 5-minute hourly maximum SO2 concentrations for 2013-2015 in all six urban areas 

17 evaluated were generally low during nighttime and approached maxima values during daytime 

18 hours (second draft ISA, section 2.5.3.3, Figures 2-23 and 2-24). The timing and duration of 

19 daytime maxima in the six sites evaluated were likely related to a combination of source 

20 emissions and meteorological parameters (second draft ISA, section 2.5.3.3; U.S. EPA 2008, 

21 section 2.5.1). For example, SO2 emitted from elevated point sources (e.g., power plants and 

22 industrial sources) may be entrained into the mixed boundary layer, which expands during the 

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

24 2.3.2.3 Relationship Between 1-hour and 5-minute Concentrations

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

26 source can greatly exceed mean concentrations across the plume (second draft ISA, section 

27 2.5.4). Further, measured 5-minute concentrations at a particular location can be much higher 

28 than the average concentration at the same location for the associated hour. However, as 

29 emissions travel further downwind and experience ever increasing dispersion, these differences

30 lessen both spatially and temporally. This can contribute to greater spatial and temporal 

 

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

TX, and Gila County, AZ (second draft ISA, section 2.5.2.2). These six locations were 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.
August 24, 2017 2-10 Draft – Do Not Quote or Cite

1 variability in 5-minute than in 1-hour concentrations, as is seen in the six urban locations 

2 evaluated in the ISA (second draft ISA, p. 2-52). 

3 Using monitoring data from 2013-2015, Figure 2-8 illustrates the general pattern of lower 

4 5-minute concentrations with lower 1-hour concentrations. The left panel of Figure 2-8 shows 

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

6 concentrations are relatively low, the 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,10 7

8 the distribution of maximum 5-minute concentrations is also lower. This is documented by the 

9 distinct reduction in 99th percentile daily maximum 5-minute concentrations at lower design 

10 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 150 ppb.11 11

12 This contrasts with the much higher distribution of daily maximum 5-minute concentrations at 

13 sites with design values exceeding the current standard. The 99th percentile of these daily 

14 maximum 5-minute concentrations is 365 ppb, meaning that one percent of the days at these sites 

15 has a maximum 5-minute concentration above 365 ppb (i.e., 210 occurrences).

 

10 The design value (DV) for the standard is the metric used to determine whether areas meet or exceed the NAAQS.

A design value is a statistic that describes the air quality status of a given area relative to the NAAQS. Design 

values are considered to be valid if the monitoring data used to calculate them meet the regulatory completeness 

criteria which for SO2 require four quarters of all three years of the period to have data for at least 75 percent of 

the sampling days (40 CFR 50.17 and appendix T to Part 50).

11 Additional information related to data in Figure 2-8 is presented in Appendix B.
August 24, 2017 2-11 Draft – Do Not Quote or Cite

1

2 Figure 2-8. Distributions of daily maximum 5-minute concentrations during 2013-

3 2015. Left panel presents varying distributions with varying daily maximum 

4 1-hour concentrations. Right panel presents varying distributions with varying 

5 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 6

percentile, the median, and the 75th percentile. The asterisk represents the 99th 7

8 percentile.)

9

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

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

12 having differing design values. For example, analysis of these data for the years 2013 to 2015 

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

14 75 ppb), the vast majority have zero days with a daily maximum 5-minute concentration above 

15 100 ppb or even 400 ppb. Among the few monitors with any days recording a 5-minute 

16 concentrations above 400 ppb, the maximum number of such days in a year was five; for 

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

18 of such days/year was 22 (Appendix C, Figures C-2 and C-4, lower panel).
August 24, 2017 2-12 Draft – Do Not Quote or Cite

1 REFERENCES

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

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

4 675-684. http://dx.doi.org/10.1016/S0045-6535(02)00391-0

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

6 November 2016. Available at: https://www.eia.gov/electricity/annual/pdf/epa.pdf

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

8 DOE/EIA-0035(2017-07), July 2017. Available at: 

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

10 U.S. EPA. (2008). Integrated science assessment for sulfur oxides: Health criteria [EPA Report]. 

11 EPA/600/R-08/047F. Research Triangle Park, NC: U.S. Environmental Protection 

12 Agency, Office of Research and Development, National Center for Environmental 

13 Assessment- RTP. http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=198843

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

15 (Second External Review Draft). EPA/600/R-16/351, December 2016. Available at: 

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

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

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

19 Matter. EPA-452/R-17-002, January 2017. Available at: 

20 https://www.epa.gov/naaqs/nitrogen-dioxide-no2-and-sulfur-dioxide-so2-

21 secondarystandards-planning-documents-current
August 24, 2017 3-1 External Review Draft – Do Not Quote or Cite

1 3 REVIEW OF THE PRIMARY STANDARD FOR 

2 SULFUR OXIDES 

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

4 information in the second draft ISA and draft REA. This evaluation is based on consideration of 

5 the available body of evidence assessed in the second draft ISA and of quantitative analyses of 

6 SO2 air quality, exposures and risks presented in the draft REA and in this document. Based on 

7 this information, the staff offer preliminary conclusions regarding each of the critical elements of 

8 the standard, including indicator, averaging time, form, and level. The final PA will also be 

9 informed by the advice and recommendations received from the CASAC during its review of the 

10 draft PA, and by public comments received on the draft document. The final PA is designed to 

11 help the Administrator in considering the currently available scientific and risk information and 

formulating judgments regarding the adequacy of the current primary standard.1 12 

13 3.1 APPROACH 

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

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

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

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

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

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

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

21 judgment to be made by the Administrator. 

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

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

24 health risks, including judgments about the appropriate weight to assign the range of 

25 uncertainties inherent in the evidence and analyses. Therefore, in developing conclusions in this 

26 draft PA, we are mindful that the Administrator’s judgments on the standard will reflect an 

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

28 of the strengths and limitations of that evidence and information. Our general approach to 

                                                            

1

 The basic elements of a standard include the indicator, averaging time, form, and level. 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 

obtained and averaged or cumulated. 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. The level of the standard defines 

the air quality concentration used for that purpose (i.e., an ambient air concentration of the indicator). 
August 24, 2017 3-2 External Review Draft – Do Not Quote or Cite

1 informing these judgments, discussed more fully below, recognizes that the available health 

2 effects evidence reflects a continuum from relatively higher SO2 concentrations, at which 

3 scientists generally agree that health effects are likely to occur, through lower concentrations at 

4 which the likelihood and magnitude of a response become increasingly uncertain. This approach 

5 is consistent with the requirements of sections 108 and 109 of the CAA, as well as with how the 

6 EPA and the courts have historically interpreted the Act. These provisions require the 

7 Administrator to establish primary standards that in the Administrator’s judgment are requisite to 

8 protect public health with an adequate margin of safety. In so doing, the Administrator seeks to 

9 establish standards that are neither more nor less stringent than necessary for this purpose. The 

10 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.2 11 

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

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

14 3.1.1 Approach in the Previous Review 

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

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

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

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

at-risk group and other potentially at-risk populations3 19 against an array of adverse respiratory 

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

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

22 EPA replaced the then-existing 24-hour standard with a short-term standard defined by the 3-

year average of the 99th 23 percentile of the yearly distribution of 1-hour daily maximum SO2

24 concentrations, with a level of 75 ppb. In addition to replacing the 24-hour standard with a new 

25 1-hour standard, the EPA revoked the then-existing annual standard, based largely on the lack of 

26 sufficient health evidence to support a long-term standard and a recognition that a 1-hour 

27 standard set at 75 ppb would have the effect of generally maintaining annual SO2 concentrations 

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

                                                            

2

 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. 

3

 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. 
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1 The emphasis in the 2010 review on short-term exposures of people with asthma 

2 reflected the health effects evidence that has expanded in this area over the four decades since 

3 the then-existing 24-hour and annual standards were set in 1971. A key element of the expanded 

4 evidence base was a series of controlled human exposure studies which documented effects on 

5 lung function in people with asthma exposed, while at moderate or greater levels of exertion, for 

6 periods as short as five minutes. In the 2010 review, the EPA also conducted quantitative 

7 analyses of air quality data, including 5-minute ambient air measurements, and of potential 

8 exposures for people with asthma. Consideration of these key aspects of the evidence and 

9 quantitative analyses informed the decision in the 2010 review, which additionally addressed the 

court remand4 10 to the EPA of the EPA’s 1996 decision to retain the 1971 standards without 

11 revision. 

12 The evidence-based and quantitative assessments performed for the 2010 review focused 

13 particularly on the issue of exposures to SO2 in ambient air of a duration as short as five minutes 

14 (2008 ISA; 2009 REA). The quantitative analyses documented in the REA included 

15 characterizations of the likelihood of people with asthma being exposed (while they were at 

elevated exertion5 16 ) to concentrations of SO2 from ambient air of a magnitude documented to 

17 elicit decrements in lung function (2009 REA). These analyses were performed both for air 

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

19 associated with just meeting potential alternative standards. The REA additionally included air 

20 quality analyses that explored the extent to which potential alternative standards with 1-hour, 24-

21 hour, and annual averaging times might be expected to control 5-minute ambient air 

22 concentrations (2009 REA, section 7.3). Together the evidence-based and quantitative 

23 assessments informed the policy options considered by the Administrator in that review. 

24 Considerations, conclusions and judgments by the Administrator that provided the basis for her 

25 decisions in the 2010 review are summarized below. 

26 3.1.1.1 Considering the Need for Revision 

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

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

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

                                                            

4

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

5

 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 

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

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

REA and draft PA for this review generally uses the phrase “elevated ventilation” to refer to the same occurrence. 
August 24, 2017 3-4 External Review Draft – Do Not Quote or Cite

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

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

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

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

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

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

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

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

9 5.2). Supporting evidence was provided by epidemiologic studies of a broader range of 

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

11 quantification of the exposure concentration-response relationship, potential confounding by co12 pollutants, and other areas (75 FR 35535-35536, June 22, 2010; 2008 ISA, section 5.3). 

13 In the controlled human exposure studies of exercising individuals with asthma, a dose14 response relationship was documented, with both the percentage of individuals affected and the 

15 severity of the response increasing with increasing SO2 concentrations (75 FR 35525, June 22, 

16 2010). The evidence from these studies documents the occurrence of SO2-related decrements in 

17 lung function based on reductions in forced expiratory volume (FEV1) and increases in specific 

resistance of the airways (sRaw). Moderate6 18 or greater decrements in lung function were reported 

19 in response to short (5- to 10-minute) exposures to concentrations as low as 200 to 300 ppb in 

20 approximately 5-30% of exercising individuals with asthma. In response to exposures at or above 

21 400 ppb, approximately 20-60% experienced such decrements, frequently accompanied by 

22 respiratory symptoms; in many studies, responses at these concentrations were often statistically 

significant at the group mean level7 23 (75 FR 35525-35526, June 22, 2010). 

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

25 10-minute controlled exposures, the Administrator considered guidelines from the American 

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

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

                                                            

6

 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). 

7

 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). 
August 24, 2017 3-5 External Review Draft – Do Not Quote or Cite

1 35536, June 22, 2010). Based on these considerations, the Administrator judged that the effects 

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

3 200 ppb, especially at or above 400 ppb, can result in adverse health effects (75 FR 35536, June 

4 22, 2010). In so doing, she recognized that effects reported for exposures below 400 ppb are 

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

6 In applying the health effects evidence to her consideration of the adequacy of the then7 existing standards, the Administrator gave particular attention to the quantitative analyses that 

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

9 magnitude associated with adverse effects under air quality conditions that just met the then10 existing standards. In addition to comparison of 5-minute air concentrations in 40 U.S. counties 

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

12 400 ppb), the analyses included a population exposure-based assessment in two study areas, St. 

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

14 people with asthma while at elevated exertion levels. The 5-minute exposure concentrations were 

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

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

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

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

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

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

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

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

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

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

25 and 200 ppb while engaged in activities causing them to be at elevated exertion levels. The 

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

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

substantial percentages of children with asthma at moderate or greater exertion8 28 would be 

29 exposed, at least once annually, to air quality exceeding the 200 ppb and 400 ppb 5-minute 

30 benchmarks (75 FR 35536, June 22, 2010). The Administrator judged these 5-minute exposures 

31 to be significant from a public health perspective due to their estimated frequency: 

32 approximately 24% of children with asthma in St. Louis were estimated to be exposed while at 

33 moderate or greater exertion at least once per year to air quality exceeding the 5-minute 400 ppb 

                                                            

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). 
August 24, 2017 3-6 External Review Draft – Do Not Quote or Cite

1 benchmark. Additionally, approximately 73% of children with asthma in St. Louis at moderate or 

2 greater exertion were estimated to be exposed at least once per year to air quality exceeding the 

3 5-minute 200 ppb benchmark (75 FR 35536, June 22, 2010). 

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

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

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

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

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

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

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

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

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

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

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

15 3.1.1.2 Approach for Considering Revisions to the Standards 

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

17 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 18 percentile of the yearly distribution of 1-hour daily maximum 

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

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

21 3.1.1.2.1 Indicator 

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

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

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

25 appropriate indicator for gaseous sulfur oxides because the available scientific information 

26 regarding health effects was overwhelmingly indexed by SO2. Although the presence of gaseous 

27 SOX species other than SO2 in ambient air had been recognized, no alternative to SO2 had been 

28 advanced as a more appropriate surrogate for ambient gaseous SOX (75 FR 35536, June 22, 

29 2010). Controlled human exposure studies and animal toxicological studies provided specific 

30 evidence for health effects following exposures to SO2, and epidemiologic studies typically 

31 reported effects associated with SO2 concentrations. Based on the information available in the 

32 last review and consistent with the views of the CASAC that “for indicator, SO2 is clearly the 

33 preferred choice” (Samet, 2009, p. 14), the Administrator concluded it was appropriate to 

34 continue to use SO2 as the indicator for a standard that was intended to address effects associated 

35 with exposure to SO2, alone or in combination with other gaseous sulfur oxides (75 FR 35536, 
August 24, 2017 3-7 External Review Draft – Do Not Quote or Cite

1 June 22, 2010). In so doing, the EPA recognized that measures leading to reductions in 

2 population exposures to SO2 will also likely reduce exposures to other sulfur oxides (75 FR 

3 35536, June 22, 2010). 

4 3.1.1.2.2 Averaging Time 

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

6 conclusion, based on conclusions in the ISA, advice from the CASAC, and air quality analyses, 

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

8 24 hours (75 FR 35539, June 22, 2010). Based on air quality analyses presented in the REA, the 

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

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

11 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 12 Accordingly, 

13 she considered other averaging times. 

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

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

16 5-minute peak SO2 concentrations, likely over-controlling in some areas, while under-controlling 

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

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

19 REA, section 10.5.2.2.). Drawing on this information, the Administrator concluded that a 1-hour 

20 standard, with the appropriate form and level, would be likely to substantially reduce 5- to 10-

21 minute peaks of SO2 that had been shown in controlled human exposure studies to result in 

22 increased prevalence of respiratory symptoms and/or decrements in lung function in exercising 

23 people with asthma (75 FR 35539, June 22, 2010). Further she found that a 1-hour standard 

24 could substantially reduce the upper end of the distribution of SO2 concentrations in ambient air 

25 that were more likely to be associated with respiratory outcomes (75 FR 35539, June 22, 2010). 

26 The Administrator additionally took note of advice from the CASAC. The CASAC stated 

27 that the REA had presented a “convincing rationale” for a 1-hour standard, and that “a one-hour 

28 standard is the preferred averaging time” (Samet, 2009, pp. 15, 16). The CASAC further stated 

29 that it was “in agreement with having a short-term standard and finds that the REA supports a 

30 one-hour standard as protective of public health” (Samet, 2009, p. 1). Thus, in consideration of 

31 the available information summarized here and the CASAC’s advice, the Administrator 

32 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). 
August 24, 2017 3-8 External Review Draft – Do Not Quote or Cite

1 means of controlling short-term exposures to SO2 ranging from 5 minutes to 24 hours (75 FR 

2 35539, June 22, 2010). 

3 3.1.1.2.3 Form 

4 In considering the statistical form for the new short-term standard, the Administrator 

5 judged that the form of the standard should reflect the health effects evidence presented in the 

6 ISA that indicated that the percentage of people with asthma affected and the severity of the 

7 response increased with increasing SO2 concentrations (75 FR 35541, June 22, 2010). She 

8 additionally found it reasonable to consider stability (e.g., to avoid disruption of programs 

9 implementing the standard and the related public health protections from those programs) as part 

10 of her consideration of the form for the standard (75 FR 35541, June 22, 2010). In so doing, she 

11 noted that a concentration-based form averaged over three years would likely be appreciably 

12 more stable than a no-exceedance based form, which had been the form of the then-existing 24-

13 hour standard (75 FR 35541, June 22, 2010). The CASAC additionally stated that “[t]here is 

14 adequate information to justify the use of a concentration-based form averaged over 3 years” 

15 (Samet, 2009, p. 16). In consideration of this information, the Administrator judged a 

16 concentration-based form averaged over three years to be most appropriate (75 FR 35541, June 

17 22, 2010). 

18 In selecting a specific concentration-based form, the Administrator considered health 

19 evidence from the ISA as well as air quality and exposure information from the REA. In so 

20 doing, the Administrator concluded that the form of a new 1-hour standard should be especially 

21 focused on limiting the upper end of the distribution of ambient SO2 concentrations (i.e., above 

90th 22 percentile SO2 concentrations) in order to provide protection with an adequate margin of 

23 safety against effects reported in epidemiologic and controlled human exposure studies (75 FR 

24 35541, June 22, 2010). The Administrator further noted, based on results of air quality and 

exposure analyses in the REA, that a 99th 25 percentile form was likely to be appreciably more 

effective at limiting 5-minute peak exposures of concern than a 98th 26 percentile form (75 FR 

35541, June 22, 2010). Thus, the Administrator selected a 99th 27 percentile form averaged over 

28 three years (75 FR 35541, June 22, 2010). 

29 3.1.1.2.4 Level 

30 In selecting the level of a new 1-hour standard, the Administrator gave primary emphasis 

31 to the body of health effects evidence assessed in the ISA. In so doing, she noted that the 

32 controlled human exposure studies provided the most direct evidence of respiratory effects from 

33 exposure to SO2. The Administrator drew on evidence from these studies in reaching judgments 

34 on the magnitude of adverse respiratory effects and associated potential public health 
August 24, 2017 3-9 External Review Draft – Do Not Quote or Cite

1 significance for the air quality exposure and risk analysis results of air quality scenarios 

2 representing just meeting alternative levels for a new 1-hour standard. 

3 In particular, the Administrator considered effects in exercising people with asthma after 

4 5- to 10-minute exposures as low as 200 ppb to be adverse in light of the CASAC advice on 

5 relevance of these effects, conclusions on similar effects in prior NAAQS reviews, and ATS 

6 guidelines (ATS, 1985, 2000). This judgment was based on several findings from the controlled 

7 human exposures studies. Five-to 10-minute exposures to 400 ppb or greater resulted in 

8 moderate or greater decrements in lung function in 20-60% of exercising individuals with 

9 asthma. These decrements are often statistically significant at the group mean level and 

10 frequently accompanied by respiratory symptoms. Thus, exposures to SO2 concentrations at or 

11 above 400 ppb were concluded to clearly result in adverse respiratory effects based on the ATS 

12 guidelines (ATS, 1985). Further, 5- to 10-minute exposures to 200 to 300 ppb resulted in 

13 moderate or greater decrements in lung function in 5-30% of exercising individuals with asthma 

14 (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 15 or to be frequently accompanied by respiratory 

16 symptoms, the Administrator considered effects associated with exposures as low as 200 ppb to 

be adverse in light of the CASAC’s advice11 17 and similar conclusions in prior reviews as well as 

18 the ATS guidelines (ATS, 1985, 2000). 

