Environmental Engineering Reference
In-Depth Information
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FIGURE  23.30  Schematic of mortality displacement. If frail individuals have the time of their deaths
advanced by a few days due to increases in air pollution (solid arrow), the reduction of the at-risk pool will
lead to a decrease in the number of deaths over ensuing days (dotted arrow). In the absence of any further
increases, the hazard of death will return to its usual level of daily variability (dashed arrow). (Adapted from
Zanobetti, A. et al., Epidemiology , 13, 87, 2002.)
retirement center observed increased odds (3.1, 95% CI: 1.4-6.6) of decreased heart rate vari-
ability on days during indoor PM 2.5 >15 μg/m 3 compared to days with PM levels ≤15 μg/m 3 [253].
A study in 20 healthy workers (nine smokers) from an occupational cohort (ages 21-58 years)
who wore personal PM monitors for 24 h showed a 1.4% in heart rate variability per 100 μg/m 3
increase in the 3 h moving average PM 2.5 mean [256]. A study by the same investigators in 39
boilermakers who wore personal PM monitors observed that decreases in heart variability were
associated with the lead and vanadium content of the PM 2.5 aerosol (vanadium, nickel, copper,
chromium, lead, and manganese were tested) [257]. PM 2.5 mass did not show any association at
any of the lags that were evaluated (see Table 4 of Ref. [257]). Either through decreases in heart
rate variability or direct toxic effects on the conduction system of the heart, PM aerosol could
also trigger cardiac arrhythmias that could increase the risk of death [258]. Support for this pos-
sibility in humans comes from a study of patients with implanted deibrillators [258]. The odds
of increases in deibrillator discharges were associated with increases in PM 2.5 , black carbon,
NO 2 , and O 3 . The largest and most precisely estimated effects were seen for NO 2 (see Table 4 in
Ref. [258]).
Acute heart attacks are thought to be initiated by the formation of a clot that obstructs the low
of blood in a blood vessel damaged by the atherosclerotic process, and anticoagulants are used
routinely to reduce the risk of heart attacks [259]. Alterations in the coagulable state of blood have
been suggested as one mechanism through which PM aerosol could increase the risk of death [137].
At least two studies have provided support for this hypothesis. Following a 1985 4-day episode of
increased TSP and SO 2 in southern Germany, an increased risk of extreme values of plasma vis-
cosity was observed in 3256 participants in a prospective randomized study of therapy for cardiac
disease [260]. The results from this study were supported by those from a study of 112 subjects aged
60 years and older who provided repeated blood specimens over a period of 18 months (maximum
of 12 specimens) [261]. Estimated personal exposure to PM 10 over the 3 days prior to blood sampling
produced changes in a set of hematological parameters that suggested sequestration of red blood
cells in the circulation [261]. Such a phenomenon could increase the risk of clot formation in the
presence of a hypercoagulable state.
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