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Policy Assessment for the Review of the
Primary National Ambient Air Quality Standard
for Sulfur Oxides
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EPA-452/R-18-002
May 2018
Policy Assessment for the Review of the Primary National Ambient Air Quality Standard for
Sulfur Oxides
U.S. Environmental Protection Agency
Office of Air Quality Planning and Standards
Health and Environmental Impacts Division
Research Triangle Park, NC
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DISCLAIMER
This document has been prepared by staff in the Health and Environmental Impacts
Division, Office of Air Quality Planning and Standards, U.S. Environmental Protection Agency
(EPA). Any findings and conclusions are those of the authors and do not necessarily reflect the
views of the Agency. Mention of trade names or commercial products is not intended to
constitute endorsement or recommendation for use. Questions or comments related to this
document should be addressed to Dr. Nicole Hagan, U.S. Environmental Protection Agency,
Office of Air Quality Planning and Standards, C504-06, Research Triangle Park, North Carolina
27711 (email: hagan.nicole@epa.gov).
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TABLE OF CONTENTS
LIST OF APPENDICES iii
LIST OF FIGURES iv
LIST OF TABLES v
LIST 01 ACRONYMS AND ABBREVIATIONS vi
1 INTRODUCTION 1-1
1.1 Purpose 1-1
1.2 B ackground 1-2
1.2.1 Legislative Requirements 1-2
1.2.2 History of the Reviews of the Primary NAAQS for SOx 1-4
1.2.3 Current SO2 NAAQS Review 1-7
1.3 General Approach and Organization of this Document 1-19
REFERENCES 1-10
2 CURRENT AIR QUALITY 2-1
2.1 Sources to Ambient Air 2-1
2.2 Ambient Air Monitoring Methods and Network 2-3
2.3 Ambient Air Monitoring Concentrations 2-5
2.3.1 Trends 2-5
2.3.2 Current Concentrations 2-8
REFERENCES 2-13
3 REVIEW OF THE PRIMARY STANDARD FOR SULFUR OXIDES 3-1
3.1 Approach 3-1
3.1.1 Approach in the Previous Review 3-2
3.1.2 Approach for the Current Revi ew 3-11
3.2 Adequacy of the Current Standard 3-14
3.2.1 Evidence-based Considerations 3-14
3.2.2 Exposure/Risk-based Considerations 3-37
3.2.3 CASAC Advice 3-56
3.2.4 Staff Conclusions on the Current Standard 3-58
3.3 Key Uncertainties and Areas for Future Research and Data Collection 3-67
REFERENCES 3-69
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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 (2014-2016)
D. Air quality information for geographical areas of three selected U.S.
epidemiological studies
E. Derivation of design values presented in Appendix D
F. Geographic distribution of continental U.S. facilities emitting more than 1,000 tpy
SO2 and population density based on U.S. census tracts
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LIST OF FIGURES
Figure 2-1. Percent contribution of SO2 emissions by sector 2-2
Figure 2-2. National SO2 emission trends by sector 2-3
Figure 2-3. Temporal trend in number of monitors reporting 5-minute concentrations 2-5
Figure 2-4. National temporal trend in SO2 concentrations: 1980-2016 (24 sites) 2-6
Figure 2-5. Temporal trend in SO2 concentrations: 2000-2016 (193 sites) 2-7
Figure 2-6. Temporal trend in daily maximum 5-minute SO2 concentrations: 2011-2016 2-7
Figure 2-7. Concentrations of SO2 in terms of the current standard (3-year average of annual
99th percentile daily maximum 1-hour concentrations) at sites with datasets
meeting completeness requirements for 2014-2016 2-9
Figure 2-8. Distributions of daily maximum 5-minute concentrations during 2014-2016 2-12
Figure 3-1. Overview of the approach for review of the current primary standard 3-13
IV
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LIST OF TABLES
Table 1-1. History of the primary national ambient air quality standard(s) for sulfur oxides
since 1971 1-7
Table 3-1. Percentage of adults with asthma in controlled human exposure studies
experiencing sulfur dioxide-induced decrements in lung function and respiratory
symptoms 3-24
Table 3-2. 2015 National Asthma Prevalence 3-36
Table 3-3. Air quality conditions adjusted to just meet the current standard: Percent of
simulated populations of children with asthma estimated to experience at least one
daily maximum 5-minute exposure per year at or above indicated concentrations
while breathing at an elevated rate 3-45
Table 3-4. Air quality conditions adjusted to just meet the current standard: Percent of
simulated population of children with asthma estimated to experience at least one
day per year with a SCh-related increase in sRaw of 100% or more 3-46
Table 3-5. Population size near larger sources of SO2 emissions 3-55
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LIST OF ACRONYMS AND ABBREVIATIONS
AHR airway hyperresponsiveness
APEX Air Pollutants Exposure model
AQCD Air Quality Criteria Document
AQS Air Quality System
CAA Clean Air Act
CASAC Clean Air Scientific Advisory Committee
CHAD Consolidated Human Activity Database
DV design value
ED emergency department
EGU Electricity generating unit
EPA Environmental Protection Agency
FEM federal equivalent method
FEVi 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
502 sulfur dioxide
503 sulfur tri oxide
SOx oxides of sulfur
sRaw specific airway resistance
USB United States background
UVF ultraviolet fluorescence
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1 INTRODUCTION
1.1 PURPOSE
This document, Policy Assessment for the Review of the Primary National Ambient Air
Quality Standardfor Sulfur Oxides (hereafter referred to as PA), presents the policy assessment
for the U.S. Environmental Protection Agency's (EPA's) current review of the primary (health-
based) national ambient air quality standard (NAAQS) for sulfur oxides (SOx).1 The overall
plan for this review was presented in the Integrated Review Plan for the Primary National
Ambient Air Quality Standardfor Sulfur Dioxide, Final (IRP; U.S. EPA, 2014a). The IRP also
identified key policy-relevant issues to be addressed in this review and discussed the key
documents that generally inform NAAQS reviews, including an Integrated Science Assessment
(ISA), a Risk and Exposure Assessment (REA), and a Policy Assessment (PA).
The PA presents a staff evaluation of the policy implications of the key scientific and
technical information in the ISA and REA for consideration by the EPA Administrator.2
Ultimately, a final decision on the primary standard for SOx will reflect the judgments of the
Administrator. The role of the PA is to help "bridge the gap" between the Agency's scientific
assessments presented in the ISA and REA, and the judgments required of the Administrator in
determining whether it is appropriate to retain or revise the NAAQS.
In evaluating the adequacy of the current standard and whether it is appropriate to
consider alternative standards, the PA focuses on information that is most pertinent to evaluating
the basic elements of the NAAQS: indicator, averaging time, form, and level.3 These elements,
1 This review focuses on the presence in ambient air of sulfur oxides, a group of closely related gaseous compounds
that include sulfur dioxide and sulfur trioxide and of which sulfur dioxide (the indicator for the current standard)
is the most prevalent in the atmosphere and the one for which there is a large body of scientific evidence on
health effects. The health effects of particulate atmospheric transformation products of SOx, such as sulfates, are
addressed in the review of the NAAQS for particulate matter. Additionally, the ecological welfare effects of
sulfur oxides and particulate atmospheric transformation products are being considered in the review of the
secondary NAAQS for Oxides of Nitrogen, Oxides of Sulfur, and Particulate Matter (U.S. EPA, 2017a), while the
visibility, climate, and materials damage-related welfare effects of particulate sulfur compounds are being
evaluated in the review of the secondary NAAQS for particulate matter (U.S. EPA, 2016a).
2 The terms "staff," "we," and "our" throughout this document refer to the staff in the EPA's Office of Air Quality
Planning and Standards (OAQPS).
3 The indicator defines the chemical species or mixture to be measured in the ambient air for the purpose of
determining whether an area attains the standard. The averaging time defines the period over which air quality
measurements are to be averaged or otherwise analyzed. The form of a standard defines the air quality statistic
that is to be compared to the level of the standard in determining whether an area attains the standard. For
example, the form of the annual NAAQS for fine particulate matter is the average of annual mean concentrations
for three consecutive years, while the form of the 8-hour NAAQS for carbon monoxide is the second-highest 8-
hour average in a year. The level of the standard defines the air quality concentration used for that purpose.
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which together serve to define each standard, must be considered collectively in evaluating the
health protection afforded by the primary standard for SOx.
The development of the PA is also intended to facilitate advice to the Agency and
recommendations to the Administrator from an independent scientific review committee, the
Clean Air Scientific Advisory Committee (CASAC), as provided for in the Clean Air Act
(CAA). As discussed below in section 1.2.1, the CASAC is to advise on subjects including the
Agency's assessment of the relevant scientific information and on the adequacy of the current
standards, and to make recommendations as to any revisions of the standards that may be
appropriate. The EPA makes available to the CASAC and the public one or more drafts of the
PA for CASAC review and public comment.4
In this PA, we take into account the available scientific and technical information, as
assessed in the Integrated Science Assessment for Sulfur Oxides - Health Criteria (2017 ISA
[U. S. EPA, 2017b]) and Risk and Exposure Assessment for the Review of the Primary National
Ambient Air Quality Standardfor Sulfur Oxides (REA [U.S. EPA, 2018]). The evaluation and
staff conclusions in this PA have been informed by the advice received from the CASAC based
on its review of the draft PA (U.S. EPA, 2017c) and other draft Agency documents prepared thus
far in this review, and also by public comment received thus far.
Beyond informing the Administrator and facilitating the advice and recommendations of
the CASAC, the PA is also intended to be a useful reference to all parties interested in the review
of the primary NAAQS for SOx. In these roles, it is intended to serve as a source of policy-
relevant information that informs the Agency's review of the primary NAAQS for SOx, and it is
written to be understandable to a broad audience.
1.2 BACKGROUND
1.2.1 Legislative Requirements
Two sections of the CAA govern the establishment and revision of the NAAQS. Section
108 [42 U.S.C. ง 7408] directs the Administrator to identify and list certain air pollutants and
then to issue air quality criteria for those pollutants. The Administrator is to list those pollutants
"emissions of which, in his judgment, cause or contribute to air pollution which may reasonably
be anticipated to endanger public health or welfare," "the presence of which in the ambient air
4 The decision whether to prepare one or more drafts of the PA is influenced by preliminary staff conclusions, taking
into consideration CASAC advice and public comments, among other factors. Typically, a second draft PA has
been prepared in cases where the available information calls into question the adequacy of the current standard
and where analyses of potential alternative standards are developed. In such cases, a second draft PA includes
preliminary staff conclusions regarding potential alternative standards and undergoes CASAC review and public
comment prior to preparation of the final PA. When such analyses are not undertaken, a second draft PA may not
be warranted, as is the case in this review of the primary NAAQS for SOx.
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results from numerous or diverse mobile or stationary sources"; and for which he "plans to issue
air quality criteria..42 U.S.C. ง 7408(a)(1). Air quality criteria are intended to "accurately
reflect the latest scientific knowledge useful in indicating the kind and extent of all identifiable
effects on public health or welfare which may be expected from the presence of [a] pollutant in
the ambient air... " 42 U.S.C. ง 7408(a)(2).
Section 109 [42 U.S.C. ง 7409] directs the Administrator to propose and promulgate
"primary" and "secondary" NAAQS for pollutants for which air quality criteria are issued [42
U.S.C. ง 7409(a)], Section 109(b)(1) defines primary standards as ones "the attainment and
maintenance of which in the judgment of the Administrator, based on such criteria and allowing
an adequate margin of safety, are requisite to protect the public health."5 Under section
109(b)(2), a secondary standard must "specify a level of air quality the attainment and
maintenance of which, in the judgment of the Administrator, based on such criteria, is requisite
to protect the public welfare from any known or anticipated adverse effects associated with the
presence of [the] pollutant in the ambient air."6
The requirement that primary standards provide an adequate margin of safety was
intended to address uncertainties associated with inconclusive scientific and technical
information available at the time of standard setting. It was also intended to provide a reasonable
degree of protection against hazards that research has not yet identified. See Lead Industries
Association v. EPA, 647 F.2d 1130, 1154 (D.C. Cir 1980), cert, denied. 449 U.S. 1042 (1980);
American Petroleum Institute v. Costle, 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert, denied, 455
U.S. 1034 (1982); Coalition of Battery Recyclers Ass'n v. EPA, 604 F.3d 613, 617-18 (D.C. Cir.
2010); Mississippi v. EPA, 744 F. 3d 1334, 1353 (D.C. Cir. 2013). Both kinds of uncertainties
are components of the risk associated with pollution at levels below those at which human health
effects can be said to occur with reasonable scientific certainty. Thus, in selecting primary
standards that include an adequate margin of safety, the Administrator is seeking not only to
prevent pollution levels that have been demonstrated to be harmful but also to prevent lower
pollutant levels that may pose an unacceptable risk of harm, even if the risk is not precisely
identified as to nature or degree. The CAA does not require the Administrator to establish a
primary NAAQS at a zero-risk level or at background concentration levels, see Lead Industries
5 The legislative history of section 109 indicates that a primary standard is to be set at "the maximum permissible
ambient air level. . . which will protect the health of any [sensitive] group of the population," and that for this
purpose "reference should be made to a representative sample of persons comprising the sensitive group rather
than to a single person in such a group." S. Rep. No. 91-1196, 91st Cong., 2d Sess. 10 (1970).
6 Under CAA section 302(h) (42 U.S.C. ง 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 properly, and hazards to transportation, as well as effects on economic values and on personal
comfort and well-being."
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v. EPA, 647 F.2d at 1156 n.51, Mississippi v. EPA, 744 F.3d at 1351, but rather at a level that
reduces risk sufficiently so as to protect public health with an adequate margin of safety.
In addressing the requirement for an adequate margin of safety, the EPA considers such
factors as the nature and severity of the health effects involved, the size of the sensitive
population(s), and the kind and degree of uncertainties. The selection of any particular approach
to providing an adequate margin of safety is a policy choice left specifically to the
Administrator's judgment. See Lead Industries Association v. EPA, 647 F.2d at 1161-62;
Mississippi v. EPA, 744 F.3d at 1353.
In setting primary and secondary standards that are "requisite" to protect public health
and welfare, respectively, as provided in section 109(b), the EPA's task is to establish standards
that are neither more nor less stringent than necessary. In so doing, the EPA may not consider the
costs of implementing the standards. See generally, Whitman v. American Trucking Associations,
531 U.S. 457, 465-472, 475-76 (2001). Likewise, "[attainability and technological feasibility are
not relevant considerations in the promulgation of national ambient air quality standards"
{American Petroleum Institute v. Costle, 665 F.2d at 1185).
Section 109(d)(1) requires that "[n]ot later than December 31, 1980, and at five-year
intervals thereafter, the Administrator shall complete a thorough review of the criteria published
under section [108] and the national ambient air quality standards.. .and shall make such
revisions in such criteria and standards and promulgate such new standards as may be
appropriate...." Section 109(d)(2) requires that an independent scientific review committee
"shall complete a review of the criteria.. .and the national primary and secondary ambient air
quality standards... and shall recommend to the Administrator any new... standards and revisions
of existing criteria and standards as may be appropriate...." Since the early 1980s, this
independent review function has been performed by the CAS AC of the EPA's Science Advisory
Board.7
1.2.2 History of the Reviews of the Primary NAAQS for SOx
The initial air quality criteria for SOx were issued in 1969 (34 FR 1988, February 11,
1969). Based on these criteria, the EPA, in initially promulgating NAAQS for SOx in 1971,
established the indicator as SO2. The two primary standards set in 1971 were 0.14 parts per
million (ppm) averaged over a 24-hour period, not to be exceeded more than once per year, and
0.03 ppm, as an annual arithmetic mean.
7 Lists of the CASAC members and of members of the CASAC Sulfur Oxides Panel are available at:
https://vosefiiite.epa.gOv/sab/sabpeople.ns:f/WebCofiifiiitteesSiibcoiiiiiiittees/CASAC%20Siil:fni%200xides%20P
anel
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The first review of the air quality criteria and standards for SOx was completed in several
stages. In the first stage, the EPA released the Air Quality Criteria Document (AQCD) for PM
and SOx in December 1981, and an addendum presenting information from subsequently
available controlled human exposure studies in 1982 (U.S. EPA, 1982a, 1982b). The policy
aspects of the air quality criteria, and preliminary exposure analyses were evaluated by OAQPS
staff in the 1982 Staff Paper (U.S. EPA, 1982c).
In 1986, the EPA published a second addendum to the 1982 AQCD, presenting newly
available evidence from epidemiologic and controlled human exposure studies (U.S. EPA,
1986a). Policy-relevant aspects of the new evidence and staff findings from a companion
population exposure assessment were evaluated in a 1986 Addendum to the 1982 Staff Paper
(U.S. EPA, 1986b, 1986c). The CAS AC reviewed all of these documents and provided advice
and recommendations with regard to decisions for the review of the standards. Based on the
evidence in the 1982 and 1986 documents, staff evaluations and CAS AC recommendations, in
1988, the EPA proposed to retain the existing standards and solicited comment on the alternative
of retaining the existing standards while additionally establishing a 1-hour standard of 0.4 ppm to
protect against short-term exposures (53 FR 14926, April 26, 1988). In 1992, the American Lung
association brought a lawsuit to compel the EPA to review and, if appropriate, revise the primary
standards for SOx, and the remainder of the review was then completed under court order (59 FR
58962, November 15, 1994; 61 FR 25566, May 22, 1996).
In 1994, the EPA prepared a supplement to the second addendum to the 1982 AQCD in
response to publication of additional relevant controlled human studies on health effects of short-
term SO2 concentrations (1994 AQCD supplement [U.S. EPA, 1994a]). Policy-relevant aspects
of the full body of evidence, including that newly available, along with the 1986 exposure
analysis were evaluated in the 1994 Supplement to the 1982 Staff Paper (U.S. EPA, 1994b). Also
in 1994, based on the available evidence, staff evaluations, CAS AC advice, and public comment
on the 1988 proposal, the EPA re-proposed to retain the existing standards and also solicited
comment on retaining the existing standards in combination with one of three policy options to
further reduce the health risk posed by exposure to high 5-minute peaks of SO2 if additional
protection were judged to be necessary (59 FR 58958, November 15, 1994). The three
alternatives were: (1) Revising the existing primary SO2 NAAQS by adding a new 5-minute
standard of 0.60 ppm SO2, not to be exceeded more than once per calendar year; (2) establishing
a new regulatory program under section 303 of the CAA to supplement protection provided by
the existing NAAQS, with a trigger level of 0.60 ppm SO2, not to be exceeded more than once
per calendar year; and (3) augmenting implementation of existing standards by focusing on those
sources or source types likely to produce high 5-minute peak concentrations of SO2.
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This review was completed in 1996 with the EPA's decision to retain without revision the
existing standards (61 FR 25566, May 22, 1996). In reaching this decision, the Administrator
concluded, based on the staff exposure analysis, that exposure of individuals with asthma to SO2
levels that can reliably elicit adverse health effects was likely a rare event when viewed in the
context of the entire population of people with asthma. As a result, the Administrator judged that
5-minute peaks of SO2 did not pose a broad public health problem when viewed from a national
perspective, and a 5-minute standard was not promulgated (61 FR 25566, May 22, 1996).
In 1996, the American Lung Association and the Environmental Defense Fund
challenged the EPA's decision not to establish a 5-minute standard. On January 30, 1998, the
Court of Appeals for the District of Columbia ("D.C. Circuit") found that the EPA had failed to
adequately explain its determination that no revision to the SO2 NAAQS was appropriate and
remanded the decision back to EPA for further explanation. Specifically, the court determined
that the EPA had not provided adequate rationale to support the judgment that 5-minute peaks of
SO2 do not pose a public health problem from a national perspective, given that the record for
the rule indicated that these peaks would likely significantly affect a subset of individuals with
asthma (American Lung Ass 'n v. EPA, 134 F. 3d 388, 392-393 [D.C. Cir. 1998]). Following the
remand, the EPA requested that states voluntarily submit 5-minute SO2 monitoring data for the
EPA to use to gain a better understanding of the magnitude and frequency of high, 5-minute peak
SO2 concentrations.
The next and most recent review of the air quality criteria and primary standards for SOx
was completed in 2010 (75 FR 35520, June 22, 2010; 74 FR 64810, December 8, 2009). The
scientific evidence for this review was assessed in the 2008 ISA (U.S. EPA, 2008) and the
exposure/risk analyses were presented in the 2009 REA (U.S. EPA, 2009). As a result of this
review, the EPA promulgated a new 1-hour standard to provide the requisite protection for at-
risk populations such as people with asthma against respiratory health effects related to short-
term SO2 exposures. The 1-hour standard was set with SO2 as the indicator based on its common
occurrence in the atmosphere and the predominance of SO2 studies in the health effects
information for SOx. The standard was set at a level of 75 parts per billion (ppb), based on the 3-
year average of the annual 99th percentile of 1-hour daily maximum SO2 concentrations. The
EPA also revoked the then-existing 24-hour and annual primary standards based largely on the
conclusion that the 1-hour standard would also control longer-term average concentrations,
maintaining 24-hour and annual concentrations generally well below the levels of those
standards, and on the lack of evidence indicating the need for such longer-term standards. The
2010 action also addressed the remand by the D.C. Circuit in 1998. The 2010 and prior standards
are summarized in Table 1-1.
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Table 1-1. History of the primary national ambient air quality standard(s) for sulfur
oxides since 1971.
Final
Rule/Decision
Indicator
Averaging
Time
Level
Form
April 30,1971
(36 FR 8186)
S02
24 hours
140 ppba
one allowable exceedance per year
1 year
30 ppba
arithmetic average
May 22, 1996
(61 FR 25566)
Both the 24-hour and annual average standards retained without revision
June 22, 2010
(75 FR 35520)
S02
1 hour
75 ppb
99th percentile of yearly distribution of 1-hour
daily maximums, averaged over 3 years
24-hour and annual standards revoked
a Although the levels were set in terms of ppm (0.14 ppm for the 24-hour standard and 0.03 ppm for the annual standard),
they are shown here in ppb for consistency with units of current standard.
In conjunction with the 2010 revisions to the standards, the EPA revised the SO2 ambient
air monitoring regulations to require that monitoring agencies using continuous SO2 methods
report the highest 5-minute concentration for each hour of the day (along with the hourly
average); many agencies additionally report all twelve 5-minute concentrations for each hour of
the day (75 FR 35554, June 22, 2010; 40 CFR 58.16). The rationale for this requirement was to
provide additional monitoring data for use in subsequent reviews of the primary standard,
particularly in considering the extent of protection provided by the 1-hour standard against 5-
minute peak SO2 concentrations of concern (75 FR 35554, June 22, 2010).
After publication of the final rule, a number of industry groups and states filed petitions
for review arguing (1) that the EPA failed to follow notice-and-comment rulemaking procedures
because the proposal did not indicate that EPA was considering changing its method of
determining attainment from an air-monitoring approach to a hybrid approach using computer
modeling in combination with air monitoring, and (2) that the decision to establish a 1-hour SO2
NAAQS at 75 ppb was arbitrary and capricious because it was lower than statutorily authorized.
The D.C. Circuit rejected these challenges, dismissing the first argument for lack of jurisdiction
and denying the petitions with respect to the second argument, explaining that the EPA did not
act arbitrarily in setting the 2010 standard (National Environmental Developmental Association's
Clean Air Project v. EPA, 686 F. 3d 803[D.C. Cir. 2012]). Accordingly, the 2010 standard was
upheld {Id)
1.2.3 Current SO2 NAAQS Review
In May 2013, the EPA announced the initiation of the current periodic review of the air
quality criteria for SOx and the primary NAAQS for sulfur oxides and issued a call for
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information in the Federal Register (78 FR 27387, May 10, 2013). A wide range of external
experts as well as EPA staff representing a variety of areas of expertise (e.g., epidemiology,
human and animal toxicology, statistics, risk/exposure analysis, atmospheric science)
participated in a workshop, held by the EPA on June 12-13, 2013 in Research Triangle Park, NC.
The workshop provided for a public discussion of the key policy-relevant issues around which
the EPA has structured the review and of the most meaningful new scientific information that
would be available in this review to inform our understanding of these issues.
Building from the workshop discussions, the EPA developed the draft Integrated Review
Plan for the Primary National Ambient Air Quality Standards for Sulfur Dioxide, External
Review Draft (draft IRP, U.S. EPA, 2014b; 79 FR 14035, March 12, 2014) outlining the
schedule, process, and key policy-relevant questions that would guide the evaluation of the air
quality criteria for SO2 and the review of the primary NAAQS for SOx. The draft IRP was
released in March 2014 (79 FR 14035, March 12, 2014) and was the subject of a consultation
with the CASAC on April 22, 2014 (79 FR 16325, March 25, 2014). Comments received from
the CASAC and the public were considered in the preparation of the final IRP, which was
released in October 2014 (U.S. EPA, 2014a; 79 FR 66721, November 10, 2014).
The process for development of the first draft ISA included review of preliminary drafts
of key ISA chapters by subject matter experts at a public workshop hosted by the EPA's National
Center for Environmental Assessment (NCEA) on June 23-24, 2014 (79 FR 33750, June 12,
2014). Comments received from this review as well as comments from the public and the
CASAC on the draft IRP were considered in preparation of the Integrated Science Assessment
for Sulfur Oxides - Health Criteria (External Review Draft - November 2015, U.S. EPA, 2015),
released in November 2015 (80 FR 73183, November 24, 2015). The first draft IS A was
reviewed by the CASAC at a public meeting in January 2016 and a public teleconference in
April 2016 (80 FR 79330, December 21, 2015; 80 FR 79330, December 21, 2015; Diez Roux,
2016).
The EPA released the Integrated Assessment for Sulfur Oxides - Health Criteria (Second
External Review Draft - December 2016, U.S. EPA, 2016b) in December 2016, which was
reviewed by the CASAC at a public meeting in March 2017 and a public teleconference in June
2017 (82 FR 11449, February 23, 2017; 82 FR 23563, May 23, 2017). The final ISA was
released in December 2017 (U.S. EPA, 2017b; 82 FR 58600, December 13, 2017).
As part of the planning process for development of the REA, the EPA completed the
Review of the Primary National Ambient Air Quality Standardfor Sulfur Oxides: Risk and
Exposure Assessment Planning Document (REA Planning Document, U.S. EPA, 2017d) in
February 2017 (82 FR 11356, February 22, 2017), and held a consultation with the CASAC at a
public meeting in March 2017 (82 FR 11449, February 23, 2017). In consideration of CASAC
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comments at that consultation, as well as public comments, the EPA developed the draft REA
(U.S. EPA, 2017e) and the draft PA (U.S. EPA 2017c), which were released on August 24, 2017
(82 FR 43756, September 19, 2017). The draft REA and draft PA were reviewed by the CASAC
at a a public meeting on September 18-19, 2017 (82 FR 37213, August 9, 2017), with CASAC
advice and comments provided in letters to the Administrator dated April 30, 2018 (Cox and
Diez Roux, 2018a,b). Staff considered CASAC advice and public comments in completing these
documents.
The schedule for completion of this review is governed by a consent decree, which, in
relevant part, specifies signature on the notice setting forth the EPA's proposed decision
concerning its review of the primary NAAQS for SOx no later than May 25, 2018; and sign a
notice setting forth EPA's final decision concerning its review of the primary NAAQS for SOx
no later than January 28, 2019 (Consent Decree at 4, Center for Biological Diversity et al. v.
Pruitt, Case No. 3:16-cv-03796-VC (N.D. Cal. April 28, 2017), Document No. 37 entered by the
court on April 28, 2017).
1.3 GENERAL APPROACH AND ORGANIZATION OF THIS
DOCUMENT
This PA draws on the policy-relevant aspects of the scientific evidence and quantitative
air quality, exposure and risk analyses. With regard to the health effects evidence, we consider
the nature of the key effects associated with SO2 in ambient air, the types and magnitudes of
exposures associated with effects, and populations at greatest risk, as well as the uncertainties.
Based on this information, we summarize associated potential public health impacts of SO2 in
ambient air. We additionally consider the magnitude of exposures and risks estimated in the
REA, along with the associated uncertainties. This evaluation supports staff conclusions with
regard to the key policy-relevant questions for the review, including whether the currently
available information appears to call into question the adequacy of public health protection
afforded by the current standard.
Following this introductory chapter, chapter 2 focuses on current air quality, including
sources of SO2 to ambient air, the ambient monitoring network for SO2, and trends and current
conditions. Chapter 3 has three areas of focus. Section 3.1 focuses on the review of the primary
NAAQS for SOx presenting background information on the rationale for previous reviews and
the approach followed in the current review. Section 3.2 considers the evidence and exposure
and risk information for the current standard, as well as CASAC advice, and presents staff
conclusions regarding these considerations in this review. Section 3.3 identifies key uncertainties
and areas for future research.
1-9
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REFERENCES
Cox, LA; Diez Roux, A. (2018a). Letter from Louis Anthony Cox, Chair, Clean Air Scientific
Advisory Committee, and Ana Diez Roux, Immediate Past Chair, Clean Air Scientific
Advisory Committee, to Administrator E. Scott Pruitt. Re: CAS AC Review of the EPA's
Risk and Exposure Assessment for the Review of the Primary National Ambient Air
Quality Standard for Sulfur Oxides (External Review Draft - August 2017). April 30,
2018.
Cox, LA; Diez Roux, A. (2018b). Letter from Louis Anthony Cox, Chair, Clean Air Scientific
Advisory Committee, and Ana Diez Roux, Immediate Past Chair, Clean Air Scientific
Advisory Committee, to Administrator E. Scott Pruitt. Re: CAS AC Review of the EPA's
Policy Assessment for the Review of the Primary National Ambient Air Quality Standard
for Sulfur Oxides (External Review Draft - August 2017). April 30, 2018.
Diez Roux, A. (2016). Letter from Ana Diez Roux, Chair, Clean Air Scientific Advisory
Committee, to Administrator Gina McCarthy. Re: CAS AC Review of the EPA's
Integrated Science Assessment for Sulfur Oxides - Health Criteria (External Review
Draft-November 2015). April 15, 2016.
U.S. EPA. (1982a). Air quality criteria for particulate matter and sulfur oxides (final, 1982).
Environmental Criteria and Assessment Office, Washington, DC, EPA 600/8-82/029.
Available at: https://www3.epa. gov/ttn/naaqs/standards/so2/s so2 pr.htro 1
U.S. EPA. (1982b). Air quality criteria for particulate matter and sulfur oxides, volume I
addendum. Environmental Criteria and Assessment Office, Research Triangle Park, NC,
EPA-600/8-82-029a. Available at:
https://www3.epa.gov/ttn/naaqs/standards/so2/s so2 pr.html
U.S. EPA. (1982c). Review of the National Ambient Air Quality Standards for Sulfur Oxides:
Assessment of Scientific and Technical Information, OAQPS Staff Paper. Office of Air
Quality Planning and Standards, Research Triangle Park, NC, EPA-450-5-82-007.
