Traffic-related particulate matter and acute respiratory symptoms among New York City area adolescents.
ABSTRACT Exposure to traffic-related particulate matter (PM) has been associated with adverse respiratory health outcomes in children. Diesel exhaust particles (DEPs) are a local driver of urban fine PM [aerodynamic diameter < or = 2.5 microm (PM(2.5))]; however, evidence linking ambient DEP exposure to acute respiratory symptoms is relatively sparse, and susceptibilities of urban and asthmatic children are inadequately characterized.
We examined associations of daily ambient black carbon (BC) concentrations, a DEP indicator, with daily respiratory symptoms among asthmatic and nonasthmatic adolescents in New York City (NYC) and a nearby suburban community.
BC and PM(2.5) were monitored continuously outside three NYC high schools and one suburban high school for 4-6 weeks, and daily symptom data were obtained from 249 subjects (57 asthmatics, 192 nonasthmatics) using diaries. Associations between pollutants and symptoms were characterized using multilevel generalized linear mixed models, and modification by urban residence and asthma status were examined.
Increases in BC were associated with increased wheeze, shortness of breath, and chest tightness. Multiple lags of nitrogen dioxide (NO(2)) exposure were associated with symptoms. For several symptoms, associations with BC and NO(2) were significantly larger in magnitude among urban subjects and asthmatics compared with suburban subjects and nonasthmatics, respectively. PM(2.5) was not consistently associated with increases in symptoms.
Acute exposures to traffic-related pollutants such as DEPs and/or NO(2) may contribute to increased respiratory morbidity among adolescents, and urban residents and asthmatics may be at increased risk. The findings provide support for developing additional strategies to reduce diesel emissions further, especially in populations susceptible because of environment or underlying respiratory disease.
- SourceAvailable from: Patrick L Kinney[Show abstract] [Hide abstract]
ABSTRACT: Highway-building environments are prevalent in metropolitan areas. This paper presents our findings in investigating pollutant transport in a highway-building environment by combing field measurement and numerical simulations. We employ and improve the Comprehensive Turbulent Aerosol Dynamics and Gas Chemistry (CTAG) model to simulate the spatial variations of black carbon (BC) concentrations near highway I-87 and an urban school in the South Bronx, New York. The results of CTAG simulations are evaluated against and agree adequately with the measurements of wind speed, wind directions, and BC concentrations. Our analysis suggests that the BC concentration at the measurement point of the urban school could decrease by 43-54% if roadside buildings were absent. Furthermore, we characterize two generalized conditions in a highway-building environment, i.e., highway-building canyon and highway viaduct-building. The former refers to the canyon between solid highway embankment and roadside buildings, where the spatial profiles of BC depend on the equivalent canyon aspect ratio and flow recirculation. The latter refers to the area between a highway viaduct (i.e., elevated highway with open space underneath) and roadside buildings, where strong flow recirculation is absent and the spatial profiles of BC are determined by the relative heights of the highway and buildings. The two configurations may occur at different locations or in the same location with different wind directions when highway geometry is complex. Our study demonstrates the importance of incorporating highway-building interaction into the assessment of human exposure to near-road air pollution. It also calls for active roles of building and highway designs in mitigating near-road exposure of urban population.Environmental Science & Technology 11/2011; 46(1):312-9. · 5.26 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: While exposures to urban fine particulate matter (PM(2.5)) and soot-black carbon (soot-BC) have been associated with asthma exacerbations, there is limited evidence on whether these pollutants are associated with the new development of asthma or allergy among young inner city children. We hypothesized that childhood exposure to PM(2.5) and the soot-BC component would be associated with the report of new wheeze and development of seroatopy in an inner city birth cohort. As part of the research being conducted by the Columbia Center of Children's Environmental Health (CCCEH) birth cohort study in New York City, two-week integrated residential monitoring of PM(2.5), soot-BC (based on a multi-wavelength integrating sphere method), and modified absorption coefficient (Abs*; based on the smoke stain reflectometer) was conducted between October 2005 and May 2011 for 408 children at ages 5-6 years old. Residential monitoring was repeated 6 months later (n=262) to capture seasonal variability. New wheeze was identified through the International Study of Asthma and Allergies in Childhood (ISAAC) questionnaires during up to 3 years of follow-up and compared to a reference group that reported never wheeze, remitted wheeze, or persistent wheeze. Specific immunoglobulin (Ig) E against cockroach, mouse, cat, and dust mite and total IgE levels was measured in sera at ages 5 and 7 years. PM(2.5), soot-BC, and Abs* measured at the first visit were correlated moderately with those at the second visit (Pearson r>0.44). Using logistic regression models, a positive association between PM(2.5) and new wheeze was found with adjusted odds ratio [95% confidence intervals] of 1.51 [1.05-2.16] per interquartile range (IQR). Positive but non-significant association was found between the development of new wheeze and soot-BC and (OR 1.40 [0.96-2.05]), and Abs* (OR 1.57 [0.91-2.68]); Significantly positive associations were found between air pollutant measurements and new wheeze when restricting to those participants with repeat home indoor measurements 6 months apart. Associations between pollutants and IgE levels were not detected. Our findings suggest that childhood exposure to indoor air pollution, much of which penetrated readily from outdoor sources, may contribute to the development of wheeze symptoms among children ages 5 to 7 years.Environment international 05/2012; 45:44-50. · 6.25 Impact Factor
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ABSTRACT: Air pollution is comprised of a complex mixture of gaseous and particulate pollutants emitted from multiple sources. During transport in the atmosphere, emissions undergo photochemical reactions, which may change their toxicity. Toxicological and epidemiological studies have linked vehicular emissions to respiratory and cardiovascular health effects. The aim of this study was to investigate the toxicity of primary and secondary traffic particles. Male Sprague–Dawley rats were exposed to either filtered air (control group) or one of three types of atmospheres: fresh primary particles from a major traffic tunnel plenum (P); secondary organic aerosol formed from photochemical oxidation of primary tunnel gases after filtration of primary particles (SOA); or photochemically aged primary particles plus secondary organic aerosols (P + SOA). In each exposure, 80–90 % of pollutant gases were removed using a non-selective denuder. Animals were exposed for 5 h per day, with varying number of days of exposure. Outcomes included: breathing pattern, broncho-alveolar lavage (BAL), complete blood count, and in vivo chemiluminescence (IVCL). Consistent mass concentration (approximately 50 μg/m3) was achieved for all exposures. Respiratory data showed many changes with each exposure type. All exposures produced decreases in tidal volume, minute volume, inspiratory and expiratory flows. There were mild inflammatory changes in BAL, with increased neutrophils for the SOA and P + SOA exposures and lymphocytes for the P and P + SOA exposure, with no changes in any test exposure for total protein, β-NAG or IVCL. All exposures produced changes compared to filtered air. Exposures containing particles (P and P + SOA) had stronger effects than SOA.Air Quality Atmosphere & Health 6(2). · 1.98 Impact Factor
volume 118 | number 9 | September 2010 • Environmental Health Perspectives
Research | Children’s Health
Growing epidemiologic evidence indicates
that long-term exposure to traffic-related air
pollution, particularly diesel exhaust particles
(DEPs), is associated with higher prevalence
of asthma and chronic respiratory symptoms
(Kim et al. 2004; McConnell et al. 2006).
