Ambient PM2.5-bound polycyclic aromatic hydrocarbons (PAHs) associated with pro-thrombotic biomarkers among young healthy adults: A 16 times repeated measurements panel study

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Studies have shown that the cardio/cerebrovascular toxicity of ambient PM2.5 is related to its bound polycyclic aromatic hydrocarbons (PAHs). Currently, only a few studies have reported the relationship between PM2.5-bound PAHs and promoted blood coagulation and thrombosis, but there isn't a consistent conclusion. Therefore, we conducted a prospective panel study to investigate the association. Thirty-three young healthy adults participated in sixteen repeated visits from 2014 to 2018 in Tianjin, China. During each visit, three pro-thrombotic biomarkers: ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin motif 13), D-dimer and Myeloperoxidase (MPO) were measured. Before each visit, ambient PM2.5 samples were daily collected for one week. Sixteen PAHs were determined using Gas Chromatography-Mass Spectrometer, and the positive matrix factorization (PMF) model was applied to identify the sources. Linear mixed-effects models were fitted to investigate the associations between PM2.5-bound PAHs exposure and the biomarkers. Thirteen time-metrics were defined to identify significant time points of PM2.5-bound PAHs' effects. We observed that the increase of PM2.5-bound PAHs exposure was significantly associated with reduced ADAMTS13, elevated D-dimer and MPO. At lag0, each 5.7ng/m3 increase in Benzo[j]fluoranthene and per 3.4ng/m3 increase Dibenz[a,h]anthracene could make a maximum change of -19.08% in ADAMTS13 and 132.60% in D-dimer. Additionally, per 16.43ng/m3 increase in Chrysene could lead to a maximum elevation of 32.14% in MPO at lag4. The PM2.5-bound PAHs often triggered more significant changes at lag 3,4 and 6. The ambient PM2.5-bound PAHs originated from six sources: coal combustion (43.10%), biomass combustion (20.77%), diesel emission (14.78%), gasoline emission (10.95%), industrial emission (7.58%), and cooking emission (2.83%). The greatest contributors to alterations in ADAMTS13, D-dimer and MPO are industrial emission (-48.43%), biomass combustion (470.32%) and diesel emission (13.14%) at lag4. Our findings indicated that short-term exposure to ambient PM2.5-bound PAHs can induce alterations of pro-thrombotic biomarkers among healthy adults.