Association of air pollution exposure and genetic susceptibility with increased risk of thoracic aortic aneurysm and dissection

Abstract

Thoracic aortic aneurysm and dissection (TAAD) represent a serious health threat, yet the role of air pollution exposure on its development has been underexplored. Here we investigate the relationships between air pollutants and TAAD incidence. In a Cox’s proportional hazards model, hazard ratios (95% confidence intervals) of TAAD for an interquartile range increase in air pollutants were 2.15 (1.96, 2.35) for particulate matter with an aerodynamic diameter ≤2.5 μm (PM2.5; per 2.15 μg m−3 increase), 1.76 (1.61, 1.92) for PM10 (per 2.99 μg m−3 increase), 1.45 (1.34, 1.58) for NO2 (per 6.97 μg m−3 increase) and 1.40 (1.29, 1.51) for NOx (per 11.58 μg m−3 increase). These estimates remained consistent when using inverse probability weighting and generalized propensity score methods. Furthermore, this study revealed potential joint effects and interactions between air pollutants and genetic susceptibility on TAAD risk, especially the multiplicative and additive interactions between PM2.5 and genetic susceptibility. Air pollution exposure is associated with an increased TAAD risk and genetic susceptibility modifies this association. Ma et al. demonstrate that air pollution is associated with an increased risk of thoracic aortic aneurysm and dissection (TAAD), and that genetic susceptibility to TAAD amplifies this risk through multiplicative and additive interactions.