One key longitudinal study observed that
exposures to traffic-related pollutants such
as elemental carbon (EC), nitrogen dioxide
(NO2), acid vapor, and fine particulate mat-
ter [PM; aerodynamic diameter ≤ 2.5 µm
(PM2.5)] were associated with deficits in lung
function growth between 10 and 18 years of
age (Gauderman et al. 2004). More recently,
geographic indicators such as roadway prox-
imity have been associated with frequency
of asthma exacerbation (Chang et al. 2009)
and with development of allergic sensitiza-
tion and chronic respiratory symptoms in
birth cohort studies (Morgenstern et al. 2008;
Ryan et al. 2007). Studies have also demon-
strated that shorter-term increases in ambi-
ent traffic-related particles exacerbate asthma
and increase airway inflammation in children
with asthma (Delfino et al. 2006, 2008; Gent
et al. 2009; Hirshon et al. 2008). The relative
effects of ambient DEP exposure on acute
respiratory morbidity in healthy children are
less well understood.
Urban and suburban disparities in preva-
lence and acute exacerbation of asthma are
well documented (Aligne et al. 2000; Bryant-
Stephens 2009). Asthma hospitalization rates
for children and young adults are higher in
New York City (NYC) than in surround-
ing suburbs (New York State Department
of Health 2007) and are higher in NYC
communities with greater numbers of die-
sel emission sources, such as major truck-
ing thoroughfares and bus depots (Lena et al.
2002; Tonne et al. 2004). Air pollution, aller-
gens, socioeconomic status, ethnicity, health
care inequalities, and psychosocial stressors
have been implicated as risk factors for the
disproportionate burdens of asthma preva-
lence and morbidity among urban children
(Bryant-Stephens 2009). The interrelation-
ships among urban residence, ambient DEP
exposure, acute respiratory symptoms, and
susceptibility of asthmatics are not well
characterized, and assessment of health risks
associated with acute DEP exposures has been
impeded by the lack of exposure data at fine
temporal and spatial resolution in urban and
In the present study, our objective was
to characterize associations between daily
school-based measurements of ambient black
carbon (BC), an indicator of DEPs, and daily
respiratory symptoms in a longitudinal study
of asthmatic and nonasthmatic adolescents
residing in NYC and in a nearby suburban
community. Although BC is a product of
multiple combustion processes (Glaser et al.
2005), in previous studies of the participating
schools (Patel et al. 2009) and other NYC
locations (Kinney et al. 2000; Lena et al.
2002), BC was significantly associated with
volume of diesel traffic but not car traffic.
Hence, BC may serve as a suitable indica-
tor of DEPs. We also uniquely designed the
study to examine whether the effects of DEP
exposure on respiratory symptoms differed
by asthma status and urban residence. We
hypothesized that daily reports of respiratory
symptoms would be positively associated with
daily BC concentrations, and the estimated
effect of BC exposure on symptoms would be
greater among asthmatic subjects and among
Address correspondence to P.L. Kinney, Department
of Environmental Health Sciences, Mailman School
of Public Health, Columbia University, 60 Haven
Ave., B-1, New York, NY 10032 USA. Telephone:
(212) 305-3663. Fax: (212) 305-4012. E-mail: plk3@
We thank the schools and students for their
Funding was provided by the National Institute
of Environmental Health Sciences (grants
ES11379, T32ES007322, ES09600, ES09089, and
P50ES015905) and U.S. Environmental Protection
Agency (grant R827027).
M.R. and S.P. are affiliated with the community
organizations For a Better Bronx and West Harlem
Environmental Action, Inc., respectively, which
are involved in environmental justice and advo-
cacy issues in the study area. D.K. was employed
by West Harlem Environmental Action, Inc. J.C.C.
is employed by the nonprofit Fundación Santa Fe
de Bogotá. The other authors declare they have no
actual or potential competing financial interests.
Received 23 September 2009; accepted 7 May 2010.
Traffic-Related Particulate Matter and Acute Respiratory Symptoms among
New York City Area Adolescents
Molini M. Patel,1 Steven N. Chillrud,2 Juan C. Correa,3 Yair Hazi,4 Marian Feinberg,5 Deepti KC,6 Swati Prakash,6
James M. Ross,2 Diane Levy,7 and Patrick L. Kinney4
1Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, College of Physicians and Surgeons, Columbia
University, New York, New York, USA; 2Lamont-Doherty Earth Observatory, Columbia University, Palisades, New York, USA; 3Division
de Salud Communitaria, Fundación Santa Fe de Bogotá, Bogotá, Colombia; 4Department of Environmental Health Sciences, Mailman
School of Public Health, Columbia University, New York, New York, USA; 5For a Better Bronx, Bronx, New York, USA; 6West Harlem
Environmental Action, Inc., New York, New York, USA; 7Department of Biostatistics, Mailman School of Public Health, Columbia
University, New York, New York, USA
Background: Exposure to traffic-related particulate matter (PM) has been associated with adverse
respiratory health outcomes in children. Diesel exhaust particles (DEPs) are a local driver of urban
fine PM [aerodynamic diameter ≤ 2.5 µm (PM2.5)]; however, evidence linking ambient DEP expo-
sure to acute respiratory symptoms is relatively sparse, and susceptibilities of urban and asthmatic
children are inadequately characterized.
oBjectives: We examined associations of daily ambient black carbon (BC) concentrations, a DEP
indicator, with daily respiratory symptoms among asthmatic and nonasthmatic adolescents in New
York City (NYC) and a nearby suburban community.
