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(Fe, Cu, Zn, and V) might be associated with ST-segment depression, given that both these, and
OC, may have the capability to induce oxidative stress in the lung. However, when adjusted for
ABS (absorbance, a measure of EC emissions from motor vehicles), none of the metals that were
measured were associated with ST-segment depression, while the ABS associations remained
signiicant with only slight variation.
Riediker et al. (2004a,b) studied a panel of nine nonsmoking healthy male highway patrol
oficers (ages 23-30) in North Carolina over four late-shift tours of duty. Their patrol cars had air
samples that were analyzed for vapor and PM 2.5 components each day. PM 2.5 components were
correlated to cardiac and blood parameters measured 10 and 15 h after the work shift. They reported
that in-vehicle PM 2.5 mass was associated with changes in cardiac parameters—blood proteins
associated with inlammation, hemostasis, and thrombosis—and increased red blood cell (RBC)
volume. In a follow-up study, Riediker (2007) used data on PM 2.5 components. Those associated
with health-related endpoints were Ca (increased uric acid and von Willebrand factor [vWF], and
decreased protein C), Cr (increased WBC and IL-6), Cu (increased blood urea nitrogen, mean cycle
length of normal R-R intervals), and S (increased ventricular ectopic beats). Control for the gaseous
pollutants had little effect on the effect estimates.
Gent et al. (2009) studied 149 children with physician-diagnosed asthma and symptoms or
medication use within the previous 12 months who were living in New Haven, CT and vicinity.
Air sampling ilters were collected daily and analyzed for trace elements by x-ray luorescence
(XRF) and black carbon (BC) by light relectance. Using factor analysis/source apportionment, they
identiied six sources of PM 2.5 . They were motor vehicle, road dust, S (for regional PM 2.5 ), biomass
burning, oil combustion, and sea salt. They attributed 42% of the PM 2.5 to the motor vehicle source,
and 12% to road dust. Increased likelihood of symptoms and inhaler use was largest for 3 day
averaged exposures, with a 10% increased likelihood of wheeze per 5 μg/m 3 of the motor vehicle
source, and a 28% likelihood increase for shortness of breath associated with road dust. There were
no associations with increased health outcome risks for PM 2.5 per se or the other source factors.
In summary, a broad variety of short-term cardiovascular effects have been signiicantly
associated with peaks in ambient air concentrations of PM 2.5 and/or one or more of its chemical
components in panel studies. In young, healthy highway patrol oficers, PM 2.5 , but not gaseous
pollutants, was associated with changes in cardiac parameters such as Ca (vWF), Cr (WBC and
IL-6), Cu (R-R intervals). These various cardiac-related responses, while not necessarily associated
with speciic PM 2.5 components, are certainly consistent with the excess cardiovascular mortality
and morbidity in the ever-growing air pollution health effects literature.
In addition, peaks in ambient air PM were associated with a variety of pulmonary effects among
children with physician-diagnosed asthma and symptoms or medication use within the previous 12
months living in New Haven, CT, and vicinity. The sources of PM 2.5 were motor vehicle, road dust,
S for regional PM 2.5 , biomass burning, oil combustion, and sea salt, with 42% of the PM 2.5 attributed
to the motor vehicle source, and 12% to road dust. Increased likelihood of symptoms and inhaler use
was largest for 3 day averaged exposures, with a 10% increased likelihood of wheeze per 5 μg/m 3 of
the motor vehicle source, and a 28% likelihood increase for shortness of breath associated with road
dust. There were no associations with increased health outcome risks for PM 2.5 per se or the other
source factors (Gent et al. 2009).
14.2.4   l arge  P oPulation -b ased  s tudies in  H uMans  d ealing
witH  r esPonses to  PM c oMPonents
In a Hong Kong, China sulfur-in-fuel intervention study (Hedley et al., 2002), SO 2 , Ni, and V fell
promptly and substantially after the intervention, while other criteria pollutants and metals did not
fall (Hedley et al., 2004). Thus, it is possible that the large changes in the three pollutants that fell
may account for at least some of the changes in the intervention-related cardiovascular mortality
and bronchial hyperreactivity in this study.
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