Epidemiological evidence for the association between air pollutants exposure and venous thromboembolism (VTE) remains controversial. In this study, a total of 389,659 participants from the UK Biobank who were free of VTE in 2010 were included, and the annual mean concentrations of air pollutants near where participants lived were collected. During a median follow-up period of 8.25 years, 4986 VTEs were determined from the hospital admission records. The Cox proportional hazard model was used to examine the association between air pollutants and VTE. We firstly investigated the associations between air pollutants concentration and VTE and found only NO2 and NO increased VTE risk (P < 0.05). We further calculated the product of air pollutant concentrations and outdoor time to measure personal daily cumulative exposure and found that the hazard rates (HRs) of VTE for a 50-μg/m∗day increase in daily cumulative exposure to PM10, PM2.5, PM2.5-10, NO, and NO2 were 1.08 (1.05-1.12), 1.16 (1.09-1.24), 1.23 (1.11-1.37), 1.04 (1.01-1.06), and 1.05 (1.03-1.08), respectively. To measure joint exposure to various air pollutants and its effect on VTE, we created a weighted air pollutants exposure score (APES) and found a dose-response relationship between APES and VTE risk (P < 0.001 for trend). Compared with participants in the lowest quintile of APES, the HRs of VTE were 1.19 (1.08-1.30) for those within the highest quintile groups. Furthermore, we also found the effect of air pollutants on VTE was statistically significant only in individuals with low-middle VTE genetic risk score (GRS) (P < 0.05), but not in the high VTE GRS groups (P > 0.05). Our findings suggest that exposure to various air pollutants including PM2.5, PM2.5-10, PM10, NO, and NO2, either individually or jointly, were associated with an increased risk of VTE in a dose-response pattern. Our study highlights the importance of a comprehensive assessment of various air pollutants in VTE prevention.
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