Methods: BC and PM2.5 were monitored continuously outside three NYC high schools and one
suburban high school for 4–6 weeks, and daily symptom data were obtained from 249 subjects
(57 asthmatics, 192 nonasthmatics) using diaries. Associations between pollutants and symptoms
were characterized using multilevel generalized linear mixed models, and modification by urban
residence and asthma status were examined.
results: Increases in BC were associated with increased wheeze, shortness of breath, and chest
tightness. Multiple lags of nitrogen dioxide (NO2) exposure were associated with symptoms. For
several symptoms, associations with BC and NO2 were significantly larger in magnitude among
urban subjects and asthmatics compared with suburban subjects and nonasthmatics, respectively.
PM2.5 was not consistently associated with increases in symptoms.
conclusions: Acute exposures to traffic-related pollutants such as DEPs and/or NO2 may con-
tribute to increased respiratory morbidity among adolescents, and urban residents and asthmatics
may be at increased risk. The findings provide support for developing additional strategies to reduce
diesel emissions further, especially in populations susceptible because of environment or underlying
key words: asthma, black carbon, diesel traffic, respiratory symptoms, urban air pollution. Environ
Health Perspect 118:1338–1343 (2010). doi:10.1289/ehp.0901499 [Online 7 May 2010]
Diesel air pollution and respiratory health
Environmental Health Perspectives • volume 118 | number 9 | September 2010
Materials and Methods
Subject recruitment and data collection. We
conducted an individual-level longitudinal
study involving exposure and respiratory health
monitoring over a 4- to 6-week period at
each of four high schools located in the NYC
metropolitan area. The study was approved
by the Columbia University Medical Center
Institutional Review Board before the start
of the study. The NYC Board of Education
granted permission on the condition that
school identities would remain confidential.
The four participating high schools were
chosen to represent a range of exposures to
traffic-related air pollutants as previously
described (Patel et al. 2009). In 2003, moni-
toring was conducted at an NYC school (U1)
adjacent to a medium-size highway. In 2004,
monitoring was conducted at a second NYC
school (U2) adjacent to a major highway with
an annual average daily traffic 2.5 times higher
than that at U1 (New York State Department
of Transportation 2006). The third participat-
ing NYC school in 2005 (U3) was on a two-
lane street located > 500 m from a highway
that prohibits commercial traffic, including
most diesel vehicles. The fourth school was
located in a suburban town 40 km northwest
of NYC on a two-lane roadway > 3 km from a
highway. The same suburban school was mon-
itored in 2003 and 2004 concurrently with
U1 and U2, respectively. Suburban school
measurements in 2003 are referred to as S1,
and 2004 measurements are referred to as S2.
Study participants were recruited through
classroom presentations. Anonymous baseline
questionnaires were initially administered to
approximately 300 students at each school
to obtain characteristics of the student bod-
ies regarding demographics, smoking, hous-
ing, activity patterns, and histories of asthma
and chronic respiratory symptoms. Written
informed consent was obtained from partici-
pants and parents/guardians before the start
of the study. Current asthma was defined as
physician-diagnosed asthma plus symptoms
in the previous 12 months as self-reported
on baseline questionnaires, and an effort was
made to recruit at least 20 asthmatics per
school. As a result of enhanced recruitment
strategies targeted at asthmatic subjects over
the 3 years (study advertisements placed in
hallways, announcements made over public
address systems, and recruitment of subjects
by school nurses), the number of asthmatic
subjects increased each year.
Students who returned signed consent
forms (44–78 per school) were given predated
daily symptom diaries to record respiratory
symptoms and medication use. Subjects were
instructed to complete diaries every morning
by recording whether they had symptoms or
used medication for asthma on the previous
calendar day. Symptom diaries were collected
from participants on a weekly basis to mini-
mize recall of symptoms for > 7 days. Of the
students who gave informed consent, 33–70
(75–90%) per school returned diaries and
were included in the study.
Ambient pollutant data. Outdoor BC
concentrations in the PM2.5 size range were
monitored continuously at each school using a
dual-beam aethalometer (model AE-21; Magee
Scientific, Berkeley, CA, USA). Aethalometers
were placed with air inlets outside second- or
third-floor classroom windows that faced adja-
cent roadways. Ambient air was sampled at 4
L/min, and suspended PM2.5 was deposited
onto quartz fiber tape. Optical density (OD)
of deposited particles was measured every
5 min at a wavelength of 880 nm. BC mass
concentration was quantified by multiplying
differences in OD between measurements by
an absorption coefficient. At the beginning
and end of each monitoring year, aethalome-
ters were operated together in the laboratory to
confirm between-instrument agreement. The
aethalometer had a limit of detection (LOD)
of 0.16 µg/m3 at a 5-min resolution.
Outdoor PM2.5 concentrations were
monitored and recorded hourly using a beta
attenuation monitor (BAM; model 1020; Met
One Instruments Inc., Grant Pass, OR, USA)
with air inlets placed outside of the same win-
dows as aethalometers. Air was sampled at
16.7 L/min, and PM2.5 mass was calculated
as a function of the attenuation of beta rays
(electrons) passing through particles depos-
ited onto filter tape. The BAM had an LOD
of 4.8 µg/m3 at a 1-hr resolution. Once per
week, aethalometer and BAM flow rates were
checked, and data were downloaded. Raw data
were checked for aberrations and processed
according to manufacturers’ instructions.
Daily ambient NO2 and ozone (O3) data
were obtained from the U.S. Environmental
Protection Agency’s Air Quality Systems data-
base (U.S. Environmental Protection Agency
2007) for two community monitoring sites
closest to schools. The urban site was 2.2 km
from U1, 2.4 km from U2, and 9.0 km from
U3. The suburban site was 40 km from the
suburban school. Hourly concentrations were
aggregated into daily averages for NO2 and
maximum 8-hr moving averages for O3.
Statistical analysis. We performed sta-
tistical modeling using R version 2.10.0 (R
Foundation for Statistical Computing, Vienna,
Austria); results with p < 0.05 were consid-
ered statistically significant. Observations
from all schools were combined, and three-
level generalized linear mixed models were
fit (glmm function with logit link for bino-
mial outcomes) to estimate the magnitude of
association between pollutant concentrations
and daily symptom incidence. Because of the
high correlation between school-based BC
and central-site NO2 measurements, separate
models were fit with NO2 as the independent
variable. Pollutants were matched to symp-
toms by calendar date. Subject and school
were included in models as random inter-
cept terms to account for correlation among
outcome responses within subjects and nest-
ing of subjects within schools, respectively.
