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Previous studies have illustrated the pivotal role of coagulation biomarkers in the link between air pollution and cardiovascular disease (CVD). However, inconsistencies remain in the conclusions, with limited studies conducted in rural areas of China. We conducted a panel study in rural areas of Henan Province, China. Considering the potential effect modifications of atherosclerotic cardiovascular disease (ASCVD) risks, 104 participants were enrolled, comprising two matched groups: 52 with high ASCVD risks and 52 with low ASCVD risks. DNA methylation at CpG sites and coagulation indices were measured for all participants. Linear mixed-effect regression models were used to evaluate the associations between ambient air pollution, coagulation biomarkers, and DNA methylation. We observed that for every 5-day standard deviation (SD) increment of PM 2.5 (11.91 μg/m³) and PM 10 (13.65 μg/m³), fibrinogen increased by 7.70% (95%CI: 2.27, 13.12) and 8.50% (95%CI: 2.46, 14.55), respectively. SO 2 (6.95 μg/m³) was associated with 40.25% (95%CI: 14.83, 65.67) increase in plasminogen activator inhibitor-1 (PAI-1). Decreased methylation at CpG sites was associated with exposure to air pollution. However, DNA methylation did not mediate the association between ambient air pollution and coagulation. Our study revealed the harmful impact of ambient air pollution on coagulation function but found no significant mediation effects of DNA methylation. • Ambient air pollution was associated with higher coagulation risk. • Different air pollutants had distinct effects on coagulation function. • DNA methylation did not mediate the association between ambient air pollution and coagulation.
Chen et al. (Fri,) studied this question.