Abstract

Background: Ambient air pollution has been associated with activation of systemic inflammation and hypercoagulability and increased plasma homocysteine, but the chemical constituents behind the association are not well understood. Aims: We examined the relations of chemical constituents of fine particles (PM2.5) and biomarkers of inflammation, coagulation and homocysteine in the context of traffic-related air pollution. Methods: A panel of 40 healthy college students underwent biweekly blood collection for 12 times before and after relocating from a suburban campus to an urban campus with changing air pollution contents in Beijing. Blood samples were measured for circulatory biomarkers ofhigh-sensitivity C reactive protein (hs-CRP), tumor necrosis factor alpha (TNF-?), fibrinogen,plasminogen activator inhibitor type 1 (PAI-1), tissue-type plasminogen activator (t-PA), von Willebrand factor (vWF), soluble platelet selectin (sP-selectin), and total homocysteine (tHcy). Various air pollutants were measured in a central air-monitoring station in each campus and 32 PM2.5 chemical constituents were determined in the laboratory. We used mixed-effects models to estimate the effects of PM2.5 chemical constituents on circulatory biomarkers. Results:We found consistent positive associations between the following biomarkers and PM2.5 chemical constituents across different models: TNF-? with secondary organic carbon, chloride, zinc, molybdenum and stannum; fibrinogen with magnesium, iron, titanium, cobalt and cadmium; PAI-1 with titanium, cobalt and manganese; t-PA with cadmium and selenium; vWF with aluminum.We also found consistent inverse associations of vWF with nitrate, chloride and sodium, and sP-selectin with manganese. Conclusions: Our results provide clues for the potential roles that PM2.5 chemical constituents may play in the biological mechanisms through which air pollution may influence the cardiovascular system.

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