1. Full Terms & Conditions of access and use can be found at
http://www.tandfonline.com/action/journalInformation?journalCode=uawm20
Download by: [Mark Shepherd] Date: 18 October 2015, At: 18:01
Journal of the Air & Waste Management Association
ISSN: 1096-2247 (Print) 2162-2906 (Online) Journal homepage: http://www.tandfonline.com/loi/uawm20
Estimates of community exposure and health risk
to sulfur dioxide from power plant emissions using
short-term mobile and stationary ambient air
monitoring
Mark A. Shepherd, Gleb Haynatzki, Risto Rautiainen & Chandran Achutan
To cite this article: Mark A. Shepherd, Gleb Haynatzki, Risto Rautiainen & Chandran Achutan
(2015) Estimates of community exposure and health risk to sulfur dioxide from power plant
emissions using short-term mobile and stationary ambient air monitoring, Journal of the Air &
Waste Management Association, 65:10, 1239-1246, DOI: 10.1080/10962247.2015.1077174
To link to this article: http://dx.doi.org/10.1080/10962247.2015.1077174
Accepted online: 29 Jul 2015.
Submit your article to this journal
Article views: 44
View related articles
View Crossmark data

2. TECHNICAL PAPER
Estimates of community exposure and health risk to sulfur dioxide from
power plant emissions using short-term mobile and stationary ambient
air monitoring
Mark A. Shepherd,1,3
Gleb Haynatzki,2
Risto Rautiainen,3
and Chandran Achutan3,⁄
1
Topaz Power Management, L.P., Austin, TX, USA
2
Department of Biostatistics, College of Public Health, University of Nebraska Medical Center, Omaha, NE, USA
3
Department of Environmental, Agricultural and Occupational Health, College of Public Health, University of Nebraska Medical Center,
Omaha, NE, USA
⁄
Please address correspondence to: Chandran Achutan, Associate Professor, Department of Environmental, Agricultural and Occupational
Health, 984388 Nebraska Medical Center, Omaha, NE 68198-4388, USA; e-mail: cachutan@unmc.edu
To estimate plausible health effects associated with peak sulfur dioxide (SO2) levels from three coal-fired power plants in the
Baltimore, Maryland, area, air monitoring was conducted between June and September 2013. Historically, the summer months
are periods when emissions are highest. Monitoring included a 5-day mobile and a subsequent 61-day stationary monitoring
study. In the stationary monitoring study, equipment was set up at four sites where models predicted and mobile monitoring data
measured the highest average concentrations of SO2. Continuous monitors recorded ambient concentrations each minute. The 1-
min data were used to calculate 5-min and 1-hr moving averages for comparison with concentrations from clinical studies that
elicited lung function decrement and respiratory symptoms among asthmatics. Maximum daily 5-min moving average concentra-
tions from the mobile monitoring study ranged from 70 to 84 ppb (183–220 µg/m3
), and maximum daily 1-hr moving average
concentrations from the mobile monitoring study ranged from 15 to 24 ppb (39–63 µg/m3
). Maximum 5-min moving average
concentrations from stationary monitoring ranged from 39 to 229 ppb (102–600 µg/m3
), and maximum daily 1-hr average
concentrations ranged from 15 to 134 ppb (40–351 µg/m3
). Estimated exposure concentrations measured in the vicinity of
monitors were below the lowest levels that have demonstrated respiratory symptoms in human clinical studies for healthy
exercising asthmatics. Based on 5-min and 1-hr monitoring, the exposure levels of SO2 in the vicinity of the C.P. Crane, Brandon
Shores, and H.A. Wagner power plants were not likely to elicit respiratory symptoms in healthy asthmatics.
Implications: Mobile and stationary air monitoring for SO2 were conducted to quantify short-term exposure risk, to the
surrounding community, from peak emissions of three coal-fired power plants in the Baltimore area. Concentrations were
typically low, with only a few 5-min averages higher than levels indicated during clinical trials to induce changes in lung
capacity for healthy asthmatics engaged in exercise outdoors.
Introduction
Fossil fuel-fired power plants are the largest source of sulfur
dioxide (SO2) emissions in the United States. Clinical and
epidemiological studies have linked ambient SO2 concentra-
tions to respiratory effects among exercising asthmatics follow-
ing peak exposures, defined as 5–10-min exposures at
relatively high concentrations (Balmes et al., 1987; Bethel
et al., 1985; Horstman et al., 1986). Currently, high ambient
concentrations of SO2 are relatively rare and thus population
exposure is considerably less (U.S. Environmental Protection
Agency [EPA], 2008). In 2000, the American Thoracic Society
(ATS) modified its guidance on what constitutes an adverse
health effect of air pollution, concluding that air pollution–
induced changes in lung function should be considered
adverse, even if this shift does not result in immediate illness
(ATS, 2000). The changed guidance renewed interest in low-
level exposure to SO2 and associated potential health effects.