Available at: https://www3.epa. gov/ttn/naaqs/standards/so2/s so2 pr.htm 1
U.S. EPA. (1986a). Air quality criteria for particulate matter and sulfur oxides (1982):
assessment of newly available health effects information, 2nd addendum. Environmental
Criteria and Assessment Office, Office of Health and Environmental Assessment, Office
of Research and Development, Research Triangle Park, NC, EPA/600/8- 86/020F.
U.S. EPA. (1986b). Review of the national ambient air quality standard for sulfur oxides:
updated assessment of scientific and technical information. Addendum to the 1982
OAQPS Staff Paper. Environmental Criteria and Assessment Office, Office of Health and
Environmental Assessment, Office of Research and Development, Research Triangle
Park, NC, EPA-452/05 86-013. Available at:
https://www3.epa. eov/ttm/maaqs/standards/so2/s so2 pr.html
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U.S. EPA. (1986c). An Analysis of Short-Term Sulfur Dioxide Population Exposures in the
Vicinity of Utility Power Plants. Office of Air Quality Planning and Standards, Research
Triangle Park, NC. Available at:
https://www3.epa. gov/ttn/naaqs/standards/so2/s so2 pr.html
U.S. EPA. (1994a). Supplement to the second addendum (1986) to air quality criteria for
particulate matter and sulfur oxides (1982): Assessment of new findings on sulfur dioxide
acute exposure health effects in asthmatic individuals. Environmental Criteria and
Assessment Office, Office of Health and Environmental Assessment, Office of Research
and Development, Research Triangle Park, NC, EPA/600/FP-93/002, August 1994.
Available at: https://www3.epa.gov/ttm/naaqs/standards/so2/s so2 pr.html
U.S. EPA (1994b). Review of the national ambient air quality standards for sulfur oxides:
assessment of scientific and technical information. Supplement to the 1986 OAQPS Staff
Paper Addendum. Environmental Criteria and Assessment Office, Office of Health and
Environmental Assessment, Office of Research and Development, Research Triangle
Park, NC, EPA/600/FP-93/002, EPA-452/R-94-013. Available at:
https://www3.epa. gov/ttn/naaq s/standards/so2/s so2 pr.html
U.S. EPA. (2008). Integrated Science Assessment (ISA) for Sulfur Oxides - Health Criteria
(Final Report). National Center for Environmental Assessment-RTP Division, Office of
Research and Development, Research Triangle Park, NC, EPA-600/R-08/047F,
September 2008. Available at:
http: //cfpub. epa. gov/n cea/ cfm/recordi spl ay. cfm ? dei 143
U.S. EPA. (2009). Risk and Exposure Assessment to Support the Review of the SO2 Primary
National Ambient Air Quality Standard. Office of Air Quality Planning and Standards,
Research Triangle Park, NC, EPA-452/R-09-007, July 2009. Available at:
https://www3.epa.gov/ttn/naaqs/standards/so2/data/200908S02REAFin.alReport.pdf
U.S. EPA. (2014a). Integrated Review Plan for the Primary National Ambient Air Quality
Standard for Sulfur Dioxide, Final. Office of Air Quality Planning and Standards,
Research Triangle Park, NC, EPA-452/P-14-007, October 2014. Available at:
https://www3.epa.gov/ttn/naaqs/standards/so2/data/20141028so2reviewplan.pdf
U.S. EPA. (2014b). Integrated Review Plan for the Primary National Ambient Air Quality
Standard for Sulfur Dioxide, External Review Draft. Office of Air Quality Planning and
Standards, Research Triangle Park, NC, EPA-452/P-14-005, March 2014. Available at:
https://www3.epa.gov/ttn/naaqs/standards/so2/data/20140318so2reviewplan.pdf
U.S. EPA. (2015). Integrated Science Assessment (ISA) for Sulfur Oxides - Health Criteria
(External Review Draft, Nov 2015). National Center for Environmental Assessment-RTP
Division, Office of Research and Development, Research Triangle Park, NC,
EPA/600/R-15/066, November 2015. Available at:
http s: //cfpub .epa. gov/n. cea/i sa/recordi spl ay. cfm ? dei )44
U.S. EPA. (2016a). Integrated Review Plan for the Secondary National Ambient Air Quality
Standards for Particulate Matter. Office of Air Quality Planning and Standards, Research
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Triangle Park, NC, EPA-452/R-16-005, December 2016. Available at:
https://www.epa.gov/naaqs/particulate-matter-pm-standards-planning-documents-cuiTent-
review
U.S. EPA. (2016b). Integrated Science Assessment (ISA) for Sulfur Oxides - Health Criteria
(Second External Review Draft). National Center for Environmental Assessment-RTP
Division, Office of Research and Development, Research Triangle Park, NC,
EPA/600/R-16/351, December 2016. Available at:
U.S. EPA. (2017a). Integrated Review Plan for the Secondary National Ambient Air Quality
Standard for Ecological Effects of Oxides of Nitrogen, Oxides of Sulfur and Particulate
Matter. Office of Air Quality Planning and Standards, Research Triangle Park, NC, EPA-
452/R-17-002, January 2017. Available at: https://www.epa.gov/naaqs/nitrogen-dioxide-
no2-and-sulfur-dioxide-so2-secondarystandards-planning-documents-current
U.S. EPA. (2017b). Integrated Science Assessment (ISA) for Sulfur Oxides - Health Criteria
(Final). National Center for Environmental Assessment-RTP Division, Office of
Research and Development, Research Triangle Park, NC, EPA/600/R-17/451, December
2017. Available at: https://cfpub.epa.gov/n.cea/isa/recordisplav.cfm?deid=338596
U.S. EPA. (2017c). Policy Assessment for the Review of the Primary National Ambient Air
Quality Standard for Sulfur Oxides, External Review Draft. Office of Air Quality
Planning and Standards, Research Triangle Park, NC, EPA-452/P-17-003, August 2017.
Available at: https://www.epa.gov/naaqs/siilfiir-dioxide-so2.-primary-air-quality-
U.S. EPA. (2017d). Review of the Primary National Ambient Air Quality Standard for Sulfur
Oxides: Risk and Exposure Assessment Planning Document. Office of Air Quality
Planning and Standards, Research Triangle Park, NC, EPA-452/P-17-001, February
2017. Available at:
https://www3.epa.gov/ttn/naaqs/standards/so2/data/20170216so2rea.pdf
U.S. EPA. (2017e). Risk and Exposure Assessment for the Review of the Primary National
Ambient Air Quality Standard for Sulfur Oxides, External Review Draft. Office of Air
Quality Planning and Standards, Research Triangle Park, NC, EPA-452/P-17-002,
August 2017. Available at: https://www.epa.gov/naaqs/siilfiir-dioxide-so2-primary-air-
U.S. EPA. (2018). Risk and Exposure Assessment for the Review of the Primary National
Ambient Air Quality Standard for Sulfur Oxides, Final. Office of Air Quality Planning
and Standards, Research Triangle Park, NC, EPA-452/R-18-003, May 2018. Available at:
.epa.gov/ncea/isa/recordisplay.cfm?deid=326450
standards
https://www.epa. gov/naaq s/sulfur-
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2 CURRENT AIR QUALITY
This chapter presents a summary of our current understanding of SOx in ambient air
largely drawn from the more detailed discussion provided in the ISA (ISA, chapter 2). Section
2.1 summarizes the current information on sources and emissions and section 2.2 summarizes
current ambient air monitoring methods and networks. Recent concentrations of SO2 in ambient
air are summarized in section 2.3.
2.1 SOURCES TO AMBIENT AIR
In this section, we describe the most recently available information on sources and
emissions of SOx into the ambient air. The section does not provide a comprehensive list of all
sources, nor does it provide estimates of emission rates or emission factors for all source
categories. Rather, the discussion here is intended to identify the larger source categories, either
on a national or local scale, and generally describe their emissions and distribution within the
U.S. based on the U.S. EPA 2014 National Emissions Inventory (NEI).
Sulfur oxides are emitted into air from specific sources (e.g., fuel combustion processes)
and also formed in the atmosphere from other atmospheric compounds (e.g., as an oxidation
product of reduced sulfur compounds, such as sulfides). Sulfur oxides are also transformed in the
atmosphere to particulate sulfur compounds, such as sulfates. Sulfur oxides known to occur in
the troposphere include SO2 and sulfur trioxide (SO3) (ISA, section 2.3). As a result of rapid
atmospheric chemical reactions involving SO3, the most prevalent sulfur oxide in the atmosphere
is SO2 (ISA, section 2.3).
Fossil fuel combustion is the main anthropogenic source of SO2 emissions, while
volcanoes and landscape fires (wildfires as well as controlled burns) are the main natural sources
(ISA, section 2.1).1 Industrial chemical production, pulp and paper production, natural biological
activity (plants, fungi, and prokaryotes), and volcanoes are among many sources of reduced
sulfur compounds that contribute, through various oxidation reactions in the atmosphere, to the
formation of SO2 in the atmosphere (ISA, section 2.1). Anthropogenic SO2 emissions originate
primarily from point sources, including coal-fired electricity generating units (EGUs) and other
industrial facilities (ISA, section 2.2.1). The largest S02-emitting sector within the U.S. is
1 The 2008 ISA (U.S. EPA, 2008) described a modeling analysis that estimated SO2 concentrations for 2001 in the
absence of any U.S. anthropogenic emissions of SO2 (2008 ISA, section 2.5.3). Such concentrations are referred
to as United States background or USB. The 2008 ISA analysis estimated USB concentrations of SO2 to be below
0.01 ppb over much of the U.S., ranging up to a maximum of 0.03 ppb. In the U.S. Northwest, geothermal
sources (e.g., volcanoes) were estimated to be responsible for up to 80% of the ambient air concentrations
resulting solely from natural sources and sources outside of the U.S. (ISA, section 2.5.5).
2-1
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electricity generation, as shown in Figure 2-1, of which 97% of SO2 from electricity generation
is from coal combustion.
Figure 2-1. Percent contribution of SO2 emissions by sector (Source: 2014 NEI).2
Other anthropogenic sources of SO2 emissions include industrial fuel combustion and
process emissions, industrial processing, commercial marine activity, and fire used in landscape
management and agriculture (ISA, section 2.2.1). While electricity generation is the dominant
industry sector contributing to SO2 emissions on a national scale, other sectors can also have a
significant influence on local air quality. Large emissions facilities other than EGUs that may
substantially impact local air quality include copper smelters, kraft pulp mills, Portland Cement
plants, iron and steel mill plants, sulfuric acid plants, petroleum refineries, and chemical
processing plants (ISA, p. 2-5). For example, ambient air monitoring sites that have recorded
some of the highest 1-hour daily maximum SO2 concentrations in the U.S. are located near
copper smelters in Arizona (ISA, sections 2.5.2 and 2.5.4; Figure 2-11). The two smelters in this
area had estimated annual emissions of approximately 17,000 and 5,000 tpy in the 2014 NEI
(ISA, p. 2-50).
2 Total SO2 emissions from the 2014 NEI were 4,942,063 tons.
Mobile Sources
(except CMV), 1.2
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65.9
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Industrial
Processes, 12.3
2-2
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Figure 2-2 illustrates the national emissions trends from 1990 to 2016. Declines in SO2
emissions are likely related to the implementation of national control program s developed under
the Clean Air Act Amendments of 1990, including Phase I and II of the Acid Rain Program, the
Clean Air Interstate Rule, and the Cross-State Air Pollution Rule. An additional factor is changes
in market conditions, e.g., reduction in energy generation by coal (U.S. EIA, 2017).3 Declines
between 1971, when SOx NAAQS were first established, and 1990, when the Amendments were
adopted, were on the order of 5,000 tpy deriving primarily from reductions in emissions from the
metals processing sector (ISA, Figure 2-5).
25,000
20,000
15,000
10,000
5,000
1990 1995 2000 2005 2010 2015
~ Stationary fuel combustion ~ Industrial and other processes ~Transportation ฆ Miscellaneous
Figure 2-2. National SO2 emission trends by sector.
2.2 AMBIENT AIR MONITORING METHODS AND NETWORK
To promote uniform enforcement of the air quality standards set forth under the CAA, the
EPA has established federal reference methods (FRMs) and federal equivalent methods (FEMs)
for ambient air sample collection and analysis. Measurements for determinations of NAAQS
compliance must be made with FRMs or FEMs. The current SO2 monitoring network relies on
3 The reduction in energy generation by coal resulted in the use of fuels that emit less SO2 in energy generation (U.S.
EIA. 2016).
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the automated pulsed ultraviolet fluorescence (UVF) FRM (40 CFR Appendix A-l to Part 50; 40
CFR Appendix A-2 to Part 50). The UVF method is a continuous automated method that
quantifies SO2 concentrations, providing averages across desired time periods, such as 5-minute
and 1-hour averages.
Measurements of SO2 concentrations in ambient air are collected by networks of FRM
monitors, primarily operated by state and local monitoring agencies in the U.S. The main
network providing ambient data for NAAQS surveillance monitoring purposes is the State and
Local Air Monitoring Stations (SLAMS) network. In 2016, there were 363 SLAMS sites
reporting SO2 concentrations to the Air Quality System (AQS), the EPA's repository for detailed
air pollution data. For each SO2 monitoring site, the SLAMS monitoring agencies report hourly
concentrations and either the maximum 5-minute concentration in the hour (one of twelve 5-
minute periods within an hour) or all twelve 5-minute average SO2 concentrations within the
hour.
Five minute SO2 data have become much more widely available due to regulatory
requirements promulgated in 2010 (Figure 2-3).4 Although 5-minute concentration
measurements were available for fewer than 10% of monitoring sites at the time of the last
review, such data (either all 12 values in each hour or just the maximum 5-minute
concentrations) are currently available for nearly all of the SO2 sites operating nationwide,
providing a more robust foundation for characterization of 5-minute ambient air concentrations
in this review. Further, the newly available monitoring data also include more monitors reporting
the 12 consecutive 5-minute concentrations for each hour than were available in the last review
(Figure 2-3). Of the monitors reporting 5-minute data in 2016, almost 40% are reporting all
twelve 5-minute SO2 measurements in each hour while about 60% are reporting the maximum 5-
minute SO2 concentration in each hour.5
4 At SO2 NAAQS compliance monitoring sites, air monitoring agencies are now required to report, for every hour of
the day, the hourly average and either the maximum 5-minute value (one of twelve 5-minute periods) in the hour
or all twelve 5-minute averages within the hour (75 FR 35554, June 22, 2010).
5 In 2016, three sites reported both the continuous 5-minute data and the maximum 5-minute data separately.
Therefore, these monitors are included in the count for each of the categories of 5-minute measurements.
2-4
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600
500
2003 2004 2005 2006 2007 2008 2009 2010 2011 2012 2013 2014 2015 2016
0 5-min values {max/hr only) ~ 5-min values (all 12/hr) 1-hr values
Figure 2-3. Temporal trend in number of monitors reporting 5-minute
concentrations.
2.3 AMBIENT AIR MONITORING CONCENTRATIONS
This section briefly summarizes trends in ambient air SO2 concentrations and current
conditions based on recent ambient air monitoring data.
2.3.1 Trends
Ambient air concentrations of SO2 in the U.S. have declined substantially from 1980 to
2016. Figure 2-4 illustrates this decline in terms of the distribution of 3-year averages of annual
99th percentile daily maximum 1-hour concentrations6 at 24 monitoring sites that have been
operating across this period. The average of this dataset has declined by more than 82% over the
36-year period (the white line in Figures 2-4 and 2-5). Over the past 16 years, a larger dataset of
193 sites operating from 2000-2016 also indicates a decline, which is on the order of 69% for the
6 The form of the current 1-hour SO2 NAAQS is the 99th percentile of the yearly distribution of 1-hour daily
maximums, averaged over 3 years.
2-5
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average of that dataset (Figure 2-5).7 Daily maximum 5-minute SO2 concentrations have also
consistently declined over time from 2011 to 2016 (Figure 2-6).8
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Three-year average of annual 99th percentile of daily maximum 1-hour
concentrations. (Note: Dashed line indicates the current standard [75 ppb].)
7 In Figures 2-4 and 2-5, the year on the x-axis represents the last year of the 3-year average (e.g., 2015 represents
the average of 2013-2015). Additionally, the lower and upper bounds of the shaded area are the 10th and 90th
percentiles, respectively.
8 In Figure 2-6, the number of sites with monitors for 2011, 2012, 2013, 2014, 2015, and 2016 were 301, 321, 366,
359, 352, and 366, respectively.
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(Note: Dashed line indicates the current standard [75ppbj).
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2016. (N = number of measurements)
2-7
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2.3.2 Current Concentrations
2.3.2.1 Geographic Variation in Concentrations
Concentrations of SO2 vary across the U.S. and tend to be higher in areas with sources
having relatively higher SO2 emissions (e.g., EGUs).9 Consistent with the locations of larger
anthropogenic SO2 sources, higher concentrations are primarily located in the eastern half of the
continental U.S., especially in the Ohio River valley, upper Midwest, and along the Atlantic
coast (Figure 2-7). The point source nature of SO2 emissions contribute to the relatively high
spatial variability of SO2 concentrations compared with pollutants such as ozone (O3) and PM
(ISA, section 3.2.3). Another contributing factor to the spatial variability is the dispersion and
oxidation of SO2 in the atmosphere, resulting in decreasing SO2 concentrations with increasing
distance from the source. Sulfur oxides emitted from point sources tends to travel away from the
emissions source as a plume, which may or may not impact large portions of surrounding
populated areas depending on meteorological conditions and terrain (ISA, section 3.2.3).
9 Volcano emissions contribute to the elevated concentrations observed on the island of Hawaii.
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S02 Site Level DVs
2014-2016 (ppb)
/O
# 26-50
~ 76 - 246
Figure 2-7. Concentrations of SO2 in terms of the current standard (3-year average of annual 99th percentile daily
maximum 1-hour concentrations) at sites with datasets meeting completeness requirements for 2014-2016.
-------
2.3.2.2 Seasonal and Diel Variability in Concentrations
Recent (2013-2015) data indicate that 1-hour daily maximum SO2 concentrations vary
across seasons, with the greatest variations seen in the upper percentile concentrations (versus
average or lower percentiles) for each season (ISA, section 2.5.3.2). This is seen in the data
presented for six areas in the draft ISA10 (ISA, section 2.5.3.2). This variation, along with
month-to-month variations in 1-hour daily maximum SO2 concentrations also presented in the
ISA, were generally consistent with month-to-month emissions patterns and the expected
atmospheric chemistry of SO2 for a given season. For example, "summertime minima, observed
in the New York City, NY and Houston, TX, sites may correspond to enhanced oxidation of SO2
to SO42" by photochemically derived atmospheric oxidants that are more prevalent during the
humid summer (Khoder, 2002)" (ISA, p. 2-63). The differences in seasonal pattern (as well as
magnitude) of concentrations among areas studied indicate the variability of SO2 concentrations
across local and regional scales (ISA, section 2.5.3.2).
Consistent with the nationwide diel patterns reported in the last review, 1-hour average
and 5-minute hourly maximum SO2 concentrations for 2013-2015 in the six areas evaluated in
the ISA were generally low during nighttime and approached maxima values during daytime
hours (ISA, section 2.5.3.3, Figures 2-23 and 2-24). The timing and duration of daytime maxima
in the six areas evaluated were likely related to a combination of source emissions and
meteorological parameters (ISA, section 2.5.3.3; U.S. EPA 2008, section 2.5.1). For example,
SO2 emitted from elevated point sources (e.g., power plants and industrial sources) may be
entrained into the mixed boundary layer, which expands during the day with rising surface
temperatures (U.S. EPA 2008, section 2.5.1, Figures 2-23 and 2-24).
2.3.2.3 Relationship Between 1-hour and 5-minute Concentrations
Peak concentrations within a plume of SO2 downwind from, but relatively nearby to, a
source can greatly exceed mean concentrations across the plume (ISA, section 2.5.4). Further,
measured 5-minute concentrations at a particular location can be much higher than the average
concentration at the same location for the associated hour. However, as emissions travel further
downwind and experience ever increasing dispersion, these differences lessen both spatially and
temporally. This can contribute to greater spatial and temporal variability in 5-minute than in 1-
hour concentrations, as is seen in the six locations evaluated in the ISA (second draft ISA, p. 2-
56).
10 The six locations evaluated are: Cleveland, OH, Pittsburgh, PA, New York City, NY, St. Louis, MO-IL, Houston,
TX, and Gila County, AZ (ISA, section 2.5.2.2). These six locations were chosen for the ISA "focus area"
analysis based on (1) their relevance to current health studies (i.e., areas with peer-reviewed, epidemiologic
analysis), (2) the existence of four or more monitoring sites located within the area boundaries, and (3) the
presence of several diverse SO2 sources within a given focus area boundary (ISA, section 2.5.2.2).
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Using monitoring data from 2014-2016, Figure 2-8 illustrates the general pattern of lower
5-minute concentrations with lower 1-hour concentrations. The left panel of Figure 2-8 shows
that across the monitors meeting data completeness criteria, on days when the maximum 1-hour
concentrations are relatively low, the daily maximum 5-minute concentrations are also relatively
low. Similarly, as shown in the right panel of Figure 2-8, at sites with relatively lower design
values,11 the distribution of maximum 5-minute concentrations is also lower. This is documented
by the distinct reduction in 99th percentile daily maximum 5-minute concentrations at lower
design values. For example, in areas with design values at or below the current standard (75
ppb), 99.9 percent of daily maximum 5-minute concentrations are at or below approximately 131
ppb.12 This contrasts with the much higher distribution of daily maximum 5-minute
concentrations at sites with design values exceeding the current standard. The 99th percentile of
these daily maximum 5-minute concentrations is 359 ppb, meaning that one percent of the days
at these sites has a maximum 5-minute concentration above 359 ppb (i.e., 186 occurrences).
11 The design value (DV) is a statistic that describes the air quality status of a given area relative to a particular
NAAQS. A design value summarizes the concentrations of a criteria pollutant in terms of the statistical form of
the standard for that pollutant, thus indicating whether the area meets or exceeds the standard. Consistent with the
form of the SO2 standard, SO2 design values are calculated as the 3-year average of the annual 99th percentile of
the daily maximum 1-hour average concentrations (see 40 CFR 50.17). By regulation, design values calculated
from monitoring data are considered to be valid if they meet specified completeness criteria, which for SO2 are
data for at least 75 percent of the sampling days in all four quarters of all three years of the period (see Appendix
T to Part 50).
12 Additional information related to data in Figure 2-8 is presented in Appendix B, Tables B-l and B-2.
2-11
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Figure 2-8. Distributions of daily maximum 5-minute concentrations during 2014-
2016. Left panel presents varying distributions with varying daily maximum
1-hour concentrations. Right panel presents varying distributions with varying
design values; the last bin (>75 ppb) presents data for sites not meeting the
current standard. (Note: The values represented in the boxplots are the 25th
percentile, the median, and the 75th percentile. The asterisk represents the 99th
percentile.)
Analyses of the current monitoring dataset, expanded since the last review, provide
information on the occurrence of daily maximum 5-minute concentrations of interest at monitors
having differing design values. For example, analysis of these data for the years 2014 to 2016
indicates that among monitors with design values meeting the current standard (i.e., at or below
75 ppb), the vast majority have zero days with a daily maximum 5-minute concentration above
400 ppb or even 100 ppb (Appendix C). Among the few monitors with any days recording a 5-
minute concentration above 400 ppb, the maximum number of such days in a year was seven; for
monitors with any days recording 5-minute concentrations above 200 ppb, the maximum number
of such days/year was 32 (Appendix C, Figures C-2 and C-4, lower panel).
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REFERENCES
Khoder, MI. (2002). Atmospheric conversion of sulfur dioxide to particulate sulfate and nitrogen
dioxide to particulate nitrate and gaseous nitric acid in an urban area. Chemosphere 49:
675-684. http://dx.doi.org/hi i<ซl-. x0045~6535(02> i ^ ! i
U.S. EIA (U.S. Energy Information Administration). (2016). Electric Power Annual 2015. U.S.
Department of Energy, Washington, DC, November 2016. Available at:
https://www.eia.gov/electricitv/anniial/pdf/epa.pdf
U.S. EIA (U.S. Energy Information Administration). (2017). Monthly Energy Review July 2017.
U.S. Department of Energy, Washington, DC, DOE/EIA-003 5(2017-07), July 2017.
Available at: https://www.eia.gov/totalenergy/data/monthlv/pdf/mer.pdf
U.S. EPA. (2008). Integrated Science Assessment (ISA) for Sulfur Oxides - Health Criteria
(Final Report). National Center for Environmental Assessment-RTP Division, Office of
Research and Development, Research Triangle Park, NC, EPA-600/R-08/047F,
September 2008. Available at:
http://cfpiib.epa.gov/ncea/cfm/recordisplay.cfm7dei 143
U.S. EPA. (2017). Integrated Science Assessment (ISA) for Sulfur Oxides - Health Criteria
(Final). National Center for Environmental Assessment-RTP Division, Office of
Research and Development, Research Triangle Park, NC, EPA/600/R-17/451, December
2017. Available at: https://cfpub.epa.gov/ncea/isa/recordisplay.cfm?deid=338596
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3 REVIEW OF THE PRIMARY STANDARD FOR
SULFUR OXIDES
This chapter evaluates the policy implications of the key scientific and technical
information in the ISA and REA. This evaluation is based on consideration of the available body
of evidence assessed in the ISA and of quantitative analyses of SO2 air quality, exposures and
risks presented in the REA and in this document. Based on this information, the staff offer
conclusions regarding each of the critical elements of the standard, including indicator, averaging
time, form, and level. This final PA is also informed by the advice and recommendations
received from the CASAC during its review of the draft PA, and by public comments received
on the draft document. The final PA is designed to help the Administrator in considering the
currently available scientific and risk information and formulating judgments regarding the
adequacy of the current primary standard.
3.1 APPROACH
Staffs approach in this review of the primary standard for SOx takes into consideration
the approaches used in the previous review. The past and current approaches described below are
both based, most fundamentally, on using the EPA's assessment of the current scientific
evidence and associated quantitative analyses to inform the Administrator's judgment regarding
a primary standard for SOx that is requisite to protect public health with an adequate margin of
safety. In reaching conclusions on options for the Administrator's consideration, we note that the
final decision to retain or revise the current SO2 primary standard is a public health policy
judgment to be made by the Administrator.
The final decision by the Administrator will draw upon the available scientific evidence
for S02-attributable health effects, and on quantitative analyses of population exposures and
health risks, including judgments about the appropriate weight to assign the various uncertainties
inherent in the evidence and analyses. Therefore, in developing conclusions in this PA, we are
mindful that the Administrator's judgments on the standard will reflect an interpretation of the
available scientific evidence and exposure/risk information in consideration of the strengths and
limitations of that evidence and information. Our general approach to informing these judgments,
discussed more fully below, recognizes that the available health effects evidence reflects a
continuum from relatively higher SO2 concentrations, at which scientists generally agree that
health effects are likely to occur, through lower concentrations at which the likelihood and
magnitude of a response become increasingly uncertain. This approach is consistent with the
requirements of sections 108 and 109 of the CAA, as well as with how the EPA and the courts
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have historically interpreted the Act. These provisions require the Administrator to establish
primary standards that in the Administrator's judgment are requisite to protect public health with
an adequate margin of safety. In so doing, the Administrator seeks to establish standards that are
neither more nor less stringent than necessary for this purpose. The Act does not require that
primary standards be set at a zero-risk level, but rather at a level that reduces risk sufficiently so
as to protect public health with an adequate margin of safety.1
Section 3.1.1 below summarizes the approach used in the last review of the primary
NAAQS for SOx and section 3.1.2 summarizes the general approach for the current review.
3.1.1 Approach in the Previous Review
The last review of the primary NAAQS for SOx was completed in 2010 and resulted in
substantial revisions to the standards (75 FR 35520, June 22, 2010). In consideration of the
evidence of respiratory effects in people with asthma in response to exposures as short as five
minutes, the EPA established a new short-term standard to provide increased protection for this
at-risk group and other potentially at-risk populations2 against an array of adverse respiratory
effects that have been linked to short-term SO2 exposures in both controlled human exposure and
epidemiologic studies (75 FR 35525-35526, June 22, 2010; 2008 ISA, section 5.5). Specifically,
the EPA replaced the then-existing 24-hour standard with a 1-hour standard of 75 ppb in terms of
the 3-year average of the 99th percentile of the yearly distribution of 1-hour daily maximum SO2
concentrations. In addition to replacing the 24-hour standard with a new 1-hour standard, the
EPA revoked the then-existing annual standard, based largely on the lack of sufficient health
evidence to support a long-term standard and a recognition that a 1-hour standard set at 75 ppb
would have the effect of generally maintaining annual SO2 concentrations well below the level of
the revoked annual standard (75 FR 35550, June 22, 2010).
The emphasis on short-term exposures of people with asthma reflected the health effects
evidence that has expanded in this area over the four decades since the then-existing 24-hour and
annual standards were set in 1971 (2008 ISA; U.S. EPA, 1982, 1986, 1994). A key element of
the expanded evidence base was a series of controlled human exposure studies which
1 The four basic elements of the NAAQS (indicator, averaging time, level and form) are considered collectively in
evaluating the health protection afforded by the current standard.
2 As used here and similarly throughout the document, the term population refers to persons having a quality or
characteristic in common, such as a specific pre-existing illness or a specific age or lifestage. A lifestage refers to
a distinguishable time frame in an individual's life characterized by unique and relatively stable behavioral and/or
physiological characteristics that are associated with development and growth. Identifying at-risk populations
includes consideration of intrinsic (e.g., genetic or developmental aspects) or acquired (e.g., disease or smoking
status) factors that increase the risk of health effects occurring with exposure to sulfur oxides as well as extrinsic,
nonbiological factors, such as those related to socioeconomic status, reduced access to health care, or exposure.
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documented bronchoconstriction-related effects on lung function in people with asthma exposed
while breathing at elevated rates3 for periods as short as five minutes. In the 2010 review, the
EPA also conducted quantitative analyses of air quality data, including 5-minute ambient air
measurements, and of potential exposures for people with asthma. Consideration of these key
aspects of the evidence and quantitative analyses informed the decision in the 2010 review,
which additionally addressed the court remand4 to the EPA of the EPA's 1996 decision to retain
the 1971 standards without revision.