19 The Administrator then considered what the findings of the REA exposure analyses 

20 indicated with regard to varying degrees of protection that different 1-hour standard levels might 

be expected to provide against 5-minute benchmark concentrations of 200 ppb and 400 ppb.12 21 

For example, the exposure assessment for St. Louis13 22 estimated that a 1-hour standard at 100 ppb 

23 would likely protect more than 99% of children with asthma in that city from experiencing any 

24 days in a year with at least one 5-minute exposure at or above 400 ppb while at moderate or 

25 greater exertion, and approximately 97% of those children with asthma from experiencing any 

26 days in a year with at least one exposure at or above 200 ppb while at moderate or greater 

27 exertion (75 FR 35547, June 22, 2010). Results for the air quality scenario for a 1-hour standard 

                                                            

10 As summarized in section 3.2.1.1 below and described more fully in the second draft ISA for this review, study 

subjects have since been characterized as falling into two subpopulations that differ in susceptibility to SO2. 

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). 
August 24, 2017 3-10 External Review Draft – Do Not Quote or Cite

1 level of 50 ppb suggested that such a standard would somewhat further limit exposures, such that 

2 more than 99% of children at moderate or greater exertion would likely be protected from 

3 experiencing any days in a year with a 5-minute exposure at or above the 200 ppb benchmark 

4 concentration (75 FR 35542-47, June 22, 2010). 

5 In considering the implications of the exposure assessment results the Administrator 

6 noted that although she considered the health effects resulting from 5-minute SO2 exposures as 

7 low as 200 ppb to be adverse, she also recognized that such effects are appreciably less severe 

8 than those at SO2 concentrations at or above 400 ppb and found little difference between the 

9 results for standard levels of 50 and 100 ppb with regard to 5-minute exposures at or above 400 

10 ppb. She recognized that a standard level below 100 ppb may somewhat further limit 5-minute 

11 SO2 ambient air concentrations and exposures above 200 ppb, although she did not judge that a 

12 standard level of 50 ppb was warranted. 

13 Before reaching her conclusion with regard to level for the 1-hour standard, the 

14 Administrator additionally considered the epidemiological evidence among the U.S. 

15 epidemiologic studies (some conducted in multiple locations) reporting mostly positive and 

16 sometimes statistically significant associations between ambient SO2 concentrations and 

17 emergency department visits and hospital admissions. She noted there was a cluster of three 

studies for which 99th 18 percentile 1-hour daily maximum concentrations were estimated to be 

19 between 78-150 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 20 

21 Given the above considerations and the comments received on the proposal, the 

22 Administrator determined that the appropriate judgment, based on the entire body of evidence 

and information available in this review, and the related uncertainties,15 23 was a standard level of 

24 75 ppb. She concluded that such a standard, with a 1-hour averaging time and 99th percentile 

25 form, would provide a significant increase in public health protection compared to the current 

26 standards and would be expected to provide protection, with an adequate margin of safety, 

27 against the respiratory effects that have been linked with SO2 exposures in both controlled 

28 human exposure and epidemiologic studies. Specifically, she concluded that such a standard 

29 would limit 1-hour exposures at and above 75 ppb. (75 FR 35548, June 22, 2010). Such a 

30 standard was also considered likely “to maintain SO2 concentrations below those in locations 

                                                            

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). 
August 24, 2017 3-11 External Review Draft – Do Not Quote or Cite

1 where key U.S. epidemiologic studies have reported that ambient SO2 is associated with clearly 

2 adverse respiratory health effects, as indicated by increased hospital admissions and emergency 

3 department visits.” The Administrator also found that “a 1-hour standard at a level of 75 ppb is 

4 expected to substantially limit asthmatics’ exposure to 5–10 minute SO2 concentrations ≥ 200 

5 ppb, thereby substantially limiting the adverse health effects associated with such exposures.” 

6 Lastly, the Administrator noted “that a standard level of 75 ppb is consistent with the consensus 

7 recommendation of CASAC”. The Administrator also considered the likelihood of public health 

8 benefits at lower standard levels, and judged a 1-hour standard at 75 ppb to be sufficient to 

9 protect public health with an adequate margin of safety (75 FR 35547-35548, June 22, 2010). 

10 This judgment included consideration of the appropriate degree of protection with an 

11 adequate margin of safety for populations at increased risk for adverse respiratory effects from 

12 short-term exposures to SO2 for which the evidence supports a causal relationship with SO2

13 exposures. In reaching these conclusions, the Administrator considered the requirement for a 

14 standard that is neither more nor less stringent than necessary for this purpose and recognized 

15 that the CAA does not require that primary NAAQS be set at a zero-risk level or to protect the 

16 most susceptible individual, but rather at a level that reduces risk sufficiently so as to protect 

17 public health with an adequate margin of safety (75 FR 35548, June 22, 2010). 

18 3.1.1.2.5 Revoking the Then-Existing 24-Hour and Annual Standards 

19 In addition to setting a new 1-hour standard at 75 ppb, the then-current 24-hour and 

20 annual standards were revoked in the last review based largely on the recognition that a 1-hour 

21 standard set at 75 ppb would have the effect of generally maintaining 24-hour and annual SO2

22 concentrations well below the levels of those standards (75 FR 35550, June 22, 2010). In 

23 addition, the annual standard was also revoked because of the lack of evidence supporting a 

24 relationship between long-term SO2 exposures and adverse health effects. That is, the 2008 ISA 

25 judged the health evidence linking long-term SO2 exposure to adverse health effects to be 

26 “inadequate” to infer the presence or absence of a causal relationship (75 FR 35550, June 22, 

27 2010; 2008 ISA, section 5.5). 

28 3.1.2 Approach for the Current Review 

29 To evaluate whether it is appropriate to consider retaining the current SO2 primary 

30 standard, or whether consideration of revision is appropriate, we have adopted an approach in 

31 this review that builds on the general approach used in the last review and reflects the body of 

32 evidence and information now available. As summarized above, the Administrator’s decisions in 

33 the prior review were based on an integration of information on health effects associated with 

34 exposure to SO2, expert judgments on the adversity and public health significance of key health 

35 effects, air quality and related analyses and quantitative exposure and risk assessments, and 
August 24, 2017 3-12 External Review Draft – Do Not Quote or Cite

1 policy judgments as to when the standard is requisite to protect public health with an adequate 

2 margin of safety. 

3 In conducting this assessment, we draw on the current evidence and quantitative 

4 assessments of exposure pertaining to the public health risk of SO2 in ambient air. In considering 

5 the scientific and technical information, we consider both the information available at the time of 

6 the last review and information newly available since the last review, including the second draft 

7 ISA and draft REA for this review. Figure 3-1 below illustrates the basic construct of our two8 part approach in developing preliminary conclusions regarding options to consider with regard to 

9 the adequacy of the current primary standard and, as appropriate, potential alternative standards. 

10 In the boxes of Figure 3-1, the range of questions that we consider in sections 3.2.1 and 3.2.2 

11 below are represented by a summary of policy-relevant questions that frame our consideration of 

12 the scientific evidence and quantitative analyses. 
August 24, 2017 3-13 External Review Draft – Do Not Quote or Cite

1 

2 

3 

4 Figure 3-1. Overview of the approach for review of the current primary standard. 
August 24, 2017 3-14 External Review Draft – Do Not Quote or Cite

1 3.2 ADEQUACY OF THE CURRENT STANDARD 

2 In considering the adequacy of the current SO2 primary standard, the overarching 

3 question we consider is: 

4  Does the currently available scientific evidence- and exposure/risk-based 

5 information, as reflected in the ISA and REA, support or call into question the 

6 adequacy of the protection afforded by the current SO2 primary standard? 

7 To assist us in interpreting the currently available scientific evidence and the results of 

8 recent quantitative exposure/risk analyses to address this question, we have focused on a series 

9 of more specific questions, as detailed in sections 3.2.1 and 3.2.2 below. In considering the 

10 scientific and technical information, we consider both the information available at the time of the 

11 last review and information newly available since the last review which have been critically 

12 analyzed and characterized in the 2008 ISA for the last review and the second draft ISA for the 

13 current review. 

14 3.2.1 Evidence-based Considerations 

15 In considering the evidence with regard to the overarching question posed above 

16 regarding the adequacy of the current standard, we address a series of more specific questions 

17 that focus on policy-relevant aspects of the evidence. These questions begin with consideration 

18 of the available evidence regarding the health effects associated with exposure to SOX, and 

19 particularly SO2 (section 3.2.1.1). The subsequent questions consider identification of 

20 populations at-risk of SO2-related health effects (section 3.2.1.2), and the exposure durations and 

21 levels of SO2 associated with health effects (section 3.2.1.3). Important uncertainties associated 

22 with the evidence are considered in section 3.2.1.4. 

23 3.2.1.1 Health Effects Associated with Exposure to SOX

24 Among the species of SOX (a group of closely related gaseous compounds including SO2

25 and SO3), SO2 is the most commonly occurring in the atmosphere. Accordingly, the large body 

26 of scientific evidence has over the past reviews been predominantly focused on exposures to 

27 SO2. 

28  Is there newly available evidence that indicates the importance of SOX other than 

29 SO2 with regard to abundance in ambient air, and potential for human exposures 

30 and health effects? 

31 As in the last review, the health effects evidence evaluated in the second draft ISA for 

32 SOX is focused on SO2 (second draft ISA, p. 5-1). This is consistent with the conclusion that 

33 “[o]f the sulfur oxides, SO2 is the most abundant in the atmosphere, the most important in 

34 atmospheric chemistry, and the one most clearly linked to human health effects” (second draft 

35 ISA, p. 2-1). While “SO3 can be emitted by some sources, it reacts within seconds with water in 
August 24, 2017 3-15 External Review Draft – Do Not Quote or Cite

1 the stacks or immediately after release into the atmosphere to form H2SO4 and gas-phase sulfuric 

2 acid quickly condenses or contributes to particle formation” (second draft ISA, section 2.3). 

3 Thus, the second draft ISA states that “only SO2 is present at concentrations relevant for 

4 chemistry in the troposphere, boundary layer, and for human exposures” (second draft ISA, p. 2-

5 17), and also that the available health evidence for SOX is focused on SO2 (second draft ISA, p. 

6 5-1). Thus, we conclude that the current evidence, including that newly available in this review, 

7 continues to support a focus on SO2 in considering the adequacy of public health protection 

8 provided by the primary NAAQS for SOX. 

9  Does the current evidence alter our conclusions from the previous review regarding 

10 the health effects associated with exposure to SO2? 

11 Rather than altering our conclusions from the last review, the current evidence continues 

12 to support our prior conclusions regarding the key health effects associated with SO2 exposure. 

13 Specifically, the full body of evidence continues to support the conclusion that short-term SO2

14 exposures of durations as short as a few minutes are causally related to respiratory effects in at15 risk individuals (second draft ISA, section 5.2.1.9). With regard to respiratory effects and long16 term exposures, as well as total mortality and short-term exposures, the evidence available in this 

17 review is “suggestive of, but not sufficient to infer,” a causal relationship (second draft ISA, 

18 sections 5.2.2.7 and 5.5.1.6). The evidence is inadequate for reaching conclusions regarding 

causality for other categories of effects (second draft ISA, section 1.6.2).16 19 

20 Respiratory Effects 

21 As in the last review, the currently available evidence in this review supports the 

22 conclusion that there is a causal relationship between short-term SO2 exposure and respiratory 

effects, particularly in individuals with asthma (second draft ISA, p. l-16).17 23 The clearest 

24 evidence for this conclusion comes from controlled human exposure studies available at the time 

25 of the previous review and included in the 2008 ISA. These studies demonstrate lung function 

                                                            

16 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 (second draft ISA, section1.6.2). 

17 While effects have been documented for short (5 to 10 minutes) 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 or 5.0 ppm, with most studies 

reporting no respiratory symptoms at concentrations up to 2.0 ppm (second draft ISA, section 5.2.1.7). 
August 24, 2017 3-16 External Review Draft – Do Not Quote or Cite

decrements18 1 and respiratory symptoms in people with asthma exposed to SO2 for 5 to 10 

2 minutes at elevated breathing rates (second draft ISA, section 5.2.1). The epidemiologic 

3 evidence, including recent evidence not available at the time of the previous review, includes 

4 studies reporting positive associations for asthma-related hospital admissions and emergency 

5 department visits with short-term SO2 exposures (second draft ISA, section 5.2.1). These 

6 findings are generally supportive of the causal relationship conclusion for which the controlled 

7 exposure studies are the primary basis (second draft ISA, section 5.2.1.9). 

8 Sulfur dioxide is a highly reactive and water-soluble gas that once inhaled is absorbed 

almost entirely in the upper respiratory tract19 9 (second draft ISA, sections 4.2 and 4.3). Under 

10 conditions of elevated ventilation (e.g., while exercising), SO2 penetrates into the 

tracheobronchial region,20 11 where it may contribute to responses linked to asthma exacerbation in 

12 individuals with asthma (second draft ISA, sections 4.2, 4.3 and 5.2). More specifically, 

13 bronchoconstriction, which is characteristic of an asthma attack, is the most sensitive indicator of 

14 SO2-induced lung function effects. Associated with this bronchoconstriction response is an 

increase in airway resistance which is an index of airway hyperresponsiveness (AHR),21 15 

16 Exercising individuals without asthma have also been found to exhibit such responses, but at 

17 much higher SO2 exposure concentrations, above 1000 ppb (second draft ISA, section 1.5.2). 

18 Bronchoconstriction, evidenced by decrements in lung function, is observed in controlled 

19 human exposure studies after approximately 5- to 10-minute exposures and can occur at SO2

20 concentrations as low as 200 ppb in some people with asthma exposed while breathing at 

elevated ventilation, such as during exercise (second draft ISA, section 5.2.1.2).22 21 More 

22 consistent decrements in lung function are seen in such individuals with asthma following 

23 exposures to 400 ppb and greater (second draft ISA, section 5.2.1.2). In contrast, respiratory 

24 effects are not observed in other people with asthma (nonresponders) and healthy adults exposed 

                                                            

18 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) (second 

draft ISA, section 5.2.1.2). 

19 The term “upper respiratory tract” refers to the portion of the respiratory tract, including the nose, mouth and 

larynx, that precedes the tracheobronchial region (second draft ISA, sections 4.2 and 4.3). 

20 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. 

21 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 (second draft ISA, section 5.2.1.2). 

22 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 (second draft ISA, pp. 5-14 to 5-20; Johns et al., 

2010). 
August 24, 2017 3-17 External Review Draft – Do Not Quote or Cite

1 while exercising to SO2 concentrations below 1000 ppb (second draft ISA, sections 5.2.1.2 and 

2 5.2.1.7). Across studies, bronchoconstriction in response to SO2 exposure is mainly seen during 

3 conditions of increased ventilation rates, such as exercise or laboratory-facilitated rapid, deep 

breathing.23 4 These conditions lead to a shift from nasal breathing to oral/nasal breathing, which 

5 increases the concentration of SO2 reaching the tracheobronchial region of lower airways, where 

6 depending on dose and the exposed individual’s susceptibility, it may cause bronchoconstriction 

7 (second draft ISA, sections 4.1.2.2, 4.2.2 and 5.2.1.2). 

8 The evidence base of controlled human exposure studies for people with asthma is the 

9 same in this review as in the last review. Such studies reporting asthma exacerbation-related 

10 effects for individuals with asthma are summarized in Tables 5-1 and 5-2, and section 5.2.1.2 of 

11 the second draft ISA. The main responses observed include increases in specific airway 

12 resistance (sRaw) and reductions in forced expiratory volume in one second (FEV1) after 5- to 

13 10-minute exposures. As in the last review, the second draft ISA in this review quantifies the 

14 percentage of exposed study subjects with at least 100%, 200% or 300% increases in sRaw (i.e., 

15 a doubling, tripling or greater increase) and also those with at least 15%, 20% or 30% reduction 

16 in FEV1. As recognized in the last review, the results of these studies indicate that among 

17 individuals with similar disease status, some individuals have a greater response to SO2 than 

18 others (second draft ISA, p. 5-14). The SO2-induced bronchoconstriction in these studies occurs 

19 rapidly, in as little as two minutes from exposure start, and is transient, with recovery following 

20 cessation of exposure (second draft ISA, p. 5-41). 

21 The studies of subjects with asthma breathing at elevated ventilation have found effects 

22 to become more pronounced with increased exposure concentrations. Among individuals with 

23 asthma, both the percentage of individuals affected and the severity of the response increases 

24 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 moderate24 25 or greater 

26 decrements in lung function (second draft ISA, Table 5-2). At concentrations at or above 400 

27 ppb, moderate or greater decrements in lung function occurred in 20 to 60% of exercising study 

28 subjects with asthma, and compared to exposures at 200 to 300 ppb, a larger percentage of 

29 subjects experienced severe decrements in lung function (i.e., an increase in sRaw of at least 

30 200%, and/or a reduction in FEV1 of at least 20%) (second draft ISA, Table 5-2). Moreover, at 

                                                            

23 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.

24 As in the last review (described in section 3.1.1.1 above), the second draft 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 (second 

draft ISA, section 1.6.1.1). 
August 24, 2017 3-18 External Review Draft – Do Not Quote or Cite

1 the higher SO2 concentrations, moderate or greater decrements in lung function were frequently 

2 accompanied by respiratory symptoms, such as cough, wheeze, chest tightness, or shortness of 

3 breath (second draft ISA, Table 5-2). 

4 With regard to newly available epidemiological studies, there are a limited number of 

5 such studies that have investigated SO2 effects related to asthma exacerbation, with the most 

6 cohesive evidence coming from studies on asthma-related emergency department (ED) visits 

7 (second draft ISA, section 5.2.1.2). As in the last review, areas of uncertainty in the 

8 epidemiologic evidence relate to the characterization of exposure through the use of fixed site 

9 monitor concentrations as surrogates for population exposure (often over a substantially sized 

10 area and for durations greater than an hour) and the potential for confounding by PM or other 

11 copollutants (second draft ISA, section 5.2.1). In general, the pattern of associations across the 

12 newly available studies is consistent with the studies available in the last review (second draft 

13 ISA, p. 5-70). 

14 As in the last review, the evidence base for short-term SO2 exposures and respiratory 

15 effects other than asthma exacerbation is limited and inconsistent. The second draft ISA finds the 

16 evidence for an effect of SO2 exposure on allergy exacerbation, COPD exacerbation, respiratory 

17 infection, respiratory effects in healthy populations, and respiratory mortality to be inconsistent 

18 within and across disciplines and outcomes, and finds there to be uncertainty associated with the 

19 epidemiological evidence for these endpoints that is related to potential confounding by 

20 copollutants (second draft ISA, section 5.2.1.9). 