There are only a few air monitoring stations in the Baltimore
area, however, that report ambient concentrations of SO2, and
even fewer report concentrations in 5-min block averages, the
same time period used in clinical studies to estimate health
effects (EPA, 2008). As a result, there is a lack of information
necessary to estimate both low-level ambient concentrations
and potential health effects to the surrounding community.
In 2010, the EPA reduced the National Ambient Air Quality
Standards (NAAQS) for SO2 from a 140 parts per billion (ppb),
1239
Journal of the Air & Waste Management Association, 65(10):1239–1246, 2015. Copyright © 2015 A&WMA. ISSN: 1096-2247 print
DOI: 10.1080/10962247.2015.1077174 Submitted November 24, 2014; final version submitted July 21, 2015; accepted July 22, 2015.
Color versions of one or more of the figures in the article can be found online at www.tandfonline.com/uawm.
Downloadedby[MarkShepherd]at18:0118October2015

3. 24-hr standard, to a 75 ppb (196 µg/m3
), 1-hr standard. At the
same time, EPA revoked the annual average standard of 30 ppb
(Primary National Ambient Air Quality Standard for Sulfur
Dioxide, Final Rule, 2010). The change was triggered by a
legal challenge and new information that the 24-hr standard
was not protective of certain at-risk groups. An earlier study
indicated that only a small subset of asthmatics (0.7–1.7%)
were regarded as at risk when performing moderate to heavy
exercise (Burton et al., 1987), and exposures eliciting lung decre-
ment in forced expiratory volumes (forced expiratory volume in
1 sec [FEV1]) were not demonstrated in normal healthy indivi-
duals at SO2 concentrations less than 1000 ppb (Bedi et al., 1984;
Folinsbee et al., 1985; Kulle et al., 1984; Stacy et al., 1983). In
adopting the new standard, however, EPA noted that additional
clinical studies completed since the last review demonstrated that
5–10-min exposures to 400–600 ppb SO2 consistently caused
increases in respiratory symptoms and decreased lung function in
exercising asthmatics (Gong et al., 1995; Horstman et al., 1986,
Linn et al., 1983). Moderate or greater SO2-induced decrements
in lung function have also consistently been observed at 200–300
ppb SO2 in some asthmatics (Bethel et al., 1985; Linn et al.,
1987, 1988, 1990; Sheppard et al., 1981).
The objective of this study was to estimate ambient air
concentrations of SO2 and the plausible health effects asso-
ciated with peak SO2 exposure in the vicinity of three coal-
fired power plants in Baltimore, Maryland.
Methods
Air monitoring
Figure 1 shows the locations of the C.P. Crane plant (22 km
east-northeast) and Brandon Shores and H.A. Wagner power
plants (14 km southeast) with respect to downtown Baltimore.
The Brandon Shores and H.A. Wagner plants are contiguous.
The study was divided into 5-day mobile monitoring and
subsequent 61-day stationary monitoring of SO2 concentra-
tions. Samples were collected 2 m above ground level, as a
representation of exposures within the breathing zone. All
monitoring was conducted during the day to account for
expected peak electricity demands and emissions.
From June 24 to 28, 2013, mobile monitoring was con-
ducted in locations where prior modeling data indicated that
plant emissions had the greatest impact on SO2 concentrations
in the surrounding ambient air. Mobile monitoring data were
used to identify locations for subsequent longer-term stationary
monitoring (Kaplan et al., 2013). Mobile equipment was used
to measure SO2 concentrations over land and water.
Two mobile monitoring teams were used to provide more cost-
effective coverage in locating SO2 plumes from the plants. On
June 24, both monitoring teams were mobilized approximately
3.55 km (2.2 mi) north of the H.A. Wagner plant. On June 25 and
June 26, teams used boats to monitor SO2 concentrations from the
plants over the water. Team 1 monitored near the C.P. Crane
power plant and Team 2 monitored near the H.A. Wagner and
Brandon Shores power plants. On June 27, Team 1 monitored
northwest of the C.P. Crane power plant and Team 2 monitored
near the H.A. Wagner and Brandon Shores power plants. On June
27, both teams monitored near the C.P. Crane power plant.
