Cheng Yun-Jiu, Zhu Chen, Deng Hai, Wu Yang, Wei Hui-Qiang, Lin Wei-Dong, Kaisaier Wulamiding, Li Runkai, Chen Yili, Dong Yugang, Fang Xian-Hong, Liao Yi-Jian, Wu Shu-Lin, Liao Hong-Tao, Xue Yu-Mei, Wu Zexuan
Department of Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
College of Economics and Management, China Agricultural University, No. 17 Qinghuadonglu, Haidian Dist., Beijing, China.
Eur J Prev Cardiol. 2024 Dec 7. doi: 10.1093/eurjpc/zwae390.
Both genetic and environmental factors contribute to the development of ventricular arrhythmias (VAs). However, the extent to which genetic susceptibility modifies the effects of air pollutants on the risk of VAs remains poorly understood.
This study included 491,305 participants without VAs at baseline from UK Biobank. Exposure to ambient air pollutants, including particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2) and nitrogen oxides (NOX), was estimated through land use regression modelling. The associations between air pollutants and the incidence of VAs were then investigated using a Cox proportional hazards model adjusted for covariates. Additionally, we established a polygenic risk score (PRS) for VAs and assessed the joint effect of genetic susceptibility and air pollution on incident VAs.
During a median follow-up of 14.3 years, 4,333 participants were diagnosed with VAs. Increased long-term exposure to PM2.5, PM10, NO2 and NOx was significantly associated with higher risks of VAs, with hazard ratios (HR) per quintile increase of 1.07 (95% confidence interval, 95% CI: 1.03-1.11), 1.07 (1.03-1.11), 1.10 (1.06-1.14) and 1.08 (1.05-1.12) for each pollutant respectively. Notably, there were significant additive interactions between air pollutants and genetic risk. Participants with both high genetic risk and high exposure to air pollution exhibited the greatest risk of VAs, with the highest HRs observed for PM2.5 (HR, 4.51; 95% CI, 3.66-5.56), PM10 (HR, 4.28; 95% CI, 3.52-5.22), NO2 (HR, 4.90; 95% CI, 3.97-6.03), and NOx (HR, 4.56; 95% CI, 3.72-5.60), respectively.
Long-term exposure to air pollution is associated with an increased risk of VAs, especially in individuals with a high genetic risk.
遗传因素和环境因素均对室性心律失常（VAs）的发生发展有影响。然而，遗传易感性在多大程度上改变空气污染物对VAs风险的影响仍知之甚少。
本研究纳入了英国生物银行中491,305名基线时无VAs的参与者。通过土地利用回归模型估算了对包括颗粒物（PM2.5和PM10）、二氧化氮（NO2）和氮氧化物（NOX）在内的环境空气污染物的暴露情况。然后使用针对协变量进行调整的Cox比例风险模型研究空气污染物与VAs发病率之间的关联。此外，我们建立了VAs的多基因风险评分（PRS），并评估了遗传易感性和空气污染对VAs发病的联合影响。
在中位随访14.3年期间，4333名参与者被诊断出患有VAs。长期暴露于PM2.5、PM10、NO2和NOX水平升高与VAs风险显著增加相关，每种污染物每增加一个五分位数的风险比（HR）分别为1.07（95%置信区间，95%CI：1.03 - 1.11）、1.07（1.03 - 1.11）、1.10（1.06 - 1.14）和1.08（1.05 - 1.12）。值得注意的是，空气污染物与遗传风险之间存在显著的相加相互作用。遗传风险高且空气污染暴露高的参与者表现出最高的VAs风险，PM2.5（HR，4.51；95%CI，3.66 - 5.56）、PM10（HR，4.28；95%CI，3.52 - 5.22）、NO2（HR，4.90；95%CI，3.97 - 6.03）和NOX（HR，4.56；95%CI，3.72 - 5.60）的HR最高。
长期暴露于空气污染与VAs风险增加相关，尤其是在遗传风险高的个体中。