21 The evidence base for long-term SO2 exposure and respiratory effects is somewhat 

22 augmented since the last review such that the second draft ISA in the current review concludes it 

23 to be suggestive of, but not sufficient to infer, a causal relationship (second draft ISA, section 

24 5.2.2). The support for this conclusion comes mainly from the limited epidemiological study 

25 findings of associations between long-term SO2 concentrations and increases in asthma incidence 

26 combined with findings of laboratory animal studies involving newborn rodents that indicate a 

27 potential for SO2 exposure to contribute to the development of asthma, especially allergic 

28 asthma, in children (second draft ISA, section 1.6.1.2). The evidence showing increases in 

29 asthma incidence is coherent with results of animal toxicological studies that provide a 

30 pathophysiologic basis for the development of asthma. The overall body of evidence, however, 

31 lacks consistency (second draft ISA, section 1.6.1.2). Further there are uncertainties, discussed in 

32 section 3.2.1.4 below, that apply to the epidemiologic evidence, including that newly available, 

33 across the respiratory effects examined for long-term SO2 exposure (second draft ISA, section 

34 5.2.2.7).
August 24, 2017 3-19 External Review Draft – Do Not Quote or Cite

1 Other Health Effects 

2 For effects other than respiratory effects, the current evidence is generally similar to the 

3 evidence available in the last review, and is supportive of similar conclusions. With regard to a 

4 relationship between short-term SO2 exposure and total mortality, the second draft ISA reaches 

5 the same conclusion as in the previous review that the evidence is suggestive of, but not 

6 sufficient to infer, a causal relationship (second draft ISA, section 5.5.1). This conclusion is 

7 based on previous and recent multicity epidemiologic studies providing consistent evidence of 

8 positive associations, although there is uncertainty regarding the potential for SO2 to have an 

9 independent effect on mortality. While recent studies have analyzed some key uncertainties and 

10 data gaps from the previous review, uncertainties still exist, given the limited number of studies 

11 that examined copollutant confounding, the evidence for a decrease in the size of SO2-mortality 

12 associations in copollutant models with NO2 and PM10, and the lack of a potential biological 

13 mechanism for mortality following short-term SO2 exposures (second draft ISA, section 1.6.2.4). 

For other categories of health effects,25 14 the evidence is inadequate to infer the presence or 

15 absence of a causal relationship, mainly due to inconsistent evidence across specific outcomes 

16 and uncertainties regarding exposure measurement error, copollutant confounding, and potential 

17 modes of action (second draft ISA, sections 5.3.1, 5.3.2, 5.4, 5.5.1, 5.5.2, 5.6). These conclusions 

18 are consistent with those made in the previous review. 

19 In summary, rather than altering our conclusions from the previous review, the current 

20 evidence provides continued support for our previous conclusions regarding the health effects 

21 associated with exposure to SO2 and most particularly respiratory effects following short-term

22 SO2 exposure, particularly in individuals with asthma. Accordingly, as in prior reviews, this 

23 review gives primary focus to those effects most pertinent to exposures related to current 

24 concentrations in ambient air, in particular, asthma exacerbation in individuals with asthma. 

25 3.2.1.2 Populations At-Risk of SO2-Related Health Effects 

26 Populations or lifestages can be at increased risk of an air pollutant-related health effect 

27 due to one or more of a number of factors. These factors can be intrinsic, such as physiological 

28 factors that may influence the internal dose or toxicity of a pollutant, or extrinsic, such as 

29 sociodemographic, or behavioral factors. The questions considered in this section address what 

30 the currently available evidence indicates regarding which populations are particularly at risk of 

31 health effects related to exposure to SO2 in ambient air. 

                                                            

25 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 (second draft 

ISA, Table 1-1). 
August 24, 2017 3-20 External Review Draft – Do Not Quote or Cite

1  Does the current evidence alter our understanding of populations that are 

2 particularly at-risk from SO2 exposures? Is there new evidence that suggests 

3 additional at-risk populations that should be given increased focus in this review? 

4 The currently available evidence continues to support our primary conclusions from the 

5 previous review that people with asthma are at increased risk for SO2-related health effects, 

6 specifically for respiratory effects, and specifically asthma exacerbation, associated with short7 term exposures while at elevated ventilation (second draft ISA, sections 5.2.1.2 and 6.3.1). This 

8 conclusion of the at-risk status of people with asthma is based on the well-established, and well9 characterized, evidence from controlled human exposure studies, supported by the evidence on 

10 mode of action for SO2 and with limited additional support from epidemiologic studies (second 

11 draft ISA, sections 5.2.1.2 and 6.3.1). Somewhat similar to the conclusion in the last review that 

12 children and older adults are potentially susceptible populations, the second draft ISA (relying on 

13 a more systematic approach for evaluating the evidence than in the last review) indicates the 

14 evidence to be suggestive of increased risk for these groups, with some limitations and 

inconsistencies (second draft ISA, sections 6.5.1.1 and 6.5.1.2).26 15 

16 Further, the second draft ISA finds that children with asthma may be particularly at risk 

17 compared to adults with asthma (second draft ISA, section 6.3.1). This conclusion reflects 

18 several characteristics of children as compared to adults, which include their greater 

responsiveness to methacholine,27 19 a chemical that can elicit bronchoconstriction in people with 

20 asthma, as well as their greater use of oral breathing, particularly by boys (second draft ISA, 

21 sections 5.2.1.2 and 4.1.2). Oral breathing (vs nasal breathing) and increased ventilation are 

22 factors that allow for greater SO2 penetration into the tracheobronchial region of the lower 

23 airways, and reflect conditions of individuals with asthma in which bronchoconstriction-related 

24 responses have been observed in the controlled exposure studies (second draft ISA, sections 

25 4.2.2, 5.2.1.2 and 6.3.1). 

                                                            

26 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 with which there are uncertainties in the association 

with the health outcome (second draft ISA, section 6.5.1.2). 

27 The second draft 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 (second draft 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. 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 were hyperresponsive to methacholine (second draft 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 (second 

draft ISA, section 5.2.1.2; Horstman et al., 1986). 
August 24, 2017 3-21 External Review Draft – Do Not Quote or Cite

1 We additionally recognize the well-documented finding that some individuals with 

2 asthma have a greater response to SO2 than others with similar disease status (second draft ISA, 

3 section 5.2.1.2; Horstman et al., 1986; Johns et al., 2010). This occurrence is quantitatively 

4 analyzed in a study newly available in this review. This study uses the available individual 

5 subject data from five studies involving exposure of individuals with asthma to multiple 

6 concentrations of SO2 for 5 to 10 minutes while at elevated ventilation to examine the 

7 differences in lung function response (Johns et al., 2010). As noted in the second draft ISA, 

8 “these data demonstrate a bimodal distribution of airway responsiveness to SO2 in individuals 

9 with asthma, with one subpopulation that is insensitive to the bronchoconstrictive effects of SO2

10 even at concentrations as high as 1.0 ppm, and another subpopulation that has an increased risk 

11 for bronchoconstriction at low concentrations of SO2” (second draft ISA, p. 5-17). To date, the 

12 characteristics that may define the subpopulation of responders have not been identified. The 

13 current evidence for factors other than those discussed above (asthma status and lifestage) is 

14 inadequate to determine whether they might contribute to an increased risk of SO2-related effects 

15 (second draft ISA, section 6.6). 

16 3.2.1.3 Exposure Concentrations Associated with Health Effects 

17 At the time of the last review, the EPA’s conclusions regarding concentrations of SO2

18 associated with respiratory effects were based primarily on the strong evidence base of 

19 controlled human exposure studies of individuals with asthma. These studies have documented 

20 bronchoconstriction-related moderate or greater decrements in lung function following 5- to 10-

21 minute exposures during exercise. The severity of observed responses, the percentage of 

22 individuals responding, statistical significance at the study group level and the accompanying 

23 occurrence of respiratory symptoms have been found to increase with increasing exposure 

24 concentration (75 FR 35526, June 22, 2010). This information was critical in the REA analyses 

25 in the last review, the results of which were a primary consideration in reaching a conclusion on 

26 the level for the 2010 standard. 

27  Does the current evidence alter our conclusions from the previous review regarding 

28 the exposure duration and concentrations associated with health effects? 

29 The current evidence, including that newly available in this review, supports conclusions 

30 from the last review on exposure duration and concentrations associated with SO2–related health 

31 effects. These conclusions were largely based on the longstanding evidence base of controlled 

32 human exposure studies that demonstrates a relationship between 5- and 10-minute SO2 exposure 

33 concentrations and decrements in lung function (e.g., increased sRaw and reduced FEV1) in 

34 individuals with asthma exposed while at elevated ventilation rate (second draft ISA, section 
August 24, 2017 3-22 External Review Draft – Do Not Quote or Cite

1 1.6.1.1). At the higher concentrations, there are clear and consistent increases in SO2-induced 

2 respiratory symptoms (second draft ISA, Table 5-2). 

3 The available and well characterized evidence documents an effect of short-term 

4 exposures on the respiratory system. As summarized in section 3.2.1.1, SO2-induced 

5 bronchonstriction occurs rapidly in responding study subjects with asthma exposed for just a few 

6 minutes while breathing at elevated ventilation rates (second draft ISA, section 5.2.1.2). 

7 Additionally, exposures as short as 5 minutes have been found to elicit a similar 

8 bronchoconstrictive response as somewhat longer exposures. For example, during exposure to 

9 SO2 over a 30-minute period with continuous exercise, the response to SO2 has been found to 

10 develop rapidly and is maintained throughout the 30-minute exposure (second draft ISA, p. 5-

11 14). In a study involving short exercise periods within a 6-hour exposure period, the effects 

12 observed following exercise were documented to return to baseline levels within one hour after 

13 the cessation of exercise, even with continued exposure (Linn et al., 1984). In considering the 

14 epidemiological evidence with regard to the question of exposure duration, while we note the 

15 associations of asthma-related emergency room visits and hospital admissions with 1-hour to 24-

16 hour ambient air concentration metrics, we recognize that current methods are not able to address 

17 whether these associations are due to exposure on the order of hours or much shorter-term 

18 exposure to peaks in SO2 concentration. As noted in the second draft ISA, the air quality metrics 

19 in the epidemiological studies are for time periods longer than the 5- to 10-minute exposures 

20 eliciting effects in the controlled human exposure studies and may not adequately capture the 

21 spatial and temporal variation in SO2 concentrations (second draft ISA, pp. 5-47, 5-55). 

22 With regard to the evidence for exposure concentrations eliciting effects, we focus 

23 primarily on the controlled human exposure study findings for which data are available to the 

24 EPA for individual subjects with asthma that were exposed during elevated ventilation, 

summarized in Table 3-1 (second draft ISA, Table 5-2).28 25 These data demonstrate that SO2

26 concentrations as low as 200 to 300 ppb for 5 to 10 minutes elicited moderate or greater 

27 bronchoconstriction, measured as a decrease in FEV1 of at least 15% or an increase in sRaw of at 

28 least 100% in a subset of the subjects (second draft ISA, section 5.2.1). Both the percent of 

29 individuals affected and the severity of response increased with increasing SO2 concentrations. 

30 At concentrations ranging from 200 to 300 ppb, the lowest levels tested in free breathing 

31 chamber studies, 5 to 30% of exercising individuals with asthma experienced moderate or greater 

32 decrements in lung function (second draft ISA, section 5.2.1). At concentrations at or above 400 

33 ppb, moderate or greater decrements in lung function occurred in 20 to 60% of exercising 

                                                            

28 The findings summarized in Table 5-2 of the second draft ISA and in Table 3-1 of this draft 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. 
August 24, 2017 3-23 External Review Draft – Do Not Quote or Cite

1 individuals with asthma and a larger percentage of individuals with asthma experienced more 

2 severe decrements in lung function (i.e., an increase in sRaw of at least 200%, and/or a 20% or 

3 more decrease in FEV1), compared to exposures at 200 to 300 ppb (second draft ISA, section 

4 5.2.1). Additionally, at concentrations at or above 400 ppb, moderate or greater decrements in 

5 lung function were frequently accompanied by respiratory symptoms, with some of these 

6 findings reaching statistical significance (second draft ISA, section 5.2.1). 
August 24, 2017 3-24 External Review Draft 

1 Table 3-1. Percentage of adults with asthma in controlled human exposure studies experiencing sulfur 2 decrements in lung function and respiratory symptoms (adapted from Table 5-2 in the second draft IS

SO2

Conc (ppm) 

Exposure 

Duration 

(min) N 

Ventilation 

(L/min) 

Cumulative Percentage of Responders 

(Number of Subjects)a

Study 

RespiraSuppo

sRaw ≥100%  ≥200%  ≥300% 

FEV1 ≥15%  ≥20%  ≥30% 

0.2 5 23 ~48 sRaw 9% (2)b 0 0 Linn et al. (1983b) Limited 

increassymptoasthmaHorstm1983b; al., 198Schach

10 40 ~40 sRaw 7.5% (3)c 2.5% (1)c 0c Linn et al. (1987)c10 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) 

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)d10 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) Stronge

statisticin respiet al., 1Linn et 1987 ; R

10 40 ~40 sRaw 24% (9.5)c 9% (3.5)c 4% (1.5)c Linn et al. (1987)c10 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) 7.4% (1) 3.7% (1) Horstman et al. (1986) 10 28 ~40 sRaw 18% (5) 4% (1) 4% (1) Roger et al. (1985) 
August 24, 2017 3-25 External Review Draft 

SO2

Conc (ppm) 

Exposure 

Duration 

(min) N 

Ventilation 

(L/min) 

Cumulative Percentage of Responders 

(Number of Subjects)a

Study 

RespiraSuppo

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 a

SO2-ind

symptoHorstm1983b; al., 199

10 40 ~40 sRaw 34% (13.5)c 24% (9.5)c 19% (7.5)c Linn et al. (1987)c10 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)c10 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. aData presented from all references from which individual data were available in the published paper or were provided to EPA (Johns, 2009; Johns and S

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% 

function decrements are adjusted for the effects of exercise in clean air (calculated as the difference between the percent change relative to baseline wit

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 ro

following the first 10 min period of exercise. 

dAnalysis includes data from only people with mild Linn et al. (1988) and moderate Linn et al. (1990) asthma who were not receiving supplemental mediceOne 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 

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. 

fIndicates studies in which exposures were conducted using a mouthpiece rather than a chamber. 

1 

2 
August 24, 2017 3-26 External Review Draft – Do Not Quote or Cite

1 The lowest exposure concentration in Table 3-1 is 200 ppb. This is the lowest exposure 

2 concentration tested by studies in which study subjects breathed freely (e.g., without using a 

mouthpiece).29 3 In such studies that tested 200 ppb, a portion of the exercising study subjects with 

4 asthma (approximately 8 to 9%) responded with at least a doubling in sRaw or an increase in 

5 FEV1 of at least 15% (Table 3-1; Linn et al., 1983b; Linn et al., 1987). 

6 With regard to exposure concentrations below 200 ppb, the available evidence is very 

7 limited. This information is derived from studies in which the subjects were exposed by 

8 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).30 9 Additionally, some 

10 of these studies did not include an exposure to clean air while exercising that would have 

11 allowed for determining the effect of SO2 versus that of exercise in causing bronchoconstriction. 

12 In those cases, the lung function measurements (e.g., sRaw, FEV1) following SO2 exposure are 

13 assessed relative to measurements taken prior to exposure (baseline), rather than being assessed 

14 relative to measurements for a control exposure to clean air while exercising. The studies cited 

15 here, of a limited number of adults and adolescents, reported small changes in FEV1 or sRaw in 

16 the individual study subjects, with magnitudes of change appearing to be smaller than responses 

17 reported from studies at exposure concentrations of 200 ppb or more. For example, the increase 

18 in sRaw reported for two young adult subjects exposed to 100 ppb in the study by Sheppard et al. 

19 (1981) was approximately half the response of these subjects at 250 ppb. In the two studies of 

20 adolescents (aged 12 to 18 years), among the individual study subjects for which respiratory 

21 resistance increased with SO2 exposure, the magnitude of increase was less than 100% in each

22 subject (Koenig et al., 1990; Koenig et al., 1989). 

23 In considering what can be gleaned from these mouthpiece studies of 100 ppb, we note 

24 that the results of studies that utilize a mouthpiece exposure system cannot be directly compared 

25 to results from studies involving freely breathing subjects because when a mouthpiece is used, 

26 the inhaled breath completely bypasses the nasal passages where SO2 is efficiently removed, thus 

27 allowing more of the inhaled SO2 to penetrate into the tracheobronchial airways (2008 ISA, p. 3-

28 4; second draft ISA, section 4.1.2.2). This occurrence as well as limited evidence comparing 

                                                            

29 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). 

30 A subset of these studies are cited in the second draft 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 second draft ISA. 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). 
August 24, 2017 3-27 External Review Draft – Do Not Quote or Cite

1 responses by mouthpiece and chamber exposures leads to the expectation that SO2-responsive 

2 people with asthma breathing SO2 using a mouthpiece, particularly while at elevated ventilation, 

3 would experience greater lung function responses than if exposed to the same test concentration 

4 while freely breathing in an exposure chamber (second draft ISA, p. 5-22; Linn et al., 1983a). 

5 We have also considered what can be gleaned from the epidemiological studies regarding 

6 exposure concentrations associated with health effects. Although exposure concentrations 

7 eliciting respiratory responses are not available from such studies, the ambient air concentrations 

8 occurring in studies that find associations with outcomes such as asthma-related ED visits and 

9 hospitalizations have the potential to indicate ambient air concentrations that may contribute to 

10 exposures that may be eliciting effects. For example, in recognizing the general coherence of 

11 epidemiological study findings for 24-hour ambient air concentrations with the findings of the 

12 controlled human exposure studies for exercising study subjects with asthma exposed for 5 to 10 

13 minutes, the 2008 ISA recognized that “it is possible that these epidemiologic associations are 

14 determined in large part by peak exposures within a 24-h period” (2008 ISA, p. 5-5). In 

15 considering the epidemiological studies in this light, however, we note that given the important 

16 role of SO2 as a precursor to PM in ambient air, a key uncertainty in the epidemiological 

17 evidence available in the last review was potential confounding by PM (second draft ISA, p. 5-

18 5). Among the U.S. epidemiologic studies (some conducted in multiple locations) reporting 

19 mostly positive and sometimes statistically significant associations between ambient SO2

20 concentrations and emergency department visits and hospital admissions, few studies have 

21 attempted to address this uncertainty, e.g., through the use of copollutant models. For example, 

22 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).31 23 No 

24 additional such studies have been newly identified in this review. Further, the second draft ISA 

25 states that uncertainty with regard to potential confounding by PM remains in the currently 

26 available epidemiologic evidence base (second draft ISA, p. 5-144). 

27 3.2.1.4 Uncertainties in the Health Effects Evidence 

28 A number of key uncertainties and limitations were identified in the previous review with 

29 respect to the health effects evidence, as described in the 2009 REA. This section considers the 

30 currently available information, including that newly available in this review, with regard to such 

31 areas of uncertainty. 

                                                            

31 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). 
August 24, 2017 3-28 External Review Draft – Do Not Quote or Cite

1  To what extent have important uncertainties identified in the last review been 

2 reduced and/or have new uncertainties emerged? 

3 We have not identified any new uncertainties since the last review. However, we 

4 continue to recognize important uncertainties that also existed in the last review. This array of 

5 important areas of uncertainty related to the current health evidence, including that newly 

6 available in this review, is summarized below. 

7 Although the evidence clearly demonstrates that short-term SO2 exposures cause 

8 respiratory effects, particularly asthma exacerbation in exercising individuals with asthma, as in 

9 the previous review, we continue to recognize uncertainties that remain in several aspects of our 

10 understanding of these effects. Such uncertainties include those associated with severity and 

11 prevalence of responses to very short (5- to 10-minute) SO2 exposures below 200 ppb and 

12 responses of some population groups not included in the controlled exposure studies (e.g., those 

13 with more severe asthma and children). There are also uncertainties concerning the potential 

14 influence of exposure history and co-exposure to other pollutants on the relationship between 

15 short-term SO2 exposures and respiratory effects. With regard to the evidence base, we also 

16 recognize a complication associated with interpreting the epidemiologic evidence related to 

17 uncertainty in the exposure estimates. The following discussion touches on each of these types of 

18 uncertainty. 

