Health Effects of Aerosols - Aerosols: Measurement, Dosimetry, and Health Effects - page 604

Diesel exhaust

Particulate matter

Exposure

Carbon black

Deposition

Exposure

Desorption

Unique
to
diesel

Deposition

Clearance

Organic chemicals

Particle

Neutrophil

Activation

Macrophage

Reactive
oxygen
species

DNA adducts

Cytokines
growth factors
Proteases

Mutations

Initiation

Initiated cell

Promotion

Inflammation
cell injury
cell proliferation
hyperplasia

Activation of
protooncogenes
inactivation of tumor
suppressor genes

Preneoplastic
lesion

Progression

Malignant
tumor

Fibrosis

FIGURE 23.22 Postulated mechanism for carcinogenesis related to exposure to high-level diesel exhaust
concentrations in rats. (From U.S. Environmental Protection Agency (EPA), Health assessment document
for diesel engine exhaust, Report No.: EPA/600/8-90/057F, National Center for Environmental Assessment,
Washington, DC, 2002, Figure 7.3.)

23.5.4.1 Mortality
For obvious reasons, the effects of short-term increases in ambient PM have received more atten-
tion than any other PM-aerosol-related health effect. The most famous example of the mortality
associated with acute increases in PM aerosol is the London fog episode in December, 1952, which
was responsible for both acute and subacute mortality that accounted for approximately 13,000
excess deaths from the start of the fog through March 1953 [215]. Bell and Davis [215] estimated
that a 0.10 ppm increase in weekly SO 2 (surrogate for the PM aerosol) was associated with a relative
risk (RR) of mortality of 1.31 (95% CI 1.11-1.36) (Figure 23.23). Subsequent studies of mortality
in London found associations between British smoke levels [216] and acid aerosol levels [217] and
mortality. In 1994, Schwartz [218] summarized mortality TSP/British smoke/coeficient of haze
associations from 13 studies, all of which used the same statistical methodology and reported an
RR of death per 100 μg/m 3 increase in daily TSP that ranged from 1.06 to 1.08. A detailed analysis
of the causes of death in Philadelphia, PA, reveals increased RRs for deaths from chronic obstruc-
tive lung disease (COPD) (1.25 for high TSP vs. low TSP days) and pneumonia (1.13 for high vs. low
days). Risk of death from cardiovascular disease was increased, but these deaths were often accom-
panied by underlying respiratory conditions [219]. Other studies have conirmed the increased sus-
ceptibility of patients with COPD [220] and other underlying respiratory diseases to nonrespiratory