Monitoring was conducted between 11:30 a.m. and 6:00 p.m.
Monitoring equipment was calibrated at the beginning of the
day, prior to sampling, and at the end of the day if concentrations
above detection were observed. Figure 2 and Figure 3 identify the
locations where mobile monitoring was conducted.
Stationary monitoring was conducted with the same mon-
itoring equipment and methods of operation used in the mobile
monitoring study. Four stationary monitors were located near
areas where prior modeling indicated the highest ambient con-
centrations (Figures 4 and 5) and in accordance with EPA
Figure 1. Aerial view of power plant locations.
1240 Shepherd et al. / Journal of the Air & Waste Management Association 65 (2015) 1239–1246
Downloadedby[MarkShepherd]at18:0118October2015

4. guidance for siting ambient monitors (Network Design Criteria
for Ambient Air Quality, 2013). Site 1 was located 3.5 km (2.2
mi) southeast of the H.A. Wagner power plant, and Site 2 was
located 2.7 km (1.7 mi) northwest of the Brandon Shores
power plant. Site 3 was located approximately 3 km (2.1 mi)
northwest of the C.P. Crane power plant, and Site 4 was located
approximately 2.8 km (1.8 mi) west of the plant. Monitoring
began on August 1 (monitoring duration 54 days), Site 2 on
July 25 (61 days), Site 3 on August 2 (53 days), and Site 4 on
August 13 (42 days). Monitoring was completed at all sites on
September 23, 2013. During the stationary study, monitors and
support equipment were maintained in climate-controlled shel-
ters operated continuously, 24 hr per day.
In both studies, Thermo Electron TECO 43A (Waltham,
MA) and Teledyne API 100E (San Diego, CA) samplers
were used, which use ultraviolet light (UV) fluorescence to
measure ambient SO2 concentrations. Analyzers were cali-
brated for gas phase SO2 using fluorescence measurement
techniques following EPA Equivalent Method EQSA-0486-
060 and EQSA-0495-100 (Ambient Air Monitoring
Reference and Equivalent Methods, 2014). The range of the
monitoring instrument was 0.4–500 ppb (1–1317 µg/m3
),
bracketing expected emission concentrations indicated in
prior modeling. Real-time output was captured using a
Campbell Scientific CR1000 data logger (Logan, UT) to com-
pile 1-min, 15-min, and hourly averages. EPA-protocol gases
Figure 2. Mobile monitoring locations near the Brandon Shores and H.A. Wagner power plants.
Figure 3. Mobile monitoring locations near the C.P. Crane power plant.
Shepherd et al. / Journal of the Air & Waste Management Association 65 (2015) 1239–1246 1241
Downloadedby[MarkShepherd]at18:0118October2015

5. and zero air sources were used as reference standards to cali-
brate the monitoring equipment, traceable to the National
Institute of Standards and Technology (NIST), and conducted
in accordance with a Quality Air Project Plan (QAPP).
Population-based exposure
Census data from 2010 and 2012 (U.S. Census Bureau,
2012) were used to determine the number of monitors
required to represent population-based exposure. Using EPA
criteria, the number of individuals living in the core-based
statistical area (CBSA) for Baltimore-Towson (2,753,149) was
multiplied by tons of SO2 emitted from all plants (5527),
divided by 1 million, to derive a population-weighted emis-
sions index (PWEI) of 15,217 million person-tons. The PWEI
was modified to represent time periods (third quarter) and
plant emissions during which monitoring and exposure
occurred, rather than the normal annual standard typical of
permanent monitoring installations. Based on the derived
PWEIs, EPA recommends a minimum of one monitor to
represent a CBSA; four were used in the present stationary
monitoring study.
Figure 4. Plots of highest modeled SO2 concentrations and stationary monitors 1 and 2 near the H.A. Wagner and C.P. Crane power plants.
Figure 5. Plots highest modeled SO2 concentrations and stationary monitors 3 and 4 near the C.P. Crane power plant.
1242 Shepherd et al. / Journal of the Air & Waste Management Association 65 (2015) 1239–1246
Downloadedby[MarkShepherd]at18:0118October2015

6. To demonstrate that mobile monitoring occurred during the
hours of highest emissions, the SO2 concentration emitted from
each power plant unit, each hour, as recorded by continuous
emissions monitors, was reviewed. The highest periods of
emission were from 12:00 noon to 7:00 p.m., with the excep-
tion of C.P Crane where the highest periods of emissions
occurred from 10:00 a.m. to 10:00 p.m.