The quantitative assessment for the review focused particularly on the issue of exposures
to SO2 in ambient air for a duration as short as five minutes (2008 ISA; 2009 REA). The
quantitative analyses documented in the REA included characterizations of the likelihood of
people with asthma being exposed (while breathing at elevated rates, such as associated with
many common outdoor activities) to concentrations of SO2 from ambient air of a magnitude
documented to elicit decrements in lung function (2009 REA). These analyses were performed
both for air quality conditions associated with just meeting the then-existing standards and for
conditions associated with just meeting potential alternative standards. The REA additionally
included air quality analyses that explored the extent to which potential alternative standards
with 1-hour, 24-hour, and annual averaging times might be expected to control 5-minute ambient
air concentrations (2009 REA, section 7.3). The quantitative assessments together with the health
effects evidence informed the policy options considered by the Administrator. Considerations,
conclusions and judgments by the Administrator that provided the basis for her decisions in the
2010 review are summarized below.
3.1.1.1 Considering the Need for Revision
The conclusions reached by the Administrator in the last review were based on the
extensive body of scientific evidence on S02-related health effects and quantitative analyses of
air quality, exposure and risk. In her conclusion on the adequacy of the then-existing standards,
which were set in 1971, the Administrator emphasized the evidence and quantitative analyses
concerning 5-minute exposures. The Administrator gave particular attention to the robust
evidence base, comprised of findings from controlled human exposure, epidemiologic, and
animal toxicological studies that collectively were judged "sufficient to infer a causal
3 The phrase "elevated ventilation" (or "moderate or greater exertion") was used in the 2009 REA and Federal
Register notices in the last review to refer to activity levels that in adults would be associated with ventilation
rates at or above 40 liters per minute; an equivalent ventilation rate was derived in order to identify corresponding
rates for the range of ages and sizes of the simulated populations (2009 REA, section 4.1.4.4). Accordingly, these
phrases are used in this draft PA when referring to the REA from the last review. Otherwise, however, the REA
and PA for this review generally use the phrase "elevated breathing rates" to refer to the same occurrence.
4 See Am. Lung Ass 'n v. EPA, 134 F.3d 388 (D.C. Cir. 1998) (remanding the 1996 decision to EPA).
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relationship" between short-term SO2 exposures ranging from 5 minutes to 24 hours and
respiratory morbidity (75 FR 35535, June 22, 2010). The "definitive evidence" for this
conclusion came from studies of 5- to 10-minute controlled exposures that reported respiratory
symptoms and decreased lung function in exercising individuals with asthma (2008 ISA, section
5.2). Supporting evidence was provided by epidemiologic studies of a broader range of
respiratory outcomes, with uncertainty noted about the magnitude of the study effect estimates,
quantification of the exposure concentration-response relationship, potential confounding by co-
pollutants, and other areas (75 FR 35535-35536, June 22, 2010; 2008 ISA, section 5.3).
In the controlled human exposure studies of exercising individuals with asthma, a dose-
response relationship was documented for bronchoconstriction-related effects, with both the
percentage of individuals affected and the severity of the response increasing with increasing
SO2 concentrations (75 FR 35525, June 22, 2010). The evidence from these studies documents
the occurrence of S02-related decrements in lung function based on reductions in forced
expiratory volume in one second (FEVi) and increases in specific resistance of the airways
(sRaw). Moderate5 or greater decrements in lung function were reported in response to short (5-
to 10-minute) exposures to concentrations as low as 200 to 300 ppb in approximately 5-30% of
exercising individuals with asthma. In response to exposures at or above 400 ppb, approximately
20-60% experienced such decrements, frequently accompanied by respiratory symptoms; in
many studies, responses at these concentrations were often statistically significant at the group
mean level6 (75 FR 35525-35526, June 22, 2010).
In reaching conclusions regarding the significance of the reported responses to the 5- to
10-minute controlled exposures, the Administrator considered guidelines from the American
Thoracic Society (ATS), the CASAC's written advice and recommendations, and judgments
made by the EPA in considering similar effects in previous NAAQS reviews (75 FR 35526 and
35536, June 22, 2010). Based on these considerations, the Administrator judged that the effects
reported in exercising people with asthma following 5- to 10-minute SO2 exposures at or above
5 In assessments for NAAQS reviews, the lung function responses described as indicative of a moderate functional
response include increases in sRaw of at least 100% (e.g., 2008 ISA; U.S. EPA, 1994, Table 8; U.S. EPA, 1996,
Table 8-3). The moderate category has also generally included reductions in FEVi 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 FEVi is also consistent with the relationship observed between sRaw and FEVi
responses in the Linn et al. studies for which "a 100% increase in sRaw roughly corresponds to a 12 to 15%
decrease in FEVi" (U.S. EPA, 1994, p. 20). Thus, in the 2008 review, moderate or greater SCh-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 FEVi (2008 ISA, p. 3-5).
6 At concentrations of 400 to 500 ppb, the 2008 ISA notes that the evidence shows "stronger evidence with some
statistically significant increases in respiratory symptoms," and at 600 ppb to 1 ppm, the 2008 ISA notes the
evidence to show "clear and consistent increases in SO2 induced respiratory symptoms" (2008 ISA, Table 3-1).
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200 ppb, especially at or above 400 ppb, can result in adverse health effects (75 FR 35536, June
22, 2010).7 In so doing, she recognized that effects reported for exposures below 400 ppb are
appreciably less severe than those at and above 400 ppb (75 FR 35547, June 22, 2010).
In applying the health effects evidence to her consideration of the adequacy of the then-
existing standards, the Administrator gave particular attention to the quantitative analyses that
evaluated the potential for exercising individuals with asthma to experience exposures of a
magnitude associated with adverse effects under air quality conditions that just met the then-
existing standards. In addition to comparison of 5-minute air concentrations in 40 U.S. counties
to 5-minute concentrations of potential concern (benchmark concentrations ranging from 100-
400 ppb), the analyses included a population exposure-based assessment in two study areas, St.
Louis, MO and Greene County, MO. Five-minute exposure concentrations were estimated for
people with asthma while breathing at elevated rates. The 5-minute exposure concentrations
were compared to benchmark concentrations, and also used to estimate the risk of lung function
decrements in simulated at-risk populations. Among these analyses, the Administrator
emphasized those that utilized the 5-minute benchmark concentrations that were derived from
the controlled human exposure evidence and ranged from 100 ppb to 400 ppb. Based on her
judgments regarding the significance of effects associated with 5-minute concentrations at or
above 200 ppb and 400 ppb, the Administrator considered results of comparisons of exposure
estimates to those benchmark concentrations to be particularly important, giving greater
emphasis to those at or above 400 ppb (75 FR 35547, June 22, 2010).
The exposure-based assessment estimated the portion of the population with asthma in
these two areas that would be expected to experience 5-minute exposures at or above 400 ppb
and 200 ppb while engaged in activities causing them to be breathing at elevated rates. The
Administrator particularly noted the exposure analysis results for the St. Louis case study. This
analysis estimated that for air quality simulated to just meet the then-existing standards,
substantial percentages of children with asthma would be exposed at least once annually, while
engaged in activities associated with moderate or greater exertion,8 to air quality exceeding the
200 ppb and 400 ppb 5-minute benchmarks (75 FR 35536, June 22, 2010). The Administrator
judged these 5-minute exposures to be significant from a public health perspective due to their
7 The 2010 decision notice additionally stated that "[t]he Administrator notes that although these decrements in lung
function have not been shown to be statistically significant at the group mean level, or to be frequently
accompanied by respiratory symptoms, she considers effects associated with exposures as low as 200 ppb to be
adverse in light of CASAC advice, similar conclusions in prior NAAQS reviews, and the ATS guidelines" (75 FR
35546, June 22, 2010).
8 In the 2009 REA, an equivalent ventilation rate of 22 L/min-m2 was identified as the minimum value to reflect
"moderate" or greater exertion that would correspond to the elevated ventilation rate for the exercising subjects in
the controlled human exposure studies, which was 40-50 L/min (2009 REA, p. 236).
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estimated frequency: approximately 24% of children with asthma in St. Louis were estimated to
be exposed while at moderate or greater exertion at least once per year to air quality exceeding
the 5-minute 400 ppb benchmark. Additionally, approximately 73% of children with asthma in
St. Louis at moderate or greater exertion were estimated to be exposed at least once per year to
air quality exceeding the 5-minute 200 ppb benchmark (75 FR 35536, June 22, 2010).
The Administrator also took note of the CASAC conclusion that the then-existing
standards did not adequately protect public health. Specifically, the CASAC advised that: "the
current 24-hour and annual standards are not adequate to protect public health, especially in
relation to short-term exposures to SO2 (5-10 minutes) by exercising asthmatics" (Samet, 2009,
p. 15). Based on all of the considerations summarized above, the Administrator concluded that
the then-existing 24-hour and annual primary standards were not providing the requisite
protection of public health with an adequate margin of safety. In considering approaches to
revising the standards, the Administrator concluded it to be appropriate to set a new standard that
would provide requisite protection with an adequate margin of safety to people with asthma at
elevated ventilation and that would afford protection from the adverse health effects of 5-minute
to 24-hour SO2 exposures (75 FR 35536, June 22, 2010).
3.1.1.2 Approach for Considering Revisions to the Standards
With regard to revisions to provide requisite public health protection, the Administrator
concluded it was appropriate to set a 1-hour SO2 standard at a level of 75 ppb based on the 3-
year average of the 99th percentile of the yearly distribution of 1-hour daily maximum
concentrations. The rationale and approach for selecting the 1-hour standard is presented below
in terms of the individual elements of a NAAQS: indicator, averaging time, form, and level.
3.1.1.2.1 Indicator
In reaching her decision on the indicator for the new standard, the Administrator
considered the conclusions of the ISA and REA, as well as advice from the CASAC and public
comments (75 FR 35536, June 22, 2010). The EPA continued to focus on SO2 as the most
appropriate indicator for sulfur oxides because the available scientific information regarding
health effects was overwhelmingly indexed by SO2. Although the presence of SOx species other
than SO2 in ambient air had been recognized, no alternative to SO2 had been advanced as a more
appropriate surrogate for SOx (75 FR 35536, June 22, 2010). Controlled human exposure studies
and animal toxicological studies provided specific evidence for health effects following
exposures to SO2, and epidemiologic studies typically analyzed associations of health outcomes
with concentrations of SO2. Based on the information available in the last review and consistent
with the views of the CASAC that "for indicator, SO2 is clearly the preferred choice" (Samet,
2009, p. 14), the Administrator concluded it was appropriate to continue to use SO2 as the
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indicator for a standard that was intended to address effects associated with exposure to SO2,
alone or in combination with other sulfur oxides (75 FR 35536, June 22, 2010). In so doing, the
EPA recognized that measures leading to reductions in population exposures to SO2 will also
likely reduce exposures to other sulfur oxides (75 FR 35536, June 22, 2010).
3.1.1.2.2 Averaging Time
With regard to the setting of the new standard, the Administrator agreed with the staff
conclusion, based on conclusions in the ISA, advice from the CASAC, and quantitative analyses,
that the standard should be set to provide protection from short-term exposures of 5 minutes to
24 hours (75 FR 35539, June 22, 2010). Based on air quality analyses presented in the REA, the
Administrator judged that the requisite protection from 5- to 10-minute exposure events could be
provided without having a standard with a 5-minute averaging time (75 FR 35539, June 22,
2010). She judged that a standard with a 5-minute averaging time would result in significant and
unnecessary instability in public health protection (75 FR 35539, June 22, 2010).9 Accordingly,
she considered other averaging times.
Results of air quality analyses in the REA suggested that a standard based on 24-hour
average SO2 concentrations would not likely be an effective or efficient approach for addressing
5-minute peak SO2 concentrations, likely over-controlling in some areas, while under-controlling
in others (2009 REA, section 10.5.2.2). In contrast, these analyses suggested that a 1-hour
averaging time would be more efficient and effective at limiting 5-minute peaks of SO2 (2009
REA, section 10.5.2.2.). Drawing on this information, the Administrator concluded that a 1-hour
standard, with the appropriate form and level, would be likely to substantially reduce 5- to 10-
minute peaks of SO2 that had been shown in controlled human exposure studies to result in
increased prevalence of respiratory symptoms and/or decrements in lung function in exercising
people with asthma (75 FR 35539, June 22, 2010). Further she found that a 1-hour standard
could substantially reduce the upper end of the distribution of SO2 concentrations in ambient air
that were more likely to be associated with respiratory outcomes (75 FR 35539, June 22, 2010).
The Administrator additionally took note of advice from the CASAC. The CASAC stated
that the REA had presented a "convincing rationale" for a 1-hour standard, and that "a one-hour
standard is the preferred averaging time" (Samet, 2009, pp. 15, 16). The CASAC further stated
that it was "in agreement with having a short-term standard and finds that the REA supports a
one-hour standard as protective of public health" (Samet, 2009, p. 1). Thus, in consideration of
the available information summarized here and the CASAC's advice, the Administrator
concluded that a 1-hour standard (given the appropriate level and form) was an appropriate
9 Such instability could reduce public health protection by disrupting an area's ongoing implementation plans and
associated control programs (75 FR 35537, June 22, 2010).
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means of controlling short-term exposures to SO2 ranging from 5 minutes to 24 hours (75 FR
35539, June 22, 2010).
3.1.1.2.3 Form
In considering the statistical form for the new short-term standard, the Administrator
judged that the form of the standard should reflect the health effects evidence presented in the
ISA that indicated that the percentage of people with asthma affected and the severity of the
response increased with increasing SO2 concentrations (75 FR 35541, June 22, 2010). She
additionally found it reasonable to consider stability (e.g., to avoid disruption of programs
implementing the standard and the related public health protections from those programs) as part
of her consideration of the form for the standard (75 FR 35541, June 22, 2010). In so doing, she
noted that a concentration-based form averaged over three years would likely be appreciably
more stable than a no-exceedance based form, which had been the form of the then-existing 24-
hour standard (75 FR 35541, June 22, 2010). The CASAC additionally stated that "[tjhere is
adequate information to justify the use of a concentration-based form averaged over 3 years"
(Samet, 2009, p. 16). In consideration of this information, the Administrator judged a
concentration-based form averaged over three years to be most appropriate (75 FR 35541, June
22, 2010).
In selecting a specific concentration-based form, the Administrator considered health
evidence from the ISA as well as air quality and exposure information from the REA. In so
doing, the Administrator concluded that the form of a new 1-hour standard should be especially
focused on limiting the upper end of the distribution of ambient SO2 concentrations (i.e., above
90th percentile SO2 concentrations) in order to provide protection with an adequate margin of
safety against effects reported in epidemiologic and controlled human exposure studies (75 FR
35541, June 22, 2010). The Administrator further noted, based on results of air quality and
exposure analyses in the REA, that a 99th percentile form was likely to be appreciably more
effective at limiting 5-minute peak exposures of concern than a 98th percentile form (75 FR
35541, June 22, 2010). Thus, the Administrator selected a 99th percentile form averaged over
three years (75 FR 35541, June 22, 2010).
3.1.1.2.4 Level
In selecting the level of a new 1-hour standard, the Administrator gave primary emphasis
to the body of health effects evidence assessed in the ISA. In so doing, she noted that the
controlled human exposure studies provided the most direct evidence of respiratory effects from
exposure to SO2. The Administrator drew on evidence from these studies in reaching judgments
on the magnitude of adverse respiratory effects and associated potential public health
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significance for the air quality exposure and risk analysis results of air quality scenarios
representing just meeting alternative levels for a new 1-hour standard.
In particular, the Administrator considered effects in exercising people with asthma after
5- to 10-minute exposures as low as 200 ppb to be adverse in light of the CAS AC advice on
relevance of these effects, conclusions on similar effects in prior NAAQS reviews, and ATS
guidelines (75 FR 35546, June 22, 2010; ATS, 1985, 2000). This judgment was based on several
findings from the controlled human exposures studies. Five- to 10-minute exposures to 400 ppb
or greater resulted in moderate or greater decrements in lung function in 20-60% of exercising
individuals with asthma. These decrements are often statistically significant at the group mean
level and frequently accompanied by respiratory symptoms. Thus, exposures to SO2
concentrations at or above 400 ppb were concluded to clearly result in adverse respiratory effects
based on the ATS guidelines (ATS, 1985). Further, 5- to 10-minute exposures to 200 to 300 ppb
resulted in moderate or greater decrements in lung function in 5-30% of exercising individuals
with asthma (75 FR 35546, June 22, 2010). Although such effects have not been shown to be
statistically significant at the full study group mean level,10 or to be frequently accompanied by
respiratory symptoms, the Administrator considered effects associated with exposures as low as
200 ppb to be adverse in light of the CASAC's advice11 and similar conclusions in prior reviews
as well as the ATS guidelines (ATS, 1985, 2000).
The Administrator then considered what the findings of the REA exposure analyses
indicated with regard to varying degrees of protection that different 1-hour standard levels might
be expected to provide against 5-minute exposures to concentrations of 200 ppb and 400 ppb.12
For example, the exposure assessment for St. Louis13 estimated that a 1-hour standard at 100 ppb
would likely protect more than 99% of children with asthma in that city from experiencing any
days in a year with at least one 5-minute exposure at or above 400 ppb while at moderate or
greater exertion, and approximately 97% of those children with asthma from experiencing any
days in a year with at least one exposure at or above 200 ppb while at moderate or greater
10 As summarized in section 3.2.1.1 below and described more fully in the ISA for the current review, study subjects
have since been described as falling into two subpopulations that differ in susceptibility to SO2. Thus, the extent
to which the more susceptible subpopulation is represented among the full study group may influence study mean
responses.
11 The CAS AC letter on the first draft SO2 REA to the Administrator stated: "CAS AC believes strongly that the
weight of clinical and epidemiology evidence indicates there are detectable clinically relevant health effects in
sensitive subpopulations down to a level at least as low as 0.2 ppm SO2" (Henderson, 2008).
12 The Administrator additionally noted the results of the 40-county analysis of limited available 5-minute
concentration data that indicated for a 1-hour standard level of 100 ppb a maximum annual average of two days
per year with 5-minute concentrations above 400 ppb and 13 days with 5-minute concentrations above 200 ppb
(76 FR 35546, June 22, 2010).
13 St. Louis was one of two study areas assessed in the REA (2009 REA).
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exertion (75 FR 35547, June 22, 2010). Results for the air quality scenario for a 1-hour standard
level of 50 ppb suggested that such a standard would somewhat further limit exposures, such that
more than 99% of children at moderate or greater exertion would likely be protected from
experiencing any days in a year with a 5-minute exposure at or above the 200 ppb benchmark
concentration (75 FR 35542-47, June 22, 2010).
In considering the implications of the exposure assessment results the Administrator
noted that although she considered the health effects resulting from 5-minute SO2 exposures as
low as 200 ppb to be adverse, she also recognized that such effects are appreciably less severe
than those at SO2 concentrations at or above 400 ppb and found little difference between the
results for standard levels of 50 and 100 ppb with regard to 5-minute exposures at or above 400
ppb (75 FR 35547, June 22, 2010). She recognized that a standard level below 100 ppb may
somewhat further limit 5-minute SO2 ambient air concentrations and exposures above 200 ppb,
although she did not judge that a standard level of 50 ppb was warranted.
Before reaching her conclusion with regard to level for the 1-hour standard, the
Administrator additionally considered the epidemiological evidence among the U.S.
epidemiologic studies (some conducted in multiple locations) reporting mostly positive and
sometimes statistically significant associations between ambient SO2 concentrations and
emergency department visits and hospital admissions. She noted there was a cluster of three
studies for which 99th percentile 1-hour daily maximum concentrations were estimated to be
between 78 and 150 ppb and for which the SO2 effect estimate remained positive and statistically
significant in copollutant models with particulate matter (PM) (75 FR 35547, June 22, 2010).14
Given the above considerations and the comments received on the proposal, the
Administrator determined that the appropriate judgment, based on the entire body of evidence
and information available in this review, and the related uncertainties,15 was a standard level of
75 ppb. She concluded that such a standard, with a 1-hour averaging time and 99th percentile
form, would provide a significant increase in public health protection compared to the then-
existing standards and would be expected to provide protection, with an adequate margin of
safety, against the respiratory effects that have been linked with SO2 exposures in both controlled
human exposure and epidemiologic studies. Specifically, she concluded that such a standard
would limit 1-hour exposures at and above 75 ppb. (75 FR 35548, June 22, 2010). Such a
14 Regarding the monitor concentrations in these studies, the EPA noted that although they may be a reasonable
approximation of concentrations occurring in the areas, the monitored concentrations were likely somewhat lower
than the absolute highest 99th percentile 1-hour daily maximum SO2 concentrations occurring across these areas
(75 FR 35547, June 22, 2010).
15 Such uncertainties included both those with regard to the epidemiologic evidence and also those with regard to the
information from controlled human exposure studies for at-risk groups, including representation of individuals
with more severe asthma than that in study subjects (75 FR 35546, June 22, 2010).
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standard was also considered likely "to maintain SO2 concentrations below those in locations
where key U.S. epidemiologic studies have reported that ambient SO2 is associated with clearly
adverse respiratory health effects, as indicated by increased hospital admissions and emergency
department visits." The Administrator also found that "a 1-hour standard at a level of 75 ppb is
expected to substantially limit asthmatics' exposure to 5-10 minute SO2 concentrations > 200
ppb, thereby substantially limiting the adverse health effects associated with such exposures."
Lastly, the Administrator noted "that a standard level of 75 ppb is consistent with the consensus
recommendation of CASAC." The Administrator also considered the likelihood of public health
benefits at lower standard levels, and judged a 1-hour standard at 75 ppb to be sufficient to
protect public health with an adequate margin of safety (75 FR 35547-35548, June 22, 2010).
This judgment included consideration of the appropriate degree of protection with an
adequate margin of safety for populations at increased risk for adverse respiratory effects from
short-term exposures to SO2 for which the evidence supports a causal relationship with SO2
exposures. In reaching these conclusions, the Administrator considered the requirement for a
standard that is neither more nor less stringent than necessary for this purpose and recognized
that the CAA does not require that primary NAAQS be set at a zero-risk level or to protect the
most susceptible individual, but rather at a level that reduces risk sufficiently so as to protect
public health with an adequate margin of safety (75 FR 35548, June 22, 2010).
3.1.1.2.5 Revoking the Then-Existing 24-Hour and Annual Standards
In addition to setting a new 1-hour standard at 75 ppb, the then-existing 24-hour and
annual standards were revoked based largely on the recognition that a 1-hour standard set at 75
ppb would have the effect of generally maintaining 24-hour and annual SO2 concentrations well
below the levels of those standards (75 FR 35550, June 22, 2010). In addition, with regard to the
annual standard, there was a lack of evidence supporting a relationship between long-term SO2
exposures and adverse health effects. That is, the 2008 ISA judged the health evidence linking
long-term SO2 exposure to adverse health effects to be "inadequate" to infer the presence or
absence of a causal relationship (75 FR 35550, June 22, 2010; 2008 ISA, section 5.5).
3.1.2 Approach for the Current Review
For evaluation in the current review of whether it is appropriate to consider retaining the
current SO2 primary standard, or whether consideration of revision is appropriate, we have
adopted an approach that builds on the general approach used in the last review and reflects the
body of evidence and information now available. As summarized above, the Administrator's
decisions in the prior review were based on an integration of information on health effects
associated with exposure to SO2, expert judgments on the adversity and public health
significance of key health effects, air quality and related analyses and quantitative exposure and
3-11
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risk assessments, and policy judgments as to when the standard is requisite to protect public
health with an adequate margin of safety.
In conducting this assessment, we draw on the current evidence and quantitative
assessments of exposure pertaining to the public health risk of SO2 in ambient air. In considering
the scientific and technical information, we consider both the information available at the time of
the last review and information newly available since the last review, including the ISA and REA
for this review. Figure 3-1 below illustrates the basic construct of our two-part approach in
developing conclusions regarding options to consider with regard to the adequacy of the current
primary standard. In the boxes of Figure 3-1, the range of questions that we consider in sections
3.2.1 and 3.2.2 below are represented by a summary of policy-relevant questions that frame our
consideration of the scientific evidence and quantitative analyses.
3-12
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Adequacy of Current Standard
Does information
call into question
adequacy of current
standard?
Consider Retaining
Current Standard
NO
YES
Consider Potential Alternative Standards
Elements of Potential Alternative Standards
/-Indicator
/'Averaging Time
/-Form
/-Level
Exposure- and Risk-Based Considerations
/-Nature, magnitude, and importance of
estimated exposures and risks associated
with just meeting the current standard?
/-Uncertainties in the exposure and risk
estimates?
/-Does currently available evidence and related
uncertainties strengthen or call into question prior
conclusions?
ป Evidence of health effects not previously
identified?
ฆ Newly identified at-risk populations?
ฆ Evidence of health effects at lower levels or for
different exposure durations?
ป Uncertainties identified in the last review
reduced or new uncertainties emerged?
<-Does newly available information call into question
any of the basic elements of the standard?
Evidence-Based Considerations
c Potential Alternative Standards for Consideration J)
1*
Figure 3-1. Overview of the approach for review of the current primary standard.
3-13
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3.2 ADEQUACY OF THE CURRENT STANDARD
In considering the adequacy of the current SO2 primary standard, the overarching
question we consider is:
Does the currently available scientific evidence- and exposure/risk-based
information, as reflected in the ISA and REA, support or call into question the
adequacy of the protection afforded by the current SO2 primary standard?
To assist us in interpreting the currently available scientific evidence and the results of
recent quantitative exposure/risk analyses to address this question, we have focused on a series
of more specific questions, as detailed in sections 3.2.1 and 3.2.2 below. In considering the
scientific and technical information, we consider both the information available at the time of the
last review and information newly available since the last review which have been critically
analyzed and characterized in the 2008 ISA for the last review and the ISA for the current
review. In so doing, a primary consideration is whether the information newly available in this
review alters our overall conclusions from the last review regarding health effects associated
with SOx in ambient air.
3.2.1 Evidence-based Considerations
In considering the evidence with regard to the overarching question posed above
regarding the adequacy of the current standard, we address a series of more specific questions
that focus on policy-relevant aspects of the evidence. These questions begin with consideration
of the available evidence on health effects associated with exposure to SOx, and particularly SO2
(section 3.2.1.1). The subsequent questions consider identification of populations at-risk of SO2-
related health effects (section 3.2.1.2), and the exposure durations and levels of SO2 associated
with health effects (section 3.2.1.3). Important uncertainties associated with the evidence are
considered in section 3.2.1.4 and public health implications are discussed in section 3.2.1.5.
3.2.1.1 Health Effects Associated with Exposure to SOx
Among the species of SOx (a group of closely related gaseous compounds including SO2
and SO3), SO2 is the most commonly occurring in the atmosphere and the one most clearly
associated with human health effects. Accordingly, the large body of scientific evidence has over
the past reviews been predominantly focused on exposures to SO2.
Is there newly available evidence that indicates the importance of SOx other than
SO2 with regard to abundance in ambient air, and potential for human exposures
and health effects?
As in the last review, the health effects evidence evaluated in the ISA for SOx is focused
on SO2 (ISA, p. 5-1). This is consistent with the conclusion that "[o]f the sulfur oxides, SO2 is
the most abundant in the atmosphere, the most important in atmospheric chemistry, and the one
3-14
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most clearly linked to human health effects" (ISA, p. 2-1). With regard to SO3, it "is known to be
present in the emissions of coal-fired power plants, factories, and refineries, but it reacts with
water vapor in the stacks or immediately after release into the atmosphere to form H2SO4" and
"gas-phase H2SO4.. .quickly condenses onto existing atmospheric particles or participates in new
particle formation" (ISA, section 2.3). Thus, the ISA states that "only SO2 is present at
concentrations in the gas phase that are relevant for chemistry in the atmospheric boundary layer
and troposphere, and for human exposures" (ISA, p. 2-18), and also that the available health
evidence for SOx is focused on SO2 (ISA, p. 5-1). Thus, we conclude that the current evidence,
including that newly available in this review, continues to support a focus on SO2 in considering
the adequacy of public health protection provided by the primary NAAQS for SOx.
Does the current evidence alter our conclusions from the previous review regarding
the health effects associated with exposure to SO2?
Rather than altering our conclusions from the last review, the current evidence continues
to support our prior conclusions regarding the key health effects associated with SO2 exposure.
Specifically, the full body of evidence continues to support the conclusion that short-term SO2
exposures of durations as short as a few minutes are causally related to respiratory effects in at-
risk individuals (ISA, section 5.2.1.9). With regard to respiratory effects and long-term
exposures,16 as well as total mortality and short-term exposures, the evidence available in this
review is "suggestive of, but not sufficient to infer," a causal relationship (ISA, sections 5.2.2.7
and 5.5.1.6). The evidence is inadequate for reaching conclusions regarding causality for other
categories of effects (ISA, section 1.6.2).17
Respiratory Effects
As in the last review, the currently available evidence in this review supports the
conclusion that there is a causal relationship between short-term SO2 exposure and respiratory
effects, particularly in individuals with asthma (ISA, p. 1-17).18 The clearest evidence for this
conclusion comes from controlled human exposure studies available at the time of the previous
16 In evaluating the health effects studies in the ISA, the EPA has generally categorized exposures of durations
longer than a month to be "long-term" (ISA, p. 1-2).
17 Based on the currently available evidence, the ISA concluded that the evidence was inadequate to infer the
presence or absence of a causal relationship between SO2 exposures and reproductive and developmental effects;
between long-term SO2 exposures and mortality or cancer; and, between short- or long-term SO2 exposures and
cardiovascular effects (ISA, section 1.6.2).
18 While effects have been documented for short (5- to 10- minute) exposures lower than 1.0 ppm in controlled
exposure studies of individuals with asthma, the exposure concentrations consistently eliciting effects in study
subjects without asthma are higher. Such exposures are generally above 1.0, with most studies reporting no
respiratory symptoms at concentrations up to 2.0 ppm (ISA, section 5.2.1.7, pp. 116-117, 132-133).
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review and included in the 2008 ISA. These studies demonstrate asthma exacerbation-related
lung function decrements19 and respiratory symptoms in people with asthma exposed to SO2 for
5 to 10 minutes at elevated breathing rates (ISA, section 5.2.1). The epidemiologic evidence,
including recent evidence not available at the time of the previous review, includes studies
reporting positive associations for asthma-related hospital admissions and emergency department
visits with short-term SO2 exposures (ISA, section 5.2.1). These findings are generally
supportive of the causal relationship conclusion for which the controlled exposure studies are the
primary basis (ISA, section 5.2.1.9).
Sulfur dioxide is a highly reactive and water-soluble gas that once inhaled is absorbed
almost entirely in the upper respiratory tract20 (ISA, sections 4.2 and 4.3). Under conditions of
elevated breathing rates (e.g., while exercising), SO2 penetrates into the tracheobronchial
region,21 where it may contribute to responses linked to asthma exacerbation in individuals with
asthma (ISA, sections 4.2, 4.3 and 5.2). More specifically, bronchoconstriction, which is
characteristic of an asthma attack, is the most sensitive indicator of S02-induced lung function
effects. Associated with this bronchoconstriction response is an increase in airway resistance
which is an index of airway hyperresponsiveness (AHR)22 Exercising individuals without
asthma have also been found to exhibit such responses, but at much higher SO2 exposure
concentrations, above 1000 ppb (ISA, section 1.5.2).