An autoregressive covariance structure was
specified to account for temporal correla-
tion among outcomes within subjects. Other
covariates included an indicator variable for
weekend and daily maximum 8-hr average
O3 concentration. Season of monitoring and
daily pollen concentrations measured at a
National Allergy Bureau station in Brooklyn,
New York, were evaluated as confounders but
were not included in final models because they
lacked significance and did not appreciably
change pollutant effect estimates. We exam-
ined heterogeneity of effect by urban loca-
tion or by current asthma status by including
interaction terms for pollutant × urban school
or pollutant × asthma, respectively. We per-
formed stratified analyses if interaction terms
attained a significance level of p < 0.10. We
examined effects at multiple lags of exposure
using daily averages from the same day (lag 0),
previous day (lag 1), and 2-day to 5-day mov-
ing averages. Results are reported as odds ratios
(ORs) and 95% confidence intervals (CIs) per
interquartile range (IQR) increase in pollutant
concentration using the full range of concen-
trations across all schools.
Characteristics of study population. The study
population consisted of 249 mostly female
(71%), nonwhite (40% Hispanic, 35% black)
adolescents 13–20 years of age, although
distributions of several characteristics varied
among individual schools (Table 1). During
the study period, 46% of subjects reported
any wheeze, and the median (range) percent-
age of subjects reporting wheeze per day was
11% (0–50%). We observed similar frequen-
cies for shortness of breath and chest tightness
(Table 1). Use of medication for asthma was
less common, with 22% subjects reporting
any use during the study period. Cough was
the most frequently reported symptom. More
than 86% subjects reported cough at least
once during the study period, and the median
(range) percentage of subjects reporting cough
per day was 36% (15–61%).
Trends in ambient pollutants. Daily aver-
age BC concentrations were highly variable
over the study period, with the range of con-
centrations spanning near one order of mag-
nitude at each school. The median (range)
concentrations were, for U1, 2.4 (0.68–5.5)
µg/m3; U2, 2.0 (0.59–4.9) µg/m3; U3, 1.5
(0.33–2.3) µg/m3; S1, 0.60 (0.11–1.8) µg/m3;
and S2, 0.49 (0.10–2.7) µg/m3; (Table 2).
BC showed strong, positive correlations with
Patel et al.
volume 118 | number 9 | September 2010 • Environmental Health Perspectives
NO2 and weaker, negative correlations with
O3 (Table 3).
Associations between ambient pollutants
and respiratory symptoms. In analyses com-
bining data from all subjects and schools,
an IQR increase in same-day average (lag 0)
BC concentration (1.2 µg/m3) was associ-
ated with an increased OR of wheeze of 1.11
(95% CI, 1.00–1.22) (Table 4). Previous-
day (lag 1) and multiday averages of BC were
significantly associated with wheeze, with the
largest ORs observed for 4-day (1.19) and
5-day average BC (1.22). Same-day BC was
also significantly associated with shortness of
breath and chest tightness. Associations of
lag 1 and 2-day average BC with cough were
Multiple lags of NO2 exposure were sig-
nificantly associated with wheeze and shortness
of breath, and ORs increased as the number
of averaging days increased (Table 4). All eval-
uated lags of NO2 were significantly associ-
ated with shortness of breath, with ORs (per
16-ppb increase in NO2) ranging from 1.20 for
same-day NO2 to 1.35 for 5-day average NO2.
Same-day and previous-day NO2 were not
significantly associated with wheeze, whereas
associations of multiday average exposures were
borderline significant or significant. Similar
to BC, the estimated effect of lag 1 NO2 on
cough was significantly negative. Associations
of 3-day, 4-day, and 5-day average PM2.5 with
wheeze were significantly positive. Associations
of PM2.5 with cough, shortness of breath, and
chest tightness were consistently negative and
statistically significant (Table 4).
In stratified analyses that adjusted for cur-
rent asthma, the association between BC and
shortness of breath was increased for urban
subjects (OR = 1.26; 95% CI, 1.14–1.40)
but not for suburban subjects (interaction
p = 0.02) (Table 5). The estimated effect of BC
on chest tightness was also larger and statisti-
cally significant in urban subjects compared
with suburban subjects. Associations of BC
with wheeze, cough, and use of medication
for asthma did not significantly differ between
urban and suburban groups (Table 5), so strat-
ified analyses were not performed for these
outcomes. We observed a difference between
urban and suburban subjects in the association
of NO2 with shortness of breath but not with
the other outcomes examined (Table 5). As
with BC, the association between NO2 and
shortness of breath was increased among urban
subjects (OR = 1.27; 95% CI, 1.14–1.42) but
not among suburban subjects (OR = 0.98;
95% CI, 0.83–1.15).
Controlling for urban location, the BC
× asthma interaction was statistically signifi-
cant for wheeze (p = 0.07) and use of medica-
tion for asthma (p = 0.001), and the NO2 ×
asthma interaction was significant for wheeze
(p = 0.03) and chest tightness (p = 0.02).
In stratified analyses, effect estimates for
same-day average BC and NO2 were larger
in asthmatics (n = 57 from all schools) than
in nonasthmatics (n = 192 from all schools)
(Table 5). For example, the OR for the associ-
ation between BC and wheeze was 1.23 (95%
CI, 1.00–1.50) in asthmatics and 1.00 (95%
CI, 0.89–1.13) in nonasthmatics. Similarly,
the effect estimate for NO2 with wheeze was
elevated in asthmatics (OR = 1.13; 95% CI,
0.94–1.36) but not in nonasthmatics (OR =
0.90; 95% CI, 0.79–1.02). Associations of
BC with cough, shortness of breath, and chest
tightness and associations of NO2 with cough,
shortness of breath, and use of medication for
asthma were comparable between asthmatics
and nonasthmatics (Table 5). PM2.5 associa-
tions were not significantly modified by urban
residence or current asthma (0.12 ≤ p ≤ 0.84
for interaction terms; data not shown).
Table 1. Characteristics of study population.
