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Exposure to air pollution from traffic is associated with
adverse cardiovascular events. The mechanisms
for this association are unknown. Investigators
conducted a controlled exposure to dilute diesel
exhaust in patients with stable coronary heart
disease to determine the direct effect of air
pollution on myocardial, vascular, and
fibrinolytic function.
In a double-blind, randomized, crossover study, 20 men with
prior myocardial infarction were exposed, in two
separate sessions, to dilute diesel exhaust (300
mug per cubic meter) or filtered air for 1 hour
during periods of rest and moderate exercise in
a controlled-exposure facility. During the
exposure, myocardial ischemia was quantified by
ST-segment analysis using continuous 12-lead
electrocardiography. Six hours after exposure,
vasomotor and fibrinolytic function were
assessed by means of intraarterial agonist
infusions.
During both exposure sessions, the heart rate increased
with exercise (P < 0.001); the increase was
similar during exposure to diesel exhaust and
exposure to filtered air (P = 0.67).
Exercise-induced ST-segment depression was
present in all patients, but there was a greater
increase in the ischemic burden during exposure
to diesel exhaust (-22 ± 4 vs -8 ± 6 millivolt
seconds, P<0.001). Exposure to diesel exhaust
did not aggravate preexisting vasomotor
dysfunction, but it did reduce the acute release
of endothelial tissue plasminogen activator
(P=0.009; 35% decrease in the area under the
curve).
Brief exposure to dilute diesel exhaust promotes myocardial
ischemia and inhibits endogenous fibrinolytic
capacity in men with stable coronary heart
disease. The study findings point to ischemic
and thrombotic mechanisms that may explain in
part the observation that exposure to
combustion-derived air pollution is associated
with adverse cardiovascular events.
N Engl J Med 2007; 357:1075-1082
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