Bronchoconstriction, evidenced by decrements in lung function, is observed in controlled
human exposure studies in response to exposures as short as 5- to 10-minutes and can occur at
SO2 concentrations as low as 200 ppb in some people with asthma exposed while breathing at
elevated rates, such as during exercise (ISA, section 5.2.1.2).23 More consistent decrements in
lung function are seen in such individuals with asthma following exposures to 400 ppb and
greater (ISA, section 5.2.1.2). In contrast, respiratory effects are not observed in other people
with asthma (nonresponders) and healthy adults exposed while exercising to SO2 concentrations
19 The specific responses reported in the evidence base that are described in the ISA as lung function decrements are
increased specific airway resistance (sRaw) and reduced forced expiratory volume in 1 second (FEVi) (ISA,
section 5.2.1.2).
20 The term "upper respiratory tract" refers to the portion of the respiratory tract, including the nose, mouth and
larynx, that precedes the tracheobronchial region (ISA, sections 4.2 and 4.3).
21 The term "tracheobronchial region" refers to the region of the respiratory tract subsequent to the larynx and
preceding the deep lung (or alveoli). This region includes the trachea and bronchii.
22 Airway hyperresponsiveness, which is an increased propensity of the airways to narrow in response to
bronchoconstrictive stimuli, is a characteristic feature of people with asthma (ISA, section 5.2.1.2).
23 The data from controlled human exposure studies of people with asthma indicate there to be two subpopulations
that differ in their airway responsiveness to SO2, with the second subpopulation being insensitive to SO2
bronchoconstrictive effects at concentrations as high as 1.0 ppm (ISA, pp. 5-14 to 5-21; Johns et al., 2010).
3-16
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below 1000 ppb (ISA, sections 5.2.1.2 and 5.2.1.7). Across studies, bronchoconstriction in
response to SO2 exposure is mainly seen during conditions of elevated breathing rates, such as
exercise or laboratory-facilitated rapid, deep breathing.24 These conditions lead to a shift from
nasal breathing to oral/nasal breathing, which increases the concentration of SO2 reaching the
tracheobronchial region of lower airways, where depending on dose and the exposed individual's
susceptibility, it may cause bronchoconstriction (ISA, sections 4.1.2.2, 4.2.2 and 5.2.1.2).
The evidence base of controlled human exposure studies for people with asthma is the
same in this review as in the last review. Such studies reporting asthma exacerbation-related
effects for individuals with asthma are summarized in Tables 5-1 and 5-2, and section 5.2.1.2 of
the ISA. The main responses observed include increases in specific airway resistance (sRaw) and
reductions in forced expiratory volume in one second (FEVi) after 5- to 10-minute exposures. As
in the last review, the ISA in this review quantifies the percentage of exposed study subjects with
at least 100%, 200% or 300% increases in sRaw (i.e., a doubling, tripling or greater increase) and
also those with at least 15%, 20% or 30% reduction in FEVi. As recognized in the last review,
the results of these studies indicate that among individuals with asthma, some individuals have a
greater response to SO2 than others or a measurable response at lower exposure concentrations
(ISA, p. 5-14). The S02-induced bronchoconstriction in these studies occurs rapidly, in as little
as two minutes from exposure start, and is transient, with recovery following cessation of
exposure (ISA, p. 5-14).
The studies of subjects with asthma breathing at elevated rates have found effects to
become more pronounced with increased exposure concentrations. Among individuals with
asthma, both the percentage of individuals affected and the severity of the response increases
with increasing SO2 concentrations. For example, at concentrations ranging from 200 to 300 ppb,
as many as 5 to 30% of exercising study subjects with asthma experienced moderate25 or greater
decrements in lung function (ISA, Table 5-2). At concentrations at or above 400 ppb, moderate
or greater decrements in lung function occurred in 20 to 60% of exercising study subjects with
asthma, and compared to exposures at 200 to 300 ppb, a larger percentage of subjects
experienced severe decrements in lung function (i.e., an increase in sRaw of at least 200%,
and/or a reduction in FEVi of at least 20%) (ISA, Table 5-2). Moreover, at the higher SO2
concentrations, moderate or greater decrements in lung function were frequently accompanied by
24 In the laboratory, study subjects perform this rapid, deep breathing through a mouthpiece that provides a mixture
of oxygen with enough carbon dioxide to prevent the imbalance of gases in the blood usually resulting from
hyperventilation. Breathing in the laboratory with this technique is referred to as eucapnic hyperpnea.
25 As in the last review (described in section 3.1.1.1 above), the IS A describes moderate or greater lung function
decrements as the occurrence of at least a doubling in sRaw or at least a 15% reduction in FEVi (ISA, section
1.6.1.1).
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respiratory symptoms, such as cough, wheeze, chest tightness, or shortness of breath (ISA, Table
5-2).
With regard to newly available epidemiological studies, there are a limited number of
such studies that have investigated SO2 effects related to asthma exacerbation, with the most
cohesive evidence coming from studies on asthma-related emergency department (ED) visits
(ISA, section 5.2.1.2). As in the last review, areas of uncertainty in the epidemiologic evidence
relate to the characterization of exposure through the use of fixed site monitor concentrations as
surrogates for population exposure (often over a substantially sized area and for durations greater
than an hour) and the potential for confounding by PM26 or other copollutants (ISA, section
5.2.1). In general, the pattern of associations across the newly available studies is consistent with
the studies available in the last review (ISA, p. 5-75).
As in the last review, the evidence base for short-term SO2 exposures and respiratory
effects other than asthma exacerbation is limited and inconsistent (ISA, sections 5.2.1.3-5.2.1.8,
p. 5-155). The ISA finds the evidence for an effect of SO2 exposure on allergy exacerbation,
COPD exacerbation, respiratory infection, respiratory effects in healthy populations, and
respiratory mortality to be inconsistent within and across disciplines and outcomes and/or
lacking in biological plausibility (ISA, p. 5-155). Additional uncertainty associated with the
epidemiological evidence for these endpoints is related to potential confounding by copollutants
(ISA, section 5.2.1.9, p. 5-155).
The evidence base for long-term SO2 exposure and respiratory effects is somewhat
augmented since the last review such that the ISA in the current review concludes it to be
suggestive of, but not sufficient to infer, a causal relationship (ISA, section 5.2.2). The support
for this conclusion comes mainly from the limited epidemiological study findings of associations
between long-term SO2 concentrations and increases in asthma incidence combined with
findings of laboratory animal studies involving newborn rodents that indicate a potential for SO2
exposure to contribute to the development of asthma, especially allergic asthma, in children
(ISA, section 1.6.1.2). For example, the evidence showing increases in asthma incidence is
coherent with results of animal toxicological studies that provide a pathophysiologic basis for the
development of asthma. The overall body of evidence, however, lacks consistency (ISA, section
1.6.1.2). Further there are uncertainties, discussed in section 3.2.1.4 below, that apply to the
epidemiologic evidence, including that newly available, across the respiratory effects examined
for long-term SO2 exposure (ISA, section 5.2.2.7).
26 The potential for confounding by PM is of particular interest given that SO2 is a precursor to PM (ISA, p. 1-7).
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Other Health Effects
For effects other than respiratory effects, the current evidence is generally similar to the
evidence available in the last review, and leads to similar conclusions. With regard to a
relationship between short-term SO2 exposure and total mortality, the ISA reaches the same
conclusion as in the previous review that the evidence is suggestive of, but not sufficient to infer,
a causal relationship (ISA, section 5.5.1). This conclusion is based on previously available and
recent multicity epidemiologic studies providing consistent evidence of positive associations
coupled with uncertainty regarding the potential for SO2 to have an independent effect on
mortality. While recent studies have analyzed some key uncertainties and data gaps from the
previous review, uncertainties still exist, given the limited number of studies that examined
copollutant confounding, the evidence for a decrease in the size of S02-mortality associations in
copollutant models with NO2 and PM10, and the lack of a potential biological mechanism for
mortality following short-term SO2 exposures (ISA, section 1.6.2.4).
For other categories of health effects,27 the evidence is inadequate to infer the presence or
absence of a causal relationship, mainly due to inconsistent evidence across specific outcomes
and uncertainties regarding exposure measurement error, copollutant confounding, and potential
modes of action (ISA, sections 5.3.1, 5.3.2, 5.4, 5.5.2, 5.6). These conclusions are consistent with
those made in the previous review.
In summary, rather than altering our conclusions from the previous review, the current
evidence provides continued support for our previous conclusions regarding the health effects
associated with exposure to SO2 and most particularly respiratory effects following short-term
SO2 exposure, particularly in individuals with asthma. Accordingly, as in prior reviews, this
review gives primary focus to those effects most pertinent to exposures related to current
concentrations in ambient air, in particular, asthma exacerbation in individuals with asthma.
3.2.1.2 Populations At-Risk of SCh-Related Health Effects
Populations or lifestages can be at increased risk of an air pollutant-related health effect
due to one or more of a number of factors. These factors can be intrinsic, such as physiological
factors that may influence the internal dose or toxicity of a pollutant, or extrinsic, such as
sociodemographic, or behavioral factors (ISA, p. 6-1). The questions considered in this section
address what the currently available evidence indicates regarding which populations are
particularly at risk of health effects related to exposure to SO2 in ambient air.
27 The other categories evaluated in the ISA include cardiovascular effects with short or long term exposures;
reproductive and developmental effects; and cancer and total mortality with long-term exposure (ISA, Table 1-1).
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Does the current evidence alter our understanding of populations that are
particularly at-risk from SO2 exposures? Is there new evidence that suggests
additional at-risk populations that should be given increased focus in this review?
The currently available evidence continues to support our primary conclusions from the
previous review that people with asthma are at increased risk for S02-related health effects,
specifically for respiratory effects, and specifically asthma exacerbation, associated with short-
term exposures while breathing at elevated rates (ISA, sections 5.2.1.2 and 6.3.1). This
conclusion of the at-risk status of people with asthma is based on the well-established and well-
characterized evidence from controlled human exposure studies, supported by the evidence on
mode of action for SO2 and with limited additional support from epidemiologic studies (ISA,
sections 5.2.1.2 and 6.3.1). Somewhat similar to the conclusion in the last review that children
and older adults are potentially susceptible populations, the ISA (relying on a framework that is
new in this review for evaluating the evidence for risk factors) indicates the evidence to be
suggestive of increased risk for these groups, with some limitations and inconsistencies (ISA,
sections 6.5.1.1 and 6.5.1.2).28
Further, the ISA finds that children with asthma may be particularly at risk compared to
adults with asthma (ISA, section 6.3.1). This conclusion reflects several characteristics of
children as compared to adults, which include their greater responsiveness to methacholine,29 a
chemical that can elicit bronchoconstriction in people with asthma, as well as their greater use of
oral breathing, particularly by boys (ISA, sections 5.2.1.2 and 4.1.2). Oral breathing (vs. nasal
breathing) and increased breathing rate are factors that allow for greater SO2 penetration into the
tracheobronchial region of the lower airways, and reflect conditions of individuals with asthma
in which bronchoconstriction-related responses have been observed in the controlled exposure
studies (ISA, sections 4.2.2, 5.2.1.2 and 6.3.1).
We additionally recognize the well-documented finding that some individuals with
asthma have a greater response to SO2 than others with similar disease status (ISA, section
28 The current evidence for risk to older adults relative to other lifestages comes from epidemiological studies, for
which the findings are somewhat inconsistent, and studies for which there are uncertainties in the association with
the health outcome (ISA, section 6.5.1.2).
29 The ISA concluded that potential differences in airway responsiveness of children to SO2 relative to adolescents
and adults may be inferred by the responses to methacholine (ISA, section 5.2.1.2). Methacholine is a chemical
that can elicit bronchoconstriction through its action on airway smooth muscle receptors. It is commonly used to
identify people with asthma and accordingly has been used to screen subjects for studies of SO2 effects. However,
results of studies of the extent to which airway response to methacholine is predictive of SO2 responsiveness have
varied somewhat. For example, an analysis of the extent to which airway responsiveness to methacholine, a
history of respiratory symptoms, and atopy were significant predictors of airway responsiveness to SO2, found
that about 20 to 25% of subjects ranging in age from 20 to 44 years that were hyperresponsive to methacholine
were also hyperresponsive to SO2 (ISA, section 5.2.1.2; Nowak et al., 1997). Another study focused on
individuals with airway responsiveness to methacholine found only a weak correlation between airway
responsiveness to SO2 and methacholine (ISA, section 5.2.1.2; Horstman et al., 1986).
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5.2.1.2; Horstman et al., 1986; Johns et al., 2010). This occurrence is quantitatively analyzed in a
study newly available in this review. This study uses the available individual subject data from
five studies involving exposure of individuals with asthma to multiple concentrations of SO2 for
5 to 10 minutes while breathing at elevated rates to examine the differences in lung function
response (Johns et al., 2010). As noted in the ISA, "these data demonstrate a bimodal distribution
of airway responsiveness to SO2 in individuals with asthma, with one subpopulation that is
insensitive to the bronchoconstrictive effects of SO2 even at concentrations as high as 1.0 ppm,
and another subpopulation that has an increased risk for bronchoconstriction at low
concentrations of SO2" (ISA, p. 5-20). To date, the characteristics that may define the
subpopulation of responders have not been identified. The current evidence for factors other than
those discussed above (asthma status and lifestage) is inadequate to determine whether they
might contribute to an increased risk of S02-related effects (ISA, section 6.6).
3.2.1.3 Exposure Concentrations Associated with Health Effects
At the time of the last review, the EPA's conclusions regarding concentrations of SO2
associated with respiratory effects were based primarily on the strong evidence base of
controlled human exposure studies of individuals with asthma. These studies have documented
bronchoconstriction-related moderate or greater decrements in lung function following 5- to 10-
minute exposures during exercise. The severity of observed responses, the percentage of
individuals responding, statistical significance at the study group level and the accompanying
occurrence of respiratory symptoms have been found to increase with increasing exposure
concentration (75 FR 35526, June 22, 2010). This information was critical in the REA analyses
in the last review, the results of which were a primary consideration in reaching a conclusion on
the level for the 2010 standard.
Does the current evidence alter our conclusions from the previous review regarding
the exposure duration and concentrations associated with health effects?
Our understanding of exposure duration and concentrations associated with S02-related
health effects is largely based, as it was in the last review, on the longstanding evidence base of
controlled human exposure studies that demonstrates a dose-response relationship between 5-
and 10-minute SO2 exposure concentrations and decrements in lung function (e.g., increased
sRaw and reduced FEVi) in individuals with asthma exposed while breathing at elevated rates
(ISA, section 1.6.1.1). At the higher concentrations, there are clear and consistent increases in
S02-induced respiratory symptoms (ISA, Table 5-2 and pp. 5-35, 5-39).
The available and well characterized evidence documents an effect of short-term
exposures on the respiratory system. As summarized in section 3.2.1.1, S02-induced
bronchoconstriction occurs rapidly in responding study subjects with asthma exposed for just a
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few minutes while breathing at elevated rates (ISA, section 5.2.1.2). Additionally, exposures as
short as 5 minutes have been found to elicit a similar bronchoconstrictive response at somewhat
longer exposures. For example, during exposure to SO2 over a 30-minute period with continuous
exercise, the response to SO2 has been found to develop rapidly and is maintained throughout the
30-minute exposure (ISA, p. 5-14). In a study involving short exercise periods within a 6-hour
exposure period, the effects observed following exercise were documented to return to baseline
levels within one hour after the cessation of exercise, even with continued exposure (Linn et al.,
1984). In considering the epidemiological evidence with regard to the question of exposure
duration, while we note the associations of asthma-related emergency room visits and hospital
admissions with 1-hour to 24-hour ambient air concentration metrics, we recognize that current
methods are not able to address whether these associations are indicative of a potential response
to exposure on the order of hours or much shorter-term exposure to peaks in SO2 concentration.
As noted in the ISA, the air quality metrics in the epidemiological studies are for time periods
longer than the 5- to 10-minute exposures eliciting effects in the controlled human exposure
studies and also may not adequately capture the spatial and temporal variation in SO2
concentrations (ISA, pp. 5-49, 5-59, 5-25).
With regard to the evidence for exposure concentrations eliciting effects, we focus
primarily on the controlled human exposure study findings for which data are available to the
EPA for individual subjects with asthma that were exposed while breathing at elevated rates,
summarized in Table 3-1 (ISA, Table 5-2).30 These data demonstrate that SO2 concentrations as
low as 200 to 300 ppb for 5 to 10 minutes elicited moderate or greater bronchoconstriction,
measured as a decrease in FEVi of at least 15% or an increase in sRaw of at least 100%, in a
subset of the subjects (ISA, section 5.2.1). Both the percent of individuals affected and the
severity of response increased with increasing SO2 concentrations. At concentrations ranging
from 200 to 300 ppb, the lowest levels for which there are study results that provide for
assessment of the S02-related effect independent of any effect of exercise in clean air, 5 to 30%
of exercising individuals with asthma experienced moderate or greater decrements in lung
function (ISA, section 5.2.1). At concentrations at or above 400 ppb, moderate or greater
decrements in lung function occurred in 20 to 60% of exercising individuals with asthma and a
larger percentage of individuals with asthma experienced more severe decrements in lung
function (i.e., an increase in sRaw of at least 200%, and/or a 20% or more decrease in FEVi),
compared to exposures at 200 to 300 ppb (ISA, section 5.2.1). Additionally, at concentrations at
or above 400 ppb, moderate or greater decrements in lung function were frequently accompanied
30 The findings summarized in Table 5-2 of the ISA and in Table 3-1 of this PA are based on results that have been
adjusted for effects at exercise in clean air so that they have separated out any effect of exercise in causing
bronchoconstriction and reflect the SCh-specific effect.
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by respiratory symptoms, with some of these findings reaching statistical significance (ISA,
section 5.2.1).
3-23
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Table 3-1. Percentage of adults with asthma in controlled human exposure studies experiencing sulfur dioxide-induced
decrements in lung function and respiratory symptoms.
Percentage of Responders
(Number of Subjects)3
so2
Cone
Exposure
Duration
Ventil-
ation
sRaw
>100%
>200% t
>300%
(ppm)
(min)
N
(L/min)
FEVi
>15% s|/
>20% *
>30% s|/
Study
0.2
5
23
-48
sRaw
9% (2)b
0
0
Linn et al. (1983b)
10
40
-40
sRaw
7.5% (3)c
2.5% (1)c
oc
Linn et al. (1987)c
10
40
-40
FEVi
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 etal. (1985)
5
9
-80-90
sRaw
22% (2)
0
0
10
27
-42
sRaw
0
0
0
Horstman et al. (1986)
10
28
-40
sRaw
4% (1)
0
0
Roger et al. (1985)
0.3
10
20
-50
sRaw
10% (2)
5% (1)
5% (1)
Linn et al. (1988)d
10
21
-50
sRaw
33% (7)
10% (2)
0
Linn et al. (1990)d
10
20
-50
FEVi
15% (3)
0
0
Linn et al. (1988)
10
21
-50
FEVi
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)
10
40
-40
sRaw
24% (9.5)c
9% (3.5)c
4% (1.5)c
Linn et al. (1987)ฐ
10
40
-40
FEVi
27.5% (11 )c
17.5% (7)c
10% (4)c
Linn et al. (1987)ฐ
0.5
5
10
-50-60
sRaw
60% (6)
40% (4)
20% (2)
Bethel etal. (1983)
10
27
-42
sRaw
22.2% (6)
3.7% (1)
11% (3)
Horstman et al. (1986)
10
28
-40
sRaw
18% (5)
4% (1)
4% (1)
Roger et al. (1985)
Respiratory Symptoms:
Supporting Studies
Limited evidence of SC>2-induced
increases in respiratory
symptoms in some people with
asthma: Linn etal., 1983b; Linn
etal., 1987; Linn et al., 1988;
Linn et al. 1990; Schachter et al.,
1984
Stronger evidence with some
ฆ statistically significant increases
in respiratory symptoms: Balmes
ฆetal., 1987;fGong etal., 1995 ;
Linn et al., 1983b; Linn et al.,
1987 ; Roger et al., 1985
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Percentage of Responders
(Number of Subjects)3
so2
Cone
Exposure
Duration
Ventil-
ation
sRaw
>100%
>200% t
>300%
(ppm)
(min)
N
(L/min)
FEVi
>15% si/
>20% *
>30% s|/
Study
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)
10
40
-40
sRaw
34% (13.5)c
24% (9.5)c
19% (7.5)c
Linn et al. (1987)c
10
20
-50
sRaw
60% (12)
35% (7)
10% (2)
Linn et al. (1988)
10
21
-50
sRaw
62% (13)
29% (6)
14% (3)
Linn et al. (1990)
10
40
-40
FEVi
47.5% (19)c
39% (15.5)c
17.5% (7)c
Linn et al. (1987)ฐ
10
20
-50
FEVi
55% (11)
55% (11)
5% (1)
Linn et al. (1988)
10
21
-50
FEVi
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)
Respiratory Symptoms:
Supporting Studies
Clear and consistent increases in
ฆ S02-induced respiratory
symptoms: Gong et al., 1995;
ฆ Horstman et al., 1988; Linn et al.,
1983b; Linn et al., 1987; Linn et
ฆal., 1988; Linn et al., 1990
Cone = concentration; FE\A| = forced expiratory volume in 1 sec; sRaw = specific airway resistance; S02 = sulfur dioxide.
This table is adapted from ISA Table 5-2. Information in Horstman et al (1986) is an addition (ISA, pp. 5-14 and 5-19).
aData presented from all references from which individual data were available in the published paper or were provided to EPA (Johns, 2009; Johns and Simmons, 2009; Smith,
1993). Percentage of individuals who experienced greater than or equal to a 100, 200, or 300% increase in specific airway resistance, or a 15, 20, or 30% decrease in FEV-i. Lung
function decrements are adjusted for the effects of exercise in clean air (calculated as the difference between the percent change relative to baseline with exercise/S02 and the
percent change relative to baseline with exercise/clean air).
bNumbers in parenthesis represent the number of subjects experiencing the indicated effect.
ฐResponses of people with mild and moderate asthma reported in Linn et al. (1987) have been combined. Data are the average of the first and second round exposure responses
following the first 10 min period of exercise. In some cases, the average had a first decimal place value of 5, which is reported in the table to avoid a high bias in values due to
rounding. In all other cases, the calculated percentages were rounded to the nearest integer.
dAnalysis includes data from only people with mild (Linn et al., 1988) and moderate (Linn et al., 1990) asthma who were not receiving supplemental medication.
eOne subject was not exposed to 1 ppm due to excessive wheezing and chest tightness experienced at 0.5 ppm. For this subject, the values used for 0.5 ppm were also used for
1.0 ppm under the assumption that the response at 1.0 ppm would be equal to or greater than the response at 0.5 ppm.
'Indicates studies in which exposures were conducted using a mouthpiece rather than a chamber.
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The lowest exposure concentration in Table 3-1 is 200 ppb. This is the lowest exposure
concentration for which individual study subject data are available in terms of the sRaw and
FEVi metrics presented in Table 3-1 that have been calculated with assessment of the SO2 effect
versus that of exercise in clean air. In nearly all of the studies in this table (and all of the studies
for concentrations below 500 ppb), study subjects breathed freely (e.g., without using a
mouthpiece).31 In studies that tested 200 ppb, a portion of the exercising study subjects with
asthma (approximately 8 to 9%) responded with at least a doubling in sRaw or an increase in
FEVi of at least 15% (Table 3-1; Linn et al., 1983b; Linn et al., 1987).
With regard to exposure concentrations below 200 ppb, the available evidence is very
limited. In the studies testing this concentration, subjects were exposed by mouthpiece rather
than freely breathing in an exposure chamber (Sheppard et al., 1981; Sheppard et al., 1984;
Koenig et al., 1989; Koenig et al., 1990; Trenga et al., 2001).32 Additionally, only a few of these
studies included an exposure to clean air while exercising that would have allowed for
determining the effect of SO2 versus that of exercise in causing bronchoconstriction (Sheppard et
al., 1981, 1984; Koenig et al., 1989). In those cases, a limited number of adult and adolescent
study subjects were reported to experience small changes in sRaw, with the magnitudes of
change appearing to be smaller than responses reported from studies at exposure concentrations
of 200 ppb or more. For example, the increase in sRaw reported for two young adult subjects
exposed to 100 ppb in the study by Sheppard et al. (1981) was slightly less than half the response
of these subjects at 250 ppb and the results for the study by Sheppard et al. (1984) indicate that
none of the 8 study subjects experienced as much as a doubling in sRaw in response to the
mouthpiece exposure to 100 ppb, while exercising. In the study of adolescents (aged 12 to 18
years), among the three individual study subjects for which respiratory resistance appears to have
increased with SO2 exposure, the magnitude of any increase after consideration of the response
to exercise appears to be less than 100% in each subject (Koenig et al., 1989).
In considering what may be indicated by these mouthpiece studies of 100 ppb, we note
that in a mouthpiece exposure system, the inhaled breath completely bypasses the nasal passages
where SO2 is efficiently removed, thus allowing more of the inhaled SO2 to penetrate into the
31 Studies of free-breathing subjects generally make use of small rooms in which the atmosphere is experimentally
controlled such that study subjects are exposed by freely breathing the surrounding air (e.g., Linn et al., 1987).
32 A subset of these studies is cited in the ISA; additionally, three of them (Sheppard et al., 1981; Koenig et al.,
1990; Trenga et al., 2001) are cited in the 2008 ISA and a fourth (Sheppard et al., 1984) is cited in the 1986
Addendum and 1994 Supplement to the 1982 AQCD. The fifth study (Koenig et al., 1989) is not cited in the prior
AQCDs, the 2008 ISA, or the ISA for the current review. This study is an investigation involving nine adolescent
subjects with allergic asthma (positive response to a methacholine challenge test at or below 20 mg/mL) exposed
by mouthpiece to 0.1 ppm during exercise. Measurements of FEVi and Rt were taken at baseline and subsequent
to SO2 and air only exposures during exercise (Koenig et al., 1989).
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tracheobronchial airways (2008 ISA, p. 3-4; ISA, section 4.1.2.2). This occurrence, as well as
limited evidence comparing responses by mouthpiece and chamber exposures, leads to the
expectation that S02-responsive people with asthma breathing SO2 using a mouthpiece,
particularly while breathing at elevated rates, would experience greater lung function responses
than if exposed to the same test concentration while freely breathing in an exposure chamber
(ISA, p. 5-23; Linn et al., 1983a). Thus, we conclude that the set of studies for the 100 ppb
exposure concentration, while quite limited, does not indicate as much as a doubling in sRaw in
the extremely few adults and adolescents tested (Sheppard et al., 1981, 1984; Koenig et al.,
1989).
We have also considered what may be indicated by the epidemiological studies regarding
exposure concentrations associated with health effects. Although exposure concentrations
eliciting respiratory responses are not available from such studies, studies that find associations
with outcomes such as asthma-related ED visits and hospitalizations have the potential to
indicate ambient air concentrations that may contribute to exposures that may be eliciting effects.
For example, in recognizing the general coherence of epidemiological study findings for 24-hour
ambient air concentrations with the findings of the controlled human exposure studies for
exercising study subjects with asthma exposed for 5 to 10 minutes, the 2008 ISA recognized that
"it is possible that these epidemiologic associations are determined in large part by peak
exposures within a 24-h period" (2008 ISA, p. 5-5). In considering the epidemiological studies in
this light, we additionally note that given the important role of SO2 as a precursor to PM in
ambient air, a key uncertainty in the epidemiological evidence available in the last review was
potential confounding by copollutants, particularly PM (ISA, p. 5-5). Among the U.S.
epidemiologic studies reporting mostly positive and sometimes statistically significant
associations between ambient SO2 concentrations and ED visits and hospital admissions (some
conducted in multiple locations), few studies have attempted to address this uncertainty, e.g.,
through the use of copollutant models. For example, as in the last review, there are three U.S.
studies for which the SO2 effect estimate remained positive and statistically significant in
copollutant models with PM (Appendix D).33 No additional such studies have been newly
identified in this review. Such uncertainty regarding copollutant confounding, as well as
exposure measurement error, remain in the currently available epidemiologic evidence base
(ISA, p. 5-6).
33 Based on data available for specific time periods at some monitors in the areas of these studies, the 99th percentile
1-hour daily maximum concentrations were estimated in the last review to be between 78-150 ppb (Thompson
and Stewart, 2009).
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3.2.1.4 Uncertainties in the Health Effects Evidence
A number of key uncertainties and limitations were identified in the previous review with
respect to the health effects evidence, as described in the 2009 REA. This section considers the
currently available information, including that newly available in this review, with regard to such
areas of uncertainty.
To what extent have important uncertainties identified in the last review been
reduced and/or have new uncertainties emerged?
We have not identified any new uncertainties since the last review. However, we
continue to recognize important uncertainties that also existed in the last review. These important
areas of uncertainty relate to the current health evidence, including that newly available in this
review, are summarized below.
Although the evidence clearly demonstrates that short-term SO2 exposures cause
respiratory effects, particularly asthma exacerbation in exercising individuals with asthma, as in
the previous review, we continue to recognize uncertainties that remain in several aspects of our
understanding of these effects. Such uncertainties include those associated with the severity and
prevalence of responses to very short (5- to 10-minute) SO2 exposures below 200 ppb and with
the potential extent of such responses in individuals of some population groups not included in
the controlled exposure studies (e.g., those with more severe asthma and children). There are also
uncertainties concerning the potential influence of exposure history and co-exposure to other
pollutants on the relationship between short-term SO2 exposures and respiratory effects. With
regard to the evidence base, we also recognize a complication associated with interpreting the
epidemiologic evidence related to uncertainty in the exposure estimates. The following
discussion touches on each of these types of uncertainty.
With regard to the potential for and magnitude of these effects in at-risk populations
exposed to 5- to 10-minute concentrations below 200 ppb, there is very limited evidence from a
small set of studies of exposure concentrations as low as 100 ppb, as discussed in section 3.2.1.3
above. Although only a few of these studies included an exposure to clean air while exercising
that would have allowed for determining the effect of SO2 versus that of exercise, these studies
indicate the likelihood of an appreciable reduction in S02-induced response in exercising people
with asthma from that observed for exposures at 200 ppb, with no evidence provided for as much
as a doubling in sRaw at an exposure concentration of 100 ppb. Given the limited number of
subjects in these studies and study design differences from free breathing chamber studies,
however, uncertainties remain with regard to a complete characterization of the extent of
response in exercising individuals with asthma exposed through natural or free breathing to
exposure concentrations below 200 ppb. The extent to which the epidemiological evidence,
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including that newly available, can inform this area of uncertainty is limited, at best.34
Accordingly, this remains an area of uncertainty in this review.