19 With regard to the potential for and magnitude of these effects in at-risk populations 

20 exposed to 5- to 10-minute concentrations below 200 ppb, there is very limited evidence from 

21 small mouthpiece studies of exposure concentrations as low as 100 ppb, as discussed in section 

22 3.2.1.3 above. These studies indicate the likelihood of an appreciable reduction in SO2-induced 

23 response in exercising people with asthma from that observed from exposures at 200 ppb. Given 

24 the limited size of these studies and their differences from free breathing chamber studies, 

25 however, uncertainties remain with regard to a complete characterization of the extent of 

26 response in exercising individuals with asthma exposed through natural or free breathing to 

27 exposure concentrations below 200 ppb. The extent to which the epidemiological evidence, 

including that newly available, can inform this area of uncertainty also may be limited.32 28 

29 Accordingly, this remains an area of uncertainty in this review. 

30 Some uncertainty also remains with regard to the extent to which the controlled human 

31 exposure study evidence describes the responses of the populations most at risk of SO2-related 

                                                            

32 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. 
August 24, 2017 3-29 External Review Draft – Do Not Quote or Cite

1 respiratory effects (e.g., those with the most severe responses, or greatest likelihood of response). 

2 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.33 3 Further, 

4 while it is well documented that some individuals have a greater response to SO2 than others 

5 with the same disease status, the factors contributing to this greater susceptibility are not yet 

6 known (second draft ISA, pp. 5-14 to 5-20). 

7 Uncertainty also remains related to the responses for children with asthma. Although the 

8 epidemiological evidence includes a number of studies focused on health outcomes in children 

9 that are supportive of the qualitative conclusions of causality (second draft ISA, section 5.2.1.2), 

10 there are few controlled human exposure studies to inform our understanding of concentrations 

11 associated with effects. Those studies have not included subjects younger than 12 years (second 

12 draft ISA, p. 5-21). Some characteristics particular to school age children younger than 12 years, 

13 such as increased propensity for mouth breathing (second draft ISA, section 4.1.2.2), however, 

14 suggest that this age group of children with asthma might be expected to experience larger lung 

15 function decrements than adults with asthma (second draft ISA, p. 5-24). 

16 Other areas of uncertainty concerning the potential influence of SO2 exposure history and 

17 co-exposure to other pollutants on the relationship between short-term SO2 exposures and 

18 respiratory effects also remain from the last review. There is some limited evidence regarding the 

19 potential for an increased response to SO2 exposures occurring in the presence of other common 

20 pollutants (e.g., PM, nitrogen dioxide and ozone), although the studies are limited (e.g., with 

21 regard to their relevance to ambient exposures) and/or provide inconsistent results (second draft 

22 ISA, p. 5-24; 2008 ISA, section 3.1.4.7). There is also some evidence suggestive of a potential 

23 for SO2 exposure to contribute to an increased sensitivity to allergens, however the studies are 

24 very few and are limited to experimental animal models (second draft ISA, section 5.2.1.9). 

25 There are additional complications associated with interpretation of epidemiologic 

26 studies of SO2 in ambient air that pertain to exposure measurement error and copollutant 

27 confounding (second draft ISA, sections 3.4, 5.2.1.1 and 5.2.1.2). With regard to the former, a 

28 key uncertainty in the epidemiologic evidence is whether study findings reflect an independent 

29 association for SO2 given that the studies assigned exposure from fixed site monitors while SO2

30 concentrations in ambient air tend to show high spatiotemporal variability within a city, and 

                                                            

33 The second draft ISA identifies two studies that have investigated the influence of asthma severity on 

responsiveness to SO2, with one finding that a larger change in lung function observed in the moderate/severe 

asthma group was attributable to the exercise component of the study protocol while the other did not assess the 

role of exercise in differences across individuals with asthma of differing severity (Linn et al., 1987; Trenga et al., 

1999). Based on the criteria used in the study by Linn et al (1987) for placing individuals in the 

“moderate/severe” group, the ISA concluded that the asthma of these individuals “would likely be classified as 

moderate by today’s classification standards” (second draft ISA, p. 5-20; Johns et al., 2010; Reddel, 2009). 
August 24, 2017 3-30 External Review Draft – Do Not Quote or Cite

1 correlations with personal exposure are poorly characterized. Accordingly, there is uncertainty 

2 regarding the extent to which measurements at the study monitors, and the associated air quality 

3 concentration metric for the study, adequately represent the spatiotemporal variability in ambient 

4 SO2 concentrations in the study area (second draft ISA, sections 5.2.1.2 and 3.4.1.3). 

5 Further, not only is SO2 but one component of a complex mixture of pollutants present in 

6 the ambient air, an issue not unique to SO2 epidemiological studies, but SO2 is also a precursor to 

7 sulfate, which can be a principal component of PM, an air pollutant commonly occurring across 

8 the U.S. This uncertainty affects the extent to which effect estimates from epidemiologic studies 

9 reflect the independent contribution of SO2 to the adverse respiratory outcomes assessed in these 

10 studies. This area of uncertainty was recognized in the last review and remains in the current 

11 review. In first summarizing the epidemiological evidence from the last review, the second draft 

12 ISA indicated that it was strongest for increased respiratory symptoms and respiratory-related 

13 hospital admissions and ED visits, especially in children, while noting that “a key uncertainty 

14 was potential confounding by copollutants, particularly PM” (second draft ISA, p. 5-5). With 

15 regard to the newly available evidence, the second draft ISA states that “[t]he caution expressed 

16 in the 2008 SOX ISA (U.S. EPA, 2008d) related to the limitation of attributing an independent 

17 effect to SO2 (due to the relationship of SO2 levels to PM levels) is still a concern” (second draft 

ISA, p. 5-144).34 18 

19 There remains uncertainty in the evidence with regard to the potential role of long-term 

20 exposure to SO2 in eliciting SO2-related respiratory effects. As noted in section 3.2.1.1 above, 

21 the ISA has determined the evidence to be suggestive of this being a causal relationship. The 

22 strongest evidence supporting this conclusion is provided by epidemiological study findings of 

23 associations between long-term SO2 concentrations and increases in asthma incidence combined 

24 with findings of laboratory animal studies involving newborn rodents that indicate a potential for 

25 SO2 exposure to contribute to the development of asthma, especially allergic asthma, in children. 

26 However, uncertainties that relate to the limitations of the animal toxicological evidence, 

27 particularly for long-term exposure, and the potential for confounding by other pollutants is 

28 unexamined, and largely unavailable, for epidemiologic studies of asthma among children 

29 (second draft ISA, section 5.2.2.7). 

30 Another area of uncertainty recognized by the ISA, is that contributing to conclusions 

31 regarding the potential for SO2 in ambient air to contribute to health effects other than respiratory 

                                                            

34 A few recent epidemiologic studies add evidence for SO2 in copollutant models with PM, NO2, or O3, although 

the pollutants are measured at central site monitors (second draft ISA, p. 5-8). Across the full epidemiologic 

evidence base, some associations were relatively unchanged in magnitude after adjustment for a copollutant, 

while others did not persist. However, the second draft 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” (second draft ISA, p. 5-139). 
August 24, 2017 3-31 External Review Draft – Do Not Quote or Cite

1 effects. As noted in section 3.2.1.1 above, the ISA has determined the evidence to be suggestive 

2 of, but insufficient to infer, a causal relationship between short-term SO2 exposure and mortality 

3 and to be inadequate to infer the presence or absence of a causal relationship for other types of 

4 exposures and health effects for which there are studies available. 

5 In summary, a variety of uncertainties from the last review remain, including those 

6 related to the extent of effects at concentrations below those evaluated in controlled human 

7 exposure studies of exercising individuals with asthma, and the potential for greater impacts in 

8 individuals with more severe asthma and in children with asthma (second draft ISA, section 

9 5.2.1.9). 

10 3.2.1.5 Public Health Implications 

11 Implications and the magnitude of potential impacts on public health are dependent upon 

12 the type and severity of the effect, as well as the size of population affected. With regard to SO2 

13 concentrations in ambient air, the public health implications and potential public health impacts 

14 relate to the effects causally related to SO2 exposures of interest in this review. These are 

15 respiratory effects of short-term exposures, and particularly those effects associated with asthma 

16 exacerbation in people with asthma. As summarized in section 3.2.1.1, the most strongly 

17 demonstrated effects are bronchoconstriction-related effects resulting in decrements in lung 

18 function elicited by short term exposures during periods of elevated ventilation, while asthma19 related health outcomes such as ED visits and hospital admissions have also been statistically 

20 associated with ambient air SO2 concentration metrics in epidemiological studies (second draft

21 ISA, section 5.2.1.9). 

22 In considering public health implications, in addition to the difference in severity of 

23 different effects, it is important to consider aspects of the same effect with regard to its impact on 

24 population groups of differing susceptibility. For example, with regard to bronchoconstriction25 related effects, the same percentage increase in sRaw or reduction in FEV1 for two groups of 

26 individuals that differ in their baseline sRaw or FEV1 may result in the two groups being affected 

27 differently with regard to increased susceptibility to other physiological threats or challenges. 

28 Accordingly, consideration of such baseline differences and also the relative transience or 

29 persistence of such sRaw or FEV1 changes, as well as other factors, is important to 

30 characterizing implications for public health, as recognized by the American Thoracic Society in 

31 their statements on evaluating adverse health effects of air pollution (ATS, 2000; Thurston et al., 

32 2017). 

33 The most recent policy statement by the ATS on what constitutes an adverse health effect 

34 of air pollution provides a general framework for interpreting evidence that proposes a “set of 

35 considerations that can be applied in forming judgments” for this context (Thurston et al., 2017). 
August 24, 2017 3-32 External Review Draft – Do Not Quote or Cite

1 The earlier ATS statement, in addition to emphasizing clinically relevant effects, also 

2 emphasized both the need to consider changes in “the risk profile of the exposed population,” 

3 and effects on the portion of the population that may have a diminished reserve that puts its 

4 members at potentially increased risk if affected by another agent (ATS, 2000). These concepts, 

5 including the consideration of the magnitude of effects occurring in just a subset of study 

6 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.

35 7 

8 As summarized in section 3.2.1.3 above, people with asthma are the key population at 

9 risk for SO2-related effects and children with asthma are considered to be at relatively greater 

10 risk than other age groups within this at-risk population (second draft ISA, section 6.3.1). In 

11 recognizing that asthma as a disease can vary in its severity, we take note of the lack of evidence 

12 for individuals with the most severe asthma. The evidence base of controlled exposure studies of 

13 exercising people with asthma provides limited information that indicates there to be similar 

relative responses of individuals with differences in severity of their asthma,36 14 although the 

15 evidence indicates that the absolute changes in lung function are larger for individuals with more 

16 severe asthma compared to those characterized as having mild asthma. It is uncertain whether a 

17 greater response to the exercise itself (vs the SO2 exposure) played a role in such findings, 

18 however the available studies “suggest that adults with moderate/severe asthma may have more 

19 limited reserve to deal with an insult compared with individuals with mild asthma” (second draft 

20 ISA, p. 5-20; Linn et al., 1987; Trenga et al., 1999). 

21 The information below characterizes the size and other features of the populations in the 

22 U.S. concluded to be at risk of SO2-related effects, when under elevated ventilation conditions. 

23 As a whole, the discussion in this section indicates the potential for exposures to SO2 in ambient 

24 air to be of appreciable public health importance. Such considerations contributed to the basis for 

25 the 2010 decision to appreciably strengthen the primary SO2 NAAQS and to establish a 1-hour 

26 standard to protect the at-risk populations from short term exposures of concern. Such 

27 considerations remain relevant in the current review. 

                                                            

35 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). 

36 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 second draft 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 

(second draft ISA, p. 5-20 to 5-21; Johns et al., 2010; Reddel, 2009). 
August 24, 2017 3-33 External Review Draft – Do Not Quote or Cite

1  What does the information available in this review indicate with regard to the size of 

2 at-risk populations and their distribution in the U.S.? 

3 The magnitude and characterization of a public health impact is dependent upon the size 

4 and characterization of the populations affected, as well as the type or severity of the effect. As 

5 summarized above, the population group most at risk of health effects associated with exposure 

6 to SO2 in ambient air is people with asthma. The National Center for Health Statistics data for 

7 2015 indicate that approximately 8.0% of the U.S. population has asthma (Table 3-2; CDC, 

8 2017). These data indicate the size of the key at-risk population for SO2 in ambient air. It is this 

9 population that the primary NAAQS for SO2 is intended to protect. Table 3-2 below considers 

10 the currently available information that helps to characterize key features of this population. 

11 The age group for which the prevalence documented by these data is greatest is children 

12 aged five to 19, with 10.2% of children aged 15 to 19 years having asthma. In 2012 (the most 

13 recent year for which such an evaluation is available), it was the leading chronic illness affecting 

14 children (Bloom et al., 2013). The prevalence is greater for boys than girls. Among populations 

15 of different races or ethnicities, black non-Hispanic children have the highest prevalence, at 

16 13.4%. Asthma prevalence is also increased among populations in poverty (e.g., 11.1% among 

17 people living in households below the poverty level compared to 7.2% of those living above it). 

18 Population groups with relatively greater asthma prevalence might be expected to have a 

19 relatively greater potential for SO2 impacts. 

20    
August 24, 2017 3-34 External Review Draft – Do Not Quote or Cite

1 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 2,492 10.3 

Sex 

Males 9,998 6.5 

 Boys (Age <18) 3,705 9.9 

 Men (Age 18+) 6,293 5.4 

Females 14,634 9.1 

 Girls (Age <18) 2,483 6.9 

 Women (Age 18+) 12,151 9.7 

Race/Ethnicity 

White NH 3 15,244 7.8 

 Child (Age <18) 2,810 7.4 

 Adult (Age 18+) 12,435 7.9 

Black NH 3,931 10.3 

 Child (Age <18) 1,336 13.4 

 Adult (Age 18+) 2,595 9.1 

Other NH 1,793 6.9 

 Child (Age <18) 605 8.4 

 Adult (Age 18+) 1,188 6.3 

Hispanic 3,665 6.6 

 Child (Age <18) 1,438 8.0 

 Adult (Age 18+) 2,227 5.9 

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

2 
August 24, 2017 3-35 External Review Draft – Do Not Quote or Cite

1 3.2.2 Exposure/Risk-based Considerations 

2 Our consideration of the scientific evidence available in the current review, as at the time 

3 of the last review (summarized in section 3.1 above), is informed by results from a quantitative 

4 analysis of estimated population exposure and associated risk. The overarching consideration is 

5 whether the current exposure/risk information alters our overall conclusions from the previous 

6 review regarding health risk associated with exposure to SO2 in ambient air. As in our 

7 consideration of the evidence in section 3.2.1 above, we have organized the discussion regarding 

8 the exposure/risk information around a set of key questions to assist us in considering the 

9 exposure/risk analyses of at-risk populations living in three urban areas under air quality 

10 conditions simulated to just meet the existing SO2 primary standard. 

11 Prior to addressing the individual exposure/risk questions, we provide a summary of key 

12 aspects of the assessment, including the study areas, populations simulated, modeling tools and 

13 exposure and risk metrics derived (section 3.2.2.1). We then consider aspects of the questions 

14 beginning with the magnitude of exposure and risk estimated for the simulated at-risk 

15 populations (section 3.2.2.2), followed by the key uncertainties associated with the quantitative 

16 analyses with regard to drawing conclusions as to the adequacy of protection afforded by the 

17 current SO2 standard (section 3.2.2.3). Lastly, we consider the exposure and risk estimates from 

18 the quantitative assessment with regard to the extent to which such estimates may be judged to 

19 be important from a public health perspective (section 3.2.2.4). 

20 3.2.2.1 Exposure/risk analyses 

21 In the assessment conducted for this review, described in detail in the draft REA, we have 

22 estimated SO2 exposure and risk associated with air quality conditions that just meet the current 

23 standard. These analyses inform our understanding of the protection provided by the current SO2

24 standard from effects that the health effects evidence indicates to be elicited in some portion of 

25 exercising people with asthma by short (e.g., 5to 10 minutes) elevations in SO2 exposure 

26 concentrations. The analyses estimate exposure and risk for at-risk populations in three urban 

27 study areas in: (1) Fall River, MA; (2) Indianapolis, IN; and, (3) Tulsa, OK. 

28 The three study areas present a variety of circumstances with regard to population 

29 exposure to short-term peak concentrations of SO2 in ambient air. This set of study areas and the 

30 associated exposed populations are intended to be informative to the EPA’s consideration of 

31 potential exposures and risks that may be associated with the air quality conditions that meet the 

32 current SO2 standard. As discussed further in sections 3.2.2.2 and 3.2.2.4 below, the Fall River 

33 study area is found to present particularly informative exposure circumstances given that it 

34 provides an example of an area in the U.S. in which there is substantial overlap between 

35 locations that are relatively more populated and where SO2 concentrations are relatively higher 
August 24, 2017 3-36 External Review Draft – Do Not Quote or Cite

1 (draft REA, section 5.4). As such, this area represents places in the U.S. with the potential for 

2 exposures of greatest concern, making it important in considering the protection provided by the 

3 current standard. 

4 The three study areas range in total population size from approximately 180,000 to 

5 540,000 and reflect different mixtures of SO2 emissions sources, including utilities using fossil 

6 fuel and non-utility sources, such as petroleum refineries and secondary lead smelting (draft 

7 REA, section 3.1). They include locations in New England, Ohio River Valley and the Midwest, 

8 the latter two regions comprising the part of the U.S. with generally the greatest prevalence of 

9 elevated SO2 concentrations and large emissions sources (Figure 2-7, Appendix F). Additionally, 

10 continuous 5-minute ambient air monitoring data (i.e., all 12 5-minute values for each hour) are 

11 available in two of the three study areas, with hourly maximum 5-minute concentration data 

12 available in the third (draft REA, section 3.2). 

13 Asthma prevalence estimates for the populations simulated in the three study areas ranges 

14 from 8.0 to 8.7% (draft REA, section 5.1). For children, the study area prevalence rates range 

15 from 9.7 to 11.2% (draft REA, section 5.1). Variation within each studyrelated to age, sex and 

16 whether family income is above or below the poverty level was also accounted for (section 4.1.2 

and Appendix E of draft REA,).37 17 This variation is greatest in the Fall River study area, with 

18 census block level, age-specific prevalence estimates ranging from 7.9 to 18.6% for girls and 

19 from 10.7 to 21.5% for boys (draft REA, Table 4-1). 

20 In the draft REA, 1-hour SO2 concentrations were estimated across a 3-year period 

21 (consistent with the period represented by the form of the standard) using air quality modeling of 

22 SO2 emissions sources in each area, and were adjusted, as described in the draft REA, such that 

23 the air quality modeling receptor location with the highest concentrations just met the current 

standard.38 24 In addition, sensitivity analyses were performed using an alternative adjustment 

25 approach and are summarized in section 3.2.2.2. Relationships between 1-hour and 5-minute 

26 concentrations at local monitors were then used to estimate 5-minute concentrations associated 

27 with the adjusted 1-hour concentrations across the 3-year period at all receptor locations in each 

28 area (draft REA, section 3.5). 