Age (years) [median (range)]
Father’s education level
Less than high school
High school graduate
Asthmatics [no. (%)]
School asthma prevalenceb
Symptom prevalencec [median (range)]
Shortness of breath
Use of medication for asthmac
Data are presented as percentages unless otherwise specified. Eight subjects (1–3 per school) are missing demographic
data because of uncompleted baseline questionnaires but are included in the sample sizes for each school.
aAmong the subjects who returned symptom diaries, the number of subjects who reported current smoking on the
baseline questionnaire divided by the number of subjects who completed the baseline questionnaire. bThe number of
students who reported current asthma on the anonymous survey divided by the number of students who completed the
anonymous survey at each school. cOn a given day during the study period, the number of subjects reporting presence
of a symptom or use of medication divided by all subjects providing data on symptoms or medication use that day.
U1 U2S1 S2
Table 2. Distributions of daily average BC and PM2.5 concentrations.
U3Two-lane street 4/3/2005–5/8/2005
S1Two-lane street 5/5/2003–6/16/20030.11
S2Two-lane street 2/23/2004–3/21/2004
aFor 2 days measures were < LOD.
Table 3. Spearman correlation coefficients for pollutant pairs.
*p < 0.05.
Diesel air pollution and respiratory health
Environmental Health Perspectives • volume 118 | number 9 | September 2010
A key aim of this study was to analyze the
contribution of traffic-related PM2.5 to risk of
acute respiratory morbidity among adolescents
in the NYC metropolitan area. Further, by
monitoring traffic-related particles and col-
lecting symptom data from asthmatic and
nonasthmatic subjects at urban and suburban
schools, we aimed to examine whether effects
vary by current asthma and by urban residence.
Although current levels of ambient PM2.5 have
been associated with respiratory morbidity in
U.S. communities (Dominici et al. 2006; Gent
et al. 2003; Koenig et al. 2003; O’Connor et al.
2008), uncertainty exists over which compo-
nents of PM2.5 are responsible for observed
effects. The present findings demonstrate that
increases in fine BC, an indicator of DEPs, are
associated with increased probability of wheeze,
shortness of breath, and chest tightness. PM2.5
as a whole, which is a heterogeneous mix of
chemical constituents from multiple sources,
was not consistently associated with increases
in daily symptom incidence. This study makes
an important contribution to the literature by
demonstrating that exposure to fine PM com-
ponents emitted by diesel vehicles may confer
greater risk for respiratory symptoms than does
PM2.5 as a whole. Furthermore, residence in
NYC and having asthma may independently
confer susceptibility to BC-related respiratory
morbidity. Ambient NO2, an indicator of both
gasoline and diesel emissions, was also signifi-
cantly associated with respiratory symptoms.
Thus, all traffic may be an important source
of pollutants associated with respiratory symp-
toms. At two study schools, volume of diesel
traffic but not car traffic was associated with
BC (Patel et al. 2009), which provides support
for independent effects of diesel vehicle emis-
sions in increasing adverse respiratory health
effects. Nonetheless, because of the high cor-
relation between BC and NO2, it is difficult
to distinguish between the effects of diesel and
gasoline vehicle emissions in this study.
Contrary to expectations, BC, NO2, and
PM2.5 were negatively associated with cough
at several lags of exposure, which could not
be explained by negative correlations between
cough and other symptoms or by inclusion of
covariates in the model. The relatively high
prevalence of cough and weak correlation with
other symptoms (data not shown) suggest
that other unexamined meteorologic factors
or ambient exposures negatively correlated
with BC, NO2, or PM2.5 may exert greater
influence on incidence of cough. Negative
Table 4. ORsa (95% CI) for respiratory symptoms and use of medication for asthma associated with an IQRb increase in pollutant concentrations at various lags
BC (249 subjects, 6,210 person-days)c
Lag 0 1.11 (1.00–1.22)#
Lag 1 1.08 (1.03–1.13)*0.91 (0.83–0.99)*
2-day average 1.09 (0.96–1.22) 0.90 (0.81–0.99)*
3-day average1.10 (1.03–1.18)*0.91 (0.81–1.02)
4-day average1.19 (1.06–1.33)* 0.98 (0.86–1.12)
5-day average 1.22 (1.08–1.38)*1.03 (0.88–1.19)
NO2 (249 subjects, 6,555 person-days)
Lag 01.03 (0.93–1.14)0.96 (0.88–1.05)
Lag 1 1.09 (0.97–1.24)0.88 (0.80–0.98)*
2-day average1.15 (1.00–1.33)#
3-day average 1.32 (1.11–1.56)*0.88 (0.77–1.02)
4-day average 1.57 (1.29–1.91)*0.96 (0.82–1.13)
5-day average1.70 (1.36–2.13)* 1.05 (0.87–1.26)
PM2.5 (200 subjects, 4,026 person-days)
Lag 01.05 (0.94–1.16)0.86 (0.78–0.94)*
Lag 11.09 (0.98–1.21) 0.83 (0.75–0.91)*
2-day average1.10 (0.98–1.25) 0.79 (0.70–0.88)*
3-day average1.18 (1.03–1.35)* 0.78 (0.70–0.89)*
4-day average1.24 (1.06–1.44)* 0.78 (0.69–0.90)*
5-day average1.23 (1.04–1.45)*0.76 (0.65–0.88)*
Shortness of breath Chest tightnessUse of medication for asthma
aModels combine data from all schools and adjust for school, weekend, and daily maximum 8-hr average O3. bIQRs are 1.2 µg/m3 for BC, 16 ppb for NO2, and 11.3 µg/m3 for PM2.5.
cSample sizes vary among pollutant models because of differing patterns of missing pollutant measurements. *p < 0.05. #0.05 ≤ p < 0.10.
Table 5. ORs (95% CI) for respiratory symptoms and use of medication for asthma associated with an IQRa increase in same-day average pollutant concentra-
tions, stratified by locationb or asthma status.c
Pollutant and subgroup
BC × urban interactionp = 0.87p = 0.75
Urban (161; 3,917)
Suburban (88; 2,293)
BC × asthma interaction p = 0.07p = 0.73
Asthma (57; 1,350)1.23 (1.00–1.50)#
No asthma (192; 4,860) 1.00 (0.89–1.13)
NO2 × urban interaction p = 0.66p = 0.20
Suburban (88; 2,296)
NO2 × asthma interaction p = 0.03p = 0.24
Asthma (57; 1,473) 1.13 (0.94–1.36)
No asthma (192; 5,082)0.90 (0.79–1.02)
Shortness of breathChest tightness Use of medication
p = 0.02
p = 0.93
p = 0.002
p = 0.59
p = 0.71
p = 0.001
p = 0.03
p = 0.34
p = 0.33p = 0.83
p = 0.02p = 0.28
aIQRs are 1.2 µg/m3 for BC and 16 ppb for NO2. bAdjusted for weekend, daily maximum 8-hr average O3, and asthma. cAdjusted for weekend, daily maximum 8-hr average O3, and urban
location. dSample sizes refer to number of subjects and person-days of observations in each model. Person-days vary among pollutant models because of differing patterns of missing
pollutant measurements. *p < 0.05. #0.05 ≤ p < 0.10.