Estimating average exposure
IBM SPSS version 21 statistical software (Armonk, NY)
was used to calculate 5-min and 1-hr moving average SO2
concentrations for comparison with data published in human
clinical trials. The 5-min moving averages were calculated
by summing each five consecutive 1-min averages and
dividing by 5. Then, shifting forward 1 min, the next 5
min were averaged, creating a series of 5-min averages
over the whole sampling period. Similarly, 1-hr moving
averages were calculated by summing the concentrations
from each 60 consecutive 1-min time periods and dividing
by 60. Five-minute and 1-hr averages were not calculated for
time periods where there was less than 5 min or 60 min of
sample data in an hour, respectively. The maximum 5-min,
1-hr, and moving average concentrations were then com-
pared with the results of clinical studies, where concentra-
tions elicited respiratory morbidity. Respiratory morbidity
was defined to include respiratory symptoms and lung func-
tion decrement. Respiratory symptoms primarily included
bronchoconstriction, rapid shallow breathing, coughing,
wheezing, chest tightness, and shortness of breath. The end
point lung function decrement was defined as ≥100%
increase in lung airway resistance (sRAW) and/or ≥15%
decline in FEV1.
Estimating exposure variability between monitoring
sites
To evaluate whether ambient concentrations represented a
common exposure across the four stationary monitoring sites,
the Kruskal-Wallis one-way analysis of variance was used to
compare 1-hr and 5-min median concentrations at the sites.
Results
Air monitoring
The maximum 5-min average SO2 concentration measured
during mobile monitoring was 84.4 ppb (229 µg/m3
), and the
maximum 1-hr average SO2 concentration was 23.35 ppb (61
µg/m3
). Table 1 shows the results for the maximum 5-min and
1-hr averages measured during the stationary monitoring study.
During the stationary study, only at Site 2 was there a day
when a 1-hr average concentration exceeded 100 ppb
(263 µg/m3
): 134.32 ppb (354 µg/m3
), which was the lowest
exposure level demonstrating an effect in animal studies
(described in Discussion). At stationary Site 1, south of
Brandon Shores and H.A. Wagner, there were 3 days on
which 5-min average concentrations were above 100 ppb.
The highest concentration was 147 ppb (387 µg/m3
) on
September 13. At Site 2, north of Brandon Shores and H.A.
Wagner, there were 4 days where 5-min average concentrations
exceeded 100 ppb. At Site 3, northeast of C.P. Crane, there was
only 1 day with SO2 above 100 ppb. At Site 4 there were no
days where SO2 concentrations were above 100 ppb.
Exposure variability between sites
Results of Kruskal-Wallis tests indicate that there was a
significant difference in at least one of the sites 5-min average
SO2 concentration measurements (χ2
= 41714.54, P < 0.001)
and 1-hr averages (χ2
= 701.107, P < 0.001). There was greater
difference in the 5-min concentrations between sites than there
was for the 1-hr concentrations. Figure 6 shows the daily
calculated maximum 5-min and 1-hr average concentrations
for each monitoring site.
Discussion
Monitored ambient SO2 concentrations emitted from the
three coal-fired power plants in the Baltimore area were
below levels from human clinical trials that elicited respiratory
morbidity for exposed healthy asthmatics and healthy indivi-
duals without asthma. Healthy asthmatics included individuals
able to withhold the use of bronchodilators for at least 6 hr
prior to exposure and with no recent history of upper respira-
tory tract infection (EPA, 2008). Concentrations measured dur-
ing the stationary monitoring study may indicate increased risk
of lung decrement for SO2-sensitive asthmatics during elevated
activities (breathing rate ≥20 L/min), based upon several days
where 5-min average ambient concentrations were over
100 ppb (263 µg/m3
) and 1 day where it was over 200 ppb
(527 µg/m3
).
Air monitoring in relation to health criteria
Moving averages have been used extensively in air pollu-
tion studies, including research specific to SO2. Health effects
are believed to lag exposure, and the moving average is a tool
Table 1. Maximum 5-min and 1-hr moving average SO2 concentrations ppb
(µg/m3
) at the stationary monitoring sites.
Site N Mean Min. Max.