29 The exposure modeling, presented in detail in the draft REA, relied on the EPA’s Air 

30 Pollutant Exposure model (APEX), which estimates human exposure using a stochastic, event31 based microenvironmental approach. This model has a history of application, evaluation, and 

                                                            

37 As described in section 4.1.2 and Appendix E of the draft REA, asthma prevalence in the exposure modeling 

domain is estimated based on national prevalence information and study area demographic information related to 

age, sex and poverty status. 

38 As described in more detail in section 3.4 of the draft 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. 
August 24, 2017 3-37 External Review Draft – Do Not Quote or Cite

1 progressive model development in estimating human exposure and dose for reviews of NAAQS 

2 for gaseous pollutants (U.S. EPA, 2008; 2010; 2014). This general exposure modeling approach 

3 was also used in the 2009 REA for the last review of the primary standard for SOX, although a 

4 number of updates have been made to the model and various datasets used with it (2009 REA; 

5 U.S. EPA, 2017b, section 3.4). For example, exposure modeling for the draft REA includes 

6 reliance on updates to several key inputs to the model including (1) a significantly expanded 

7 Consolidated Human Activity Database (CHAD), that now has over 55,000 diaries, with over 

8 25,000 for school-aged children; (2) the updated NHANES data (2009-2014), which are the basis 

9 for the age- and sex-specific body mass distributions from which APEX samples to specify the 

10 individuals in the modeled population; (3) the algorithms used to estimate age- and sex-specific 

11 resting metabolic rate, a key input to estimating a simulated individual’s activity-specific 

12 ventilation rate; and (4) the ventilation rate algorithm itself. Further, the current model uses 

13 updated population demographic data based on the most recent Census. 

14 The APEX model probabilistically generates a sample of hypothetical individuals from 

15 an actual population database and simulates each individual’s movements through time and 

16 space (e.g., indoors at home, inside vehicles) to estimate his or her exposure to a pollutant. 

17 Population characteristics are taken into account to represent the demographic profile of the 

18 population in each study area. Age and gender demographics for the simulated at-risk population 

19 (adults and children with asthma) were drawn from the prevalence estimates provided by the 

2011-2015 National Health Interview Survey.39 20 The APEX model generates each simulated 

21 person or profile by probabilistically selecting values for a set of profile variables, including 

22 demographic variables, status and physical attributes (e.g., residence with air conditioning, 

23 height, weight, body surface area) and ventilation rate. 

24 Based on minute-by-minute activity levels, and physiological characteristics of the 

25 simulated person (see draft REA, section 4.1), APEX estimates an equivalent ventilation rate 

26 (EVR), based on normalizing the simulated individuals’ activity-specific ventilation rate to their 

27 body surface area; the EVR is used to identify exposure periods during which an individual is at 

28 or above a specified ventilation level (draft REA, section 4.1.4.4). The level specified is based on 

29 the ventilation rates of subjects in the controlled human exposure studies of exercising people 

30 with asthma (Table 3-1). The APEX simulations performed for this review have focused on 

                                                            

39 Information about the National Health Interview Survey is available at http://www.cdc.gov/nchs/nhis.htm. 
August 24, 2017 3-38 External Review Draft – Do Not Quote or Cite

exposures to SO2 emitted into ambient air that occurs in microenvironments,40 1 without additional 

contribution from indoor SO2 emissions sources.41 2 

3 As in the last review, the draft REA for this review uses the APEX model estimates of 5-

4 minute exposure concentrations for simulated individuals with asthma at elevated ventilation to 

5 characterize health risk in two ways based on information from the controlled human exposure 

6 studies on the occurrence of bronchoconstriction-related effects in some study subjects with 

7 asthma who are exposed during exercise (draft REA, section 4.5). In drawing on this evidence 

8 base for this purpose, the draft REA has given primary focus to the well-documented studies 

9 summarized in Table 5-2 and Figure 5-1 of the second draft ISA for 5- to 10-minute exposure 

10 concentrations ranging from 200 ppb to 600 ppb (Table 3-1 of this document). The first risk 

11 metric is based on comparison of the estimated 5-minute exposure concentrations individuals at 

12 elevated ventilation to 5-minute concentrations of potential concern (benchmark concentrations), 

13 and the second utilizes exposure-response information for study subjects experiencing 

14 bronchoconstriction-related effects on lung function (specifically a doubling or more in sRaw) to 

15 estimate the portion of the simulated at-risk population likely to experience one or more days 

16 with an SO2-related increase in sRaw of at least 100%. Both of these metrics are used in the draft 

17 REA to characterize health risk associated with 5-minute peak SO2 exposures among the 

18 simulated at-risk population during periods of elevated ventilation. These risk metrics were also 

19 derived in the REA for the last review and the associated estimates informed the Administrator’s 

20 2010 decision on the new standard (75 FR 35546-35547, June 22, 2010). 

21 For the benchmarks metric, the draft REA for this review, like the 2009 REA in the last 

22 review, uses benchmark concentrations that range from 400 ppb down to 100 ppb (draft REA, 

23 section 4.5.1). At the upper end of this range, 400 ppb represents the lowest concentration in 

24 free-breathing controlled human exposure studies of exercising people with asthma where 

25 moderate or greater lung function decrements occurred that were often statistically significant at 

26 the group mean level and were frequently accompanied by respiratory symptoms. The 200 ppb 

27 benchmark concentration represents the lowest level tested in studies where subjects were freely 

28 breathing in exposure chambers (moderate or greater lung function decrements in some of these 

                                                            

40 Five microenvironments (MEs) are modeled in the draft 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 draft 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 (draft REA, section 4.2). 

41 Indoor sources are generally minor in comparison to SO2 from ambient air (draft REA, sections 2.1.1 and 2.1.2). 
August 24, 2017 3-39 External Review Draft – Do Not Quote or Cite

1 subjects) (75 FR 35527, June 22, 2010). The lowest benchmark concentration (100 ppb), which 

2 is one half the lowest exposure concentration tested in free breathing exposure studies, has been 

3 included in consideration of the nonzero percentage of subjects with asthma experiencing 

4 moderate transient decrements in lung function at the 200 ppb exposure concentration 

5 (approximately 8 to 9%) and the lack of specific study data for some groups of individuals with 

asthma, such as primary-school-age children and those with more severe asthma.42 6 

7 The exposure-response (E-R) function for the risk of lung function decrements was 

8 developed from the individual subject results for sRaw from the controlled exposure studies of 

9 exercising freely breathing people with asthma exposed to SO2 concentrations from 1000 ppb 

10 down as low as 200 ppb (draft REA, Table 4-9). Beyond the assessment of these studies and 

11 their results in past reviews, there has been extensive evaluation of the individual subject results, 

12 including a data quality review in the last SO2 NAAQS review (Johns and Simmons, 2009), and 

13 detailed analysis in two subsequent publications (Johns et al., 2010; Johns and Linn, 2011). The 

14 sRaw responses reported in these studies have been summarized in the second draft ISA, as in 

15 the last review, in terms of percent of study subjects experiencing responses of a magnitude 

16 equal to a doubling or tripling or more. Across the exposure range from 200 to 1000 ppb, the 

17 percentage of exercising study subjects with asthma having at least a doubling of sRaw increases 

18 from about 8-9% (at exposures of 200 ppb) up to approximately 50-60% (at exposures of 1000 

19 ppb) (draft REA, Table 4-9). The E-R function used in the main analysis of the draft REA was 

20 derived from these data using a probit function (draft REA, section 4.5.2). 

21 In summary, while the general approach and methodology for the exposure-based 

22 assessment in this review is similar to that in the last review, there are a number of ways in 

23 which these analyses differ (see 2009 REA and draft REA for this review). In addition to the 

24 expansion in the number and type of study areas assessed, we note the number of improvements 

25 to input data and modeling approaches, including the availability of continuous 5-minute air 

                                                            

42 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 

(second draft ISA, pp. 5-20 to 5-21; 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 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” 

(second draft ISA, p. 5-21). 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 second draft 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 (second draft ISA, pp. 5-21 to 5-24). 
August 24, 2017 3-40 External Review Draft – Do Not Quote or Cite

1 monitoring data at monitors within two of the three study areas. The current draft REA extends 

2 the time period of simulation to a 3-year simulation period, consistent with the form established 

3 for the now-current standard. Further, the years simulated reflect more recent emissions and 

4 circumstances subsequent to the 2010 decision. 

5 3.2.2.2 At-risk population exposures and risk 

6 In this section, we summarize the exposure and risk estimates from the draft REA and 

7 consider the following question. 

8  What is the magnitude of population exposure and risk in at-risk populations in 

9 areas simulated to just meet the current SO2 standard? What portion of the at-risk 

10 populations are estimated to experience exposures of concern or lung function 

11 decrements at levels of potential health concern? 

12 In addressing these questions, we consider the population estimates provided by the draft 

13 REA simulations of exposure to SO2 emitted into ambient air (draft REA, Chapters 5 and 6). In 

14 considering these REA estimates for air quality conditions just meeting the current standard, we 

15 particularly focus on the extent of protection provided by the standard from SO2 exposures of 

16 potential concern. As described in the prior section, the draft REA presents two sets of risk 

17 estimates for the 3-year simulation in each study area: (1) the number (and percent) of simulated 

18 persons experiencing exposures at or above the particular benchmark concentrations of interest, 

19 while at elevated ventilation; and (2) the number and percent of people estimated to experience 

20 at least one SO2-related lung function decrement in a year and the number and percent of people 

21 experiencing multiple lung function decrements associated with SO2 exposures. 

22 In presenting the exposure and risk estimates, the draft REA recognizes that the approach 

23 applied to adjust air quality to conditions just meeting the current standard can have important 

24 impacts on the risk and exposures estimates (draft REA, section 6.2.2). Because of this, the draft 

25 REA presents results for two different approaches to adjusting air quality. The first approach 

26 uses the highest design value across all modeled air quality receptors to adjust the air quality 

27 concentrations in each area to just meet the standard (draft REA, section 3.4). This is done by 

28 estimating the amount of SO2 concentration reduction needed for this highest receptor to be

29 adjusted to the current SO2 standard, and based on this amount, all other receptors impacted by 

30 the highest source(s) are adjusted accordingly. The second approach is included as a sensitivity 

31 analysis that recognizes the potential uncertainty associated with the modeled concentrations, 

32 particularly the very highest modeled concentrations. Accordingly, the second approach uses the 

air quality receptor having the 99th 33 percentile of the distribution of design values (instead of the 

34 receptor having the maximum design value) to estimate the SO2 concentration reductions needed 

35 to adjust the air quality to just meet the standard (draft REA, section 6.2.2.1). In study areas in 

36 which modeled concentrations at a very small number of receptors are substantially higher than 
August 24, 2017 3-41 External Review Draft – Do Not Quote or Cite

1 those at all other air quality receptors, these two different approaches can result in very different 

2 SO2 concentrations across an area. In such study areas, in particular, the first approach generally 

3 results in much more significant reductions being applied to reduce SO2 concentrations at the 

4 small group of highest modeled receptors such that concentrations at those receptors are just at or 

5 just below the standard and concentrations at the other receptors across the area are appreciably 

6 lower. Given that these two approaches to adjusting air quality can result in important 

7 differences in the magnitude of risk to at-risk populations in areas simulated to just meet the 

current standard, the tables below present estimates based on both approaches.43 8 

9 Of the two types of risk metrics derived in the draft REA, we turn first to the results for 

10 the benchmark-based risk metric with regard to the percent of the study area populations with 

11 asthma estimated to experience at least one daily maximum 5-minute exposure per year at or 

12 above the different benchmark concentrations while at elevated ventilation (Table 3-3). Under air 

13 quality conditions just meeting the current standard across the three study areas, approximately 

14 20 to 25% of children with asthma, on average across the 3-year period, are estimated to 

15 experience one or more days per year with a 5-minute exposure at or above 100 ppb while 

16 breathing at elevated ventilation rates (Table 3-3). With regard to the 200 ppb benchmark, as 

17 many as 0.7 percent of the simulated population of children with asthma, on average across the 

18 3-year period, was estimated to experience a single day with a 5-minute exposure at or above 

19 200 ppb while breathing at elevated ventilation rates (Table 3-3). The percentage in a single year 

20 ranged up to 2.2% for a single day, while less than 0.1% of children with asthma were estimated 

21 to experience more than a single day with an exposure at or above 200 ppb while at elevated 

22 ventilation (draft REA, Tables 6-5 and 6-6). No simulated children with asthma were estimated 

23 to experience a day with a 5-minute exposure at or above 300 or 400 ppb. The estimates for 

24 adults are lower, generally due to the lesser amount and frequency of time spent outdoors (draft 

25 REA, section 5.2). 

                                                            

43 Details regarding these sensitivity analyses focused on the impact of the adjustment approach are presented in the 

draft REA, section 6.2.2.1. 
August 24, 2017 3-42 External Review Draft – Do Not Quote or Cite

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

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

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

4 concentrations while at elevated ventilation. 

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 <0.1B – 0.1 0.1 – 0.4 

> 200 <0.1 – 0.7 0 – <0.1 0 

> 300 0 0 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 6-5 of the draft REA). 

B <0.1 is used to represent nonzero estimates below 0.1%. A value of zero (0) indicates there were no individuals 

having the selected exposure in any year.

5 

6 We next consider the estimates for risk of lung function decrements in terms of a 

7 doubling or more in sRaw (Table 3-4). Under conditions just meeting the current standard in the 

8 three study areas, as many as 1.1% of children with asthma, on average across the 3-year period, 

9 were estimated to experience at least one day per year with a SO2-related increase in sRaw of 

10 100% or more in the study area with the highest estimates (Table 3-4, Fall River). The 

11 corresponding percent estimated to experience two or more such days ranged as high as 0.6%, on 

12 average across the 3-year simulation period (draft REA, Table 6-8). Additionally, in the same 

13 study area, as much as 0.2% of the simulated populations of children with asthma, on average 

14 across the 3-year period, was estimated to experience a single day with a SO2-related increase in 

15 sRaw of 200% or more. The estimates for adults are very slightly lower, again, generally due to 

16 the lesser time spent outdoors (draft REA, section 5.3). 
August 24, 2017 3-43 External Review Draft – Do Not Quote or Cite

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

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

3 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 0 <0.1 B - <0.1 

> 200% 0.1 – 0.2 0 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 draft 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.

4 

5 In understanding these results, we note that the three study areas selected provide a 

6 variety of circumstances with regard to population exposure to short-term peak concentrations of 

7 SO2 in ambient air. These three study areas reflect different combinations of different types of 

8 SO2 emissions sources, including utilities using fossil fuels and non-utility sources, and provide 

9 three different patterns of exposure to SO2 concentrations in a populated area in the U.S. In this 

10 way, the three areas provide a variety of examples of exposure patterns that can be informative to 

11 the EPA’s consideration of potential exposures and risks that may be associated with air quality 

12 conditions occurring under the current SO2 standard. As indicated by the discussion above and 

13 also recognized in section 3.2.2.3 below, there is variability in the estimated magnitude of 

14 exposure and associated risk across study areas and uncertainties associated with these estimates. 

15 In developing the air quality scenarios for the current standard in the three study areas, 

16 the draft REA recognizes that these scenarios of adjusted air quality provide representations of 

17 the pattern of air quality that might occur in each study area under conditions that just meet the 

18 current standard. Where such conditions include relatively large spatial extents of higher 

19 concentrations – i.e., areas with design values in proximity to the level of the standard – that 

20 overlap with the more populated parts of the study area, exposure and risk results are relatively 

21 higher (draft REA, section 5.4). Among the three study areas, this best describes the Fall River 

22 study area, which is an area where source characteristics contribute to a sizeable spread of 

23 source-influenced relatively higher concentrations that coincide or overlap with locations where 

24 people reside and/or frequent. This association between concentrations and population in Fall 

25 River is illustrated in Figure 5-4 of the draft REA. Inclusion of an area with these characteristics 

26 in the REA provides some insight into the potential exposure and risk associated with other areas 

27 across the U.S. with similar characteristics and is therefore particularly informative to evaluation 

28 of the level of protection provided by the standard. 
August 24, 2017 3-44 External Review Draft – Do Not Quote or Cite

1 The other two study areas (Indianapolis and Tulsa) provide examples of areas where the 

2 higher SO2 concentrations that result from the sizeable SO2 sources in the study area do not 

3 strongly coincide with parts of the area in which people reside and/or frequent (draft REA, 

4 section 5.4). This relationship between SO2 concentrations and population is these two areas is 

5 illustrated in Figures 5-5 and 5-6 of the draft REA. Accordingly, the corresponding exposure and 

6 risk estimates for these area are lower than those estimated for the Fall River study area, even 

7 though the populations are larger (draft REA, sections 5.1 and 5.4). 

8 As discussed above, among the three study areas, the Fall River study area presents the 

9 exposure circumstances associated with highest SO2-related exposures and risk for the current 

10 standard air quality scenario. Because of this, we recognize that the Fall River study area is of 

11 particular importance in considering the adequacy of the protection afforded by the current 

12 standard. Recognizing this, we note that the draft REA indicates that the percent of children with 

13 asthma that might be expected to experience 5-minute SO2 concentrations at or above the 200 

14 ppb benchmark concentration, in an urban area that just meets the current standard, may be as 

15 high as 0.7%, on average across the three years, and 2.2% in a single-year period. With regard to 

16 the lung function risk, the draft REA indicates the percent of children that might be expected to 

17 experience at least a doubling of specific airway resistance, under conditions just meeting the 

18 current standard, may be as high as 1.1%, on average across the three-year period, and 1.9% in a 

19 single year. Thus, these results indicate that, in the single year with the highest concentrations 

20 across the 3-year period, nearly 98% of the population of children with asthma in the Fall River 

21 study area, would not be expected to experience a day with a 5-minute exposure at or above the 

22 200 ppb and 400 ppb benchmarks and would not be expected to experience as much as a 

23 doubling in sRaw, 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).44 24 

25 On average across the 3-year period, the corresponding percentage is nearly 99% (Tables 3-3 and 

26 3-4, above).

                                                            

44 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, 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 draft REA, we note that the single year estimates for the Fall 

River study area in the current draft REA fall between the estimates for the two most similar air quality scenarios 

assessed in the last review. 
August 24, 2017 3-45 External Review Draft – Do Not Quote or Cite

1 3.2.2.3 Uncertainties 

2 In this section, we consider the uncertainties associated with the quantitative estimates of 

3 exposure and risk, including those recognized by the characterization of uncertainty in the draft 

4 REA (draft REA, section 6.2). The characterization in the draft REA is based on an approach 

5 intended to identify and compare the relative impact that important sources of uncertainty may 

6 have on the exposure and risk estimates. The approach used has been applied in REAs for past 

7 NAAQS reviews for ozone, nitrogen oxides, carbon monoxide (U.S. EPA, 2008; 2010; 2014) 

8 and SOX (U.S. EPA, 2009). In the characterization of uncertainty for the current analysis, the 

9 draft REA utilized a qualitative uncertainty characterization approach adapted from the WHO 

10 approach for characterizing uncertainty in exposure assessment (WHO, 2008) accompanied by 

11 quantitative sensitivity analyses of key aspects of the assessment approach. This characterization 

12 and analyses are described in detail in chapter 6 of the draft REA. The approach used in the draft 

13 REA varies from that of WHO (2008) in that the draft REA approach placed a greater focus on 

14 evaluating the direction and the magnitude of the uncertainty (i.e., qualitatively rating how the 

15 source of uncertainty, in the presence of alternative information, may affect the estimated 

16 exposures and health risk results). 