Patel et al.
volume 118 | number 9 | September 2010 • Environmental Health Perspectives
associations of PM2.5 with shortness of breath
and chest tightness could not be explained
by negative correlations between PM2.5 and
other pollutants in either pooled or individ-
ual school data. However, ORs for associa-
tions of same-day average PM2.5 with wheeze,
shortness of breath, and use of medication
for asthma were > 1.0, and associations of
3- to 5-day average PM2.5 with wheeze were
positive and significant, suggesting that at cer-
tain lags PM2.5 exposure may increase risk of
respiratory symptoms. PM2.5 was not meas-
ured at S1, and data were missing for most of
the study period at S2 because of equipment
malfunctions. Because of fewer person-days of
observations and domination of PM2.5 analy-
ses with observations from urban subjects, the
PM2.5 findings may not be representative of
the general population.
Our results are consistent with those from
other recent studies that demonstrate adverse
respiratory health effects in association with
traffic-related exposures in populations not
limited to children with asthma (Gauderman
et al. 2004; Kim et al. 2004; Ryan et al. 2007;
Salam et al. 2007). A strength of our study is
its longitudinal design, involving continuous
measurement of ambient BC concentrations
and collection of daily respiratory symptom
data from individual subjects. Each subject
served as his or her own control, thus mini-
mizing confounding from between-subject
differences in time-invariant factors such as
sex and ethnicity. BC concentrations spanned
nearly an order of magnitude at schools and
displayed acute changes day-to-day (Patel
et al. 2009), which increased power to esti-
mate their effect on changing daily incidence
of symptoms. In a longitudinal study of asth-
matics by Delfino et al. (2003), daily con-
centrations of EC, which is similar to BC,
were associated with daily respiratory symp-
toms ascertained from diaries, and same-day
averages were more strongly associated with
symptoms, compared with previous-day aver-
ages. Symptoms vary day to day and thus may
be a sensitive indicator of the effects of daily
changes in air pollution on respiratory health.
The results of both studies highlight the
importance of obtaining daily data, which are
subject to less recall error, compared with his-
torical questionnaire data. With self-admin-
istered diaries, it is difficult to assess whether
subjects record symptoms on a daily basis.
The school-based study provided the oppor-
tunity to address this limitation by having
teachers remind students to complete symp-
tom diaries at the beginning of class each day.
Another advantage of the school-based study
was accessibility of study staff to subjects’
classrooms to collect diaries and reinforce the
importance of completing diaries daily.
In this study, BC measurements were
limited to school locations, which may not
accurately represent subjects’ exposures in
other locations given the high spatial hetero-
geneity in BC observed in NYC (Kinney et al.
2000; Lena et al. 2002) and the wide range of
distances between school and home observed
among subjects. School-based BC exposures
were significantly associated with respiratory
symptoms, and potential error in the meas-
urement of personal exposures would be ran-
dom and result in the underestimation of BC
associations. Together with findings from
other school-based studies (Janssen et al. 2003;
Kim et al. 2004), the present findings indicate
that recurrent exposures during the 6- to 7-hr
school day may be independent risk factors for
adverse respiratory health effects and provide
rationale for policies to reduce children’s expo-
sures to traffic-related pollutants by limiting
time spent outdoors or limiting new school
construction adjacent to major roadways.
Alternatively, given the high urban-to-subur-
ban correlation in daily BC at concurrently
monitored study schools (Patel et al. 2009),
high correlation between serial measurements
of school and personal EC exposures in NYC
students (Spira-Cohen et al. 2010), and high
infiltration of ambient BC indoors (Sarnat
et al. 2006), school-based measurements of BC
may serve as reasonable estimates of personal
exposure in longitudinal analyses.
Because ambient NO2 concentrations are
spatially heterogeneous, the degree of measure-
ment error may vary among schools because of
varying distance to central site. The greatest
NO2 measurement error potentially occurred
at U3, where BC correlation with NO2 was
the lowest. We obtained larger ORs for mul-
tiday averages of NO2, in which single-day
measurement errors may be smoothed, sug-
gesting that measurement error could have
biased results to the null and led to underes-
timation of NO2 associations. However, mul-
tiday averages of BC also had larger estimated
effects on symptoms, and for most symptoms,
ORs in pooled and subgroup analyses were
similarly significant for BC and NO2 and
had CIs of similar width. Also, daily values in
school-based BC and central-site NO2 were
highly correlated at all schools but U3. These
observations suggest that misclassification of
NO2 exposure arising from use of central site
measurements did not strongly affect findings.
Significant heterogeneity in BC and
NO2 associations by urban school location,
controlling for current asthma, suggests that
urban residents may have increased suscep-
tibility to the effects of traffic-related pollut-
ants on respiratory symptoms, independent of
asthma. Associations may vary between urban
and suburban locations because of differences
in the mix of ambient pollutants, allergens,
and other environmental exposures (Matsui
et al. 2008; Simons et al. 2007). Also, esti-
mated effects may be larger in magnitude in
urban subjects because of higher BC concen-
trations or interactions between BC and other
urban risk factors for increased respiratory
morbidity. In suburban-only analyses, most
ORs for symptoms were close to 1.0, and
the widths of CIs were not much larger than
those for urban-only analyses, suggesting that
lack of significance in suburban schools was
not simply due to lack of power from smaller
sample size. Pollutants other than BC and/
or NO2 may have been important risk fac-
tors for respiratory symptoms in the suburban
subjects during the study period.
