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

IF 10.8 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Yudiyang Ma, Jianing Wang, Linxi Tang, Feipeng Cui, Lei Zheng, Meiqi Xing, Yaohua Tian
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引用次数: 0

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.

空气污染暴露和遗传易感性与胸主动脉瘤和夹层风险增加的关系。
胸主动脉瘤及夹层(TAAD)是一种严重的健康威胁,但空气污染暴露在其发展中的作用尚未得到充分探讨。本文研究了空气污染物与TAAD发病率之间的关系。在Cox比例风险模型中,空气污染物在四分位数范围内增加的TAAD风险比(95%置信区间)分别为:空气动力学直径≤2.5 μm的颗粒物(PM2.5;每增加2.15 μg m-3)为2.15 (1.96,2.35),PM10(每增加2.99 μg m-3)为1.76 (1.61,1.92),NO2(每增加6.97 μg m-3)为1.45 (1.34,1.58),NOx(每增加11.58 μg m-3)为1.40(1.29,1.51)。当使用逆概率加权和广义倾向评分方法时,这些估计保持一致。此外,本研究揭示了空气污染物与遗传易感性对TAAD风险的潜在联合效应和相互作用,特别是PM2.5与遗传易感性之间的乘法和加性相互作用。空气污染暴露与TAAD风险增加有关,遗传易感性改变了这种关联。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
5.70
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