17 The characterization and analyses in the draft REA involve consideration of the various 

18 types of inputs and approaches that together result in the exposure and risk estimates for the three 

19 study areas. In so doing, the draft REA considers the limitations and uncertainties underlying 

20 these inputs and approaches and the extent of their influence on the resultant exposure/risk 

21 estimates. Consistent with the WHO (2008) guidance, the overall impact of the uncertainty is 

22 scaled by considering the extent or magnitude of the impact of the uncertainty as implied by the 

23 relationship between the source of the uncertainty and the exposure/risk output. The draft REA 

24 also evaluated the direction of influence, indicating how the source of uncertainty was judged to 

25 affect the exposure/risk estimates (e.g., likely to over- or under-estimation). 

26  What are the key uncertainties associated with the exposure and risk estimates, 

27 including those of particular significance with regard to drawing conclusions as to 

28 the adequacy of the protection afforded by the current SO2 standard? 

29 Based on the uncertainty characterization and associated analyses in the draft REA and 

30 consideration of associated policy implications, we recognize several areas of uncertainty as 

31 particular important in our consideration of the exposure and risk estimates, as was also the case 

32 in the last review. Generally, these areas include estimation of the spatial distribution of SO2

33 concentrations across each study area under air quality conditions just meeting the existing 

34 standard, including the fine-scale temporal pattern of 5-minute concentrations. We additionally 

35 recognize the uncertainty with regard to population groups and exposure concentrations for 

36 which the health effects evidence base is limited or lacking. 
August 24, 2017 3-46 External Review Draft – Do Not Quote or Cite

1 With regard to the spatial distribution of SO2 concentrations, the draft REA recognizes 

2 some uncertainty associated with the approach used to adjust the air quality surface to 

3 concentrations just meeting the current standard. Accordingly, the draft REA has investigated the 

4 potential quantitative impact of this uncertainty on the exposure and risk estimates by deriving 

5 estimates based on an alternative adjustment approach (described in section 6.2.2.1 of the draft 

6 REA). Given the results of this sensitivity analysis, we have considered estimates from both 

7 approaches in summarizing the draft REA estimates in section 3.2.2.2 above. Additionally, we 

8 recognize uncertainty in the estimates of 5-minute concentrations in ambient air across the 

9 modeling receptors in each study area. While the ambient air monitoring dataset available to 

10 inform these estimates is much expanded in this review over the dataset available in the last 

11 review, we are still drawing on relationships occurring at one location and over one range of 

12 concentrations to estimate the fine-scale temporal pattern in concentrations at other locations. 

13 This is an important area of uncertainty in the draft REA results because the ambient air 5-

14 minute concentrations are integral to the 5-minute estimates of exposure. While we recognize 

15 this as an important area of uncertainty, the approach used has taken into account the currently 

16 available information and is considered to provide a reasonable representation of fine-scale 

17 temporal variability in the three study areas. 

18 An additional area of uncertainty affecting our interpretation of the exposure and risk 

19 results for the set of study areas assessed concerns our understanding of, and the prevalence 

20 across the U.S. of, the different exposure circumstances they represent. As noted in section 

21 3.2.2.2, the circumstances particularly pertinent to consideration of the adequacy of protection of 

22 the current standard include those in which areas where populations reside and/or exercise 

23 overlap with concentrations of SO2 that are near, albeit just under, the level of the standard. Such 

24 circumstances are influenced by source characteristics and meteorological conditions, as well as 

25 housing and recreational area patterns in urban areas. While there is some uncertainty in our 

26 understanding of the prevalence of the exposure circumstances represented by the three study 

27 areas, including those for the Fall River study area, the available information indicates there to 

28 be many densely-populated areas in the U.S. in which there are facilities with sizeable SO2

emissions (e.g., Appendix F).45 29 

30 We also recognize an important area of uncertainty that is particular to our interpretation 

31 of the lung function risk estimates. This area concerns estimates of lung function risk derived for 

32 exposure concentrations below those represented in the evidence base. The exposure-response 

                                                            

45 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 (second draft ISA, section 2.5.2.2). 
August 24, 2017 3-47 External Review Draft – Do Not Quote or Cite

1 function on which the primary risk estimates are based generates non-zero predictions of a 

2 percent of the at-risk population exposure expected to experience a day with at least a doubling 

3 of sRaw for all exposures experienced while at elevated ventilation. In considering these 

4 estimates, we recognize that the uncertainty in the response estimates increases substantially with 

5 decreasing exposure concentration below those supported by study data. In so doing, we note the 

6 contribution to the risk estimates of exposure concentrations below 200 ppb. Additionally, we 

7 note that the assessment focuses on the daily maximum 5-minute exposure during elevated 

8 ventilation, summarizing results in terms of the days on which the magnitude of such exposure 

9 exceeds a benchmark or contributes to increased sRaw. While the health effects evidence 

10 indicates the lack of a cumulative effect of multiple exposures over several hours or a day 

11 (second draft ISA, section 5.2.1.2), and a reduced response to repeated exercising exposure 

12 events over an hour (second draft ISA, section 5.2.1.2; Kehrl et al., 1987), information is 

13 somewhat limited with regard to the length of time after recovery from one exposure by which a 

14 repeat exposure would elicit a similar effect as that of the initial event.

15 Another area of uncertainty, which remains from the last review and is important to our 

16 consideration of the draft REA results, concerns the extent to which the quantitative results 

17 represent the populations at greatest risk of effects associated with exposures to SO2 in ambient 

18 air. As recognized in sections 3.2.1.1 and 3.2.1.4, the controlled human exposure study evidence 

19 base does not include studies of children younger than 12 years old or studies of people with 

more severe asthma.46 20 The limited evidence that informs our understanding of potential risk to 

21 these groups indicates the potential for them to experience greater effects than other population 

22 groups with asthma under similar exposure circumstances, as summarized in section 3.2.1.4 

23 above. Further we note the lack of information on the factors contributing to increased 

24 susceptibility to SO2-induced bronchoconstriction among some people with asthma. Thus, there 

25 is uncertainty associated with our interpretation of the exposure/risk estimates with regard to the 

26 extent to which they represent the populations at greatest risk of SO2-related respiratory effects 

27 that is important to consideration of the exposure and risk results with regard to the adequacy of 

28 protection provided by the current standard. 

29 In summary, among the multiple uncertainties and limitations in data and tools that affect 

30 the quantitative estimates of exposure and risk and their interpretation in the context of 

31 considering the current standard, we recognize several here as particularly important. These 

32 include uncertainties related to estimation of 5-minute concentrations in ambient air; the lack of 

33 information from controlled human exposure studies for the lower, more prevalent, 

                                                            

46 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 draft REA. 
August 24, 2017 3-48 External Review Draft – Do Not Quote or Cite

1 concentrations of SO2 and limited information regarding multiple exposure episodes within a 

2 day; the prevalence of different exposure circumstances represented by the three study areas; 

3 and, characterization of particular subgroups of people with asthma that may be at greater risk. 

4 3.2.2.4 Potential public health implications 

5 In considering public health implications of the quantitative exposure and risk estimates 

6 that may inform the Administrator’s judgments in this area, this section discusses the information 

7 pertaining to the following question. 

8  To what extent are the estimates of exposures and risks to at-risk populations that 

9 remain under conditions just meeting the current SO2 standard important from a 

10 public health perspective? 

11 Several factors are important to consideration of public health implications. These 

12 include the magnitude or severity of the effects associated with the exposures estimated in the 

13 draft REA, as well as their adversity at the individual and population scale. Other important 

14 considerations include the size of the population estimated to experience such effects or to 

15 experience exposures associated with such effects. These considerations are discussed below. 

16 Based on the currently available evidence which is largely consistent with that available 

17 in the last review (as summarized in section 3.2.1 above), the quantitative exposure and risk 

18 analyses focus on the potential for lung function decrements in people with asthma exposed to 

19 SO2 while at elevated ventilation. Additionally, we have again focused on estimates for two 

20 types of risk metrics, one involving comparison to benchmark concentrations and the second 

21 involving estimates of lung function risk with regard to moderate or greater increases in sRaw. In 

22 considering these estimates, we recognize that although the lung function decrements, which are 

23 related to bronchoconstriction, are expected to be transient, we additionally recognize that such 

24 decrements, while occurring, may contribute to a diminished reserve in lung function (second 

25 draft ISA, p. 1-17, section 5.2.1.2). For population groups already at diminished reserve, such as 

26 those with more severe asthma, this may be particularly important. Thus, the discussion here 

27 reflects consideration of the health evidence, and exposure and risk estimates, as well as the 

28 consideration of potential public health implications in previous NAAQS decisions and ATS 

29 policy statements (as also discussed in section 3.2.1.5). 

30 In light of the conclusion that among all people with asthma, children may be particularly 

31 at risk (summarized in section 3.2.1.2 above) and the draft REA findings of higher exposures and 

32 risks for children (in terms of percent of that population), we have focused the discussion here on 

33 children. We recognize that the draft REA results for air quality conditions just meeting the 

34 current standards indicate that, on average across the 3-year period simulated (consistent with the 

35 form of the current standard), less than 1% of the simulated population of children with asthma 
August 24, 2017 3-49 External Review Draft – Do Not Quote or Cite

1 might be expected to experience a single day with a 5-minute exposure at or above 200 ppb 

2 while breathing at elevated ventilation rates. The draft REA simulations also estimated no 

3 children with asthma to experience any days in a 3-year simulation period with a 5-minute 

4 exposure at or above 300 or 400 ppb. With regard to the lowest benchmark considered (100 ppb), 

5 the draft REA also indicates that in some areas of the U.S., approximately 25% of children with 

6 asthma, on average across the 3-year period, might be expected to experience one or more days 

7 per year with a 5-minute exposure at or above 100 ppb while breathing at elevated ventilation 

8 rates, with higher percentages in some years. With regard to estimates of lung function 

9 decrements, the draft REA indicates that in some areas, approximately 1% of children with 

10 asthma, on average across a 3-year period, might be expected to experience at least one day per 

11 year with a SO2-related increase in sRaw of 100% or more; the estimate for two or more days is 

12 appreciably lower, at 0.4% (draft REA, Table 6-8). Additionally, under such conditions (just 

13 meeting the current standard), the estimated percent of children with asthma that might be 

14 expected to experience a single day per year with a SO2-related increase in sRaw of 200% or 

15 more, on average across the 3-year period, is 0.2% (Table 3-4). 

16 In considering the severity of responses associated with the REA estimates, we take note 

17 of the health effects evidence for the different benchmark concentrations and judgments made 

18 with regard to the severity of these effects in the last review. As in the last review, we recognize 

19 that the responses documented for exposures of 400 ppb are frequently accompanied by 

20 respiratory symptoms and thus are appropriately considered to be adverse respiratory effects 

21 consistent with past and recent ATS position statements. With regard to the lower benchmark 

22 concentration of 200 ppb, we recognize that, while the responses documented in studies of 

23 exercising subjects with asthma are not consistently accompanied by respiratory symptoms, 

24 conclusions in past NAAQS reviews recognized that moderate decrements in lung function can 

25 be clinically significant in some individuals with asthma (75 FR 35526, June 22, 2010). 

26 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, 47 27 ATS statements and conclusions in 

28 past NAAQS reviews. While noting the lack of information for some populations groups with 

29 asthma, including primary-school-age children and people with more severe asthma, we 

30 additionally recognize the uncertainty with regard to effects that might be associated with 

31 exposures as low as 100 ppb (as discussed in section 3.2.1.3 and 3.2.1.4 above). 

32 As indicated in section 3.1 above, the at-risk population in this review is people with 

33 asthma, as was the case in the last review. Further, children with asthma are identified as 

                                                            

47 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). 
August 24, 2017 3-50 External Review Draft – Do Not Quote or Cite

1 particularly at risk. The size of the at-risk population in the U.S. is substantial. As summarized in 

2 section 3.2.1.5, nearly eight percent of the U.S. population (more than 24 million people) and 

3 8.4% of U.S. children have asthma. The prevalence in U.S. child populations of different races or 

4 ethnicities ranges from 7.4% to 13.4% (Table 3-2 above). This is well reflected in the draft REA 

5 study areas in which the asthma prevalence ranged from 8% to 8.7% of the total populations and 

6 9.7% to 11.2% of the children, with the highest prevalence represented in the Fall River study 

7 area. In Fall River, the prevalence varies among census tracts, with the highest tract having a 

8 prevalence in boys of 21.5% (draft REA, Table 4-1). 

9 In considering the three study areas and the variation in exposure/risk estimates among 

10 them, we recognize the Fall River study area to be particularly informative to consideration of 

11 public health risk associated with and public health protection provided by the current standard. 

12 This is because, as summarized in section 2.2.2.2 above, the source characteristics and 

13 population distribution in the area cause the locations of relatively higher SO2 concentrations in 

14 ambient air across the area (i.e., those closest to just meeting the standard) to overlap with 

15 locations of higher population density. These exposure circumstances contribute to higher 

16 exposure and risk estimates than in the other study areas (draft REA, section 5.4), making 

17 estimates for Fall River important in considering the adequacy of protection provided by the 

18 current standard. Thus, we have given particular attention to estimates for this study area. 

19 Although exposure and risk estimates were not available in the last review for air quality 

20 conditions just meeting the now-current standard, the findings and considerations summarized 

21 here are generally similar to those considered in the last review, and indicate a level of protection 

22 consistent with that described in the 2010 decision. The exposure and risk estimates for the three 

23 study areas assessed in the draft REA for this review reflect differences in exposure 

24 circumstances among those areas and illustrate the exposures and risk that might be expected to 

25 occur in other areas with such circumstances under air quality conditions that just meet the 

26 current standard. Thus, the draft REA estimates indicate the magnitude of exposure and risk that 

27 might be expected in some areas and illustrate the importance to consideration of the public 

28 health protection afforded by the current standard of those areas where locations of relatively 

29 higher SO2 concentrations in ambient air across the area coincide with the locations of higher 

30 population density. These considerations, and others raised above, are important to conclusions 

31 regarding the public health significance of the draft REA results. We recognize that such 

32 conclusions also depend in part on public health policy judgments that will weigh in the 

33 Administrator’s decision in this review with regard to the adequacy of protection afforded by the 

34 current standard. Such judgments include those concerning the public health significance of 

35 effects at exposures for which evidence is limited or lacking, such as effects at the lower 
August 24, 2017 3-51 External Review Draft – Do Not Quote or Cite

1 benchmark concentrations considered and lung function risk estimates associated with exposure 

2 concentrations lower than those tested in the controlled exposure studies. 

3 3.2.3 Preliminary Staff Conclusions on the Current Standard 

4 This section describes preliminary staff conclusions regarding the adequacy of the current 

5 primary SO2 standard. These preliminary conclusions are based on considerations described 

6 above, and in the discussion below regarding the currently available scientific evidence (as 

7 summarized in the second draft ISA, and the ISA and AQCDs from prior reviews), and the risk 

8 and exposure information drawn from the draft REA. Conclusions in the final PA will draw upon 

9 the final ISA, developed in consideration of CASAC review and public comment on the second 

10 draft ISA, and on the final REA, developed in consideration of CASAC review and public 

11 comment on the draft REA. Further, staff conclusions presented in the final PA will take into 

12 account advice from the CASAC and public comment on the draft PA and on these preliminary 

13 conclusions. 

14 Taking into consideration the discussions responding to specific questions above in this 

15 and the prior chapter, this section addresses the following overarching policy question. 

16  Does the currently available scientific evidence- and exposure/risk-based 

17 information, as reflected in the ISA and REA, support or call into question the 

18 adequacy of the protection afforded by the current SO2 standard? 

19 In considering this question, we recognize as an initial matter that, as is the case in 

20 NAAQS reviews in general, the extent to which the current primary SO2 standard is judged to be 

21 adequate will depend on a variety of factors inclusive of science policy judgments and public 

22 health policy judgments. These factors include public health policy judgments concerning the 

23 appropriate benchmark concentrations on which to place weight, as well as judgments on the 

24 public health significance of the effects that have been observed at the exposures evaluated in the 

25 health effects evidence. The factors relevant to judging the adequacy of the standards also 

26 include the interpretation of, and decisions as to the weight to place on, different aspects of the 

27 results of the exposure assessment for the three areas studied and the associated uncertainties. 

28 Thus, we recognize that the Administrator’s conclusions regarding the adequacy of the current 

29 standard will depend in part on public health policy judgments, science policy judgments 

30 regarding aspects of the evidence and exposure/risk estimates, as well as, judgments about the 

31 level of public health protection with an adequate margin of safety that is requisite under the 

32 Clean Air Act. 

33 Our response to this question takes into consideration the discussions that address the 

34 specific policy-relevant questions in prior sections of this document (see sections 3.2.1-3.2.2) 

35 and the approach described in section 3.1 that builds on the approach from the last review. We 
August 24, 2017 3-52 External Review Draft – Do Not Quote or Cite

1 focus first on consideration of the evidence, including that newly available in this review, and the 

2 extent to which it alters key conclusions supporting the current standard. We then turn to 

3 consideration of the quantitative exposure and risk estimates drawn from the draft REA, 

4 including associated limitations and uncertainties, and the extent to which they indicate differing 

5 conclusions regarding the magnitude of risk, as well as level of protection from adverse effects, 

6 associated with the current standard. We additionally consider the key aspects of the evidence 

7 and exposure/risk estimates emphasized in establishing the now-current standard, and the 

8 associated public health policy judgments and judgments about the uncertainties inherent in the 

9 scientific evidence and quantitative analyses that are integral to decisions on the adequacy of the 

10 current primary SO2 standard. 

11 In considering the currently available evidence, staff gives great weight to the long12 standing body of health effects evidence for SO2, augmented in some aspects since the last 

13 review, that provides the foundation of our understanding of the health effects of SO2 in ambient 

14 air. In so doing, we give particular attention to the evidence from controlled human exposure 

15 studies that demonstrates that very short exposures to less than 1000 ppb SO2, while breathing at 

16 elevated ventilation rates, induces bronchoconstriction in some people with asthma; and, 

17 supports the identification of people with asthma as the population at risk from short-term peak 

18 concentrations in ambient air (second draft ISA; 2008 ISA; 1994 AQCD supplement). 

19 Further, while the evidence base has been augmented since the time of the last review, we 

20 note that the newly available evidence does not lead to different conclusions regarding the 

21 primary health effects of SO2 in ambient air or regarding exposure concentrations associated

22 with those effects; nor does it identify different populations at risk of SO2 -related effects. In this 

23 way, the health effects evidence available in this review is consistent with evidence available in 

24 the last review when the current standard was established. This strong evidence base continues to 

25 demonstrate a causal relationship between short-term SO2 exposures and respiratory effects, 

26 particularly in people with asthma. This conclusion is primarily based on evidence from 

27 controlled human exposure studies available at the time of the last review that reported lung 

28 function decrements and respiratory symptoms in people with asthma exposed to SO2 for 5 to 10 

29 minutes while breathing at elevated ventilation. Support is provided by the epidemiological 

30 evidence that is coherent with the controlled exposure studies. The epidemiological evidence, 

31 including that recently available, includes studies reporting positive associations for asthma32 related hospital admissions and emergency department visits (of individuals of all ages, 
August 24, 2017 3-53 External Review Draft – Do Not Quote or Cite

1 including adults and children) with short-term SO2 exposures (second draft ISA, section 

5.2.1.2).48 2 

3 The health effects evidence newly available in this review also does not extend our 

4 understanding of the range of 5-minute exposure concentrations eliciting effects in people with 

5 asthma exposed while breathing at elevated ventilation rates beyond what was understood in the 

6 last review. As in the last review, 200 ppb remains the lowest concentration tested in exposure 

7 studies where study subjects are freely breathing in exposure chambers. At that exposure 

8 concentration, approximately eight to nine percent of study subjects with asthma, breathing at 

9 elevated ventilation rates, experienced moderate or greater lung function decrements following 

10 5- to 10-minute controlled exposures. The limited information available for lower exposure 

11 concentrations, while not amenable to direct quantitative comparisons, generally indicates 

12 somewhat lesser response. In considering what may be gleaned from the epidemiological 

13 evidence with regard to exposure concentrations eliciting effects, we recognize complications 

14 associated with interpretation of epidemiologic studies of SO2 in ambient air that relate to 

15 whether measurements at the study monitors adequately represent the spatiotemporal variability 

16 in ambient SO2 concentrations in the study areas and associated population exposures (second 

17 draft ISA, section 5.2.1.9). 