The associations of BC and NO2 with
respiratory symptoms were larger in asthmatics
than in nonasthmatics, independent of urban
location. Asthmatics may be more sensitive
to BC exposures a result of increased deposi-
tion and retention of particles in airways and/
or greater sensitivity to release proinflamma-
tory cytokines (Lay et al. 2009; Quaedvlieg
et al. 2006). In NYC and the United States,
asthma exacerbations are a leading cause of
school absenteeism and source of health care
expenditures (Garg et al. 2003). Accumulating
evidence of greater health risks associated with
exposure to traffic-related pollutants among
asthmatics has important implications for
developing policies to reduce acute asthma
morbidity and the associated public health
consequences. The estimated effect of BC on
wheeze was larger among asthmatics than
among nonasthmatics and was borderline
significant only in asthmatics. The estimated
effect of NO2 on wheeze was larger among
asthmatics but not significant. The CIs associ-
ated with these ORs in asthmatics were wider
compared with those in pooled analyses. The
relatively small sample size of asthmatics in
all schools except for U3 may have resulted
in reduced power to detect significant asso-
ciations. Lack of sufficient power may also
explain why we did not observe associations of
BC with shortness of breath and chest tight-
ness that differed significantly between asth-
matics and nonasthmatics despite significant
associations in pooled analyses.
The study population comprised mostly
nonwhite participants, although the distri-
butions of race and ethnicity varied among
the five school cohorts. The heterogeneity in
time-invariant characteristics among subjects
and schools did not likely confound analysis
of within-subject exposure–response associa-
tions over time, although the findings may
not be generalizable to the general U.S. pop-
ulation or other populations that differ in
distribution of demographic characteristics.
Study participants differed from the schools’
student bodies according to many factors,
including sex, smoking, and current asthma
prevalence. The voluntary nature of participa-
tion may have also contributed to sampling
bias in the study. However, we did not aim to
Diesel air pollution and respiratory health
Environmental Health Perspectives • volume 118 | number 9 | September 2010
obtain representative populations but rather
to oversample asthmatics and examine differ-
ences in susceptibility between asthmatics and
DEPs are a heterogeneous mixture of EC,
sulfates, nitrates, metals, trace elements, organic
compounds, and particles of various sizes. In
experimental studies, various components in
isolation have been shown to stimulate release
of proinflammatory cytokines and immuno-
globulin E (Bömmel et al. 2003; Inoue et al.
2007; Kleinman et al. 2007). Although BC
accounts for most DEPs by mass, BC may be
serving as a surrogate for another DEP compo-
nent that is a causal risk factor for respiratory
morbidity. Alternatively, although BC concen-
trations at schools in the present study (Patel
et al. 2009) were significantly associated with
local diesel traffic volume, BC may be serving
as a surrogate for other mobile and station-
ary combustion sources that emit BC (Glaser
et al. 2005). Ambient concentrations of BC
and PM2.5 were higher at urban schools than
at suburban schools (Patel et al. 2009), and
differences in PM2.5 were only partly explained
by differences in BC. Therefore, other source
components of PM2.5 are also likely to differ
between urban and suburban locations and
may also be important risk factors for respi-
ratory morbidity. Identifying specific PM2.5
components and sources that are causally asso-
ciated with adverse health effects has important
implications for future air quality standards
and control programs.
Exposures from other combustion sources
such as domestic cooking, environmental
tobacco smoke, and transportation may also
be important risk factors for respiratory mor-
bidity in this study population. In a subset
of 18 U3 subjects, smoking exposures and
gas stove use were stable over time within
subjects and were uncorrelated with temporal
trends in school-based BC concentrations.
Total commute time and time spent in each
mode of transport varied temporally but
were uncorrelated with BC (data not shown).
Based on this subset of the data, it is not likely
that these factors confounded the association
between BC and respiratory symptoms.
The findings of the present study contribute
to furthering understanding of the respiratory
health effects associated with specific compo-
nents of PM2.5 by demonstrating that increases
in respiratory morbidity are associated with
acute increases in BC, an indicator of DEPs,
but not with PM2.5 as a whole. The results fur-
ther suggest that asthmatics and urban popula-
tions may be more susceptible to exposure to
traffic-related pollutants. Although the effect
estimates for BC exposures were relatively
small, they may be especially significant when
considering population-level risks, given the
large numbers of people exposed to high vol-
umes of truck and bus traffic in high-density
metropolitan areas and the high prevalence of
asthma among their residents.
Aligne AC, Auinger P, Byrd RS, Weitzman M. 2000. Risk factors
for pediatric asthma. Contributions of poverty, race, and
urban residence. Am J Respir Crit Care Med 162:873–877.
Bömmel H, Haake M, Luft P, Horejs-Hoeck J, Hein H, Bartels J,
et al. 2003. The diesel exhaust component pyrene induces
expression of IL-8 but not of eotaxin. Int Immunopharmacol
Bryant-Stephens T. 2009. Asthma disparities in urban environ-
ments. J Allergy Clin Immunol 123:1199–1206.
Chang J, Delfino RJ, Gillen D, Tjoa T, Nickerson B, Cooper D.
2009. Repeated respiratory hospital encounters among
children with asthma and residential proximity to traffic.
Occup Environ Med 66:90–98.
Delfino RJ, Gong H, Linn WS, Pellizzari ED, Hu Y. 2003. Asthma
symptoms in Hispanic children and daily ambient expo-
sures to toxic and criteria air pollutants. Environ Health
Delfino RJ, Staimer N, Gillen D, Tjoa T, Sioutas C, Fung K, et al.
2006. Personal and ambient air pollution exposure is asso-
ciated with increased exhaled nitric oxide in children with
asthma. Environ Health Perspect 114:1736–1743.
Delfino RJ, Staimer N, Tjoa T, Gillen D, Kleinman MT, Sioutas C,
et al. 2008. Personal and ambient air pollution exposures
and lung function decrements in children with asthma.
Environ Health Perspect 116:550–558.
Dominici F, Peng RD, Bell ML, Pham L, McDermott A, Zeger SL,
et al. 2006. Fine particulate air pollution and hospital
admission for cardiovascular and respiratory diseases.
Garg R, Karpati A, Leighton J, Perrin M, Shah M. 2003. Asthma
Facts. 2nd ed. New York State Department of Health and
Mental Hygiene. Available: http://www.nyc.gov/html/doh/
downloads/pdf/asthma/facts.pdf [accessed 24 August
Gauderman WJ, Avol E, Gilliland F, Vora H, Thomas D,
Berhane K, et al. 2004. The effect of air pollution on lung
development from 10 to 18 years of age. N Engl J Med
Gent JF, Koutrakis P, Belanger K, Triche E, Holford TR,
Bracken MB, et al. 2009. Symptoms and medication use
in children with asthma and traffic-related sources of fine
particulate matter. Environ Health Perspect 117:1168–1174.