5-min
1 75,917 2 (6) BDL 147 (387)
2 86,138 1 (4) BDL 228 (600)
3 76,176 1 (4) BDL 104 (274)
4 59,211 0.4 (1) BDL 38 (102)
1-hr
1 75,862 2 (5) BDL 61 (160)
2 86,083 1 (4) BDL 134 (351)
3 76,121 2 (3) BDL 38 (100)
4 59,156 0.4 (1) BDL 15 (39)
Notes: Site 2 recorded the highest reading and Site 4 the lowest.
Shepherd et al. / Journal of the Air & Waste Management Association 65 (2015) 1239–1246 1243
Downloadedby[MarkShepherd]at18:0118October2015

7. used to estimate the cumulative impact of pollutant concentra-
tions and is more consistent with actual exposure than the
block averages typically used in compliance monitoring
(Amancio et al., 2012; Kloog et al., 2012; Mar et al., 2005;
Mcbride et al., 2011). The time span most relevant to human
exposure in clinical trials is 5–10 min, as only one study
reviewed reported respiratory effects under 5 min (Horstman
et al., 1988). Because no other studies were found that demon-
strated a shorter period between similar exposures and effects,
the shortest average exposure time estimated in this study was
5 min.
Human clinical trial studies used for comparison did not pre-
sent exposure data to concentrations as low as those measured in
the mobile monitoring study. The Agency for Toxic Substances
and Disease Registry (ATSDR) published the Toxicological
Profile for Sulfur Dioxide (ATSDR, 1998) wherein clinical stu-
dies sought to establish a no observable adverse effect level
(NOAEL) or a lowest adverse effect level (LOAEL) for respira-
tory effects. The ATSDR reported an estimate of 100 ppb for a 15-
min LOAEL and 200 ppb for 5-min and 1-hr NOAELs (Koenig
et al., 1990; Linn et al., 1983, 1987). The studies, however, are not
representative of risk for certain vulnerable groups. EPA found
that human clinical studies in relatively healthy asthmatics are
useful in characterizing the concentration-response relationship,
but cannot be used to evaluate potential population thresholds
directly, as controlled human exposure studies have not been
conducted at SO2 concentrations below 200 ppb and do not
include the most sensitive asthmatics (EPA, 2008).
A slightly different risk profile is seen when comparing sta-
tionary monitoring results with concentrations reported in
human clinical trials. We focused on 1-hr and 5-min exposures,
instead of 24-hr exposures typical of epidemiological studies,
because EPA noted that it is possible that epidemiological
associations were determined in large part by peak exposures
within a 24-hr period, and because clinical studies demonstrated
5–10-min exposure-effect thresholds (EPA, 2009). At SO2 con-
centrations between 200 and 300 ppb, 5–30% of exercising
asthmatic adults experienced moderate to large decrements in
lung function following 5–10-min exposures to SO2, during
moderate to heavy exercise. There is limited evidence that
exposures below 300 ppb induce increases in respiratory symp-
toms. Exposure times of 1–6 hr did not result in different out-
comes unless there was concurrent exposure to inhaled
allergens, nitrogen dioxide (NO2), or ozone (O3). There were
no studies found describing respiratory symptoms or decrements
in lung function in resting asthmatics or healthy adults.
Limited data from animal studies indicate that repeated expo-
sure to concentrations as low as 100 ppb can exacerbate airway
hyper responsiveness following allergic sensitization (EPA,
2008). In one animal study, exposures between 100 and 160
ppb were associated with local allergic sensitization and inflam-
mation of bronchial and lung tissue (Park et al., 2001). Although
concentrations are similar to the maximum concentrations mea-
sured during the stationary monitoring study, the exposure time
periods in the animal studies were repeated for significantly
longer periods. It is uncertain as to whether these results are
representative for humans in that one human clinical study
demonstrated airway hyper responsiveness only when there
was concurrent exposure (6 hr) to 200 ppb SO2 and 400 ppb
NO2. Interestingly, concurrent exposure triggered a response in
resting asthmatics (EPA, 2008). The longest measured exposure
to a concentration above 200 ppb in the current study was 10
min, and none of the mobile or stationary monitoring results
suggest prolonged or repeated exposures to concentrations
greater than 200 ppb, although exposures can exceed this con-
centration for very brief time periods (instantaneous, 1 min, 5
min, and 1 hr). Although 1-min averages may indicate potential
for concentrations over 5-min and 1-hr thresholds, they are
below averaging times used in human clinical trials to establish
health effects. Finally, several studies have noted that there is a
refractory period after exposure to SO2 during which there is no
further response.
