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. We examined the relations of various chemical constituents of fine particles (PM_2.5) 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 their relocation from a suburban campus to an urban campus with changing air pollution contents in Beijing. Blood samples were measured for circulatory biomarkers of high-sensitivity C reactive protein (hs-CRP), tumor necrosis factor alpha (TNF-α), 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 PM_2.5 chemical constituents were determined in the laboratory. We used three different mixed-effects models (single-constituent model, constituent-PM_2.5 joint model and constituent residual model) controlling for potential confounders to estimate the effects of PM_2.5 chemical constituents on circulatory biomarkers. Results: We found consistent positive associations between the following biomarkers and PM_2.5 chemical constituents across different models: TNF-α 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. Two positive associations of zinc with TNF-α and of cobalt with fibrinogen, and two inverse associations of nitrate with vWF, and of manganese with sP-selectin, were independent of the other constituents in two-constituent models using constituent residual data. We only found weak air pollution effects on hs-CRP and tHcy. Conclusions: Our results provide clues for the potential roles that PM_2.5 chemical constituents may play in the biological mechanisms through which air pollution may influence the cardiovascular system.

Exposure to airborne fine particulate matter (PM2.5) has been associated with a variety of adverse health outcomes including chronic obstructive pulmonary disease (COPD). However, the linkages between PM2.5 exposure, PM2.5-related biomarkers, COPD-related biomarkers and COPD remain poorly elucidated. To investigate the linkages between PM2.5 exposure and COPD outcome by using the meet-in-middle strategy based on urinary metabolic biomarkers. A cross-sectional study was designed to illustrate the mentioned quadripartite linkages. Indoor PM2.5 and its element components were assessed in 41 Chinese elderly participants including COPD patients and their healthy spouses. Metabolic biomarkers involved in PM2.5 exposure and COPD were identified by using urinary metabolomics. The associations between PM2.5- and COPD-related biomarkers were investigated by statistics and metabolic pathway analysis. Seven metabolites were screened and identified with significant correlations to PM2.5 exposure, which were majorly involved in purine and amino acid metabolism as well as glycolysis. Ten COPD-related metabolic biomarkers were identified, which suggested that amino acid metabolism, lipid and fatty acid metabolism, and glucose metabolism were disturbed in the patients. Also, PM2.5 and its many elemental components were significantly associated with COPD-related biomarkers. We observed that the two kinds of biomarkers (PM2.5- and COPD-related) integrated in a locally connected network and the alterations of these metabolic biomarkers can biologically link PM2.5 exposure to COPD outcome. Our study indicated the modification of PM2.5 to COPD via both modes of action of lowering participants' antioxidation capacity and decreasing their lung energy generation; this information would be valuable for the prevention strategy of COPD.