Some uncertainty also remains with regard to the extent to which the controlled human
exposure study evidence describes the responses of the populations most at risk of S02-related
respiratory effects (e.g., those with the greatest likelihood of the most severe response or of
responding at the lowest exposure concentration). For example, the available studies have
generally involved subjects with mild or moderate asthma, such that the response of individuals
with more severe asthma is unknown.35 Further, while it is well documented that some
individuals have a greater response to SO2 than others with the same disease status, the factors
contributing to this greater susceptibility are not yet known (ISA, pp. 5-14 to 5-21).
Uncertainty also remains related to the responses for children with asthma. Although the
epidemiological evidence includes a number of studies focused on health outcomes in children
that are supportive of the qualitative conclusions of causality (ISA, section 5.2.1.2), there are few
controlled human exposure studies to inform our understanding of exposure concentrations
associated with effects in this population group. Those studies have not included subjects
younger than 12 years (ISA, p. 5-22). Some characteristics particular to school age children
younger than 12 years, such as increased propensity for mouth breathing (ISA, p. 4-5), however,
suggest that this age group of children with asthma might be expected to experience larger lung
function decrements than adults with asthma (ISA, p. 5-25).
Other areas of uncertainty concerning the potential influence of SO2 exposure history and
co-exposure to other pollutants on the relationship between short-term SO2 exposures and
respiratory effects also remain from the last review. There is some limited evidence regarding the
potential for an increased response to SO2 exposures occurring in the presence of other common
pollutants such as PM (potentially including particulate sulfur compounds), nitrogen dioxide and
34 As associations reported in the epidemiologic analyses are associated with air quality concentration metrics as
surrogates for the actual pattern of exposures experienced by study population individuals over the period of a
particular study, the studies are limited in what they can convey regarding the specific patterns of exposure
circumstances (e.g., magnitude of concentrations over specific durations and frequency) that might be eliciting
reported health outcomes.
35 The ISA identifies two studies that have investigated the influence of asthma severity on responsiveness to SO2,
with one finding that a larger change in lung function observed in the moderate/severe asthma group was
attributable to the exercise component of the study protocol while the other did not assess the role of exercise in
differences across individuals with asthma of differing severity (Linn et al., 1987; Trenga et al., 1999). The ISA
states, "[hjowever, both studies suggest that adults with moderate/severe asthma may have more limited reserve
to deal with an insult compared with individuals with mild asthma" (ISA, p. 5-22). Based on the criteria used in
the study by Linn et al (1987) for placing individuals in the "moderate/severe" group, the ISA concluded that the
asthma of these individuals "would likely be classified as moderate by today's classification standards" (ISA, p.
5-22; Johns et al., 2010; Reddel, 2009).
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ozone, although the studies are limited (e.g., with regard to their relevance to ambient exposures)
and/or provide inconsistent results (ISA, pp. 5-23 to 5-26, pp. 5-143 to 5-144; 2008 ISA, section
3.1.4.7). For example, "studies of mixtures of particles and sulfur oxides indicate some enhanced
effects on lung function parameters, airway responsiveness, and host defense," however, "some
of these studies lack appropriate controls and others involve [sulfur-containing species] that may
not be representative of ambient exposures" (ISA, p.5-144).36 There is also some evidence
suggestive of a potential for SO2 exposure to contribute to an increased sensitivity to allergens;
however, the studies are very few and are limited to experimental animal models (ISA, section
5.2.1.9).
There are additional complications associated with interpretation of epidemiologic
studies of SO2 in ambient air that pertain to exposure measurement error and copollutant
confounding (ISA, sections 3.4, 5.2.1.1 and 5.2.1.2). With regard to the former, a key uncertainty
in the epidemiologic evidence is whether study findings reflect an independent association for
SO2 given that the studies assigned exposure from fixed site monitors while SO2 concentrations
in ambient air tend to show high spatiotemporal variability within a city, and correlations with
personal exposure are poorly characterized. Accordingly, there is uncertainty regarding the
extent to which measurements at the study monitors, and the associated air quality concentration
metric for the study, adequately represent the spatiotemporal variability in ambient SO2
concentrations in the study area (ISA, sections 5.2.1.2 and 3.4.1.3).
With regard to copollutant confounding, not only is SO2 but one component of a complex
mixture of pollutants present in the ambient air, an issue not unique to SO2 epidemiological
studies, but SO2 is also a precursor to sulfate, which can be a principal component of PM, an air
pollutant commonly occurring across the U.S. (ISA, section 2.3; U.S. EPA, 2009, Table 3-2 and
section 3.3.2). This uncertainty affects the extent to which effect estimates from epidemiologic
studies reflect the independent contribution of SO2 to the adverse respiratory outcomes assessed
in these studies. This area of uncertainty was recognized in the last review and remains in the
current review. In first summarizing the epidemiological evidence from the last review, the ISA
36 These toxicological studies in laboratory animals, which were newly available in the last review, were discussed
in greater detail in the 2008 ISA. That ISA stated that "[rjespiratory responses observed in these experiments
were in some cases attributed to the formation of particular sulfur-containing species" yet, "the relevance of these
animal toxicological studies has been called into question because concentrations of both PM (1 mg/m3 and
higher) and SO2 (1 ppm and higher) utilized in these studies are much higher than ambient levels" (2008 ISA, p.
3-30). The 2008 ISA further stated that "the SCh-adsorbed PM utilized in some of these studies is not
representative of ambient PM," providing the example that "some of the laboratory-generated aerosols contained
sulfite but atmospheric chemistry studies do not indicate significant amounts of sulfite ion in atmospheric PM"
(2008 ISA, p. 3-30). Thus, the 2008 ISA concluded that "animal toxicological studies conducted since the [prior]
review suggest that SO2 effects may be potentiated by coexposure to PM but the relevance of these results to
ambient exposures is not clear" (2008 ISA, p. 3-30).
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indicated that it was strongest for increased respiratory symptoms and respiratory-related
hospital admissions and ED visits, especially in children, while noting that "a key uncertainty
was potential confounding by copollutants, particularly PM" (ISA, p. 5-5). With regard to the
newly available evidence, "uncertainties related to exposure measurement error and copollutant
confounding remain" (ISA, p. 5-6).37
There remains uncertainty in the evidence with regard to the potential role of long-term
exposure to SO2 in eliciting SCh-related respiratory effects. As noted in section 3.2.1.1 above,
the ISA has determined the evidence to be suggestive of this being a causal relationship. The
strongest evidence supporting this conclusion is provided by epidemiological study findings of
associations between long-term SO2 concentrations and increases in asthma incidence combined
with findings of laboratory animal studies involving newborn rodents that indicate a potential for
SO2 exposure to contribute to the development of asthma, especially allergic asthma, in children.
However, "some uncertainty remains regarding an independent effect of long-term SO2 exposure
on the development of asthma" and "potential confounding by other pollutants is unexamined,
and largely unavailable, for epidemiologic studies of asthma among children" (ISA, p. 5-182).
Another area of uncertainty recognized by the ISA relates to conclusions regarding the
potential for SO2 in ambient air to contribute to health effects other than respiratory effects. As
noted in section 3.2.1.1 above, the ISA has determined the evidence to be suggestive of, but
insufficient to infer, a causal relationship between short-term SO2 exposure and mortality and to
be inadequate to infer the presence or absence of a causal relationship for other types of
exposures and health effects for which there are studies available (ISA, section 1.6.2).
In summary, a variety of uncertainties from the last review remain, including those
related to the extent of effects at concentrations below those evaluated in controlled human
exposure studies of exercising individuals with asthma, and the potential for greater impacts in
individuals with more severe asthma and in children with asthma, as well as exposure
measurement error and potential copollutant confounding in the epidemiologic studies (ISA,
section 5.2.1.9).
3.2.1.5 Public Health Implications
In general, implications and the magnitude of potential impacts on public health are
dependent upon the type and severity of the effect, as well as the size of population affected.
37 With regard to asthma-related outcomes, "a small number of epidemiologic studies examined copollutant models"
and while "[s]ome associations were relatively unchanged in magnitude after adjustment for a copollutant; others
did not persist" (ISA, p. 5-154). The ISA concludes that "inference from copollutant models is limited given
potential differences in exposure measurement error for SO2 compared to NO2, CO, PM, and O3 and in many
cases, high copollutant correlations" (ISA, p. 5-154). The evidence for nonasthma-related outcomes is described
as "limited and inconsistent" (ISA, pp. 5-155 to 5-156).
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With regard to SO2 concentrations in ambient air, the public health implications and potential
public health impacts relate to the effects causally related to SO2 exposures of interest in this
review. These are respiratory effects of short-term exposures, and particularly those effects
associated with asthma exacerbation in people with asthma. As summarized in section 3.2.1.1,
the most strongly demonstrated effects are bronchoconstriction-related effects resulting in
decrements in lung function elicited by short term exposures during periods of elevated breathing
rate, while asthma-related health outcomes such as ED visits and hospital admissions have also
been statistically associated with ambient air SO2 concentration metrics in epidemiological
studies (ISA, section 5.2.1.9).
In considering public health implications, in addition to the difference in severity of
different effects, it is important to consider aspects of the same effect with regard to its impact on
population groups of differing susceptibility. For example, with regard to bronchoconstriction-
related effects, the same percentage increase in sRaw or reduction in FEVi for two groups of
individuals that differ in their baseline sRaw or FEVi may result in the two groups being affected
differently with regard to increased susceptibility to other physiological threats or challenges.
Accordingly, consideration of such baseline differences and also the relative transience or
persistence of these responses, as well as other factors, is important to characterizing
implications for public health, as recognized by the ATS in their statements on evaluating
adverse health effects of air pollution (ATS, 2000; Thurston et al., 2017).
Building on the earlier policy statement by the ATS that was considered in the last review
(ATS, 2000), the recent policy statement by the ATS on what constitutes an adverse health effect
of air pollution provides a general framework for interpreting evidence that proposes a a "set of
considerations that can be applied in forming judgments" for this context (Thurston et al., 2017).
The earlier ATS statement, in addition to emphasizing clinically relevant effects (e.g., the
adversity of small transient changes in lung function metrics in combination with respiratory
symptoms), also emphasized both the need to consider changes in "the risk profile of the exposed
population," and effects on the portion of the population that may have a diminished reserve that
puts its members at potentially increased risk if affected by another agent (ATS, 2000). The
consideration of effects on individuals with pre-existing diminished lung function continues to be
recognized as important in the more recent ATS statement (Thurston et al., 2017). For example,
in adding emphasis in this area, this statement conveys the view that "small lung function
changes" in individuals with compromised function, such as that resulting from asthma, should
be considered adverse, even without accompanying respiratory symptoms (Thurston et al.,
2017). All of these concepts, including the consideration of the magnitude of effects occurring in
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just a subset of study subjects, continue to be recognized as important in the more recent ATS
statement (Thurston et al., 2017) and continue to be relevant to the evidence base for SO2.38
As summarized in section 3.2.1.3 above, people with asthma are the key population at
risk for SCh-related effects and children with asthma are considered to be at relatively greater
risk than other age groups within this at-risk population (ISA, section 6.3.1). In recognizing that
asthma as a disease can vary in its severity, we take note of the relative lack of evidence for
individuals with the most severe asthma. The evidence base of controlled exposure studies of
exercising people with asthma provides limited information that indicates there to be similar
relative responses of individuals with differences in severity of their asthma,39 although the
evidence from one study indicates that the absolute changes in lung function are larger for
individuals with more severe asthma compared to those characterized as having mild asthma. In
that study, the larger absolute change in lung function was attributable to a larger response to the
exercise component of the exposure protocol in the moderate/severe asthma group compared to
the mild asthma group (ISA, p. 5-22; Linn et al., 1987). Because the role of exercise was not
determined in the second study, it is unclear whether a greater response to the exercise itself (vs
the SO2 exposure) played a role in its findings (ISA, p. 5-22; Trenga et al., 1999). However, the
two available studies "suggest that adults with moderate/severe asthma may have more limited
reserve to deal with an insult compared with individuals with mild asthma" (ISA, p. 5-22; Linn et
al., 1987; Trenga etal., 1999).
The information below characterizes the size and other features of the populations in the
U.S. concluded to be at risk of S02-related effects (when breathing at elevated rates). As a
whole, the discussion in this section indicates the potential for exposures to SO2 in ambient air to
be of appreciable public health importance. Such considerations contributed to the basis for the
2010 decision to appreciably strengthen the primary SO2 NAAQS and to establish a 1-hour
standard to protect the at-risk populations from short term exposures of concern. Such
considerations remain relevant in the current review.
38 In the Administrator's judgments on the then-existing standard in the last review, as well as on the appropriate
level for the new 1-hour standard, the Administrator considered the 2000 ATS policy statement, as well as advice
from CAS AC and recommendations and judgments made by EPA in previous NAAQS reviews (section 3.1.1
above).
39 These studies categorized with regard to asthma severity based mainly on the individual's use of medication to
control asthma, such that individuals not regularly using medication were classified as minimal/mild, and those
regularly using medication as moderate/severe (Linn et al., 1987). The ISA indicates that the moderate/severe
grouping would likely be classified as moderate by today's asthma classification standards due to the level to
which their asthma was controlled and ability to engage in moderate to heavy levels of exercise (ISA, p. 5-22;
Johns et al., 2010; Reddel, 2009).
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What does the information available in this review indicate with regard to the size of
at-risk populations and their distribution in the U.S.?
The magnitude and characterization of a public health impact is dependent upon the size
and characterization of the populations affected, as well as the type or severity of the effect. As
summarized above, the population group most at risk of health effects associated with exposure
to SO2 in ambient air is people with asthma.40 The National Center for Health Statistics data
from the National Health Information Survey (NHIS)41 for 2015 indicate that approximately 8%
of the U.S. population has asthma (Table 3-2; CDC, 2017). These data indicate the size of the
key at-risk population for SO2 in ambient air. It is this population that the primary NAAQS for
SO2 is intended to protect. Table 3-2 below considers the currently available information that
helps to characterize key features of this population.
Population groups with relatively greater asthma prevalence might be expected to have a
potential for relatively greater population-level SO2 impacts. Among all U.S. adults, asthma
prevalence is estimated to be 7.6%, with women having a higher estimate (9.7%) than men
(5.4%). The estimated prevalence is greater in children (less than 18 years of age) than adults
(Table 3-2). Asthma was the leading chronic illness affecting children in 2012, the most recent
year for which such an evaluation is available (Bloom et al., 2013).
Among all U.S. children, the asthma prevalence estimate is greater for boys (9.9%) than
girls (6.9%>), and, with regard to age, is generally greatest in young teenagers (Table 3-2).
Among populations of different races or ethnicities, black non-Hispanic and Puerto Rican
Hispanic children are estimated to have the highest estimated prevalences, at 13.4% and 13.9%,
respectively. For the age group 5-14 years, the estimates are 16.3% and 14.7% for black non-
40 We additionally note, that some individuals with asthma have a greater response to SO2 than others with asthma
(ISA, p. 5-14). Analyses of publicly available primary data from five studies demonstrated a bimodal distribution
of SO2 responses in study subjects with asthma, "with one subpopulation that is insensitive to the
bronchoconstrictive effects of SO2 even at concentrations as high as 1.0 ppm, and another subpopulation that has
an increased risk of bronchoconstriction ... at low concentrations" (ISA, p. 5-19 to 5-20; Johns et al., 2010).
41 The NHIS is conducted annually by the U.S. Centers for Disease Control and Prevention. The NHIS collects
health information from a nationally representative sample of the noninstitutionalized U.S. civilian population
through personal interviews. Participants (or parents of participants if the survey participant is a child) who have
ever been told by a doctor or other health professional that the participant had asthma and reported that they still
have asthma were considered to have current asthma. Data are weighted to produce nationally representative
estimates using sample weights; estimates with a relative standard error greater than or equal to 30% are generally
not reported (Mazurek and Syamlal, 2018). The NHIS estimates described here are drawn from the 2015 NHIS,
Table 4-1 (https://www.cdc.gov/asthma/nhis/2015/table4-l.htm) and current asthma prevalence table
(https ://www. cdc .gov/asthma/most_recent_data. htm).
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Hispanic and Puerto Rican children, respectively (Table 3-2).42 Asthma prevalence is also
increased among populations in poverty (e.g., 11.1% among people living in households below
the poverty level compared to 7.2% of those living above it).43
The information on which to base estimates of asthma prevalence in other subgroups of
children is much more limited (e.g., as discussed in the REA, section 4.1.2). For example, the
more limited information from the National Health Information Survey (NHIS) for 2011-2015
indicates there to be a greater prevalence of asthma in children that are obese compared to those
that are not (REA, section 4.1.2, Figure 4-2).44
42 Interestingly, in black, non-Hispanic children aged 5 to 14 years, the estimated asthma prevalence is greater in
boys (19.0%) than girls (13.5%). While in Puerto Rican children aged 5 to 14 years, the estimated prevalence is
greater in girls (18.5%) than boys (11.6%) (https://www.cdc.gov/asthma/nhis/2015/table4-l.htm).
43 There is also a correlation between asthma prevalence and obesity (REA, section 4.1.2).
44 In consideration of the limited information regarding factors related to breathing habit (whether one is breathing
through their nose or mouth) and recognizing the lack of evidence from controlled human exposure studies of
S02-induced lung function decrements in children, approximately 5 to 11 years of age, with asthma, the ISA
suggests that this age group of children and "particularly boys and perhaps obese children, might be expected to
experience greater responsiveness (i.e., larger decrements in lung function) following exposure to SO2 than
normal-weight adolescents and adults" (ISA, p. 4-7 and 5-36). However, the ISA does not find the evidence to be
adequate to conclude differential risk status for subgroups of children with asthma (ISA, Chapter 6).
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Table 3-2.
2015 National Asthma Prevalence.
Number with Current
Percent with Current
onaractenstic 1
Asthma (in thousands)2
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
10.0
12-14 years
1,272
10.3
15-17 years
1,219
9.8
Sex
Males
9,998
6.5
Boys (Age <18)
3,705
9.9
Boys (Age 5-14)
2,428
11.6
Men (Age 18+)
6,293
5.4
Females
14,634
9.1
Girls (Age <18)
2,483
6.9
Girls (Age 5-14)
1,605
8.0
Women (Age 18+)
12,151
9.7
Race/Ethnicity
White NH3
15,244
7.8
Child (Age <18)
2,810
7.4
Child (Age 5-14)
1,750
8.2
Adult (Age 18+)
12,435
7.9
Black NH
3,931
10.3
Child (Age <18)
1,336
13.4
Child (Age 5-14)
911
16.3
Adult (Age 18+)
2,595
9.1
Other NH
1,793
6.9
Child (Age <18)
605
8.4
Child (Age 5-14)
389
9.4
Adult (Age 18+)
1,188
6.3
Hispanic, all
3,665
6.6
Child (Age <18)
1,438
8.0
Child (Age 5-14)
983
9.7
Adult (Age 18+)
2,227
5.9
Hispanic, Puerto Rican
715
13.7
Child (Age<18)
198
13.9
Child (Age 5-14)
117
14.7
Adult (Age 18+)
516
13.6
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Characteristic1
Number with Current
Percent with Current
Asthma (in thousands)2
Asthma
Hispanic, Mexican/Mexican-American
2,126
6.0
Child (Age<18)
Child (Age 5-14)
Adult (Age 18+)
899
646
1,226
7.3
9.2
5.3
Federal Poverty Threshold
Below 100% of poverty level
5,086
11.1
100% to less than 250% of poverty level
7,664
8.4
250% to less than 450% of poverty level
4,989
6.3
450% of poverty level or higher
6,894
6.9
1 Numbers within selected characteristics may not sum to total due to rounding
2 Includes persons who answered "yes" to the questions "Have you EVER been told by a doctor or other health
professional that you had asthma" and "Do you still have asthma?"
3NH = non-Hispanic
Adapted from https://www.cdc.gov/asthma/most_recent_data.htm and
https://www.cdc.gov/asthma/nhis/2015/table4-1.htm (CDC, 2017).
3.2.2 Exposure/Risk-based Considerations
Our consideration of the scientific evidence available in the current review, as at the time
of the last review (summarized in section 3.1 above), is informed by results from a quantitative
analysis of estimated population exposure and associated risk. The overarching consideration is
whether the current exposure/risk information alters our overall conclusions from the previous
review regarding health risk associated with exposure to SO2 in ambient air. As in our
consideration of the evidence in section 3.2.1 above, we have organized the discussion regarding
the exposure/risk information around a set of key questions to assist us in considering the
exposure/risk analyses of at-risk populations living in three urban areas under air quality
conditions simulated to just meet the existing SO2 primary standard.
Prior to addressing the individual exposure/risk questions, we provide a summary of key
aspects of the assessment, including the study areas, populations simulated, modeling tools and
exposure and risk metrics derived (section 3.2.2.1). We then consider aspects of the questions
beginning with the magnitude of exposure and risk estimated for the simulated at-risk
populations (section 3.2.2.2), followed by the key uncertainties associated with the quantitative
analyses with regard to drawing conclusions as to the adequacy of protection afforded by the
current SO2 standard (section 3.2.2.3). Lastly, we consider the exposure and risk estimates from
the quantitative assessment with regard to the extent to which such estimates may be judged to
be important from a public health perspective (section 3.2.2.4).
3.2.2.1 Exposure/Risk Analyses
In the assessment conducted for this review, described in detail in the REA, we have
estimated SO2 exposure and risk associated with air quality conditions that just meet the current
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standard. These analyses inform our understanding of the protection provided by the current SO2
standard from effects that the health effects evidence indicates to be elicited in some portion of
exercising people with asthma by short (e.g., 5- to 10-minute) elevations in SO2 exposure
concentrations. The analyses estimate exposure and risk for at-risk populations in three urban
study areas in: (1) Fall River, MA; (2) Indianapolis, IN; and, (3) Tulsa, OK. The three study
areas present a variety of circumstances with regard to population exposure to short-term peak
concentrations of SO2 in ambient air. This set of study areas and the associated exposed
populations are intended to be informative to the EPA's consideration of potential exposures and
risks that may be associated with the air quality conditions that meet the current SO2 standard.
The three study areas range in total population size from approximately 180,000 to
540,000 and reflect different mixtures of SO2 emissions sources, including utilities using fossil
fuel and non-utility sources, such as petroleum refineries and secondary lead smelting (REA,
section 3.1). The three study areas - in Massachusetts, Indiana and Oklahoma -are in three
different climate regions of the U.S.: the Northeast, Ohio River Valley (Central), and South (Karl
and Koss, 1984). The latter two regions comprise the part of the U.S. with generally the greatest
prevalence of elevated SO2 concentrations and large emissions sources (Figure 2-7, Appendix F).
Additionally, continuous 5-minute ambient air monitoring data (i.e., all 12 5-minute values for
each hour) are available in all three study areas (REA, section 3.2).
Consistent with the health effects evidence in this review (summarized in section 3.2.1
above), the focus of the REA is on short-term exposures of individuals in the population with
asthma during times when they are breathing at an elevated rate. Exposure and risk is
characterized for two population groups: adults (individuals older than 18 years) with asthma and
school-aged children (aged 5 to 18 years)45 with asthma. The focus on these populations is
consistent with the ISA's identification of individuals with asthma as the population at risk of
S02-related effects, and its conclusion that within this population, children with asthma may be
at greater risk than adults with asthma (ISA, section 6.6). Asthma prevalence estimates for the
populations simulated in the three study areas ranges from 8.0 to 8.7% (REA, section 5.1). For
children, the study area prevalence rates range from 9.7 to 11.2% (REA, section 5.1). Variation
within each study area related to age, sex and family income was also accounted for (section
4.1.2 and Appendix E of REA)46 For children, this variation is greatest in the Fall River study
45 The child population group focuses on ages 5 to 18 in recognition of data limitations and uncertainties, including
those related to accurately simulating activities performed, estimating physiological attributes, as well as
challenges in asthma diagnoses for very young children.
46 As described in section 4.1.2 and Appendix E of the REA, asthma prevalence in the exposure modeling domain is
estimated based on national prevalence information and study area demographic information related to age, sex
and family income from the NHIS.
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area, with census block level, age-specific prevalence estimates ranging from 7.9 to 18.6% for
girls and from 10.7 to 21.5% for boys (REA, Table 4-2).
In the REA, 1-hour SO2 concentrations were estimated across a 3-year period (consistent
with the period represented by the form of the standard) using air quality modeling of SO2
emissions sources in each area,47 and were adjusted, as described in the REA, such that the air
quality modeling receptor location with the highest concentrations just met the current
standard.48 In addition, sensitivity analyses were performed using an alternative adjustment
approach and are summarized in section 3.2.2.2. Relationships between 1-hour and 5-minute
concentrations at local monitors were then used to estimate 5-minute concentrations associated
with the adjusted 1-hour concentrations across the 3-year period at all receptor locations in each
area (REA, section 3.5).
The exposure modeling, presented in detail in the REA, relied on the EPA's Air Pollutant
Exposure model (APEX), which estimates human exposure using a stochastic, event-based
microenvironmental approach. This model has a history of application, evaluation, and
progressive model development in estimating human exposure and dose for reviews of NAAQS
for gaseous pollutants (U.S. EPA, 2008; 2010; 2014). This general exposure modeling approach
was also used in the 2009 REA for the last review of the primary standard for SOx, although a
number of updates have been made to the model and various datasets used with it (2009 REA;
U.S. EPA, 2017b, section 3.4). For example, exposure modeling for the REA includes reliance
on updates to several key inputs to the model including (1) a significantly expanded
Consolidated Human Activity Database (CHAD), that now has over 55,000 diaries, with over
25,000 for school-aged children; (2) the updated NHANES data (2009-2014), which are the basis
for the age- and sex-specific body mass distributions from which APEX samples to specify the
individuals in the modeled population; (3) the algorithms used to estimate age- and sex-specific
resting metabolic rate, a key input to estimating a simulated individual's activity-specific
ventilation (or breathing) rate; and (4) the ventilation rate algorithm itself. Further, the current
model uses updated population demographic data based on the most recent Census.
The APEX model probabilistically generates a sample of hypothetical individuals from
an actual population database and simulates each individual's movements through time and
space (e.g., indoors at home, inside vehicles) to estimate his or her exposure to a pollutant.
47 As described in chapter 3 of the REA, the air quality modeling utilized emissions estimates and meteorological
data for the years 2011 through 2013 as conditions in this time period are close to those just meeting the current
standard, thus requiring a smaller adjustment to create the current standard scenario.
48 As described in more detail in section 3.4 of the REA, the adjustments were implemented with a focus on
reducing emissions from the source contributing to the standard exceedances until the areas just met the standard.
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Population characteristics are taken into account to represent the demographic profile of the
population in each study area. Age and gender demographics for the simulated at-risk population
(adults and children with asthma) were drawn from the prevalence estimates provided by the
2011-2015 National Health Interview Survey.49 The APEX model generates each simulated
person or profile by probabilistically selecting values for a set of profile variables, including
demographic variables, status and physical attributes (e.g., residence with air conditioning,
height, weight, body surface area) and ventilation rate.
Based on minute-by-minute activity levels, and physiological characteristics of the
simulated person (see REA, section 4.1), APEX estimates an equivalent ventilation rate (EVR),
based on normalizing the simulated individuals' activity-specific ventilation rate to their body
surface area; the EVR is used to identify exposure periods during which an individual is at or
above a specified ventilation level (REA, section 4.1.3.3). The level specified is based on the
ventilation rates of subjects in the controlled human exposure studies of exercising people with
asthma (Table 3-1). The APEX simulations performed for this review have focused on exposures
to SO2 emitted into ambient air that occurs in microenvironments,50 without additional
contribution from indoor SO2 emissions sources.51
As in the last review, the REA for this review uses the APEX model estimates of 5-
minute exposure concentrations for simulated individuals with asthma while breathing at
elevated rates to characterize health risk in two ways based on information from the controlled
human exposure studies on the occurrence of bronchoconstriction-related effects in some study
subjects with asthma who are exposed during exercise (REA, section 4.6). In drawing on this
evidence base for this purpose, the REA has given primary focus to the well-documented studies
summarized in Table 5-2 and Figure 5-1 of the ISA for 5- to 10-minute exposure concentrations
ranging from 200 ppb to 600 ppb (Table 3-1 of this document). The first risk metric is based on
comparison of the estimated 5-minute exposure concentrations for individuals breathing at
elevated rates to 5-minute concentrations of potential concern (benchmark concentrations), and
the second utilizes exposure-response information for study subjects experiencing
49 Information about the National Health Interview Survey is available at http://www.cdc.gov/nchs/nhis.htm.
50 Five microenvironments (MEs) are modeled in the REA as representative of a larger number of
microenvironments. The 2009 REA results indicated that the majority of peak SO2 exposures occurred while
individuals were within outdoor microenvironments (2009 REA, Figure 8-21). Based on that finding and the
objective (i.e., understanding how often and where short-term peak SO2 exposures occur), the approach
implemented in the REA recognizes the added efficiency of minimizing the number of MEs, particularly indoor
MEs, that are parameterized and included in the modeling. Accordingly, the number of MEs was aggregated to
address exposures of ambient origin that occur within a core group of indoor, outdoor, and vehicle MEs (REA,
section 4.4).
51 Indoor sources are generally minor in comparison to SO2 from ambient air (ISA, p. 3-6; REA, sections 2.1.1 and
2.1.2).
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bronchoconstriction-related effects on lung function (specifically a doubling or more in sRaw) to
estimate the portion of the simulated at-risk population likely to experience one or more days
with an SCh-related increase in sRaw of at least 100%. Both of these metrics are used in the REA
to characterize health risk associated with 5-minute peak SO2 exposures among the simulated at-
risk population during periods of elevated breathing rates. These risk metrics were also derived
in the REA for the last review and the associated estimates informed the Administrator's 2010
decision on the new standard (75 FR 35546-35547, June 22, 2010).
