Abstract
BACKGROUND: Current evidence regarding the relationship between air pollution and pulmonary embolism (PE) is not definitive.</p>
OBJECTIVES: This investigation aimed to scrutinize the association between exposure to various air pollutants and PE incidence, taking into account the moderating effect of genetic susceptibility.</p>
METHODS: This prospective cohort study enrolled 362,672 individuals from the UK Biobank who had no history of PE and had complete genotyping profiles at baseline. Cox proportional hazards models were conducted to assess the relationship between individual air pollutant, the air pollution score, the polygenic risk score (PRS), and PE incidence. Subgroup analyses and sensitivity analyses were performed to validate results robutness.</p>
RESULTS: Over a median follow-up duration of 14.2 years, 5586 incident PEs were documented. The HRs (95% CIs) for PE incidence per interquartile range increment in PM2.5, PM2.5-10, PM10, NO2, and NOx were 1.08 (1.02-1.15), 1.01 (0.95-1.08), 1.10 (1.02-1.19), 1.13 (1.04-1.23), and 1.13 (1.05-1.20). Participants in the highest quartile of air pollution score had an HR (95% CI) of 1.33 (1.10-1.62) for incident PE compared with those in the lowest quartile. Moreover, we also found that persons with high genetic predisposition and air pollution score were at nearly twice the risk of PE (HR 2.15, 95% CI: 1.56-2.96), in contrast to those with low genetic risk and air pollution exposure.</p>
CONCLUSION: This investigation revealed that extended combined exposure to air pollutants was linked to an elevated incidence of PE, particularly in those with a high genetic predisposition.</p>