18 In this review, as in the last review, we recognize some uncertainty with regard to 

19 exposure levels eliciting effects in some population groups not studied, such as individuals with 

20 severe asthma, as well as uncertainty in the extent of effects at exposure levels below those 

21 studied. Collectively, these aspects of the evidence and associated uncertainties contribute to a 

22 recognition that for SO2, as for other pollutants, the available evidence base in a NAAQS review 

23 generally reflects a continuum, consisting of ambient levels at which scientists generally agree 

24 that health effects are likely to occur, through lower levels at which the likelihood and magnitude 

25 of the response become increasingly uncertain. 

26 As at the time of the last review, the exposure and risk estimates developed from 

27 modeling exposures to SO2 emitted into ambient air are critically important to consideration of 

28 the potential for exposures and risks of concern under air quality conditions of interest, and 

29 consequently are critically important to judgments on the adequacy of public health protection 

30 provided by the current standard. In considering the public health implications of estimated 

31 occurrences of exposures of different magnitudes, we take note of guidance from the ATS, the 

32 CASAC’s written advice and recommendations in past reviews, and judgments made by the EPA 

33 in considering similar effects in previous NAAQS reviews (75 FR 35526 and 35536, June 22, 

                                                            

48 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 evidence 

continue to provide support for the conclusion on the causal relationship (second draft ISA, section 5.2.1.2). 
August 24, 2017 3-54 External Review Draft – Do Not Quote or Cite

1 2010). As recognized in section 3.2.1.5, an additional publication by the ATS that further 

2 addresses judgments on what constitutes an adverse health effect of air pollution is newly 

3 available in this review (Thurston et al., 2017). The more recent statement expands upon the 

4 2000 statement, that was considered in the last SO2 NAAQS review, and recognizes additional 

5 considerations with regard to such judgments that remain consistent with the EPA’s judgments in 

6 the 2010 review. In that review, the Administrator judged that the effects reported in exercising 

7 people with asthma following 5- to 10-minute SO2 exposures at or above 200 ppb, and especially 

8 at or above 400 ppb (often accompanied by respiratory symptoms and for which the evidence is 

9 stronger), can result in adverse health effects (75 FR 35536, June 22, 2010). In so doing, she also 

10 recognized that effects reported for exposures below 400 ppb are less severe than those at and 

11 above 400 ppb (75 FR 35547, June 22, 2010). 

12 In considering the draft REA analyses available in this review, we are aware of a number 

13 of ways in which these analyses differ from those available in the last review. In addition to the 

14 expansion in the number and type of study areas assessed, we note the number of improvements 

15 to input data and modeling approaches, including the availability of continuous 5-minute air 

16 monitoring data at monitors within two of the three study areas. The current draft REA extends 

17 the time period of simulation by including a 3-year simulation period consistent with the form 

18 established for the now-current standard. Further, the years simulated reflect more recent 

19 emissions and circumstances subsequent to the 2010 decision. In considering the draft REA 

20 results, we also take note of the array of emissions and exposure circumstances represented by 

21 the three study areas. As summarized in section 3.2.2 above, the areas fall into three different 

22 geographic regions of the U.S. They range in total population size from approximately 180,000 

23 to approximately one half million, and vary in population demographic characteristics. 

24 Additionally, the types of large sources of SO2 emissions represented in the three study areas 

25 vary with regard to emissions characteristics and include EGUs, petroleum refineries, glass26 making facilities, secondary lead smelters (from battery recycling), and chemical manufacturing. 

27 As at the time of the last review, people with asthma are the population at risk of SO2-

28 related respiratory effects. Children with asthma may be particularly at risk (section 3.2.1.2 

29 above). While there are more adults in the U.S. with asthma than children with asthma, the draft 

30 REA results in terms of percent of the simulated at-risk populations, indicates higher exposures 

31 and risks for children with asthma as compared to adults. This finding relates to children’s 

32 greater frequency and duration of occasions outdoors (section 3.2.2.2 above). In light of these 

33 conclusions and findings, we have focused our consideration of the draft REA results here on 

34 children. 

35 As can be seen by the variation in exposure estimates, the three study areas in the draft 

36 REA represent an array of exposure circumstances, including those contributing to relatively 
August 24, 2017 3-55 External Review Draft – Do Not Quote or Cite

1 higher and relatively lower exposures and associated risk. As recognized in the draft REA, the 

2 analyses there are not intended to provide a comprehensive national assessment. Rather, the 

3 analyses for this array of study areas are intended to indicate the magnitude of exposures and 

4 risks that may be expected in areas of the U.S. that just meet the current standard but that may 

5 differ in ways affecting population exposures of interest. In that way, the draft REA is intended 

6 to be informative to the EPA’s consideration of potential exposures and risks associated with the 

7 current standard and the Administrator’s decision on the adequacy of protection provided by the 

8 current standard. As discussed in sections 3.2.2.2 and 3.2.2.4 above, consideration of exposures 

9 occurring in those areas where locations of relatively higher SO2 concentrations in ambient air 

10 across an area that just meets the current standard coincide with the locations of higher 

11 population density are particularly important to consideration of the public health protection 

12 afforded by the current standard. 

13 With regard to the draft REA representation of air quality conditions associated with just 

14 meeting the current standard, while we note reduced uncertainty in a few aspects of the approach 

15 for developing this air quality scenario, we recognize the uncertainty associated with the 

16 application of adjustments to the highest model receptor in the study area. As summarized in 

17 sections 3.2.2.2 and 3.2.2.3 above, sensitivity analyses described in section 6.2.2 of the draft 

18 REA indicate the quantitative impact potentially associated with area of uncertainty. Given the 

19 importance of this aspect of the REA to consideration of the level of protection provided by the 

20 current standard, we have considered the results for each study area in terms of a range bounded 

21 on the low end by the results for the main analysis and on the upper end by those based on the 

22 alternative adjustment approach used in the sensitivity analysis. In this context, we note that 

23 across all three study areas, which provide an array of SO2 emissions and exposure situations, the 

24 percent of children with asthma estimated to experience at least one day with as much as a 

25 doubling in sRaw (attributable to SO2), on average across the 3-year period, ranges from 0.9 to 

26 1.1%; the highest estimate is just under 2% for the highest single year. Less than 1% of children 

27 with asthma are estimated to experience, while at elevated ventilation, a daily maximum 5-

28 minute exposure per year at or above 200 ppb, on average across the 3-year period, with a 

29 maximum of approximately 2% in the highest single year. Further, no child (or adult) with 

30 asthma is estimated to experience, while at elevated ventilation, a daily maximum 5-minute 

31 exposure per year at or above 400 ppb (in any of the three years simulated across the three study 

32 areas). Thus, in light of current ATS guidance, as well as conclusions and CASAC advice in 

33 prior NAAQS reviews, the draft REA exposure and risk estimates for the current review indicate 

34 that the current standard is likely to provide effective protection from SO2-related health effects 

35 to at-risk populations of children and adults with asthma. 
August 24, 2017 3-56 External Review Draft – Do Not Quote or Cite

1 In summarizing the information discussed thus far, we reflect on the key aspects of the 

2 2010 decision that established the current standard. As an initial matter, effects associated with 

3 5- to 10-minute exposures as low as 200 ppb of people with asthma while breathing at elevated 

4 ventilation were considered to be adverse; this judgment was based on consideration of CASAC 

5 advice and EPA decisions in prior NAAQS reviews, as well as ATS guidance. We note that the 

6 newly available information in this review includes an additional statement from ATS on 

7 adversity which is generally consistent with the earlier statement (available at the time of the 

8 2010 decision). While recognizing the differences between the current and past analyses, 

9 including the lack of an air quality scenario specific to the now-current standard in the last 

10 review, as well as uncertainties associated with such analyses, we note a rough consistency of the 

11 associated estimates when considering the array of study areas in both reviews. Overall, the 

12 newly available quantitative analyses appear to comport with the conclusions reached in the last 

13 review regarding control expected to be exerted by the now-current 1-hour standard on 5-minute 

14 exposures of concern. With regard to the results for the REA in the last review (which were for a 

15 single-year simulation), the 2010 decision recognized those results to indicate that a one-hour 

16 standard of 75 ppb might be expected to protect more than 97% of children with asthma (and 

17 somewhat less than 100%) from experiencing exposures at or above a 200 ppb benchmark 

18 concentration, and more than 99% of that population group from experiencing exposures at or 

19 above a 400 ppb benchmark. Single-year results for study areas assessed in the current draft REA 

20 indicate protection of approximately 98 to more than 99% of the populations of children with 

21 asthma from experiencing exposures at or above a 200 ppb benchmark concentration and of all 

22 of the study area at-risk populations from exposures at or above 400 ppb. Additionally, the 2010 

23 decision also took note of the magnitude of the ambient air SO2 concentrations in U.S. 

24 epidemiological studies of associations between ambient air concentrations and emergency 

25 department visits and hospital admissions, for which the effect estimate remained positive and 

26 statistically significant in copollutant models with PM. In considering these studies, the 

27 Administrator judged that the level chosen for the new 1-hour standard provided an adequate 

28 margin of safety. No additional such studies are available in the current review. Thus, in 

29 considering the key aspects of the decision in the last review, we find the currently available 

30 information to be consistent with that on which the decision establishing the current standard was 

31 based. 

32 Based on all of the above, and taking into consideration related information, limitations 

33 and uncertainties, such as those recognized above, we draw preliminary conclusions regarding 

34 the extent to which the newly available information in this review supports or calls into question 

35 the adequacy of protection afforded by the current standard. In considering the conclusions that 

36 may be supported by the exposure and risk estimates, we take note of the more than 24 million 
August 24, 2017 3-57 External Review Draft – Do Not Quote or Cite

1 people with asthma in the U.S., including more than 6 million children. We additionally note the 

2 uncertainties or limitations of the current evidence base with regard to the exposure levels at 

3 which effects may be elicited in some population groups (e.g., children with asthma and 

4 individuals with severe asthma), as well as the severity of the effects. In so doing, we recognize 

5 that the controlled human exposure studies, on which the depth of our understanding of SO2-

6 related health effects is based, do not provide information with regard to responses in people 

7 with more severe asthma or in children younger than 12 years. Additionally, some aspects of our 

8 understanding continue to be limited; among these aspects are the potential for effects in some 

9 people with asthma exposed to concentrations below 200 ppb, as well as the potential for other 

10 air pollutants to affect responses to SO2. In light of this we note the draft REA results for the 

11 lowest benchmark that indicate that in some areas of the U.S. with air quality conditions that just 

12 meet the current standard, appproximately 20 to 25% of children with asthma may experience 

13 one or more exposures, on average across a 3-year period, to concentrations at or above 100 ppb 

14 while at elevated ventilation. Thus, the evidence and exposure/risk information related to the 

15 lowest exposures studied lead us to conclude that the combined consideration of the body of 

16 evidence and the quantitative exposure estimates continue to provide support for a standard as 

17 protective as the current one. 

18 Further, we recognize that conclusions regarding the adequacy of the current standard 

19 depend in part on public health policy judgments identified above and judgments about the level 

20 of public health protection with an adequate margin of safety. In so doing, we take note of the 

21 long-standing health effects evidence that documents the effects of SO2 exposures as short as a 

22 few minutes on people with asthma that are exposed while breathing at elevated ventilation rates 

23 and recognize that such effects have been documented in the lowest concentration studied in 

24 exposure chambers with appropriate clean-air controls (200 ppb). In so doing, we recognize the 

25 limitations, and associated uncertainty, in the evidence available for lower exposure 

26 concentrations (e.g., 100 ppb), as was the case in the last review, and we note the lower 

27 responses reported. Thus, in focusing on the potential for 5-minute exposures at and above 200 

28 ppb, that have been previously recognized as adverse (June 22, 2010; 75 FR 35547), we take 

29 note of the draft REA results that indicate the current standard may be expected to protect 

30 approximately 98% to nearly 99% of at-risk populations with asthma from experiencing any 

31 days with such exposures, in a single- and 3-year period, respectively. We additionally note the 

32 draft REA finding of no children (or adults) estimated to experience any days with a 5-minute 

33 exposure of 300 ppb or higher. In light of ATS guidance, CASAC advice and EPA conclusions 

34 in past NAAQS reviews, these results indicate effective protection of at-risk populations from 

35 SO2-related health effects that we note is consistent with the level of protection specified when 

36 the standard was set. Thus, we reach the preliminary conclusion that the currently available 
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1 evidence and quantitative information, including the associated uncertainties, do not call into 

2 question the adequacy of protection provided by the current standard, and thus support 

3 consideration of retaining the current standard, without revision. 

4 In summary, the newly available health effects evidence, critically assessed in the ISA as 

5 part of the full body of evidence, reaffirms conclusions on the respiratory effects recognized for 

6 SO2 in the last review. Further, we observe the general consistency of the current evidence with 

7 the evidence that was available in the last review with regard to key aspects on which the current 

8 standard is based. We additionally note the quantitative exposure and risk estimates for 

9 conditions just meeting the current standard that indicate a similar level of protection, for at-risk 

10 populations from respiratory effects considered to be adverse, as that described in the last review 

11 for the now-current standard. We also recognize, as in the last review, the limitations and 

12 uncertainties associated with the available information. Collectively, these considerations 

13 (including those discussed above) provide the basis for the preliminary staff conclusion that 

14 consideration should be given to retaining the current standard, without revision. Accordingly, 

15 and in light of this preliminary staff conclusion that it is appropriate to consider the current 

16 standard to be adequate, we have not identified any potential alternative standards for 

17 consideration in this review. 

18 3.3 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH 

19 AND DATA COLLECTION 

20 In this section, we highlight key uncertainties associated with reviewing and establishing 

21 the primary NAAQS for sulfur oxides. Such key uncertainties and areas for future research, 

22 model development, and data gathering are outlined below. In some cases, research in these 

23 areas can go beyond aiding standard setting to aiding in the development of more efficient and 

24 effective control strategies. We note, however, that a full set of research recommendations to 

25 meet standards implementation and strategy development needs is beyond the scope of this 

26 discussion. Rather, listed below are key uncertainties, research questions and data gaps that have 

27 been thus far highlighted in this review of the primary standard. 

28  A critical aspect of our consideration of the evidence and the quantitative dose estimates 

29 is our understanding of SO2 effects below the lowest concentrations studied in controlled 

30 human exposure studies. Additional information related in several areas would reduce 

31 uncertainty in our interpretation of the available information for purposes of risk 

32 characterization. These areas include the following. 

33  Our understanding of whether and to what extent some population groups, 

34 including children or people with severe asthma, are more responsive to peak SO2

35 exposures (or responsive to lower concentrations), while breathing at elevated 

36 ventilation rates, than the groups that have been studied. 
August 24, 2017 3-59 External Review Draft – Do Not Quote or Cite

1  A better understanding of the effects and the shape of the exposure-response 

2 relationship at lower 5-minute exposure concentrations (i.e., below 200 ppb) 

3 would help to reduced uncertainty in our estimates of lung function effects and, 

4 accordingly, in characterizing SO2-related health effects. 

5  Little information is available on the factors contributing to the susceptibility to 

6 lower concentrations of SO2 of a subgroup of people with asthma, termed 

7 “responders” in the second draft ISA (second draft ISA, section 5.2.1.2; Johns and 

8 Linn, 2011). 

9  There is also only very limited evidence regarding the potential influence of 

10 history of exposure and co-occurring exposure to other air pollutants, including 

11 particulate matter. Further research is needed in this area to better inform our 

12 characterization of health risk related to SO2. 

13  An understanding of the fine-scale spatial and temporal gradients of ambient air SO2

14 concentrations in residential areas, as well as near sources of SO2 emissions, is a key 

15 element in our assessment of exposure and risk. Additional information in this area is 

16 needed. Current limitations in this area additionally contribute to uncertainty in 

17 characterization of ambient air SO2 levels in the risk assessment and the resulting 

18 exposure and risk estimates. Further characterization of the fine-scale spatial and 

19 temporal variation in ambient air SO2 concentrations in different environments and 

20 related to different sources, as well as different air quality conditions that just meet the 

21 existing standard, would help to reduce this uncertainty. 

22  Uncertainties with regard to other aspects of the health effects evidence include that 

23 regarding what can be gleaned from the epidemiologic studies showing an association 

24 between short-term SO2 exposures and asthma-related hospital admission and emergency 

25 department visits. Uncertainty remains regarding the extent of copollutant confounding in 

26 these studies, particularly by PM. Additionally, there is uncertainty related to the 

27 representation of exposure through fixed site monitors and capturing peak SO2

28 concentrations that limits the informativeness of the ambient air concentrations analyzed 

29 in the studies to standards reviews. 

30  While the CHAD is much expanded over the last review, limited information and 

31 associated uncertainty remain in several aspects of the available data. Additional 

32 information would reduce uncertainty in these aspects of our exposure and risk estimates. 

33  Collection and analysis of multiday activity patterns that consider the attributes 

34 most influential to determining long-term activity patterns. Further research 

35 would assist in better evaluating and improving existing approaches used to 

36 generate longitudinal activity profiles (as discussed in the draft REA, section 

37 4.1.5.1). 

38  Activity data for some population subgroups, such as people with severe asthma 

39 and very young children. 
August 24, 2017 3-60 External Review Draft – Do Not Quote or Cite

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24 Gong, H, Jr; Lachenbruch, PA; Harber, P; Linn, WS. (1995). Comparative short-term health 

25 responses to sulfur dioxide exposure and other common stresses in a panel of asthmatics. 

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27 Henderson R. (2008). Clean Air Scientific Advisory Committee’s (CASAC) Peer Review of 

28 EPA's Risk and Exposure Assessment to Support the Review of the SO2 Primary 

29 National Ambient Air Quality Standards (First Draft, July 2008). EPA-CASAC-08-019. 

30 Available at: https://www3.epa.gov/ttn/naaqs/standards/so2/s_so2_cr.html

31 Horstman, D; Roger, LJ; Kehrl, H; Hazucha, M. (1986). Airway sensitivity of asthmatics to 

32 sulfur dioxide. Toxicol Ind Health 2: 289-298. 

33 Horstman, DH; Seal, E, Jr; Folinsbee, LJ; Ives, P; Roger, LJ. (1988). The relationship between 

34 exposure duration and sulfur dioxide-induced bronchoconstriction in asthmatic subjects. 

