Particulate air pollution and vascular reactivity: the bus stop study
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Particulate air pollution is associated with cardiovascular morbidity but mechanisms are not well understood. We tested the effects on vascular reactivity of exposure to fine particulates matter mass (PM2.5), number of particles ≤1 μm/m3 (PM1.0) and nitrogen dioxide concentration (NO2).
About 39 healthy volunteers sat outside for 2 h at two different Ottawa bus stops. Flow-mediated vasodilation (FMD) of the brachial artery was then measured by ultrasound and expressed as: (maximum artery diameter after release of a blood pressure cuff inflated above systolic pressure—baseline resting diameter)/baseline resting diameter.
A 30 μg/m3 increase in PM2.5 exposure corresponded to a 0.48% reduction in FMD, P = 0.05 representing a 5% relative change in the maximum ability to dilate. Results were consistent between the two bus stops and not sensitive to type of analysis. No significant association was found between FMD and NO2, PM1.0 or traffic density.
PM2.5 may reduce the capacity to vasodilate, a potential explanation for the documented association with cardiovascular morbidity.
KeywordsArteries Endothelin Epidemiology Vasodilation Pollution
Particulates matter mass
Number of particles ≤1 μm/m3
Nitrogen dioxide concentration
Chronic obstructive pulmonary disease
Thermo Environmental Instruments Inc.
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