For the benchmarks metric, the REA for this review, like the 2009 REA in the last
review, uses benchmark concentrations that range from 400 ppb down to 100 ppb (REA, section
4.6.1). At the upper end of this range, 400 ppb represents the lowest concentration in free-
breathing controlled human exposure studies of exercising people with asthma where moderate
or greater lung function decrements occurred that were often statistically significant at the group
mean level and were frequently accompanied by respiratory symptoms, including statistically
significant increased occurrences (ISA, section 5.2.1.2). At 300 ppb, statistically significant
increases in lung function decrements (specifically reduced FEVi) have been documented in
analyses of the subset of controlled human exposure study subjects with asthma that are
responsive to SO2 at concentrations below 600 or 1000 ppb (ISA, p. 153 and Table 5-21; Johns
et al., 2010). The 200 ppb benchmark concentration represents the lowest level tested in studies
where subjects were freely breathing in exposure chambers, and where comparisons with
exposures to clean air while exercising were conducted, thus providing for conclusions regarding
S02-attributable responses. At this concentration, moderate or greater lung function decrements
occurred in a percentage of exercising study subjects and there was also limited evidence of SO2-
related respiratory symptoms (ISA, section 5.2.1.2). For exposure concentrations below 200 ppb,
limited data are available that while not completely comparable to the data at higher
concentrations do not indicate responses on the order of a doubling in sRaw (section 3.2.1.3
above). However, in consideration of the nonzero percentage of subjects with asthma
experiencing moderate transient decrements in lung function at the 200 ppb exposure
concentration (approximately 8 to 9%) and the scarcity or lack of specific controlled human
exposure study data for some groups of individuals with asthma, such as primary-school-age
children and those with more severe asthma,52 a benchmark concentration of 100 ppb (one half
52 Recognizing that even the study subjects described as "moderate/severe" group (had well-controlled asthma, were
generally able to withhold medication, were not dependent on corticosteroids, and were able to engage in
moderate to heavy levels of exercise) would likely be classified as moderate by today's classification standards
(ISA, pp. 5-22; Johns et al., 2010; Reddel, 2009), we have considered the evidence with regard to the response of
individuals with severe asthma that are not generally represented in the full set of controlled human exposure
studies. There is no evidence to indicate such individuals would experience moderate or greater lung function
decrements at lower SO2 exposure concentrations than individuals with moderate asthma. With regard to the
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the lowest exposure concentration for which the ISA provides quantified SCh-attributable
responses resulting from free breathing exposure studies), has been included.
The exposure-response (E-R) function for the risk of lung function decrements was
developed from the individual subject results for sRaw from the controlled exposure studies of
exercising freely breathing people with asthma exposed to SO2 concentrations from 1000 ppb
down as low as 200 ppb (REA, Table 4-12). Beyond the assessment of these studies and their
results in past reviews, there has been extensive evaluation of the individual subject results,
including a data quality review in the last SO2 NAAQS review (Johns and Simmons, 2009), and
detailed analysis in two subsequent publications (Johns et al., 2010; Johns and Linn, 2011). The
sRaw responses reported in these studies have been summarized in the ISA, as in the last review,
in terms of percent of study subjects experiencing responses of a magnitude equal to a doubling
or tripling or more. Across the exposure range from 200 to 1000 ppb, the percentage of
exercising study subjects with asthma having at least a doubling of sRaw increases from about 8-
9% (at exposures of 200 ppb) up to approximately 50-60% (at exposures of 1000 ppb) (REA,
Table 4-11). The E-R function used in the main analysis of the REA was derived from these data
using a probit function (REA, section 4.6.2).
In summary, while the general approach and methodology for the exposure-based
assessment in this review is similar to that in the last review, there are a number of ways in
which these analyses differ (see 2009 REA and REA for this review). In addition to the
expansion in the number and type of study areas assessed, we note the number of improvements
to input data and modeling approaches, including the availability of continuous 5-minute air
monitoring data at monitors within the three study areas. The REA for the current review extends
the time period of simulation to a 3-year simulation period, consistent with the form established
for the now-current standard. Further, the years simulated reflect more recent emissions and
circumstances subsequent to the 2010 decision.
3.2.2.2 At-Risk Population Exposures and Risk
In this section, we summarize the exposure and risk estimates from the REA and consider
the following question.
severity of the response, the limited data that are available indicate a similar magnitude SCh-specific response (in
sRaw) as that for individuals with less severe asthma, although the individuals with more severe asthma are
indicated to have a greater response to exercise prior to SO2 exposure, indicating that those individuals "may have
more limited reserve to deal with an insult compared with individuals with mild asthma" (ISA, p. 5-22). As noted
in sections 3.2.1.3 and 3.2.1.4 above, evidence from controlled human exposure studies are not available for
children younger than 12 years old, and the ISA indicates that the information regarding behavior and
methacholine responsiveness for the subset of this age group that is of school age (e.g., 5-12 years) indicates a
potential for greater response (ISA, pp. 5-22 to 5-25).
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What is the magnitude of population exposure and risk in at-risk populations in
areas simulated to just meet the current SO2 standard? What portion of the at-risk
populations are estimated to experience exposures of concern or lung function
decrements at levels of potential health concern?
Given these overarching questions, the air quality scenario analyzed in the REA focuses
on air quality conditions that just meet the current standard. In addressing these questions, we
consider the population estimates provided by the REA simulations (REA, Chapters 5 and 6) and
in considering these REA estimates, we particularly focus on the extent of protection provided
by the standard from SO2 exposures of potential concern. As described in the prior section, the
REA presents two sets of risk estimates for the 3-year simulation in each study area: (1) the
number (and percent) of simulated persons experiencing exposures at or above the particular
benchmark concentrations of interest, while breathing at elevated rates; and (2) the number and
percent of people estimated to experience at least one S02-related lung function decrement in a
year and the number and percent of people estimated to experience multiple lung function
decrements associated with SO2 exposures.
As an initial matter, we note that, as indicated by the use of a case study approach
(summarized in section 3.2.2.1 above), the REA analyses are not intended to provide a
comprehensive national assessment. The REA objective is not to present an exhaustive analysis
of exposure and risk in the areas that currently just meet the current standard and/or of exposure
and risk associated with air quality adjusted to just meet the current standard in areas that
currently do not meet the standard. Rather, the analyses are intended to provide assessments of
an air quality scenario just meeting the current standard for a small, diverse set of study areas and
associated exposed at-risk populations. The purpose is to assess, based on current tools and
information, the potential for exposures and risks beyond those indicated by the information
available at the time the standard was established. Accordingly, capturing an appropriate
diversity in study areas and air quality conditions (that reflect the current standard scenario)53 is
important to the role of the REA in informing the EPA's conclusions on the public health
protection afforded by the current standard.
In this light, we present the REA results from two different approaches to adjusting air
quality. The first approach uses the highest design value across all modeled air quality receptors
to adjust the air quality concentrations in each area to just meet the standard (REA, section 3.4).
53 A broad variety of spatial and temporal patterns of SO2 concentrations can exist when ambient air concentrations
just meet the current standard. These patterns will vary due to many factors including the types of emissions
sources in a study area and several characteristics of those sources, such as magnitude of emissions and facility
age, use of various control technologies, patterns of operation, and local factors, as well local meteorology.
Variability and uncertainty in these patterns is indicated by the estimates derived by the particular analytical
approaches and methodologies used to describe the study area-specific air quality.
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This is done by estimating the amount of SO2 concentration reduction needed for concentrations
at this highest receptor to be adjusted to just meet the current standard, and based on this amount,
all other receptors impacted by the highest source(s) are adjusted accordingly. The second
approach is included in the REA as a sensitivity analysis in recognition of the potential
uncertainty associated with the estimated concentrations across the modeling domain,
particularly the very highest concentrations. Accordingly, the second approach uses the air
quality receptor having the 99th percentile of the distribution of design values (instead of the
receptor having the maximum design value) to estimate the SO2 concentration reductions needed
to adjust the air quality to just meet the standard (REA, section 6.2.2.1). In study areas in which
estimated concentrations at a very small number of receptors are substantially higher than those
at all other air quality receptors, these two different approaches can result in very different SO2
concentrations across an area. In such study areas in particular, the first approach generally
results in much more significant reductions being applied to reduce SO2 concentrations at the
small group of highest receptor locations such that concentrations at those receptors are just at or
just below the standard and concentrations at the other receptors across the area are appreciably
lower. We have represented both sets of results in the tables below in recognition of the
uncertainty and variability inherent in representing air quality conditions just meeting the current
standard.54
Of the two types of risk metrics derived in the REA, we turn first to the results for the
benchmark-based risk metric with regard to the percent of the simulated populations of children
with asthma estimated to experience at least one daily maximum 5-minute exposure per year at
or above the different benchmark concentrations while breathing at elevated rates under air
quality conditions just meeting the current standard (Table 3-3). The estimates for adults are
lower, generally due to the lesser amount and frequency of time spent outdoors (REA, section
5.2). As an initial matter, we note that the estimates for the Tulsa study area are much lower than
those for the other two areas. For Tulsa, the fraction of the simulated child population with
asthma was less than 0.5% for the 100 ppb benchmark and zero for the other benchmarks.
Under air quality conditions just meeting the current standard in the other two study areas
(Indianapolis and Fall River), approximately 20% to just over 25% of a study area's simulated
children with asthma, on average across the 3-year period, are estimated to experience one or
more days per year with a 5-minute exposure at or above 100 ppb while breathing at elevated
rates (Table 3-3). With regard to the 200 ppb benchmark, the two study areas' estimates are as
54 Details regarding the sensitivity analyses focused on the impact of the adjustment approach are presented in the
REA, section 6.2.2.1.
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high as 0.7 percent,55 on average across the 3-year period, and range up to as high as 2.2%56 in a
single year (Table 3-3). Less than 0.1% of either area's children with asthma were estimated to
experience multiple days with such an exposure at or above 200 ppb (REA, Table 6-9).
Additionally, in the study area with the highest estimates (Indianapolis), approximately a quarter
of a percent of simulated children with asthma were estimated to experience a day with a 5-
minute exposure at or above 300, on average across the 3-year period; the percentage was 0.1%
for the 400 ppb benchmark (Table 3-3). Across all three areas, no children were estimated to
experience multiple days with a daily maximum 5-minute exposure (while breathing at an
elevated rate) at or above 300 ppb (REA, Table 6-9).
Table 3-3. Air quality conditions adjusted to just meet the current standard: Percent of
simulated populations of children with asthma estimated to experience at least
one daily maximum 5-minute exposure per year at or above indicated
concentrations while breathing at an elevated rate.
5-minute
Exposure
Concentration
(ppb)
Percent (%) of Population of Children (5-18 years) with Asthma
Average per yearA
Fall River, MA
Indianapolis, IN
Tulsa, OK
>100
19.4-26.7
22.4-23.0
O
I
o
>200
A
O
CO
I
O
0.6-0.7ฐ
0
>300
0
0.2-0.3ฐ
0
>400
0
<0.1 -0.1ฐ
0
AThe values presented in each cell are the average of the results for the three years simulated based on the two
approaches to air quality adjustment (drawn from Table 6-8 of the REA).
B <0.1 is used to represent nonzero estimates below 0.1%. A value of zero (0) indicates there were no individuals
estimated to have the selected exposure in any year.
c The highest single year result for 200 ppb was for Fall River where the estimate ranged up to 2.2% (for the
second air quality adjustment approach in REA, Table 6-8).
D The highest single year results for 300 and 400 ppb were for Indianapolis where the estimates ranged up to
0.8% and 0.3%, respectively (REA, Table 6-8).
We next consider the estimates for risk of lung function decrements in terms of a
doubling or more in sRaw, focusing on results for children with asthma (Table 3-4). The
estimates for the Tulsa study area are lower than for the other two areas (Table 3-4), the results
for which are summarized next.
55 This percentage in the Fall River study area corresponds to 28 children with asthma, while in the larger
Indianapolis study area, it corresponds to 71 such children (REA, section 5.2 and Appendix J).
56 This percentage, estimated for the Fall River study area, corresponds to 88 children with asthma (REA, Appendix
J).
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Under air quality conditions just meeting the current standard in the Indianapolis and Fall
River study areas, as many as 1.3% and 1.1%, respectively,57 of children with asthma, on
average across the 3-year period, were estimated to experience at least one day per year with a
S02-related doubling in sRaw (Table 3-4). The corresponding percentage estimates for
experiencing two or more such days ranged as high as 0.7%, on average across the 3-year
simulation period, and 1% in a single year (REA, Table 6-11). Additionally, as much as 0.2%
and 0.3%), in Fall River and Indianapolis, respectively, of the simulated populations of children
with asthma, on average across the 3-year period, was estimated to experience a single day with
a S02-related tripling in sRaw (Table 3-4), with 0.2% or less estimated to experience multiple
such days (REA, Table 6-11).
Table 3-4. Air quality conditions adjusted to just meet the current standard: Percent of
simulated population of children with asthma estimated to experience at least
one day per year with a SCh-related increase in sRaw of 100% or more.
Lung function
decrement
(increase in sRaw)
Percent (%) of Population of Children (5-18 years) with Asthma*
Average per year
Fall River, MA
Indianapolis, IN
Tulsa, OK
>100%
0.9-1.1 c
CO
I
CO
<0.1B - <0.1
>200%
0.1 -0.2ฐ
0.3-0.3ฐ
0
AThe values presented in each cell are the average of the results for the three years simulated based on two
approaches to air quality adjustment (drawn from Table 6-7 of the REA).
B <0.1 is used to represent nonzero estimates below 0.1%. A value of zero (0) indicates there were no individuals
estimated to have the selected decrement in any year.
c The highest single year result for at least 100% increase in sRaw was for Fall River where the estimate ranged
up to 1.9% (for the second air quality adjustment approach in REA, Table 6-10).
D The highest single year results for at least 200% increase in sRaw were for Indianapolis and Fall River where
the estimates ranged up to 0.4%,(REA, Table 6-10).
In understanding these results, we note that the three study areas provide a variety of
circumstances with regard to population exposure to short-term peak concentrations of SO2 in
ambient air. These three study areas reflect different combinations of different types of SO2
emissions sources, including utilities using fossil fuels and non-utility sources (REA, section
3.1), and illustrate three different patterns of exposure to SO2 concentrations in a populated area
in the U.S. (REA, section 5.1). In this way, the three areas provide a variety of examples of
exposure patterns that can be informative to the EPA's consideration of potential exposures and
risks that may be associated with air quality conditions occurring under the current SO2 standard.
57 The 1.3% estimate in the Indianapolis study area corresponds to approximately 140 children with asthma, and the
1.1% estimate for Fall River corresponds to 55 such children (REA, section 5.3 and Appendix J).
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While the same conceptual air quality scenario is simulated in all three study areas (i.e.,
conditions that just meet the existing standard), source and population characteristics in the study
areas contribute to variability in the estimated magnitude of exposure and associated risk across
study areas.
Where the higher SO2 concentrations that result from the sizeable SO2 sources in a study
area do not strongly coincide with parts of the area in which people reside and/or frequent, the
exposure and risk estimates for the 3-year period are relatively lower. The Tulsa study area
provides an example of such an area (REA, section 5.4). The relationship between SO2
concentrations and population in this area is illustrated in Figure 5-7 of the REA, which
illustrates the relationships between population distribution and locations with relatively lower
design values that contribute to this study area having exposure and risk estimates that are lower
than those estimated for the other two study areas (REA, section 5.1). These differences occur
even though total study area population size is similar to that for the Fall River study area (REA,
sections 5.1 and 5.4).
Where the simulated air quality conditions for a study area includes relatively large
spatial extents of higher concentrations - i.e., areas with design values in proximity to the level
of the standard - that overlap with the more populated parts of the study area, exposure and risk
results are relatively higher (REA, section 5.4). Among the three study areas, this best describes
the Fall River and Indianapolis study areas, which are areas where source characteristics
contribute to a sizeable spread of source-influenced relatively higher concentrations that coincide
or overlap with locations where people reside and/or frequent. This association between
concentrations and population in these two areas is illustrated in Figures 5-5 and 5-6 of the REA.
Inclusion of areas with these characteristics in the REA provides some insight into the potential
exposure and risk associated with other areas across the U.S. with similar characteristics and is
therefore particularly informative to evaluation of the level of protection provided by the
standard.
The REA provides exposure and risk estimates associated with air quality that might
occur in an area under conditions that just meet the current standard and, in so doing, it illustrates
the differences likely to occur across various locations with such air quality as a result of area-
specific differences in emissions and population characteristics. In the context of the overarching
question for the review regarding whether the currently available information calls into question
the adequacy of the current standard (see section 3.1.2 above), our discussions here and in the
sections below, accordingly, focus particularly on results for the areas with combinations of
emissions and population characteristics that contribute to relatively higher exposures and risk
(Indianapolis and Fall River).
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For these areas, the REA indicates that the percent of children with asthma that might be
expected to experience 5-minute SO2 concentrations at or above the 200 ppb benchmark
concentration, in an urban area that just meets the current standard, may be as high as 0.7%, on
average across the three years, and 2.2% in a single-year period (Table 3-3). With regard to the
300 ppb and 400 ppb benchmarks, these percentages may be as high, respectively, as 0.3 and
O.P/o on average across the three years and 0.8%> and 0.3% in a single-year period (Table 3-3).
With regard to the lung function risk, the REA indicates the percent of children that might be
expected to experience at least a doubling of specific airway resistance, under conditions just
meeting the current standard, may be as high as 1.3%, on average across the 3-year period, and
1.9% in a single year (Table 3-4).
In framing these same exposure estimates from the perspective of estimated protection
indicated to be provided by the current standard, these results for the Fall River and Indianapolis
study areas indicate that, in the single year with the highest concentrations across the 3-year
period, nearly 98% to just over 99% of the population of children with asthma would not be
expected to experience such a day with an exposure at or above the 200 ppb; between 99.1% and
just over 99.9% would not be expected to experience such a day with exposure at or above the
400 ppb benchmark. These and the similar estimates for a doubling or more in sRaw are of a
magnitude roughly consistent with the level of protection that was described in establishing the
now-current standard in 2010 (as summarized in section 3.1.1.2.4 above).58 As noted in section
3.2.2.1 above, the current REA additionally provides estimates for a 3-year simulation period,
consistent with the form established for the now-current standard. Such estimates for the
Indianapolis study area, on average across the 3-year period, indicate that 99.9% and 99.3% of
the population of children with asthma would not be expected to experience a day with an
exposure at or above 400 ppb and 200 ppb, respectively (Table 3-3 above).
3.2.2.3 Uncertainties
In this section, we consider the uncertainties associated with the quantitative estimates of
exposure and risk, including those recognized by the characterization of uncertainty in the REA
58 Although the 2009 REA did not include an air quality scenario representing the now-current standard, among the
scenarios it did include were single-year air quality scenarios representing standard levels of 100 and 50 ppb. For
the single-year scenario representing a standard level of 100 ppb in the study area with the highest population
exposure and risk (St. Louis), the 2009 REA estimated 2.7% of children with asthma to experience at least one
day with exposure at or above 200 ppb, while at elevated ventilation (2.1-2.9% to experience one or more SO2-
attributable increases in sRaw of at least 100%); this estimate was 0.09% for the scenario representing a standard
level of 50 ppb (0.4-0.9% to experience one or more SCh-attributable increases in sRaw of at least 100%) (2009
REA, Table 9-8 and Appendix B). While we recognize a number of differences between the 2009 REA and the
quantitative modeling and analyses performed in the current REA, we note that the single year estimates for the
Indianapolis and Fall River study areas in the current REA fall between the estimates for the two most similar air
quality scenarios assessed in the last review.
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(REA, section 6.2). The characterization in the REA is based on an approach intended to identify
and compare the relative impact that important sources of uncertainty may have on the exposure
and risk estimates. The approach used has been applied in REAs for past NAAQS reviews for
ozone, nitrogen oxides, carbon monoxide (U.S. EPA, 2008; 2010; 2014) and SOx (U.S. EPA,
2009). In the characterization of uncertainty for the current analysis, the REA utilized a
qualitative uncertainty characterization approach adapted from the WHO approach for
characterizing uncertainty in exposure assessment (WHO, 2008) accompanied by quantitative
sensitivity analyses of key aspects of the assessment approach. This characterization and
analyses are described in detail in chapter 6 of the REA. The approach used in the REA varies
from that of WHO (2008) in that the REA approach placed a greater focus on evaluating the
direction and the magnitude of the uncertainty (i.e., qualitatively rating how the source of
uncertainty, in the presence of alternative information, may affect the estimated exposures and
health risk results).
The characterization and analyses in the REA involve consideration of the various types
of inputs and approaches that together result in the exposure and risk estimates for the three
study areas. In so doing, the REA considers the limitations and uncertainties underlying these
inputs and approaches and the extent of their influence on the resultant exposure/risk estimates.
Consistent with the WHO (2008) guidance, the overall impact of the uncertainty is scaled by
considering the extent or magnitude of the impact of the uncertainty as implied by the
relationship between the source of the uncertainty and the exposure/risk output. The REA also
evaluated the direction of influence, indicating how the source of uncertainty was judged to
affect the exposure/risk estimates (e.g., likely to over- or under-estimation).
What are the key uncertainties associated with the exposure and risk estimates,
including those of particular significance with regard to drawing conclusions as to
the adequacy of the protection afforded by the current SO2 standard?
Based on the uncertainty characterization and associated analyses in the REA and
consideration of associated policy implications, we recognize several areas of uncertainty as
particularly important in our consideration of the exposure and risk estimates, as was also the
case in the last review. Generally, these areas include estimation of the spatial distribution of SO2
concentrations across each study area under air quality conditions just meeting the existing
standard, including the fine-scale temporal pattern of 5-minute concentrations. Among other
areas, we additionally recognize the uncertainty with regard to population groups and exposure
concentrations for which the health effects evidence base is limited or lacking.
With regard to the spatial distribution of SO2 concentrations, the REA recognizes some
uncertainty associated with the model estimates of 1-hour concentrations and the approach used
to adjust the air quality surface to concentrations just meeting the current standard. The REA
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analyzed the potential quantitative impact of this uncertainty on the exposure and risk estimates
by deriving estimates based on an alternative adjustment approach (described in section 6.2.2.1
of the REA). As discussed in section 3.2.2.2 above, we have considered estimates from both
approaches in summarizing the REA estimates. Additionally, we recognize uncertainty in the
estimation of concentrations associated with SO2 emissions sources not explicitly modeled (e.g.,
REA, Table 6-3) and in the estimates of 5-minute concentrations in ambient air across the
modeling receptors in each study area. While the ambient air monitoring dataset available to
inform these estimates is much expanded in this review over the dataset available in the last
review, we are still drawing on relationships occurring at one location and over one range of
concentrations to estimate the fine-scale temporal pattern in concentrations at other locations.
This is an important area of uncertainty in the REA results because the ambient air 5-minute
concentrations are integral to the 5-minute estimates of exposure. While we recognize this as an
important area of uncertainty, the approach used has taken into account the currently available
information and is considered to provide a reasonable representation of fine-scale temporal
variability in the three study areas.
We also recognize an important area of uncertainty that is particular to our interpretation
of the lung function risk estimates. This area concerns estimates of lung function risk derived for
exposure concentrations below those represented in the evidence base. The exposure-response
function on which the primary risk estimates are based generates non-zero predictions of a
percent of the at-risk population exposure expected to experience a day with at least a doubling
of sRaw for all exposures experienced while breathing at an elevated rate. In considering these
estimates, we recognize that the uncertainty in the response estimates increases substantially with
decreasing exposure concentration below those supported by study data. In so doing, we note the
appreciable contribution to the risk estimates of exposure concentrations below 200 ppb; the
large majority of 5-minute exposure concentrations contributing to estimated occurrences of a
doubling or more in sRaw were between 50 and 150 ppb, while none were below 40 ppb (REA,
section 5.3).
Other areas of uncertainty concern the potential influence of SO2 exposure history and
co-exposure to other pollutants on the relationship between short-term SO2 exposures and
respiratory effects. With regard to the former, we note that the assessment focuses on the daily
maximum 5-minute exposure during a period of elevated breathing rate, summarizing results in
terms of the days on which the magnitude of such exposure exceeds a benchmark or contributes
to increased sRaw. While the health effects evidence indicates the lack of a cumulative effect of
multiple exposures over several hours or a day (ISA, section 5.2.1.2), and a reduced response to
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repeated exercising exposure events over an hour (Kehrl et al., 1987),59 information is somewhat
limited with regard to the length of time after recovery from one exposure by which a repeat
exposure would elicit a similar effect as that of the initial event. With regard to the potential
influence of copollutants on SCh-related health risk, we note the very limited information
regarding the potential for the presence of other commonly occurring pollutants to affect
individual response to SO2, as summarized in section 3.2.1.4 above.
Another area of uncertainty, which remains from the last review and is important to our
consideration of the REA results, concerns the extent to which the quantitative results represent
the populations at greatest risk of effects associated with exposures to SO2 in ambient air. As
recognized in sections 3.2.1.1 and 3.2.1.4, the controlled human exposure study evidence base
does not include studies of children younger than 12 years old, and is extremely limited with
regard to studies of people with more severe asthma.60 The limited evidence that informs our
understanding of potential risk to these groups is uncertain but indicates the potential for them to
experience greater effects or have lesser reserve to protect against such effects than other
population groups with asthma under similar exposure circumstances, as summarized in section
3.2.1.4 above. Further we note the lack of information on the factors contributing to increased
susceptibility to SCh-induced bronchoconstriction among some people with asthma. Thus, there
is uncertainty associated with our interpretation of the exposure/risk estimates with regard to the
extent to which they represent the populations at greatest risk of S02-related respiratory effects
that is important to consideration of the exposure and risk results with regard to the adequacy of
protection provided by the current standard.
In summary, among the multiple uncertainties and limitations in data and tools that affect
the quantitative estimates of exposure and risk and their interpretation in the context of
considering the current standard, we recognize several here as particularly important, noting that
they are generally similar to uncertainties recognized in the last review. These include
uncertainty related to estimation of the spatial and temporal pattern of 5-minute concentrations in
ambient air for the current standard scenario; the prevalence of different exposure circumstances
represented by the three study areas; the lack of information from controlled human exposure
studies for the lower, more prevalent, concentrations of SO2; and, characterization of risk for
particular subgroups of people with asthma that may be at greater risk.
59 This study exposed mild asthmatic males to 1.0 ppm SO2 during three 10-minute exercise periods separated by
15-minute rest periods within the chamber. The sRaw response to SO2 decreased linearly from the first to the
second and the third SO2 exposures with the response following the third exposure being statistically less than
after the first (Kehrl et al., 1987).
60 We additionally recognize that limitations in the activity pattern information for children younger than five years
old precluded their inclusion in the populations of children simulated in the REA.
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3.2.2.4 Potential Public Health Implications
In considering public health implications of the quantitative exposure and risk estimates
that may inform the Administrator's judgments in this area, this section discusses the information
pertaining to the following question.
To what extent are the estimates of exposures and risks to at-risk populations that
remain under conditions just meeting the current SO2 standard important from a
public health perspective?
Several factors are important to consideration of public health implications. These
include the magnitude or severity of the effects associated with the exposures estimated in the
REA, as well as their adversity at the individual and population scale. Other important
considerations include the size of the population estimated to experience such effects or to
experience exposures associated with such effects. These considerations are discussed below.
Based on the currently available evidence which is largely consistent with that available
in the last review (as summarized in section 3.2.1 above), the quantitative exposure and risk
analyses focus on the potential for lung function decrements in people with asthma exposed to
SO2 while breathing at an elevated rate. Additionally, we have again focused on estimates for
two types of risk metrics, one involving comparison to benchmark concentrations and the second
involving estimates of lung function risk with regard to moderate or greater increases in sRaw. In
considering these estimates, we recognize that although the lung function decrements, which are
related to bronchoconstriction, are expected to be transient, we additionally recognize that such
decrements, while occurring, may contribute to a diminished reserve in lung function (ISA, p. 1-
17, section 5.2.1.2). For population groups already at diminished reserve, such as those with
more severe asthma, this may be particularly important. Thus, the discussion here reflects
consideration of the health evidence, and exposure and risk estimates, as well as the
consideration of potential public health implications in previous NAAQS decisions and ATS
policy statements (as also discussed in section 3.2.1.5).
In light of the conclusion that among all people with asthma, children may be particularly
at risk (summarized in section 3.2.1.2 above) and the REA findings of higher exposures and risks
for children (in terms of percent of that population), we have focused the discussion here on
children. We recognize that the REA estimates indicate that in some areas of the U.S. where SO2
concentrations just meet the current standard, on average across the 3-year period simulated
(consistent with the form of the current standard), less than 1%, 0.3% and 0.1% of the simulated
population of children with asthma might be expected to experience a single day per year with a
5-minute exposure at or above 200 ppb, 300 ppb and 400 ppb, respectively, while breathing at an
elevated rate. With regard to the lowest benchmark considered (100 ppb), the corresponding
percentage is approximately 20 to 25%, with higher percentages in some individual years.
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With regard to estimates of lung function decrements, the REA indicates that in some
such areas, approximately 1% of children with asthma, on average across a 3-year period, might
be expected to experience at least one day per year with a S02-related increase in sRaw of 100%
or more; the estimate for two or more days is lower, at 0.4% (REA, Table 6-8). Additionally,
under such conditions (just meeting the current standard), the estimated percent of children with
asthma that might be expected to experience a single day per year with a S02-related increase in
sRaw of 200% or more, on average across the 3-year period, is 0.2 to 0.3% (Table 3-4).
In considering the severity of responses associated with the REA estimates, we take note
of the health effects evidence for the different benchmark concentrations and judgments made
with regard to the severity of these effects in the last review. As in the last review, we recognize
that the responses documented for exposures of 400 ppb are frequently accompanied by
respiratory symptoms and thus are appropriately considered to be adverse respiratory effects
consistent with past and recent ATS position statements. At 300 ppb, statistically significant
increases in lung function decrements (specifically reduced FEVi) have been documented in
analyses of the subset of controlled human exposure study subjects with asthma that are
responsive to SO2 at concentrations below 600 or 1000 ppb (ISA, p. 153 and Table 5-21; Johns
et al., 2010). With regard to the lower benchmark concentration of 200 ppb, we recognize that,
while the responses documented in studies of exercising subjects with asthma are not
consistently accompanied by respiratory symptoms, conclusions in pastNAAQS reviews
recognized that moderate decrements in lung function can be clinically significant in some
individuals with asthma (75 FR 35526, June 22, 2010). Accordingly, the Administrator in the last
review considered effects associated with exposures as low as 200 ppb to be adverse in light of
CASAC advice,61 ATS statements and conclusions in past NAAQS reviews (75 FR 35546, June
22, 2010). While noting the very limited or lack of such information for some population groups
with asthma, including primary-school-age children and people with more severe asthma, we
additionally recognize the uncertainty with regard to effects that might be associated with
exposures as low as 100 ppb (as discussed in section 3.2.1.3 and 3.2.1.4 above).
The size of the at-risk population (people with asthma, particularly children) in the U.S.
is substantial. As summarized in section 3.2.1.5, nearly eight percent of the total U.S. population
(more than 24 million people) and 8.4% of U.S. children have asthma. The asthma prevalence in
U.S. child populations of different races or ethnicities ranges from 7.4% to 13.4% (Table 3-2
above). This is well reflected in the REA study areas in which the asthma prevalence ranged
from 8% to 8.7% of the total populations and 9.7% to 11.2% of the children, with the highest
61 In the last review, the CASAC letter on the first draft SO2 REA to the Administrator stated: "CASAC believes
strongly that the weight of clinical and epidemiology evidence indicates there are detectable clinically relevant
health effects in sensitive subpopulations down to a level at least as low as 0.2 ppm SO2" (Henderson, 2008).
