Fine
particulate matter air pollution plus
ozone impairs vascular function and raises
diastolic blood pressure. We aimed to determine the mechanism and air pollutant responsible. The effects of pollution on
heart rate variability,
blood pressure, biomarkers, and
brachial flow-mediated dilatation were determined in 2
randomized,
double-blind,
crossover studies. In Ann Arbor, 50 subjects were exposed to
fine particles (150 microg/m(3)) plus
ozone (120 parts per billion) for 2 hours on 3 occasions with pretreatments of an
endothelin antagonist (
Bosentan, 250 mg),
antioxidant (
Vitamin C, 2 g), or
placebo. In Toronto, 31 subjects were exposed to 4 different conditions (particles plus
ozone, particles,
ozone, and
filtered air). In Toronto,
diastolic blood pressure significantly increased (2.9 and 3.6 mm Hg) only during particle-containing exposures in association with
particulate matter concentration and reductions in
heart rate variability. Flow-mediated dilatation significantly decreased (2.0% and 2.9%) only 24 hours after particle-containing exposures in association with
particulate matter concentration and increases in
blood tumor necrosis factor alpha. In Ann Arbor,
diastolic blood pressure significantly similarly increased during all of the exposures (2.5 to 4.0 mm Hg), a response not mitigated by pretreatments. Flow-mediated dilatation remained unaltered.
Particulate matter, not
ozone, was responsible for increasing
diastolic blood pressure during air pollution
inhalation, most plausibly by instigating acute autonomic imbalance. Only particles from urban Toronto additionally
impaired endothelial function, likely via slower
proinflammatory pathways. Our findings demonstrate credible mechanisms whereby fine
particulate matter could trigger acute
cardiovascular events and that aspects of exposure location may be an important determinant of the health consequences.