35 AIHA J 49: 38-47. http://dx.doi.org/10.1080/15298668891379341 
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1 Johns, D. (2009). Presentation and analysis of controlled human exposure data described in 

2 Table 3-1 of the 2008 Integrated Science Assessment (ISA) for Sulfur Oxides. 

3 Memorandum to Sulfur Oxides NAAQS Review Docket. April 29, 2009. Available in 

4 Regulations.gov, EPA-HQ-OAR-2007-0352-0043. 

5 Johns, D; Simmons, K. (2009). Quality assurance review of individual subject data presented in 

6 Table 3-1 of the 2008 Integrated Science Assessment (ISA) for Sulfur Oxides. 

7 Memorandum to Sulfur Oxides NAAQS Review Docket. October 2, 2009. Available in 

8 Regulations.gov, EPA-HQ-ORD-2006-0260-0036. 

9 Johns, DO; Svendsgaard, D; Linn, WS. (2010). Analysis of the concentration-respiratory 

10 response among asthmatics following controlled short-term exposures to sulfur dioxide. 

11 Inhal Toxicol 22: 1184-1193. 

12 Kehrl, HR; Roger, LJ; Hazucha, MJ; Horstman, DH. (1987). Differing response of asthmatics to 

13 sulfur dioxide exposure with continuous and intermittent exercise. Am J Respir Crit Care 

14 Med 135: 350-355. 

15 Koenig, JQ; DS Covert; Pierson, WE. (1989). Effects of inhalation of acidic compounds on 

16 pulmonary function in allergic adolescent subjects. Env Health Persp 79: 173-178. 

17 Koenig, JQ; Covert, DS; Hanley, QS; Van Belle, G; Pierson, WE. (1990). Prior exposure to 

18 ozone potentiates subsequent response to sulfur dioxide in adolescent asthmatic subjects. 

19 Am J Respir Crit Care Med 141: 377-380. 

20 Linn, WS; Shamoo, DA; Spier, CE; Valencia, LM; Anzar, UT; Venet, TG; Hackney, JD. 

21 (1983a). Respiratory effects of 0.75 ppm sulfur dioxide in exercising asthmatics: 

22 Influence of upper-respiratory defenses. Environ Res 30: 340-348. 

23 Linn, WS; Venet, TG; Shamoo, DA; Valencia, LM; Anzar, UT; Spier, CE; Hackney, JD. 

24 (1983b). Respiratory effects of sulfur dioxide in heavily exercising asthmatics: A dose25 response study. Am Rev Respir Dis 127: 278-283. 

26 Linn, WS; Avol, EL; Shamoo, DA; Venet, TG; Anderson, KR; Whynot, JD; Hackney, JD. 

27 (1984). Asthmatics' responses to 6-hr sulfur dioxide exposures on two successive days. 

28 Arch Environ Health 39: 313-319. http://dx.doi.org/10.1080/00039896.1984.10545856

29 Linn, WS; Avol, EL; Peng, RC; Shamoo, DA; Hackney, JD. (1987). Replicated dose-response 

30 study of sulfur dioxide effects in normal, atopic, and asthmatic volunteers. Am Rev 

31 Respir Dis 136: 1127-1134. http://dx.doi.org/10.1164/ajrccm/136.5.1127 

32 Linn, WS; Avol, EL; Shamoo, DA; Peng, RC; Spier, CE; Smith, MN; Hackney, JD. (1988). 

33 Effect of metaproterenol sulfate on mild asthmatics' response to sulfur dioxide exposure 

34 and exercise. Arch Environ Occup Health 43: 399-406. 

35 http://dx.doi.org/10.1080/00039896.1988.9935858 

36 Linn, WS; Shamoo, DA; Peng, RC; Clark, KW; Avol, EL; Hackney, JD. (1990). Responses to 

37 sulfur dioxide and exercise by medication-dependent asthmatics: Effect of varying 
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1 medication levels. Arch Environ Occup Health 45: 24-30. 

2 http://dx.doi.org/10.1080/00039896.1990.9935920 

3 Magnussen, H; Jorres, R; Wagner, HM; von Nieding, G. (1990). Relationship between the 

4 airway response to inhaled sulfur dioxide, isocapnic hyperventilation, and histamine in 

5 asthmatic subjects. Int Arch Occup Environ Health 62: 485-491. 

6 http://dx.doi.org/10.1007/BF00381178 

7 Nowak, D; Jorres, R; Berger, J; Claussen, M; Magnussen, H. (1997). Airway responsiveness to 

8 sulfur dioxide in an adult population sample. Am J Respir Crit Care Med 156: 1151-

9 1156. http://dx.doi.org/10.1164/ajrccm.156.4.9607025

10 Reddel, HK. (2009). Characterizing asthma phenotypes: Predictors and outcomes at the extremes 

11 of asthma severity [Editorial]. Respirology 14: 778-780. 

12 Roger, LJ; Kehrl, HR; Hazucha, M; Horstman, DH. (1985). Bronchoconstriction in asthmatics 

13 exposed to sulfur dioxide during repeated exercise. J Appl Physiol 59: 784-791. 

14 Samet J. (2009). Clean Air Scientific Advisory Committee’s (CASAC) Review of EPA's Risk 

15 and Exposure Assessment (REA) to Support the Review of the SO2 Primary National 

16 Ambient Air Quality Standards: Second Draft. EPA-CASAC-09-007. Available at: 

17 https://www3.epa.gov/ttn/naaqs/standards/so2/s_so2_cr.html

18 Sheppard, D; Saisho, A; Nadel, JA; Boushey, HA. (1981). Exercise increases sulfur dioxide19 induced bronchoconstriction in asthmatic subjects. Am Rev Respir Dis 123: 486-491. 

20 Sheppard, D; Eschenbacher, WL; Boushey, HA; Bethel, RA. (1984). Magnitude of the 

21 interaction between the bronchomotor effects of sulfur dioxide and those of dry (cold) air. 

22 Am Rev Respir Dis 130: 52-55. 

23 Smith, E. (1993). Subject Data Supplied by the Researchers for the Recent Controlled Human 

24 Studies Analyzed in the Staff Paper Supplement and Accompanying Memorandum. 

25 Memorandum to SO2 Doeket (A-84-25). August 11, 1993.Strickland, MJ; Darrow, LA; 

26 Klein, M; Flanders, WD; Sarnat, JA; Waller, LA; Sarnat, SE; Mulholland, JA; Tolbert, 

27 PE. (2010). Short-term associations between ambient air pollutants and pediatric asthma 

28 emergency department visits. Am J Respir Crit Care Med 182: 307-316. 

29 http://dx.doi.org/10.1164/rccm.200908-1201OC

30 Thurston, GD; Kipen, H; Annesi-Maesano, I; et al. (2017). A joint ERS/ATS policy statement: 

31 what constitutes an adverse health effect of air pollution? An analytical framework. Eur 

32 Respir J 2017; 49: 1600419 [https://doi.org/10.1183/13993003.00419-2016]. 

33 Trenga, CA; Koenig, JQ; Williams, PV. (1999). Sulphur dioxide sensitivity and plasma 

34 antioxidants in adult subjects with asthma. Occup Environ Med 56: 544-547. 

35 Trenga, CA; Koenig, JQ; Williams, PV. (2001). Dietary antioxidants and ozone-induced 

36 bronchial hyperresponsiveness in adults with asthma. Arch Environ Occup Health 56: 

37 242-249. 
August 24, 2017 3-63 External Review Draft – Do Not Quote or Cite

1 U.S. EPA. (1994). Supplement to the Second Addendum (1986) to Air Quality Criteria for 

2 Particulate Matter and Sulfur Oxides (1982). Research Triangle Park, NC: Office of 

3 Health and Environmental Assessment, Environmental Criteria and Assessment Office. 

4 EPA-600/FP-93/002. 

5 U.S. EPA. (1996). Air Quality Criteria for Ozone and Related Photochemical Oxidants. 

6 Washington, DC: Office of Research and Development. EPA/600/P-93/004aF 

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

8 (Final Report). EPA-600/R-08/047F. Available at: 

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

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

11 National Ambient Air Quality Standard. EPA-452/R-09-007, July 2009. Available at: 

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

13 U.S. EPA. (2010). Quantitative Risk and Exposure Assessment for Carbon Monoxide - 

14 Amended. Office of Air Quality Planning and Standards, U.S. Environmental Protection 

15 Agency, Research Triangle Park, NC, 27711. EPA-452/R-10-006. Available at: 

16 https://www.epa.gov/naaqs/carbon-monoxide-co-standards-risk-and-exposure17 assessments-current-review 

18 U.S. EPA. (2014). Health Risk and Exposure Assessment for Ozone. Office of Air Quality 

19 Planning and Standards, U.S. Environmental Protection Agency, Research Triangle Park, 

20 NC, 27711. EPA-452/R-14-004a. Available at: https://www.epa.gov/naaqs/ozone-o3-

21 standards-risk-and-exposure-assessments-current-review

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

23 (Second External Review Draft). EPA/600/R-16/351, December 2016. Available at: 

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

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

26 Ambient Air Quality Standard for Sulfur Oxides, External Review Draft. EPA-452/P-17-

27 002, August 2017. Available at: https://www.epa.gov/naaqs/sulfur-dioxide-so2-primary28 air-quality-standards 

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

30 Oxides: Risk and Exposure Assessment Planning Document. EPA-452/P-17-001, 

31 February 2017. Available at: 

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

33 WHO. (2008). WHO/IPCS Harmonization Project Document No. 6. Part 1: Guidance Document 

34 on Characterizing and Communicating Uncertainty in Exposure Assessment. Geneva, 

35 World Health Organization, International Programme on Chemical Safety. Available at: 

36 http://www.who.int/ipcs/methods/harmonization/areas/exposure/en/ 
August 24, 2017 A-1 External Review Draft – Do Not Quote or Cite

1 APPENDIX A

2 PREPARATION OF DATA FILES FOR GENERATION OF FIGURES IN CHAPTER 2

3

4 The raw data came from pre-generated AQS extract files. Files are located at 

5 http://www.epa.gov/airquality/airdata/ad_data.html. Documentation of files is located at 

6 http://aqsdr1.epa.gov/aqsweb/aqstmp/airdata/FileFormats.html. Hourly Data Files were used. A 

7 separate Hourly Data File for each parameter and year combination was run. The type of SO2

8 data is determined by the parameter code and duration code and is coded as follows:

9  1-hour values data - parameter code = 42401 and duration code = 1

10  5-minute data (12 observations per hour) - parameter code = 42401 and duration code = H

11  5-minute data (hourly max) – parameter code = 42406 and duration code = 1

12

13 For the 1-hour data at a Site/POC to be used, it must have met the following 

14 completeness criteria:

15  75% or more of the hourly observations in a day (18 or more) must be present.

16  75% or more of the days in a quarter must be present and complete:

 1

st 17 Quarter – 68 observations or 69 observations in leap year

 2

nd 18 Quarter – 69 observations

 3

rd 19 Quarter – 69 observations

 4

th 20 Quarter – 69 observations

21  4 quarters for each of at least 3 of the 5 years (2011-2015) must be present and complete. 

22 For this analytical purpose, the three years do not have to be consecutive. This dataset 

23 was prepared in June 2016.

24

25 After completeness criteria were applied, the following data screens were also performed 

26 to account for some outliers in the 5-minute data:

27  Only 5 minute data with a corresponding hourly value in AQS (parameter 42401 and 

28 duration code 1) were kept.

29  Only 5 minute values with an hourly mean value under 120% of the hourly value in AQS 

30 (parameter 42401 and duration code 1) were kept.

31  Only hours where a 5-minute max hourly value (AQS parameter 42406 and duration code 

32 1) was reported and fell between 1 and 12 times the AQS hourly value (parameter 42401 

33 and duration code 1) were kept.
August 24, 2017 B-1 Draft – Do Not Quote or Cite

1 APPENDIX B

2 ADDITIONAL INFORMATION ON DATASETS PRESENTED IN FIGURE 2-8

3

4 Table B-1. Summary statistics (in ppb) for distributions of daily maximum 5-minute 

5 SO2 concentrations on days with differing daily maximum 1-hour SO2 

6 concentrations.

Bin Daily Maximum 1-hour Concentration (ppb)

<=25 >25-50 >50-75 >75

N 315964 5486 1521 1435

25th percentile 1 46.6 95 170.1

Median 2.0 62 122.6 220

Mean 5 74 140 259

75th percentile 5.2 88 167.2 294.25

95th percentile 22.0 152.5 259 502.9

99th percentile 44 225.6 389 822.5

When the three data sets for sites with DVs at or below 75 ppb are combined, the 

99th percentile is 58.3 ppb and the 99.9th percentile is 150 ppb.

7

8

9 Table B-2. Summary statistics (in ppb) for distributions of daily maximum 5-minute 

10 SO2 concentrations at sites with differing design values.

Bin Design Value (ppb)

<=25 >25-50 >50-75 >75

N 225863 59011 18504 21028

25th percentile 0.8 2 2 2.3

Median 1.7 5 7 8

Mean 3 10 20 41

75th percentile 3.8 13 26 40

95th percentile 12.2 37 82.6 199.6

99th percentile 28.3 68 146.1 365

11
August 24, 2017 B-2 External Review Draft – Do Not Quote or Cite

1 Figure B-1. Monitoring data for sites meeting the current standard: Frequency of daily 

2 maximum 5-minute values on days with differing daily maximum 1-hour concentrations

3 (2013-2015).

4

5

6

7

8 Figure B-2. Monitoring data for sites not meeting the current standard: Frequency of daily 

9 maximum 5-minute values on days with differing daily maximum 1-hour concentrations 

10 (2013-2015).

11

12

0

50

100

150

200

250

300

350

<=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

1400

<=25 >25-50 >50-75 >75

Number of Occurrences

Maximum Hourly Concentrations (ppb)

# >100 ppb # >200 ppb # >300 ppb # >400 ppb
August 24, 2017 C-1 External Review Draft – Do Not Quote or Cite

1 APPENDIX C

2 OCCURRENCES OF 5-MINUTE SO2 CONCENTRATIONS OF INTEREST

3 IN THE RECENT AMBIENT AIR MONITORING DATA (2013-2015)

4

5 Figure C-1. As is (unadjusted) SO2 monitoring data (2013-2015). Mean number of days/year 

6 (top panel) and maximum number of days/year (bottom panel) with daily maximum 5-minute 

7 concentrations of SO2 above 100 ppb.

8

9

10

11

12 Observation: For DV < 75, are monitors in the dataset with 

13 as many as 70 days w. a 5-min concentration >100 ppb.

14

15

16
August 24, 2017 C-2 External Review Draft – Do Not Quote or Cite

1 Figure C-2. As is (unadjusted) SO2 monitoring data (2013-2015). Mean number of days/year 

2 (top panel) and maximum number of days/year (bottom panel) with daily maximum 5-minute 

3 concentrations of SO2 above 200 ppb.

4

5

6

7

8

9

10

11 Observation: For DV < 75, are monitors in the dataset with

12 as many as 22 days with a 5-min concentration >200 ppb.

13

14
August 24, 2017 C-3 External Review Draft – Do Not Quote or Cite

1 Figure C-3. As is (unadjusted) SO2 monitoring data (2013-2015). Mean number of days/year 

2 (top panel) and maximum number of days/year (bottom panel) with daily maximum 5-minute 

3 concentrations of SO2 above 300 ppb.

4

5

6

7 

8

9

10

11

12

13 Observation: For DV < 75, are monitors in the dataset with 

14 as many as 8 days w. a 5-min concentration >300 ppb.

15
August 24, 2017 C-4 External Review Draft – Do Not Quote or Cite

1 Figure C-4. As is (unadjusted) SO2 monitoring data (2013-2015). Mean number of days/year 

2 (top panel) and maximum number of days/year (bottom panel) with daily maximum 5-minute 

3 concentrations of SO2 above 400 ppb.

4

5

6

7 

8

9

10

11

12

13

14

15 Observation: For DV < 75, are monitors in the dataset with

16 as many as 5 days w. a 5-min concentration >400 ppb.
August 24, 2017 C-5 External Review Draft – Do Not Quote or Cite

1 Figure C-5. Monitoring data (2013-2015), unadjusted. Total number of days across 3-year 

2 period with daily maximum 5-minute concentrations of SO2 above 100, 200, 300 and 400 ppb

3 across monitors grouped by design value.

4

0

500

1000

1500

2000

2500

3000

DV <25 DV >25-50 DV >50-75 DV >75

Number of Occurrences

# >100 ppb # >200 ppb # >300 ppb # >400 ppb
August 24, 2017 C-6 External Review Draft – Do Not Quote or Cite

1 Figure C-6. Monitoring data (2013-2015) adjusted to just meet the current standard (75 

ppb as a 3-year average of annual 99th 2 percentile 1-hour daily maximum concentrations).

3 Mean number of days/year (top panel) and maximum number of days/year (bottom panel) with 

4 daily maximum 5-minute concentrations of SO2 above 100, 200, 300 and 400 ppb.

5

6

7

8

9

10

11

12

13

14 10% of monitors in dataset:

15  average 1 to 5 days per year when the maximum 

16 5-minute concentration is above 200 ppb.

17  average 1 to 3 days per year when the maximum 

18 5-minute concentration is above 300 ppb.

19  average <1 to 2 days per year when maximum 

20 5-minute concentration is above 400 ppb. 

21

22

23

24

25

26

27

28

29

30

31

32

33

34

35 At 10% of monitors in the dataset:

36  there are as many as 3–15 days per year when 

37 the maximum 5-minute concentration is above 200 ppb.

38  there are as many as 1–6 days per year when 

39 the maximum 5-minute concentration is above 300 ppb.

40  there are as many as 1–5 days per year when 

41 the maximum 5-minute concentration is above 400 ppb.
August 24, 2017 D-1 External Review Draft – Do Not Quote or Cite

APPENDIX D

AIR QUALITY INFORMATION FOR GEOGRAPHICAL AREAS

OF THREE SELECTED U.S. EPIDEMIOLOGICAL STUDIES
August 24, 2017 D-2 External Review Draft – Do Not Quote or Cite

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).
August 24, 2017 D-3 External Review Draft – Do Not Quote or Cite

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, M. (2009). Air Quality Statistics for Cities Referenced in Key U.S. and 

Canadian Epidemiological Studies of Hospital Admissions and Emergency Department 

Visits for All Respiratory Causes and Asthma. OAQPS Staff Memorandum to Ozone 

NAAQS Review, March 25. Washington, DC: Office of Air Radiation. (EPA docket 

number EPA-HQ-OAR-2007-0352). Available at: 

https://www3.epa.gov/ttn/naaqs/standards/so2/data/2009_03_Thompson_AirQuality.pdf
August 24, 2017 E-1 External Review Draft – Do Not Quote or Cite

APPENDIX E 

DERIVAITON 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 Site Parameter POC City 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 Site Parameter POC City 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
August 24, 2017 F-1 External Review Draft – Do Not Quote or Cite

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
August 24, 2017 F-2 External Review Draft – Do Not Quote or Cite

Figure F-1. Continental U.S.: Facilities emitting more than 1,000 tpy SO2 (n=619 in 2011 NEI) and population density.
August 24, 2017 F-3 External Review Draft – Do Not Quote or Cite

Figure F-2. Northeast U.S.: Facilities emitting more than 1,000 tpy SO2 and population density.
August 24, 2017 F-4 External Review Draft – Do Not Quote or Cite

Figure F-3. Southeast U.S.: Facilities emitting more than 1,000 tpy SO2 and population density.
August 24, 2017 F-5 External Review Draft – Do Not Quote or Cite

Figure F-4. Northwest U.S.: Facilities emitting more than 1,000 tpy SO2 and population density.
August 24, 2017 F-6 External Review Draft – Do Not Quote or Cite

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/P-17-003

August, 2017