Gent JF, Triche EW, Holford TR, Belanger K, Bracken MB,
Beckett WS, et al. 2003. Association of low-level ozone
and fine particles with respiratory symptoms in children
with asthma. JAMA 290:1859–1867.
Glaser B, Dreyer A, Bock M, Fiedler S, Mehring M, Heitmann T.
2005. Source apportionment of organic pollutants of a
highway-traffic-influenced urban area in Bayreuth
(Germany) using biomarker and stable carbon isotope
signatures. Environ Sci Technol 39:3911–3917.
Hirshon JM, Shardell M, Alles S, Powell JL, Squibb K, Ondov J,
et al. 2008. Elevated ambient air zinc increases pediatric
asthma morbidity. Environ Health Perspect 116:826–831.
Inoue K-I, Takano H, Yanagisawa R, Sakurai M, Abe S,
Yoshino S, et al. 2007. Effects of components derived from
diesel exhaust particles on lung physiology related to anti-
gen. Immunopharmacol Immunotoxicol 29:403–412.
Janssen NA, Brunekreef B, van Vliet P, Aarts F, Meliefste K,
Harssema H, et al. 2003. The relationship between air
pollution from heavy traffic and allergic sensitization,
bronchial hyperresponsiveness, and respiratory symp-
toms in Dutch schoolchildren. Environ Health Perspect
Kim JJ, Smorodinsky S, Lipsett M, Singer BC, Hodgson AT,
Ostro B. 2004. Traffic-related air pollution near busy roads:
the East Bay Children’s Respiratory Health Study. Am J
Respir Crit Care Med 170:520–526.
Kinney PL, Aggarwal M, Northridge ME, Janssen NA, Shepard P.
2000. Airborne concentrations of PM2.5 and diesel exhaust
particles on Harlem sidewalks: a community-based pilot
study. Environ Health Perspect 108:213–218.
Kleinman MT, Sioutas C, Froines JR, Fanning E, Hamade A,
Mendez L, et al. 2007. Inhalation of concentrated ambient
particulate matter near a heavily trafficked road stimu-
lates antigen-induced airway responses in mice. Inhal
Koenig JQ, Jansen K, Mar TF, Lumley T, Kaufman J, Trenga CA,
et al. 2003. Measurement of offline exhaled nitric oxide in
a study of community exposure to air pollution. Environ
Health Perspect 111:1625–1629.
Lay JC, Alexis NE, Zeman KL, Peden DB, Bennett WD. 2009.
In vivo uptake of inhaled particles by airway phagocytes
is enhanced in patients with mild asthma compared with
normal volunteers. Thorax 64:313–320.
Lena TS, Ochieng V, Carter M, Holguin-Veras J, Kinney PL.
2002. Elemental carbon and PM2.5 levels in an urban com-
munity heavily impacted by truck traffic. Environ Health
Matsui EC, Hansel NN, McCormack MC, Rusher R, Breysse PN,
Diette GB. 2008. Asthma in the inner city and the indoor
environment. Immunol Allergy Clin North Am 28:665–686.
McConnell R, Berhane K, Yao L, Jerrett M, Lurmann F,
Gilliland F, et al. 2006. Traffic, susceptibility, and childhood
asthma. Environ Health Perspect 114:766–772.
Morgenstern V, Zutavern A, Cyrys J, Brockow I, Koletzko S,
Kramer U, et al. 2008. Atopic diseases, allergic sensitiza-
tion, and exposure to traffic-related air pollution in chil-
dren. Am J Respir Crit Care Med 177:1331–1337.
New York State Department of Health. 2007. New York State
Asthma Surveillance Summary Report. Statewide Planning
and Research Cooperative System. Albany:New York State
Department of Health.
New York State Department of Transportation. 2006.Welcome
to 511NY. Traffic Data Viewer. Available: http://www.trav-
elinfony.com/tdv/# [accessed 6 August 2006].
O’Connor GT, Neas L, Vaughn B, Kattan M, Mitchell H, Crain EF,
et al. 2008. Acute respiratory health effects of air pollution
on children with asthma in US inner cities. J Allergy Clin
Patel MM, Chillrud SN, Correa JC, Feinberg M, Hazi Y, KC D,
et al. 2009. Spatial and temporal variations in traffic-
related particulate matter at New York City high schools.
Atmos Environ 43:4975–4981.
Quaedvlieg V, Henket M, Sele J, Louis R. 2006. Cytokine pro-
duction from sputum cells in eosinophilic versus non-
eosinophilic asthmatics. Clin Exp Immunol 143:161–166.
Ryan PH, Lemasters GK, Biswas P, Levin L, Hu S, Lindsey M,
et al. 2007. A comparison of proximity and land use regres-
sion traffic exposure models and wheezing in infants.
Environ Health Perspect 115:278–284.
Salam MT, Gauderman WJ, McConnell R, Lin P-C, Gilliland FD.
2007. Transforming growth factor-1 C-509T polymorphism,
oxidant stress, and early-onset childhood asthma. Am J
Respir Crit Care Med 176:1192–1199.
Sarnat SE, Coull BA, Ruiz PA, Koutrakis R, Suh HH. 2006. The
influences of ambient particle composition and size on
particle infiltration in Los Angeles, CA, residences. J Air
Waste Manag Assoc 56:186–196.
Simons E, Curtin-Brosnan J, Buckley T, Breysse P, Eggleston P.
2007. Indoor environmental differences between inner city
and suburban homes of children with asthma. J Urban
Spira-Cohen A, Chen LC, Kendall M, Sheesley R, Thurston GD.
2010. Personal exposures to traffic-related particle pollu-
tion among children with asthma in the South Bronx, NY.
J Expo Sci Environ Epidemiol 20(5):446–456.
Tonne CC, Whyatt RM, Camann DE, Perera FP, Kinney PL. 2004.
Predictors of personal polycyclic aromatic hydrocarbon
exposures among pregnant minority women in New York
City. Environ Health Perspect 112:754–759.
U.S. Environmental Protection Agency. 2007. AirData: Access
to Air Pollution Data. Available: http://www.epa.gov/air/
data/index.html [accessed 22 February 2007].