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prevalence represented in the Fall River study area. In each study area, the prevalence varies
among census tracts, with the highest tract in Fall River having a prevalence in boys of 21.5%
and the highest tract in Indianapolis having a prevalence in girls of 19.4% (REA, Table 4-1).
In considering the public health implications of the REA estimates, we recognize that
current SO2 concentrations measured in ambient air in all three of the REA study areas are lower
than those simulated in the air quality assessed. In so doing, we note the purpose for the study
areas is to provide examples of exposure circumstances that may occur in areas that just meet the
current standard, and not to estimate exposure and risk associated with conditions occurring in
those specific locations today. However, concentrations in numerous areas across the U.S.
contribute to air quality that is near or above the existing standard. For example, 15 core-based
statistical areas62 were identified with 2014-2016 design values above the existing standard level
of 75 ppb, including areas with sizeable populations.63 Accordingly, we recognize that, while
concentrations in the specific areas simulated in the REA may be lower today than the three year
period simulated in the assessment, the exposure and risk estimates for these areas are
informative to consideration of exposures and risks in areas still existing across the U.S. that
have source and population characteristics similar to the study areas assessed, and with ambient
concentrations of SO2 that just meet the current standard today or that will be reduced to do so at
some period in the future. Thus, such air quality and exposure circumstances are of particular
importance in considering whether the currently available information calls into question the
adequacy of public health protection afforded by the current standard.
In considering the potential extent of similar areas is in the U.S. today, we recognize that
the monitoring network information on SO2 concentrations in populated areas across the U.S.
provides evidence of the occurrence of such exposure circumstances of interest in multiple
regions of the U.S. (as indicated by the 2014-2016 design values referenced above). There are,
however, limitations with regard to the extent that it might be expected to capture all areas with
the potential to exceed the standard and uncertainty related to the extent to which monitors in the
SO2 monitoring network are located in populated areas with air quality impacted by large sources
of SO2 emissions. In recognition of this limitation, we also examined the proximity of
populations to sizeable SO2 point sources using the most recently available emissions inventory
62 Core-based statistical area (CBSA) is a geographic area defined by the U.S. Office of Management and Budget to
consist of an urban area of at least 10,000 people in combination with its surrounding or adjacent counties (or
equivalents) with which there are socioeconomic ties through commuting. Populations in the 15 CBS As referred
to here range from approximately 30,000 to more than a million (based on 2016 U.S. Census Bureau estimates).
63 Table 5c. Monitoring Site Listing for Sulfur Dioxide 1-Hour NAAQS in the Excel file labeled
So2_designvalues_20142016_final_07_ 19_ 16. xlsx downloaded from https ://www. epa.gov/air-trends/air-quality-
design-values on January 26, 2018.
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information (2014). For example, this information indicates there to be many densely-populated
areas in the U.S. in which there are facilities with sizeable SO2 emissions (e.g., Appendix F).64
Information is not currently available to estimate numbers of children with asthma in such areas,
making it difficult to estimate the numbers of people potentially at risk. However, the available
information indicates that there are more than 300,000 children living within 1 km of facilities
emitting at least 1,000 tpy of SO2 and more than a million within 5 km (Table 3-5). Simply
considering the asthma prevalence at the national scale of approximately 8%, this information
indicates on the order of 24,000 to more than 100,000 children with asthma living in areas with
sources such as those assessed in the REA. It is important to clarify, however, that ambient air
concentrations of SO2 in the vast majority of the U.S. are well below the current standard, as
indicated by Figure 2-7 above.65 Thus, while the population counts in Table 3-5 may convey
information regarding the size of populations living near sources, the concentrations in most
areas are currently well below the conditions assessed in the REA.
Table 3-5. Population size near larger sources of SO2 emissions.
Sources emitting at least 1,000 tpy (N = 527 facilities)
Population within:
1 km
2 km
3 km
5 km
10 km
All Ages
1,309,212
1,529,478
2,625,196
6,067,574
23,161,915
Younger Than 18 Years
300,966
341,817
603,261
1,440,466
5,436,439
Sources emitting at least 2,000 tpy (N = 372 facilities)
Population within:
1 km
2 km
3 km
5 km
10 km
All Ages
248,007
438,760
1,281,473
2,969,007
14,280,740
Younger Than 18 Years
61,823
103,169
308,289
713,235
3,401,327
Sources: SO2 Facilities - NEI 2014 v2, Population - U.S. Census 2010
tpy = tons per year
64 Although source characteristics and meteorological conditions - in addition to magnitude of emissions - influence
the distribution of concentrations in ambient air, Appendix F focuses on the distribution of large sources, rather
than ambient concentrations, due to limitations in the available information with regard to spatial (and temporal)
patterns of SO2 concentrations in the proximity of such sources in urban areas (ISA, section 2.5.2.2).
65 As discussed in the ISA, "the point source nature of these emissions contributes to the relatively high spatial
variability of SO2 concentrations (both ambient and exposure)" and "[a]nother contributing factor to spatial
variability is the dispersion and oxidation of SO2 in the atmosphere" which results in "decreasing ambient SO2
concentrations with increasing distance from sources" (ISA, section 3.2.3). The ISA additionally notes that "SO2
from point sources travels as a plume, which may or may not impact portions of an urban area depending on
meteorological conditions" (ISA, section 3.2.3).
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Although exposure and risk estimates were not available in the last review for air quality
conditions just meeting the now-current standard, the findings and considerations summarized
here are generally similar to those considered in the last review, and indicate a level of protection
consistent with that described in the 2010 decision. The exposure and risk estimates for the three
study areas assessed in the REA for this review reflect differences in exposure circumstances
among those areas and illustrate the exposures and risk that might be expected to occur in other
areas with such circumstances under air quality conditions that just meet the current standard.
Thus, the REA estimates indicate the magnitude of exposure and risk that might be expected in
some areas and illustrate the importance to consideration of the public health protection afforded
by the current standard of those areas where locations of relatively higher SO2 concentrations in
ambient air across the area coincide with the locations of higher population density.
In summary, the considerations raised here are important to conclusions regarding the
public health significance of the REA results. We recognize that such conclusions also depend in
part on public health policy judgments that will weigh in the Administrator's decision in this
review with regard to the adequacy of protection afforded by the current standard. Such
judgments that are common to NAAQS decisions include those related to public health
implications of effects of differing severity (75 FR 355260 and 35536, June 22, 2010; 76 FR
54308, August 31, 2011; 80 FR 65292, October 26, 2015). Such judgments also include those
concerning the public health significance of effects at exposures for which evidence is limited or
lacking, such as effects at the lower benchmark concentrations considered and lung function risk
estimates associated with exposure concentrations lower than those tested in the controlled
exposure studies.
3.2.3 CASAC Advice
In our consideration of the adequacy of the current standard, in addition to the evidence-
and risk/exposure-based information discussed above, we have also considered the advice and
recommendations of the CASAC, based on their review of the ISA, the REA Planning
Document, the draft REA, and the earlier draft of this document, as well as comments from the
public on the earlier draft of this document.
A limited number of public comments have been received in this review to date,
including comments focused on the draft IRP, the REA Planning Document, the draft REA or
the draft PA. Of the five commenters that addressed adequacy of the current primary SO2
standard, two are in agreement with staff conclusions in the draft PA. One expressed the view
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that the standard should be revised to be more restrictive and two others recommended
consideration be given to a less restrictive standard.66
In their comments on the draft PA, the CAS AC SOx Panel concurred with staffs overall
preliminary conclusions that it is appropriate to consider retaining the primary current standard
without revision, stating that "the current scientific literature does not support revision of the
primary NAAQS for SO2" (Cox and Diez Roux, 2018, p. 1 of letter). The CAS AC further noted
that "the new scientific information in the current review does not lead to different conclusions
from the previous review" (Cox and Diez Roux, 2018, p. 3 of letter). Thus, the CAS AC stated
that "based on review of the current state of the science, the CASAC supports retaining the
current standard, and specifically recommends that all four elements (indicator, averaging time,
form, and level) should remain the same" (Cox and Diez Roux, 2018, p. 3 of letter). The CASAC
further stated the following (Cox and Diez Roux, 2018, p. 3 of the letter):
With regard to indicator, SO 2 is the most abundant of the gaseous SOx species.
Because, as the PA states, "the available scientific information regarding health
effects was overwhelmingly indexed by SO2 ", it is the most appropriate indicator.
The CASAC affirms that the one-hour averaging time will protect against high 5-
minute exposures and reduce the number of instances where the 5-minute
concentration poses risks to susceptible individuals. The CASAC concurs that the
99th percentile form is preferable to a 98th percentile form to limit the upper end
of the distribution of 5-minute concentrations. Furthermore, the CASAC concurs
that a three-year averaging time for the form is appropriate.
The choice of level is driven by scientific evidence from the controlled human
exposure studies used in the previous NAAQS review, which show a causal effect
of SO 2 exposure on asthma exacerbations. Specifically, controlledfive-minute
average exposures as low as 200ppb lead to adverse health effects. Although
there is no definitive experimental evidence below 200ppb, the monotonic dose-
response suggests that susceptible individuals could be affected below 200 ppb.
Furthermore, short-term epidemiology studies provide supporting evidence even
though these studies cannot rule out the effects of co-exposures and are limited by
the available monitoring sites, which do not adequately capture population
exposures to SO2. Thus, the CASAC concludes that the 75ppb average level,
based on the three-year average of 99th percentile daily maximum one-hour
concentrations, is protective and that levels above 75 ppb do not provide the same
level of protection.
The comments from the CASAC also took note of the uncertainties that remain in this
review, stating that the PA "clearly identifies most of the key uncertainties," while additionally
66 All written comments submitted to the Agency will be available in the docket for this rulemaking, as will be
CASAC letters reflecting its review of the earlier draft of this document, of the REA Planning Document and
draft REA and of drafts of the ISA.
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recognizing several additional uncertainties, including uncertainties in quantifying risk to some
subpopulations of people with asthma for which there may be potential for increased SO2
sensitivity but for which the scientific evidence is limited or lacking. In so doing, it stated that
the "CASAC notes that there are many susceptible subpopulations that have not been studied and
which could plausibly be more affected by SO2 exposures than adults with mild to moderate
asthma," providing as examples people with severe asthma and obese children with asthma, and
citing physiologic and clinical understanding (Cox and Diez Roux, 2018b, p. 3 of letter). The
CASAC stated that "[i]t is plausible that the current 75 ppb level does not provide an adequate
margin of safety in these groups[, hjowever because there is considerable uncertainty in
quantifying the sizes of these higher risk subpopulations and the effect of SO2 on them, the
CASAC does not recommend reconsideration of the level at this time" (Cox and Diez Roux,
2018b, p. 3 of letter).
The CASAC additionally recognized a number of areas for future research and data
gathering that would inform the next primary SO2 NAAQS review (Cox and Diez Roux, 2018).
These are reflected in section 3.3 below.
3.2.4 Staff Conclusions on the Current Standard
This section describes staff conclusions regarding the adequacy of the current primary
SO2 standard. These conclusions are based on considerations described in the sections above,
and in the discussion below regarding the currently available scientific evidence (as summarized
in the ISA, and the ISA and AQCDs from prior reviews), and the risk and exposure information
drawn from the REA. Further, these staff conclusions have taken into account advice from the
CASAC and public comment on the draft PA and the associated preliminary staff conclusions.
Taking into consideration the discussions responding to specific questions above in this
and the prior chapter, this section addresses the following overarching policy question.
Does the currently available scientific evidence- and exposure/risk-based
information, as reflected in the ISA and REA, support or call into question the
adequacy of the protection afforded by the current SO2 standard?
In considering this question, we recognize as an initial matter that, as is the case in
NAAQS reviews in general, the extent to which the current primary SO2 standard is judged to be
adequate will depend on a variety of factors, including science policy judgments and public
health policy judgments. These factors include public health policy judgments concerning the
appropriate benchmark concentrations on which to place weight, as well as judgments on the
public health significance of the effects that have been observed at the exposures evaluated in the
health effects evidence. The factors relevant to judging the adequacy of the standards also
include the interpretation of, and decisions as to the weight to place on, different aspects of the
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results of the exposure assessment for the three areas studied and the associated uncertainties.
Thus, we recognize that the Administrator's conclusions regarding the adequacy of the current
standard will depend in part on public health policy judgments, science policy judgments
regarding aspects of the evidence and exposure/risk estimates, and judgments about the level of
public health protection with an adequate margin of safety that is requisite under the Clean Air
Act.
Our response to the overarching question above takes into consideration the discussions
that address the specific policy-relevant questions in prior sections of this document (see sections
3.2.1-3.2.2) and the approach described in section 3.1 that builds on the approach from the last
review. We focus first on consideration of the evidence, including that newly available in this
review, and the extent to which it alters key conclusions supporting the current standard. We
then turn to consideration of the quantitative exposure and risk estimates drawn from the REA,
including associated limitations and uncertainties, and the extent to which they indicate differing
conclusions regarding the magnitude of risk, as well as level of protection from adverse effects,
associated with the current standard. We additionally consider the key aspects of the evidence
and exposure/risk estimates emphasized in establishing the now-current standard, and the
associated public health policy judgments and judgments about the uncertainties inherent in the
scientific evidence and quantitative analyses that are integral to decisions on the adequacy of the
current primary SO2 standard.
As an initial matter, we recognize the support in the current evidence for SO2 as the
indicator for SOx. As recognized in section 3.2.1.1 above, "[o]f the sulfur oxides, SO2 is the
most abundant in the atmosphere, the most important in atmospheric chemistry, and the one most
clearly linked to human health effects" (ISA, p. 2-1). Controlled human exposure studies and
animal toxicological studies provided specific evidence for health effects following exposures to
SO2, and epidemiologic studies typically analyzed associations of health outcomes with
concentrations of SO2. The advice received from the CASAC in this review concurs with the use
of SO2 as the indicator for the standard. We additionally note that measures taken to meet the
standard in terms of SO2 that may reduce population exposures to SO2 are also likely to reduce
exposures to other sulfur oxides. Thus, we conclude that the current evidence, including that
newly available in this review, continues to support a focus on SO2 for the primary NAAQS for
SOx.
In considering the currently available evidence, staff gives great weight to the long-
standing body of health effects evidence for SO2, augmented in some aspects since the last
review, that provides the foundation of our understanding of the health effects of SO2 in ambient
air. In so doing, we give particular attention to the evidence from controlled human exposure
studies that demonstrates that very short exposures to less than 1000 ppb SO2, while breathing at
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an elevated rate, induces bronchoconstriction in some people with asthma; and, supports the
identification of people with asthma as the population at risk from short-term peak
concentrations in ambient air (ISA; 2008 ISA; 1994 AQCD supplement).
It is such effects associated with short-term exposures against which the current standard,
with its averaging time of one hour, was established to protect. As summarized in section 3.2.1
above and addressed in detail in the ISA, the evidence base in this review does not include new
evidence of effects associated with other exposure durations. Thus, in considering the
information available at this time, we continue to focus on short-term exposures as those of
importance in this review. Air quality analyses summarized in chapter 2 above demonstrate the
relationship between 1-hour and 5-minute SO2 concentrations in ambient air as did those
available at the time the standard was set. Further, the chapter 2 analyses indicate the appreciably
lower prevalence of elevated 5-minute concentrations in areas meeting the current standard
compared to those that do not (e.g., Figure 2-8 above). As discussed below, protection is also
provided against exposures associated with such ambient air concentrations.
Further, while the evidence base has been augmented since the time of the last review, we
note that the newly available evidence does not lead to different conclusions regarding the
primary health effects of SO2 in ambient air or regarding exposure concentrations associated
with those effects; nor does it identify different populations at risk of S02-related effects. In this
way, the health effects evidence available in this review is consistent with evidence available in
the last review when the current standard was established. This strong evidence base continues to
demonstrate a causal relationship between short-term SO2 exposures and respiratory effects,
particularly in people with asthma. This conclusion is primarily based on evidence from
controlled human exposure studies available at the time of the last review that reported lung
function decrements and respiratory symptoms in people with asthma exposed to SO2 for 5 to 10
minutes while breathing at an elevated rate. Support is also provided by the epidemiological
evidence that is coherent with the controlled exposure studies. The epidemiological evidence,
including that recently available, includes studies reporting positive associations for asthma-
related hospital admissions and emergency department visits (of individuals of all ages,
including adults and children) with short-term SO2 exposures (ISA, section 5.2.1.2).67
The health effects evidence newly available in this review also does not extend our
understanding of the range of 5-minute exposure concentrations that elicit effects in people with
asthma exposed while breathing at an elevated rate beyond what was understood in the last
review. As in the last review, 200 ppb remains the lowest concentration tested in exposure
67 While uncertainties remain related to the potential for confounding by PM or other co-pollutants and the
representation of fine-scale temporal variation in personal exposures, the findings of the epidemiological studies
continue to provide supporting evidence for the conclusion on the causal relationship (ISA, section 5.2.1.2).
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studies where study subjects are freely breathing in exposure chambers. At that exposure
concentration, approximately eight to nine percent of study subjects with asthma, breathing at an
elevated rate, experienced moderate or greater lung function decrements following 5- to 10-
minute controlled exposures. The limited information available for exposure concentrations
below 200 ppb, while not amenable to direct quantitative comparisons with information from
studies at higher concentrations, generally indicates somewhat lesser response. In considering
what may be indicated by the epidemiological evidence with regard to exposure concentrations
eliciting effects, we recognize complications associated with interpretation of epidemiologic
studies of SO2 in ambient air that relate to whether measurements at the study monitors
adequately represent the spatiotemporal variability in ambient SO2 concentrations in the study
areas and associated population exposures (ISA, section 5.2.1.9).
In this review, as in the last review, we recognize some uncertainty with regard to
exposure levels eliciting effects in some population groups not included in the available
controlled human exposure studies, such as individuals with severe asthma, as well as
uncertainty in the extent of effects at exposure levels below those studied. Collectively, these
aspects of the evidence and associated uncertainties contribute to a recognition that for SO2, as
for other pollutants, the available evidence base in a NAAQS review generally reflects a
continuum, consisting of ambient levels at which scientists generally agree that health effects are
likely to occur, through lower levels at which the likelihood and magnitude of the response
become increasingly uncertain.
As at the time of the last review, the exposure and risk estimates developed from
modeling exposures to SO2 emitted into ambient air are critically important to consideration of
the potential for exposures and risks of concern under air quality conditions of interest, and
consequently are critically important to judgments on the adequacy of public health protection
provided by the current standard. In considering the public health implications of estimated
occurrences of exposures of different magnitudes, we take note of guidance from the ATS, the
CASAC's written advice and recommendations in past reviews, and judgments made by the EPA
in considering similar effects in previous NAAQS reviews (75 FR 35526 and 35536, June 22,
2010). As recognized in section 3.2.1.5, an additional publication by the ATS that further
addresses judgments on what constitutes an adverse health effect of air pollution is newly
available in this review (Thurston et al., 2017). The more recent statement expands upon the
2000 statement, that was considered in the last SO2 NAAQS review, and recognizes additional
considerations with regard to such judgments that remain consistent with the EPA's judgments in
the 2010 review. In that review, the Administrator judged that the effects reported in exercising
people with asthma following 5- to 10-minute SO2 exposures at or above 200 ppb, and especially
at or above 400 ppb (often accompanied by respiratory symptoms and for which the evidence is
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stronger), can result in adverse health effects (75 FR 35536, June 22, 2010). In so doing, she also
recognized that effects reported for exposures below 400 ppb are less severe than those at and
above 400 ppb (75 FR 35547, June 22, 2010).
In considering the REA analyses available in this review, we are aware of a number of
ways in which these analyses differ from and improve upon those available in the last review. In
addition to the expansion in the number and type of study areas assessed, we note the number of
improvements to input data and modeling approaches, including the availability of continuous 5-
minute air monitoring data at monitors within the three study areas. The current REA extends the
time period of simulation by including a 3-year simulation period consistent with the form
established for the now-current standard. Further, the years simulated reflect more recent
emissions and circumstances subsequent to the 2010 decision. In considering the REA results,
we also take note of the array of emissions and exposure circumstances represented by the three
study areas. As summarized in section 3.2.2 above, the areas fall into three different geographic
regions of the U.S. They range in total population size from approximately 180,000 to
approximately one half million, and vary in population demographic characteristics.
Additionally, the types of large sources of SO2 emissions represented in the three study areas
vary with regard to emissions characteristics and include EGUs, petroleum refineries, glass-
making facilities, secondary lead smelters (from battery recycling), and chemical manufacturing.
As at the time of the last review, people with asthma are the population at risk of
respiratory effects related to SO2 in ambient air. Children with asthma may be particularly at risk
(section 3.2.1.2 above). While there are more adults in the U.S. with asthma than children with
asthma, the REA results in terms of percent of the simulated at-risk populations, indicate higher
exposures and risks for children with asthma as compared to adults. This finding relates to
children's greater frequency and duration of outdoor activity (section 3.2.2.2 above). In light of
these conclusions and findings, we have focused our consideration of the REA results here on
children.
As can be seen by the variation in exposure estimates, the three study areas in the REA
represent an array of exposure circumstances, including those contributing to relatively higher
and relatively lower exposures and associated risk. As recognized in the REA and in section
3.2.2.2 above, the analyses in the REA are not intended to provide a comprehensive national
assessment. Rather, the analyses for this array of study areas and air quality patterns are intended
to indicate the magnitude of exposures and risks that may be expected in areas of the U.S. that
just meet the current standard but that may differ in ways affecting population exposures of
interest. In that way, the REA is intended to be informative to the EPA's consideration of
potential exposures and risks associated with the current standard and the Administrator's
decision on the adequacy of protection provided by the current standard. As discussed in sections
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3.2.2.2 and 3.2.2.4 above, consideration of exposures occurring in those areas where locations of
relatively higher SO2 concentrations in ambient air across an area that just meets the current
standard coincide with the locations of higher population density are particularly important to
consideration of the public health protection afforded by the current standard, particularly to the
overarching question concerning the availability of information that calls into question the
standard's adequacy.
With regard to the REA representation of air quality conditions associated with just
meeting the current standard, while we note reduced uncertainty in a few aspects of the approach
for developing this air quality scenario, we recognize the uncertainty associated with the
application of adjustments to the highest model receptor in the study area. As summarized in
sections 3.2.2.2 and 3.2.2.3 above, sensitivity analyses described in section 6.2.2 of the REA
indicate the quantitative impact potentially associated with this area of uncertainty, which
appears to be generally small for the Indianapolis study area and somewhat higher for Fall River.
Given the importance of this aspect of the REA to consideration of the level of protection
provided by the current standard, we have considered the results for each study area in terms of a
range bounded on the low end by the results for the main analysis and on the upper end by those
based on the alternative adjustment approach used in the sensitivity analysis.
In this context for the air quality scenario for the current standard, with its 1-hour
averaging time and 99th percentile form, we note that across all three study areas, which provide
an array of SO2 emissions and exposure situations, the percent of children with asthma estimated
to experience at least one day with as much as a doubling in sRaw (attributable to SO2), on
average across the 3-year period, ranges from <0.1 % to 1.3%; the highest study area estimate is
just under 2% for the highest single year (Table 3-4). Accordingly, results for the three case
study areas indicate 98.7% or more of at-risk populations to be protected from a S02-related
doubling in sRaw, as an average across the 3-year period, and approximately 98% or more
protected from as much as a single occurrence in a single year. Greater protection (e.g., 99% or
more) is indicated for multiple occurrences and more severe sRaw increases.
With regard to exposures compared to benchmark concentrations, less than 1% of
children with asthma are estimated to experience, while breathing at an elevated rate, a daily
maximum 5-minute exposure per year at or above 200 ppb, on average across the 3-year period,
with a maximum for the study area with the highest estimates just over 2% in the highest single
year (Table 3-3). Further, the percentage for at least one day with such an exposure above 400
ppb is O.P/o or less, as an average across the 3-year period (and 0.3% or less in each of the three
years simulated across the three study areas). No simulated at-risk individuals were estimated to
experience multiple such days. Thus, in light of current ATS guidance and CASAC advice, as
well as EPA conclusions in prior NAAQS reviews, the REA exposure and risk estimates for the
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current review indicate that the current standard is likely to provide a high level of protection
from S02-related health effects to at-risk populations of children and adults with asthma.
As recognized above, the protection afforded by the current standard stems from its
elements collectively, including the level of 75 ppb, the averaging time of one hour and the form
of the 99th percentile of daily maximum concentrations averaged across three years. The current
evidence as considered in the ISA, the current air quality information as analyzed in the REA
and earlier in this document, and the current risk and exposure information presented in the REA
and summarized here provide continued support to these elements, as well as to the current
indicator, as discussed earlier in this section.
In summarizing the information discussed thus far, we reflect on the key aspects of the
2010 decision that established the current standard. As an initial matter, effects associated with
5- to 10-minute exposures as low as 200 ppb of people with asthma while breathing at an
elevated rate were considered to be adverse; this judgment was based on consideration of the
CASAC's advice and EPA decisions in prior NAAQS reviews, as well as ATS guidance (75 FR
35546, June 22, 2010). We note that the newly available information in this review includes an
additional statement from ATS on adversity which is generally consistent with the earlier
statement (available at the time of the 2010 decision).
While recognizing the differences between the current and past analyses, including the
lack of an air quality scenario specific to the now-current standard in the last review, as well as
uncertainties associated with such analyses, we note a rough consistency of the associated
estimates when considering the array of study areas in both reviews. Overall, the newly available
quantitative analyses appear to comport with the conclusions reached in the last review regarding
control expected to be exerted by the now-current 1-hour standard on 5-minute exposures of
concern. With regard to the results for the REA in the last review (which were for a single-year
simulation), the 2010 decision recognized those results for the area with the highest estimates
and largest population (St. Louis) to indicate that a one-hour standard with a level between the
two levels assessed (50 and 100 ppb) might be expected to protect more than 97% of children
with asthma (and somewhat less than 100%) from experiencing exposures at or above a 200 ppb
benchmark concentration, and more than 99% of that population group from experiencing
exposures at or above a 400 ppb benchmark. Single-year results in the current REA for the two
study areas with the highest estimates (including the area with the most sizeable population,
Indianapolis) indicate protection of approximately 98 to 99% of the populations of children with
asthma from experiencing exposures at or above a 200 ppb benchmark concentration and 99.1%
or more of the study area at-risk populations from exposures at or above 400 ppb. Additionally,
the 2010 decision also took note of the magnitude of the SO2 concentrations in ambient air in
U.S. epidemiological studies of associations between ambient air concentrations and emergency
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department visits and hospital admissions, for which the effect estimate remained positive and
statistically significant in copollutant models with PM. In considering these studies, the
Administrator judged that the level chosen for the new 1-hour standard provided an adequate
margin of safety. No additional such studies are available in the current review (as noted in
section 3.2.1.3 above). Thus, in considering the main aspects of the decision in the last review,
we find the currently available information to be consistent with that on which the decision
establishing the current standard was based.
Based on all of the above, and taking into consideration related information, limitations
and uncertainties, such as those recognized above, we draw conclusions regarding the extent to
which the newly available information in this review supports or calls into question the adequacy
of protection afforded by the current standard. In considering the conclusions that may be
supported by the exposure and risk estimates, we take note of the more than 24 million people
with asthma in the U.S., including more than 6 million children, with potentially 100,000 living
within 5 km of large sources of SO2 emissions. We additionally note the uncertainties or
limitations of the current evidence base with regard to the exposure levels at which effects may
be elicited in some population groups (e.g., children with asthma and individuals with severe
asthma), as well as the severity of the effects. In so doing, we recognize that the controlled
human exposure studies, on which the depth of our understanding of SCh-related health effects is
based, provide little or no information with regard to responses in people with more severe
asthma or in children younger than 12 years. Additionally, some aspects of our understanding
continue to be limited; among these aspects are the potential for effects in some people with
asthma exposed to concentrations below 200 ppb, as well as the potential for other air pollutants
to affect responses to SO2. In light of this we note the REA results for the lowest benchmark that
indicate that in some areas of the U.S. with air quality conditions that just meet the current
standard, approximately 20 to 25% of children with asthma may experience one or more
exposures, on average across a 3-year period, to concentrations at or above 100 ppb while
breathing at an elevated rate. Thus, the evidence and exposure/risk information related to the
lowest exposures studied lead us to conclude that the combined consideration of the body of
evidence and the quantitative exposure estimates continue to provide support for a standard as
protective as the current one.
We additionally recognize that conclusions regarding the adequacy of the current
standard depend in part on public health policy judgments identified above and judgments about
the level of public health protection that is appropriate, allowing for an adequate margin of
safety. In so doing, we take note of the long-standing health effects evidence that documents the
effects of SO2 exposures as short as a few minutes on people with asthma that are exposed while
breathing at elevated rates and recognize that such effects have been documented in the lowest
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concentration studied in exposure chambers with appropriate clean-air controls (200 ppb). In so
doing, we recognize the limitations, and associated uncertainty, in the evidence available for
lower exposure concentrations (e.g., 100 ppb), as was the case in the last review, and we note the
lower responses reported. Thus, in focusing on the potential for 5-minute exposures at and above
200 ppb, and recognizing that it has been previously recognized that exposures to such
concentrations can result in adverse health effects in people with asthma (June 22, 2010; 75 FR
35547), we take note of the REA results that indicate the current standard may be expected to
protect approximately 98% and nearly 99% of populations of children with asthma from
experiencing any days with such exposures, in a single- and 3-year period, respectively. We
additionally note the REA results that indicate protection of at least 99.1% and 99.9% of children
with asthma from experiencing any days with a 5-minute exposure of 400 ppb or higher in a
single and 3-year period, respectively. In light of ATS guidance, CAS AC advice and EPA
conclusions in pastNAAQS reviews, these results indicate a high level of protection of at-risk
populations from SCh-related health effects that we note is consistent with the level of protection
specified when the standard was set. Thus, we reach the conclusion that the currently available
evidence and quantitative information, including the associated uncertainties, do not call into
question the adequacy of protection provided by the current standard, and thus support
consideration of retaining the current standard, without revision.
In summary, the newly available health effects evidence, critically assessed in the ISA as
part of the full body of evidence, reaffirms conclusions on the respiratory effects recognized for
SO2 in the last review. Further, we observe the general consistency of the current evidence with
the evidence that was available in the last review with regard to key aspects on which the current
standard is based. We additionally note the quantitative exposure and risk estimates for
conditions just meeting the current standard that indicate a similar level of protection, for at-risk
populations from respiratory effects considered to be adverse, as that described in the last review
for the now-current standard. We also recognize, as in the last review, the limitations and
uncertainties associated with the available information. Collectively, these considerations
(including those discussed above) provide the basis for the staff conclusion that consideration
should be given to retaining the current standard of 75 ppb SO2, as the 99th percentile of daily
maximum 1-hour concentrations averaged across three years, without revision. Accordingly, and
in light of this conclusion that it is appropriate to consider the current standard to be adequate,
we have not identified any potential alternative standards for consideration in this review.