Exposure variability between sites
There was a great deal of variability in 5-min and 1-hr
concentrations between the four sites. The large variance in
concentration averages measured between stationary monitor-
ing sites may indicate that short-term exposures (minutes,
hours, days, and weeks) are not the same and makes it difficult
to make inferences on those timescales for the larger commu-
nity. Reasons for the large variability in 5-min and 1-hr average
concentrations likely include the limited time period during
which the study was conducted and shifting wind conditions
during the study, often dramatically, possibly moving SO2
plumes away from monitoring locations.
Strengths and limitations
There are several limitations to interpreting risks associated
with measured ambient concentrations, primarily related to the
short-term study period. A longer-term monitoring program is
Figure 6. Graph showing the highest daily 5-min average SO2 concentrations
measured at each stationary monitoring site.
1244 Shepherd et al. / Journal of the Air & Waste Management Association 65 (2015) 1239–1246
Downloadedby[MarkShepherd]at18:0118October2015

8. necessary to better characterize the frequency and duration of
hours where 5-min average concentrations are greater than 100
ppb. Most of the variability in measured concentrations appears
to be due to rapidly changing meteorological conditions, but it
may also be related to the presence of large water bodies in
close proximity. These two variables may act to increase or
reduce ambient concentrations, including times other than sum-
mer peak emission periods (i.e., during very cold winter days
when electricity generation is maximum).
Another limitation is that very few clinical trials studied
exposures to SO2 concentrations less than 200 ppb, thus leav-
ing uncertainty as to risks associated with low-level exposures.
Several epidemiological studies have shown associations with
respiratory symptoms for children and elderly adult asthmatics
at concentrations much lower than 100 ppb (Atkinson et al.,
1999; Wilson et al., 2005); however, EPA noted that the
ubiquitous presence of confounders and the lack of a threshold
exposure made these epidemiological studies less reliable.
The results of this study emphasize what other researchers
have also found, namely, that there is rarely a correlation in
ambient concentrations between monitoring sites for primary
pollutants emitted from stacks, especially for short-term meso-
scale and micro-scale studies. Monitoring over longer periods of
time may help to reduce variability and improve risk estimates.
Conclusion
Based on 5-min and 1-hr monitoring, the exposure levels of
SO2 in the vicinity of the C.P. Crane, Brandon Shores, and
H.A. Wagner power plants were not likely to elicit respiratory
symptoms in healthy asthmatics. However, there are insuffi-
cient data to conclude that exposure levels will not lead to
decreases in lung function for some SO2-sensitive asthmatics,
when engaged in heavy to moderate exercise.
References
Agency for Toxic Substances and Disease Registry (ATSDR). 1998.
Toxicological Profile for Sulfur Dioxide. Atlanta, GA: U.S. Department of
Health and Human Services, Public Health Service. http://www.atsdr.cdc.
gov/toxprofiles/tp.asp?id=253&tid=46 (accessed November 12, 2013)
Amancio, C.T., and L.F.C. Nascimento. 2012. Association of sulfur dioxide
exposure with circulatory system deaths in a medium-sized city in Brazil.
Braz. J. Med. Biol. Res. 45:1080–1085. doi:10.1590/S0100-
879X2012007500131
Ambient Air Quality Surveillance—Network Design Criteria for Ambient Air
Quality. 2013. Title 40 U.S. Code of Federal Regulations, Pt. 40, Appendix
D & E.
Ambient Air Monitoring Reference and Equivalent Methods. 2014. Title 40
CFR U.S. Code of Federal Regulations, Pt. 53. http://www.ecfr.gov/cgi-bin/
text-idx?SID=fcb1d06a560ef8a1363197d14035a2e0&node=40:6.0.1.1.
1&rgn=div5 (accessed October 10, 2013).
American Thoracic Society. 2000. What constitutes an adverse health effect of
air pollution? Am. J. Respir. Crit. Care Med. 161:665–673.
Atkinson, R.W., H.R. Anderson, D.P. Strachan, J.M. Bland, S.A. Bremner, and
A. Ponce de Leon. 1999. Short-term associations between outdoor air
pollution and visits to accident and emergency departments in London for
respiratory complaints. Eur. Respir. J. 13:257–265. doi:10.1183/
09031936.99.13225799
Balmes, J.R., J.M. Fine, and D. Sheppard. 1987. Symptomatic bronchoconstric-
tion after short-term inhalation of sulfur dioxide. Am. Rev. Respir. Dis.
