Health Effects of Aerosols - Aerosols: Measurement, Dosimetry, and Health Effects - page 600

Another cohort study that has contributed important data on the effects of long-term exposure to
ambient PM aerosol is the Adventist Health Study of Smog (AHSMOG), which recruited subjects
from the Adventist community in California [194,195]. This study had the advantage that cigarette
smoking was virtually nonexistent as a result of religious prohibition and the fact that investiga-
tors had developed algorithms for the estimation of personal exposure of subjects to ambient PM
[196]. Unlike the Harvard and ACS studies, AHSMOG reported exposure as the number of days
on which PM 10 was above 100 μg/m 3 as well as in terms of mean PM 10 ; results were comparable for
both metrics (see Table 3 of Ref. [194]). The initial publication from AHSMOG reported increased
risk of death (1977-1992) from “any mention of non-malignant respiratory disease” for both sexes
(1.28, 1.10, males and females, respectively, per interquartile range of PM 10 of days [42.6 IQR] above
100 and 24.1 μg/m 3 for mean PM 10 ). Lung cancer risks were associated with PM only for males.
Similar effects were observed for nonmalignant respiratory deaths in both sexes and lung cancer in
males. Mean nitrogen dioxide and sulfur dioxide were associated with lung cancer in females. Thus,
this study gives a less clear picture than the Harvard and ACS studies with regard to PM effects
[189,190,192]. A later publication tried to partition the PM effects between PM 2.5 (partly estimated
from airport visibility data) and PM 10-25 [195]. Effects were largely conined to the ine fraction,
with risk ratios similar to those for PM 10 .
Subjects from the prospective study of diet in the Netherlands have been evaluated to determine
the effect of living near roads with heavy trafic and mortality [197]. The general results from this
study were summarized in Table 23.8. Mortality risk increased for those living near major roads
(100 m from a freeway or 50 m from a major nonfreeway road) compared to those who did not (e.g.,
RR for cardiovascular death per 10 μg/m 3 increase in black smoke: near, 1.95 (1.09-3.51); not near,
1.34 (0.68-2.64) [197].
Thus, there is agreement among the prospective cohort studies with regard to associations
between PM and mortality. The differences in the results in relation to gaseous pollutants remain to
be explained. Given the difference in the summertime pollutant mixtures between California and
more eastern portions of the United States [19], it is not likely that ozone is acting as a surrogate
for PM-related pollutants as has been suggested for the eastern United States [198]. In addition,
although both the Harvard study and the ACS studies pointed to sulfate as the potentially relevant
component of the PM aerosol that is associated with mortality, neither of these studies, nor the
AHSMOG study, conducted a comprehensive evaluation of this issue. Thus, the relevant physi-
cal and chemical components of the PM aerosol that are related to these effects remain virtually
unexplained.
23.5.3.3 Atopic Allergy and Asthma
Over the past several decades, there has been a steady increase in the prevalence across all age
groups, especially in the very young [109]. While there is a large body of data to support the fact
that asthma symptoms are worsening on days with increased PM aerosol (see the section on acute
effects), there are few prospective studies that have provided data on the extent to which PM aerosol
contributes to the onset of new asthma or the onset of related atopic allergy as might be expected
from data on PM mechanisms discussed previously.
In 1992, the Medical Research Council (MRC) of Great Britain reported a 36-year follow-up
of a 1946 national birth cohort [199] (Table 23.12). Exposure was based on annual coal consump-
tion during the irst 11 years of life. Although not a direct measure of PM aerosol, domestic coal
consumption in the United Kingdom was a major contributor to PM through the time of the great
London fog of 1954 [200]. “Air pollution attributable risk” for asthma/wheeze at age 36 was
6.7% and 8.8% for exposure between birth and ages 2-11, respectively. This study is unique in
that it tries to partition risk between air pollution, smoking, and history of childhood respiratory
illness in a single population in which all of these exposures were measured repeatedly over a
long period of time. The major limitation of this study was the lack of data on maternal smoking
during pregnancy and childhood, both of which have been shown to be important risk factors