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3.3 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH
AND DATA COLLECTION
In this section, we highlight key uncertainties associated with reviewing and establishing
the primary NAAQS for sulfur oxides. Such key uncertainties and areas for future research,
model development, and data gathering are outlined below. In some cases, research in these
areas can go beyond aiding standard setting to aiding in the development of more efficient and
effective control strategies. We note, however, that a full set of research recommendations to
meet standards implementation and strategy development needs is beyond the scope of this
discussion. Rather, listed below are key uncertainties, research questions and data gaps that have
been thus far highlighted in this review of the primary standard.
A critical aspect of our consideration of the evidence and the quantitative dose estimates
is our understanding of SO2 effects below the lowest concentrations studied in controlled
human exposure studies. Additional information in several areas would reduce
uncertainty in our interpretation of the available information for purposes of risk
characterization and, accordingly, reduce uncertainty in characterization of SCh-related
health effects.
- A key area of uncertainty relates to whether and to what extent some population
groups, including young children or people with severe asthma, are more
responsive to peak SO2 exposures (or responsive to lower concentrations), while
breathing at elevated rates, than the groups that have been studied.
- Additional information that might improve our understanding of the effects
(severity and occurrence) and the shape of the exposure-response relationship
expected at lower 5-minute exposure concentrations (i.e., below 200 ppb) would
help to reduce uncertainty in the estimates of lung function effects and,
accordingly, in characterizing S02-related health effects.
- A better understanding of the demographic characteristics of people with asthma
would facilitate greater detail in our characterization of SO2 exposure and risk for
at-risk populations with asthma. For example, the CASAC has identified people
with asthma who are obese and/or African American, as well as young children
and those with severe asthma as population groups for which such information is
needed.
- Little information is available on the factors contributing to the susceptibility to
lower concentrations of SO2 of a subgroup of people with asthma, termed
"responders" in the ISA (ISA, section 5.2.1.2, Table 5-21; Johns and Linn, 2011).
New and innovative studies focused on characterizing this subgroup would
contribute to improved characterization of S02-related risk.
- There is also only very limited evidence regarding the potential influence of
history of exposure and potential for enhanced effects associated with co-
occurring exposure to other air pollutants, such as particulate matter, including
particulate sulfur compounds (as recognized in section 3.2.1.4 above). Further
research is needed in this area to better inform our characterization of health risk
related to SO2.
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Characterization of the fine-scale spatial and temporal gradients of ambient air SO2
concentrations in residential areas, as well as near sources of SO2 emissions in areas with
air quality that just meets the current standard, is a key element in our assessment of
exposure and risk. Additional information in this area is needed to address current
limitations that contribute to uncertainty in characterization of ambient air SO2 levels in
the risk assessment and the resulting exposure and risk estimates.
- Ambient air monitoring data that provides more detailed characterization of the
fine-scale spatial and temporal variation in ambient air SO2 concentrations in
different environments and related to different sources would help reduce this
uncertainty and might support further evaluation of air quality model performance
in describing fine-scale spatial variation.
- Additional fine-scale temporal monitoring data (e.g., reporting of all 12 5-minute
concentrations for each hour at all ambient air monitors) would help to reduce
uncertainty in our estimation of fine-scale temporal variation.
Uncertainties with regard to other aspects of the health effects evidence include that
regarding what may be indicated with regard to exposure concentrations eliciting effects
by the epidemiologic studies that show an association between short-term SO2 exposures
and asthma-related hospital admission and emergency department visits. Uncertainty
remains regarding the extent of copollutant confounding in these studies, particularly by
PM. Additionally, there is uncertainty related to the representation of exposure through
fixed site monitors and capturing peak SO2 concentrations that limits the informativeness
of the ambient air concentrations analyzed in the studies to standard reviews.
National surveys provide information that supports national and regional estimates of
asthma prevalence. Additional clarity in this survey information regarding asthma
prevalence in additional population subgroups, such as those with obesity, as well as
clarity with regard to the extent of the potential for underestimation related to people with
undiagnosed asthma, would address some uncertainties noted in this review.
While the CHAD is much expanded over the last review, limited information and
associated uncertainty remain in several aspects of the available human activity data.
Additional information would reduce uncertainty in these aspects of our exposure and
risk estimates.
- Collection and analysis of multiday activity patterns that consider the attributes
most influential to determining long-term activity patterns, as well as related
research, would improve our ability to better evaluate and improve on existing
approaches used to generate longitudinal activity profiles (as discussed in the
REA, section 4.3.4).
- Activity data for some population subgroups, such as people with severe asthma
and very young children with asthma, as well as people with asthma of different
ethnic backgrounds, including African Americans, and also people with asthma
who are obese, would address limitations in the information needed to address
questions related to the potential for activity patterns and, accordingly, exposures
to differ for such groups.
3-68
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3-73
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APPENDIX A
PREPARATION OF DATA FILES FOR GENERATION OF FIGURES IN CHAPTER 2
The raw data came from pre-generated AQS extract files. Files are located at
https://aqs.epa.gov/aqsweb/airdata/download files.html. Documentation of files is located at
http://aqsdrl.epa.gov/aqsweb/aqstmp/airdata/FileFormats.html. Hourly Data Files were used. A
separate Hourly Data File for each parameter and year combination was run. The type of SO2
data is determined by the parameter code and duration code and is coded as follows:
1-hour values data - parameter code = 42401 and duration code = 1
5-minute data (12 observations per hour) - parameter code = 42401 and duration code = H
5-minute data (hourly max) - parameter code = 42406 and duration code = 1
For the 1-hour data at a Site/POC to be used, it must have met the following
completeness criteria:
75% or more of the hourly observations in a day (18 or more) must be present.
75% or more of the days in a quarter must be present and complete:
1st Quarter - 68 observations or 69 observations in leap year
- 2nd Quarter - 69 observations
- 3rd Quarter - 69 observations
- 4th Quarter - 69 observations
4 quarters for each of at least 3 of the 5 years (2011-2016) must be present and complete.
For this analytical purpose, the three years do not have to be consecutive. This dataset
was prepared in February 2018.
After completeness criteria were applied, the following data screens were also performed
to account for some outliers in the 5-minute data:
Only 5 minute data with a corresponding hourly value in AQS (parameter 42401 and
duration code 1) were kept.
Only 5 minute values with an hourly mean value under 120% of the hourly value in AQS
(parameter 42401 and duration code 1) were kept.
Only hours where a 5-minute max hourly value (AQS parameter 42406 and duration code
1) was reported and fell between 1 and 12 times the AQS hourly value (parameter 42401
and duration code 1) were kept.
A-l
-------
APPENDIX B
ADDITIONAL INFORMATION ON DATASETS PRESENTED IN FIGURE 2-8
Table B-l. Summary statistics (in ppb) for distributions of daily maximum 5-minute
SO2 concentrations on days with differing daily maximum 1-hour SO2
concentrations for 2014-2016.
Daily Maximum 1-hour Concentration (ppb)
<=25 >25-50 >50-75 >75
N
339471
4732
1338
1272
25th percentile
0.8
47.2
95.8
170.1
Median
1.2
62.8
122.6
218.0
Mean
4.4
73.7
137.4
259.5
75th percentile
4.2
88.0
164.2
293.6
95th percentile
19.0
150.0
254.5
512.4
99th percentile
40.5
213.2
352.4
829.6
When the three data sets for sites with DVs at or below 75 ppb are combined, the
99th percentile is 53.3 ppb and the 99.9th percentile is 131 ppb.
Table B-2. Summary statistics (in ppb) for distributions of daily maximum 5-minute
SO2 concentrations at sites with differing design values for 2014-2016.
Bin
<=25
Design Value (ppb)
>25-50 >50-75
>75
N
259617
48951
19634
18611
25th percentile
0.6
1.5
2.0
2.0
Median
1.5
4.0
6.0
6.0
Mean
3.1
9.8
18.5
38.3
75th percentile
3.1
11.3
23.0
35.7
95th percentile
11.0
36.3
75.0
192.0
99th percentile
26.0
72
130.3
359.3
B-l
-------
Figure B-l. Monitoring data for sites meeting the current standard: Frequency of daily
maximum 5-minute values on days with differing daily maximum 1-hour concentrations
(2014-2016).
o
o
O
250
200
150
25-50 >50-75
Maximum Hourly Concentrations (ppb)
>75
#>100 ppb h# >200 ppb Hi1 #>300 ppb a #>400 ppb
Figure B-2. Monitoring data for sites not meeting the current standard: Frequency of daily
maximum 5-minute values on days with differing daily maximum 1-hour concentrations
(2014-2016).
1200
1000
800
o
o
O
4)
-Q
ฃ
600
400
200
<=25 >25-50 >50-75
Maximum Hourly Concentrations (ppb)
>75
#>1G0ppb n # >200 ppb flu # >300 ppb ฆ # >400 ppb
B-2
-------
APPENDIX C
OCCURRENCES OF 5-M1NUTE S02 CONCENTRATIONS OF INTEREST
IN THE RECENT AMBIENT AIR MONITORING DATA (2014-2016)
As Is Air Quality (2014-2016): Mean Number of Days per Year
Daily Maximum 5-minute S02 At or Above 100 ppb
E
=3
E
X
CO
100
03
Q
i_
(T3
ฃ
CD
CL
to
>*
OJ
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o
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<
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<
oJ
0
CO
c
E
1
LD
TO
<1)
20
-r
Observation: For DV < 75,
are monitors in the dataset
with, on average, as many
as 36 days with a 5-minute
;
:
concentration >100 ppb.
-
|
I
:
:
i
%
. - ,
' 1 1 1
1111
25 50 75 100 125
Ambient Monitor 1-hr Design Value (ppb)
150
As Is Air Quality (2014-2016): Maximum Number of Days per
Year Daily Maximum 5-minute S02 At or Above 100 ppb
03
O
i_
03
ฃ
i_
CD
Q_
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03
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100
80
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00
E ~
E
13
E
X
TO
LO
E
-
Observation: For DV < 75,
are monitors in the dataset
with as many as 80 days
with a 5-minute
-r
concentration >100 pp
3.
|
;
:
.
1
1
V
1111
1111
1111
1111
25 50 75 100 125
Ambient Monitor 1-hr Design Value (ppb)
150
Figure C-l. As is (unadjusted) SO2 monitoring data (2014-2016). Mean number of days/year
(top panel) and maximum number of days/year (bottom panel) with daily maximum 5-minute
concentrations of SO2 at or above 100 ppb.
C-l
-------
As Is Air Quality (2014-2016): Mean Number of Days per Year
Daily Maximum 5-minute S02 At or Above 200 ppb
E
=3
E
X
03
03
Q
v_
03
ฃ
L_
O
_Q
<
O
4-ป
<
200 ppb.
-
|
I
;
:
1
>***~.\ >*
25 50 75 100 125
Ambient Monitor 1-hr Design Value (ppb)
150
As Is Air Quality (2014-2016): Maximum Number of Days per
Year Daily Maximum 5-minute S02 At or Above 200 ppb
03
Q
i_
03
ฃ
s_
<1)
Q_
*
03
Q
d)
_Q
E
E
=3
E
X
03
_Q
Q_
Q_
O
O
fN
CU
>
o
_Q
<
O
4-ป
<
CM
o
LT>
C
E
ฆ
LO
E
100
90
80
70
60
50
40
30
20
10
0
-
Observation: For DV < 75,
are monitors in the dataset
with as many as 32 days
with a 5-minute
concentration >200 ppt
).
;
i
:
;
%
.
V >
1 1 1 1
25 50 75 100 125
Ambient Monitor 1-hr Design Value (ppb)
150
Figure C-2. As is (unadjusted) SO2 monitoring data (2014-2016). Mean number of days/year
(top panel) and maximum number of days/year (bottom panel) with daily maximum 5-minute
concentrations of SO2 at or above 200 ppb.
C-2
-------
As Is Air Quality (2014-2016): Mean Number of Days per Year
Daily Maximum 5-minute S02 At or Above 300 ppb
E
=3
E
X
03
03
Q
v_
03
ฃ
L_
o
_Q
<
O
4-ป
<
300 ppb.
-r
-
|
I
;
:
1
ป*l
1
ซซi
1 1
1111
25 50 75 100 125
Ambient Monitor 1-hr Design Value (ppb)
150
As Is Air Quality (2014-2016): Maximum Number of Days per
Year Daily Maximum 5-minute S02 At or Above 300 ppb
03
O
i
03
2
i_
CD
Q_
LO
>*
03
o
CD
_Q
_Q
CL
Q.
O
O
ro
a;
>
o
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<
i
O
4'
<
oJ
o
LT)
100
E
=3
E
X
03
E
ฆ
LO
E
E
X
03
70
-r
Observation: For DV < 75,
are monitors in the dataset
with as many as 17 days
with a 5-minute
concentration >200 ppb.
i
:
;
*
ป*|
iซ*i
1 ' 1 '
25
50
75
100 125
Ambient Monitor 1-hr Design Value (ppb)
150
Figure C-3. As is (unadjusted) SO2 monitoring data (2014-2016). Mean number of days/year
(top panel) and maximum number of days/year (bottom panel) with daily maximum 5-minute
concentrations of SO2 at or above 300 ppb.
C-3
-------
As Is Air Quality (2014-2016): Mean Number of Days per Year
Daily Maximum 5-minute S02 At or Above 400 ppb
E
=3
E
X
03
100
03
Q
v_
03
2
L_
O
_Q
<
O
4-ป
<
400 ppb.
:
-
;
;
\
;
l
]+ป% f 1
1 1
1 1 1 ป
25 50 75 100 125
Ambient Monitor 1-hr Design Value (ppb)
150
As Is Air Quality (2014-2016): Maximum Number of Days per
Year Daily Maximum 5-minute S02 At or Above 400 ppb
03
O
i
03
2
i_
CD
Q_
LO
>*
03
o
CD
_Q
E
=3
E
X
03
_Q
Q_
Q.
O
O
CD
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O
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<
i
O
4'
<
oJ
o
LO
c
E
ฆ
LO
E
Z5
E
X
03
100
90
80 -ฃ
70
Observation: For DV < 75,
are monitors in the dataset
--
win 1 11 idi ly di 1 uaya
with a 5-minute
concentration >400 ppt
).
i
:
;
*
: . -
P *
lซ )- *!
1 1
1 1 1 ~ 4
25 50 75 100 125
Ambient Monitor 1-hr Design Value (ppb)
150
Figure C-4. As is (unadjusted) SO2 monitoring data (2014-2016). Mean number of days/year
(top panel) and maximum number of days/year (bottom panel) with daily maximum 5-minute
concentrations of SO2 at or above 400 ppb.
C-4
-------
As Is Ambient Monitors (2014-2016)
QJ
+->
3500
c
E
1
3000
LO
E
03
2500
E
E
X
-C
fU
(J
c
CD
2000
>
CO
'ro
a;
>
1500
Q
0
(/>
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>-
03
ro
1000
O
O
4
-M
O
s_
OJ
rsi
500
cu
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V)
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0
=3
JS
.0
> 100 ppb
> 200 ppb
ฆ > 300 ppb
ฆ > 400 ppb
n
i_
J
J
DV < 25 ppb 25 < DV < 50 50 < DV < 75
PPb ppb
Design Value Category
DV > 75 ppb
Figure C-5. Monitoring data (2014-2016), unadjusted. Total number of days across 3-year
period with daily maximum 5-minute concentrations of SO2 above 100, 200, 300 and 400 ppb
across monitors grouped by design value.
C-5
-------
All Ambient Monitors Adjusted to Meet Current Standard (2014-
2016): Mean Number of Days
100
90
80
4-ป
4-ป
-------
APPENDIX D
AIR QUALITY INFORMATION FOR GEOGRAPHICAL AREAS
OF THREE SELECTED U.S. EPIDEMIOLOGICAL STUDIES
D-l
-------
Table D-l. 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 QualityA
Study Area
Study Time
Period
Study
Reference
SO 2
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
Design Value
for Current NAAQS
(3-year average of annual
99th percentile daily
maximum 1-hour
concentrations),
ppm
Mean
Upper
Percentiles
value (ppb)
(monitor ID)
Bronx County,
Jan 1999-Dec 2000
ATSDR 2006 ฐ
24-hr ave
2 monitors collecting
12
78ฐ
1999
-
E
NY
data in series
2000
1999
78
1999-2001
73
New York City,
Jan1999-Dec2002
Itoetal 2007
24-hr ave
Average across all
7.8
75th=10
82 F
2000
71
(36-061-0056)
NY
(19) monitors
95th=17
2001
71
2000-2002
69
2002
65
(36-061-0056)
Average across all
(6) monitors
75th =38.2
90th=60.7
1988
159
147
(09-009-1123)
New Haven, CT
Jan1988-Dec1990
Schwartz, 1995
24-hr ave
29.8
150 G
1989
167
1988-1990
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 Itoetal., 2007) and Table 5-14 (for Schwartz, 1995). Where
multiple monitors contribute data, these are the arithmetic mean and percentiles of the dataset of daily multi-monitor average concentrations for the full study period.
C This study was cited as NY DOH, 2006 in the 2008 ISA.
D This statistic is for combined dataset of 2 monitoring sites due to construction at the initial site (Thompson and Stewart, 2009). Data are from the first monitor (36-005-0073) for the period Jan 1 to
July 14,1999. Data are from the second monitor (36-005-0110), approximately 1/2 mile northeast of first, for the period Sept 2,1999 to Nov 22,2000.
E Due to incomplete quarters or years, there is not a valid design value for a monitor in the Bronx any of the 3-year periods that include the study period.
F This statistic is based on monitor 36-061-0080 (Thompson and Stewart, 2009), for which five quarters of data are available during the study period (from 1999 through first quarter of 2000).
G This statistic is based on monitor 09-009-1123 (Thompson and Stewart, 2009), for which 12 quarters of data are available during the study period (1988 through 1990).
D-2
-------
REFERENCES
ATSDR (Agency for Toxic Substances and Disease Registry). (2006). A study of ambient air
contaminants and asthma in New York City: Part A and B. Atlanta, GA: U.S. Department
of Health and Human Services.
http://permanent.access.gpo.gov/lps88357/ASTHMA_BRONX_FINAL_REPORT.pdf
Ito, K; Thurston, GD; Silverman, RA. (2007). Characterization of PM2.5, gaseous pollutants,
and meteorological interactions in the context of time-series health effects models. J
Expo Sci Environ Epidemiol 17: S45-S60. http://dx.doi.org/10.1038/sj.jes.7500627
Schwartz, J; Morris, R. (1995). Air pollution and hospital admissions for cardiovascular disease
in Detroit, Michigan. Am J Epidemiol 142: 23-35.
Thompson, R; Stewart, MJ. (2009). Memorandum to Sulfur Dioxide Review Docket (EPA-HQ-
OAR-2007-0352). Air Quality Statistics for Cities Referenced in Key U.S. and Canadian
Hospital Admission and Emergency Department Visits for All Respiratory Causes and
Asthma. Docket ID No. EPA-HQ-OAR-2007-352-0018.
D-3
-------
APPENDIX E
DERIVATION OF DESIGN VALUES PRESENTED IN APPENDIX D
E-l
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UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
User ID: DST DESIGN VALUE REPORT
Report Request ID: 1565153 Report Code: AMP480 Jun. 20, 2017
GEOGRAPHIC SELECTIONS
Tribal
EPA
Code State County Site
Parameter POC City AQCR
UAR
CBSA
CSA
Region
09 009
PROTOCOL SELECTIONS
Parameter
Classification Parameter Method Duration
DESIGN VALUE 424 01
SELECTED OPTIONS
Option Type
Option Value
SINGLE EVENT PROCESSING EXCLUDE REGIONALLY CONCURRED EVENTS
WORKFILE DELIMITER
USER SITE METADATA STREET ADDRESS
MERGE PDF FILES YES
QUARTERLY DATA IN WORKFILE NO
AGENCY ROLE PQAO
DATE CRITERIA
Start Date
1990
End Date
1990
APPLICABLE STANDARDS
Standard Description
S02 1-hour 2010
Selection Criteria Page 1
-------
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 Report Date: Jun. 20, 2 017
AIR QUALITY SYSTEM
PRELIMINARY DESIGN VALUE REPORT
Pollutant: Sulfur dioxide(42401)
Standard Units: Parts per billion(008)
NAAQS Standard: S02 1-hour 2 010
Statistic: Annual 99th Percentile
Level: 75
Design Value Year: 1990
REPORT EXCLUDES MEASUREMENTS WITH REGIONALLY CONCURRED EVENT FLAGS.
State Name:
Connecticut
Site ID
09-009-0010
09-009-0017
09-009-1003
09-009-1123
09-009-2123
09-009-3008
STREET ADDRESS
EGAN CENTER, MATHEW ST
LOMBARD STREET
ANIMAL SHELTER, COMMERCE ST
715 STATE STREET
Bank St at Meadow St (see c
LYDIA STREET EXTENTION
1990
1
1989
1
1988
1 3_
Year
Comp.
99th
Cert&
Comp.
99th
Cert&
Comp.
99th
Cert&
Design
Valid
Qrtrs
Percentile
Eval
| Qrtrs
Percentile
Eval
| Qrtrs
Percentile
Eval
Value
Ind.
3
114 *
Y
4
113
3
118 *
115
N
3
112 *
4
113
113
N
4
68
Y
4
99
4
95
87
Y
4
116
Y
4
167
4
159
147
Y
4
83
Y
4
97
4
85
88
Y
3
93 *
Y
4
110
4
100
101
Y
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
-------
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
AIR QUALITY SYSTEM
PRELIMINARY DESIGN VALUE REPORT
Report Date: Jun. 20, 2017
CERTIFICATION EVALUATION AND CONCURRENCE FLAG MEANINGS
FLAG MEANING
M The monitoring organization has revised data from this monitor since the
most recent certification letter received from the state.
N 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.
S 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.
U 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.
X Certification is not required by 40 CFR 58.15 and no conditions apply to be
the basis for assigning another flag value
Y 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).
Notes: 1.
2 .
3 .
Computed design values are a snapshot of the data at the time the report was run (may not be all data for year).
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.
Annual Values not meeting completeness criteria are marked with an asterisk ('*') .
Page 3 of 3
-------
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
User ID: DST DESIGN VALUE REPORT
Report Request ID: 1565370 Report Code: AMP480 Jun. 21, 2017
GEOGRAPHIC SELECTIONS
Tribal
EPA
Code State County Site
Parameter POC City AQCR
UAR
CBSA
CSA
Region
36 005
36 047
36 061
36 081
36 085
PROTOCOL SELECTIONS
Parameter
Classification Parameter Method Duration
DESIGN VALUE 424 01
SELECTED OPTIONS
Option Type
Option Value
SINGLE EVENT PROCESSING
EXCLUDE REGIONALLY CONCURRED EVENTS
WORKFILE DELIMITER
,
USER SITE METADATA
STREET ADDRESS
MERGE PDF FILES
YES
QUARTERLY DATA IN WORKFILE
NO
AGENCY ROLE
PQAO
APPLICABLE STANDARDS
Standard Description
S02 1-hour 2010
DATE CRITERIA
Start Date End Date
2000 2002
Selection Criteria Page 1
-------
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 Report Date: Jun. 21, 2 017
AIR QUALITY SYSTEM
PRELIMINARY DESIGN VALUE REPORT
Pollutant: Sulfur dioxide(42401)
Standard Units: Parts per billion(008)
NAAQS Standard: S02 1-hour 2 010
Statistic: Annual 99th Percentile
Level: 75
Design Value Year: 2000
REPORT EXCLUDES MEASUREMENTS WITH REGIONALLY CONCURRED EVENT FLAGS.
State Name:
New York
2000
Comp. 99th
Certfc
Comp.
1999
99th
Certfc
Comp.
1998
99th
Certfc
3-Year
Design Valid
Site ID
STREET ADDRESS 1
Qrtrs
Percentile Eval
I Qrtrs
Percentile
Eval
| Qrtrs
Percentile
Eval
i Value
Ind
36-005-0073
1
IS 155, 470 JACKSON AV.
1
2
68
*
Y
4
70
Y
1
69
N
36-005-0080
MORRISANIA CENTER, 1225-57
1
94
*
4
77
Y
4
69
Y
80
N
36-005-0083
2 0 0TH STREET AND SOUTHERN B
2
62
*
62
N
36-005-0110
IS 52 681 KELLY ST
4
86
1
98
*
Y
92
N
36-047-0011
3 01 GREENPOINT AVENUE
3
51
*
Y
4
42
Y
47
N
36-047-0076
PS 321 180 7TH AV,
0
36
*
4
54
Y
3
59 *
Y
50
N
36-061-0010
MABEL DEAN HIGH SCH.ANNEX,
3
72
*
4
79
Y
3
64 *
Y
72
N
36-061-0056
PS 59, 228 E. 57TH STREET,
4
71
4
78
Y
4
69
Y
73
Y
36-081-0097
56TH AVE AT SPRINGFIELD BLV
4
50
4
53
Y
2
52 *
Y
52
N
36-085-0067
SUSAN WAGNER HS, 12 0 0 MAN
1
54
*
4
46
Y
4
46
Y
49
N
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
-------
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY Report Date: Jun. 21, 2 017
AIR QUALITY SYSTEM
PRELIMINARY DESIGN VALUE REPORT
Pollutant: Sulfur dioxide(42401)
Standard Units: Parts per billion(008)
NAAQS Standard: S02 1-hour 2 010
Statistic: Annual 99th Percentile
Level: 75
Design Value Year: 2001
REPORT EXCLUDES MEASUREMENTS WITH REGIONALLY CONCURRED EVENT FLAGS.
State Name:
New York
2001
Comp. 99th
Certfc
Site ID
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
STREET ADDRESS
IS 155, 470 JACKSON AV.
MORRISANIA CENTER, 1225-57
2 0 0TH STREET AND SOUTHERN B
IS 52 681 KELLY ST
3 01 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, 12 0 0 MAN
Qrtrs Percentile Eval
71
81
69
71
50
57
Y
Y
Y
Y
Y
Y
2000
Comp. 99th Cert&
Qrtrs Percentile Eval
94 *
62 *
86
36 *
72 *
71
50
54 *
Comp.
Qrtrs
2
1999
99th Cert&
Percentile Eval
68 *
77
98 *
51 *
54
79
78
53
46
Y
Y
Y
Y
Y
Y
Y
Y
3-Year
Design Valid
Value Ind.
68
86
67
88
51
45
73
73
51
57
50
N
N
N
N
N
N
N
Y
Y
N
N
Notes: 1.
2 .
3 .
Computed design values are a snapshot of the data at the time the report was run (may not be all data for year).
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.
Annual Values not meeting completeness criteria are marked with an asterisk ('*') .
Page 3 of 5
-------
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY Report Date: Jun. 21, 2 017
AIR QUALITY SYSTEM
PRELIMINARY DESIGN VALUE REPORT
Pollutant: Sulfur dioxide(42401)
Standard Units: Parts per billion(008)
NAAQS Standard: S02 1-hour 2 010
Statistic: Annual 99th Percentile
Level: 75
Design Value Year: 2002
REPORT EXCLUDES MEASUREMENTS WITH REGIONALLY CONCURRED EVENT FLAGS.
State Name:
New York
Site ID
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
STREET ADDRESS
MORRISANIA CENTER, 1225-57
2 0 0TH 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, 12 0 0 MAN
2002
Comp. 99th Certfc
Qrtrs Percentile Eval
62
67
65
57
Y
Y
2001
Comp. 99th Cert&
Qrtrs Percentile Eval
71
81
69
71
50
57
Y
Y
Y
Y
Y
Y
2000
Comp. 99 th Cert&
Qrtrs Percentile Eval
1 94 *
2 62 *
4 86
0 36 *
3 72 *
4 71
4 50
1 54 *
3-Year
Design Valid
Value Ind.
94
65
78
36
71
69
50
57
54
N
N
N
N
N
Y
N
N
N
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
-------
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY
AIR QUALITY SYSTEM
PRELIMINARY DESIGN VALUE REPORT
Report Date: Jun. 21, 2017
CERTIFICATION EVALUATION AND CONCURRENCE FLAG MEANINGS
FLAG MEANING
M The monitoring organization has revised data from this monitor since the
most recent certification letter received from the state.
N 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.
S 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.
U 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.
X Certification is not required by 40 CFR 58.15 and no conditions apply to be
the basis for assigning another flag value
Y 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).
Notes: 1.
2 .
3 .
Computed design values are a snapshot of the data at the time the report was run (may not be all data for year).
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.
Annual Values not meeting completeness criteria are marked with an asterisk ('*') .
Page 5 of 5
-------
APPENDIX F
GEOGRAPHIC DISTRIBUTION OF CONTINENTAL
U.S. FACILITIES EMITTING MORE THAN 1,000 TPY S02
AND POPULATION DENSITY BASED ON U.S. CENSUS TRACTS
F-l
-------
Sources emitting 1.000 tpy or more
Population Density 2010 (People/Sq. Mile)
o to 389
390 to 2.612
2,613 to 5,548
5,549 to 9,977
ฆ 9,978 to 191,050
Figure F-l. Continental U.S.: Facilities emitting more than 1,000 tpy SO2 (11=619 in 2011 NEI) and population density.
F-2
-------
Sources emitting 1,000 tpy or more
Population Density 2010 (People/Sq. Mile)
0 to 389
390 to 2.612
| 2,613 to 5,548
5.549 to 9,977
ฆ 9,978 to 191,050
Figure F-2. Northeast U.S.: Facilities emitting more than 1,000 tpy SO2 and population density.
F-3
-------
NEI 2011
Sou roes em itti ng 1,000 tpy ormore
Population Density 2010 (People/Sq. Mile)
0 to 389
390 to 2,612
2.613 to 5 .548
5,549 to 9,977
ฆ 9.978 to 191,050
Figure F-3. Southeast U.S.: Facilities emitting more than 1,000 tpy SO2 and population density.
F-4
-------
Sources emitting 1.000 tpy or more
Population Density 2010 (People/Sq. Mile)
0 to 389
390 to 2,612
J 2,613 to 5,548
5,549 to 9,977
ฆ 9,978 to 191,050
Figure F-4. Northwest U.S.: Facilities emitting more than 1,000 tpy SO2 and population density.
-------
NEI 2011
Sources emitting 1.000 tpy or more
Population Density 2010 (Peopie/Sq. Mile)
o to 389
390 to 2,612
2,613 to 5,548
5 549 t0 9 977
ฆ 9,978 to 191,050
Figure F-5. Southwest U.S.: Facilities emitting more than 1,000 tpy SO2 and population density.
F-6
-------
United States Office of Air Quality Planning and Standards Publication No. EPA-452/R-18-002
Environmental Protection Health and Environmental Impacts Division May 2018
Agency Research Triangle Park, NC
------- |