136:1117–1121. doi:10.1164/ajrccm/136.5.1117
Bedi, J.F., L.J. Folinsbee, and S.M. Horvath. 1984. Pulmonary function effects
of 1.0 and 2.0 ppm sulfur dioxide exposure in active young male non-
smokers. J. Air Pollut. Control Assoc. 34:1117–1121. doi:10.1080/
00022470.1984.10465861
Bethel, R.A., D. Sheppard, B. Geoffroy, E. Tam, J.A. Nadel, and H.A.
Boushey. 1985. Effect of 0.25 ppm sulfur dioxide on airway resistance in
freely breathing, heavily exercising, asthmatic subjects. Am. Rev. Respir.
Dis. 131:659–661.
Burton, C.S., T.E. Stockenius, T.S. Stocking, E.L. Carr, B.S. Austin, and R.L.
Roberson. 1987. Assessment of Exposures of Exercising Asthmatics to
Short-Term SO2 Levels as a Result of Emissions from U.S. Fossil-fueled
Power Plants. Publication No. 87/176. San Rafael, CA: Systems
Applications Inc., September 23, 1987.
Folinsbee, L.J., J.F. Bedi, and S.M. Horvath. 1985. Pulmonary response to
threshold levels of sulfur dioxide (1.0 ppm) and ozone (0.3 ppm). J. Appl.
Physiol. 58:1783–1787.
Gong, H., Jr., P.A. Lachenbruch, P. Harber, and W.S. Linn. 1995. Comparative
short-term health responses to sulfur dioxide exposure and other common
stresses in a panel of asthmatics. Toxicol. Ind. Health 11:467–487.
doi:10.1177/074823379501100502
Horstman, D., L.J. Roger, H. Kehrl, and M. Hazucha. 1986. Airway sensitivity
of asthmatics to sulfur dioxide. Toxicol. Ind. Health 2:289–298.
doi:10.1177/074823378600200307
Horstman, D.H., E. Seal, L.J. Folinsbee, P. Ives, and L.J. Roger. 1988. The
relationship between exposure duration and sulfur dioxide-induced bronch-
oconstriction in asthmatic subjects. Am. Ind. Hyg. Assoc. J. 49:38–47.
doi:10.1080/15298668891379341
Kaplan, M., R. Paine, and R. Iwanchuk. 2013. Mobile SO2 monitoring study
and case-study AERMOD modeling near Wagner and Crane generating
stations. Unpublished consultant report. Chelmsford, MA: AECOM.
Kloog, I., B.A. Coull, A. Zanbetii, P. Koutrakis, and J. Schwartz. 2012. Acute
and chronic effects of particles on hospital admissions in New-England.
PLoS ONE 7:e34664. doi:10.1371/journal.pone.0034664
Koenig, J.Q., D.S. Covert, Q.S. Hanley, G. van Belle, and W.E. Pierson. 1990.
Prior exposure to ozone potentiates subsequent response to sulfur dioxide in
adolescent asthmatic subjects. Am Rev Respir Dis. 141:377–380.
doi:10.1164/ajrccm/141.2.377
Kulle, T.J., L.R. Sauder, F. Shanty, H.D. Kerr, B.P. Farrell, W.R. Miller, and J.
H. Milman. 1984. Sulfur dioxide and ammonium sulfate effects on pul-
monary function and bronchial reactivity in human subjects. Am. Ind. Hyg.
Assoc. J. 45:156–161. doi:10.1080/15298668491399569
Linn, W.S., E.L. Avol, R.C. Peng, D.A. Shamoo, and J.D. Hackney. 1987.
Replicated dose-response study of sulfur dioxide effects in normal, atopic,
and asthmatic volunteers. Am. Rev. Respir. Dis. 136:1127–1134.
doi:10.1164/ajrccm/136.5.1127
Linn, W.S., E.L. Avol, D.A. Shamoo, C.E. Spier, M.N. Smith, and J.D.
Hackney. 1988. Effect of metaproterenol sulfate on mild asthmatics’
response to sulfur dioxide exposure and exercise. Arch. Environ. Health
43:399–406. doi:10.1080/00039896.1988.9935858
Linn, W.S., D.A. Shamoo, R.C. Peng, K.W. Clark, E.L. Avol, and J.D.
Hackney. 1990. Response to sulfur dioxide and exercise by medication-
dependent asthmatics: Effect of varying medication levels. Arch. Environ.
Health 45:24–30. doi:10.1080/00039896.1990.9935920
Linn W.S., T.G. Venet, D.A. Shamoo, L.M. Valencia, U.T. Anzar, C.E. Spier,
and J.D. Hackney. 1983. Respiratory effects of sulfur dioxide in heavily
exercising asthmatics. A dose-response study. Am Rev Respir Dis.
127:278–283.
Mar, T.F., K. Jansen, K. Shepherd, T. Lumley, T.V. Larson, and J.Q. Koenig.
2005. Exhaled nitric oxide in children with asthma and short-term PM2.5.
Environ. Health Perspect. 113:1791–1794. doi:10.1289/ehp.7883
Shepherd et al. / Journal of the Air & Waste Management Association 65 (2015) 1239–1246 1245
Downloadedby[MarkShepherd]at18:0118October2015

9. Mcbride, S.J., G.A. Norris, R.W. Williams, and L.M. Neas. 2011. Bayesian
hierarchical modeling of cardiac response to particulate matter exposure.
J. Expos. Sci. Environ. Epidemiol. 21:74–91. doi:10.1038/jes.2009.58
Network Design Criteria for Ambient Air Quality. 2013. Title 40 U.S. Code of
Federal Regulations, Pt. 58, Appendix D&E. http://www.ecfr.gov/cgi-bin/
text-idx?SID=12826113f7c3749222e1af3759ce7f32&mc=true&tpl=/ecfr
browse/Title40/40cfr58_main_02.tpl (accessed October 12, 2013).
Park, J.K., Y.K. Kim, S.R. Lee, S.H. Cho, K.U. Min, and Y.Y. Kim. 2001.
Repeated exposure to low levels of sulfur dioxide (SO2) enhances the
development of ovalbumin-induced asthmatic reactions in guinea pigs.
Ann. Allergy Asthma Immunol. 86:62–67. doi:10.1016/S1081-1206(10)
62358-7
Primary National Ambient Air Quality Standard for Sulfur Dioxide; Final Rule.
75 Federal Register 119 (22 June 2010), pp. 35520–35603.
Sheppard, D., A. Saisho, J.A. Nadel, and H.A. Boushey. 1981. Exercise
increases sulfur dioxide-induced bronchoconstriction in asthmatic subjects.
Am. Rev. Respir. Dis. 123:486–491.
Stacy, R.W., E. Seal Jr., D.E. House, J. Green, L.J. Roger, and L. Raggio. 1983.
A survey of effects of gaseous and aerosol pollutants on pulmonary func-
tion of normal males. Arch. Envrion. Health 38:104–115.
U.S. Census Bureau. Annual Estimates of the Population of Metropolitan and
Micropolitan Statistical Areas: April 1, 2010 to July 1, 2012 (CBSA-
EST2012-01). http://www.census.gov/popest/data/metro/totals/2012/index.
html (accessed February 4, 2013).
U.S. Environmental Protection Agency. 2008. Technology Transfer Network
National Ambient Air Quality Standards (2008, September). Integrated
Science Assessment for Sulfur Oxides—Health Criteria. EPA/600/R-08/
047FA. http://www.epa.gov/ttn/naaqs/standards/so2/s_so2_index.html
(accessed June 1, 2013).
U.S. Environmental Protection Agency. 2009. Technology Transfer Network
National Ambient Air Quality Standards (2009, August). Risk and
Exposure Assessment to Support the Review of the SO2 Primary NAAQS
—Final Report. EPA-452/R-09-007. http://www.epa.gov/ttn/naaqs/stan
dards/so2/s_so2_index.html (accessed June 1, 2013).
Wilson, A.M., C.P. Wake, T. Kelly, and J.C. Salloway. 2005. Air pollution,
weather, and respiratory emergency room visits in two northern New
England cities: An ecological time-series study. Environ. Res. 97:312–
321. doi:10.1016/j.envres.2004.07.010
About the Authors
Mark A. Shepherd is vice president of Environmental Health and Safety at
Topaz Power Management, LP, Austin, Texas, and a graduate of the
Department of Environmental, Agricultural & Occupational Health, College
of Public Health, University of Nebraska Medical Center.
Gleb Haynatzki is a professor in the Department of Biostatistics, College of
Public Health, University of Nebraska medical Center.
Risto Rautiainen is a professor in the Department of Environmental, Agricultural
& Occupational Health, College of Public Health, University of Nebraska Medical
Center.
Chandran Achutan is an associate professor in the Department of
Environmental, Agricultural & Occupational Health, College of Public
Health, University of Nebraska Medical Center.
1246 Shepherd et al. / Journal of the Air & Waste Management Association 65 (2015) 1239–1246
Downloadedby[MarkShepherd]at18:0118October2015