Ministry of Education Key Laboratory of Environment and Health, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department of Maternal and Child Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Environ Health Perspect. 2024 Oct;132(10):107002. doi: 10.1289/EHP14291. Epub 2024 Oct 10.
Unraveling gene-environment interaction can provide a novel insight into early disease prevention. Nevertheless, current understanding of the interplay between genetic predisposition and air pollution in relation to myocardial infarction (MI) risk remains limited. Furthermore, the potential long-term influence of air pollutants on MI incidence risk warrants more conclusive evidence in a community population.
We investigated interactions between genetic predisposition and exposure to air pollutants on MI incidence.
This study incorporated a sample of 456,354 UK Biobank participants and annual mean air pollution (, , , and ) from the UK Department for Environment, Food and Rural Affairs (2006-2021). The Cox proportional hazards model was employed to explore MI incidence after chronic air pollutants exposure. By quantifying genetic risk through the calculation of polygenic risk score (PRS), this study further examined the interactions between genetic risk and exposure to air pollutants in the development of MI on both additive and multiplicative scales.
Among 456,354 participants, 9,114 incident MI events were observed during a median follow-up of 12.08 y. Chronic exposure to air pollutants was linked with an increased risk of MI occurrence. Specifically, the hazard ratios (per interquartile range) were 1.12 (95% CI: 1.10, 1.13) for , 1.20 (95% CI: 1.19, 1.22) for , 1.13 (95% CI: 1.12, 1.15) for , and 1.12 (95% CI: 1.11, 1.13) for . In terms of the joint effects, participants with high PRS and high level of air pollution exposure exhibited the greatest risk of MI among all study participants ( to 324%). Remarkably, both multiplicative and additive interactions were detected in the ambient air pollutants exposure and genetic risk on the incidence of MI.
There were interactions between exposure to ambient air pollutants and genetic susceptibility on the risk of MI onset. Moreover, the joint effects of these two exposures were greater than the effect of each factor alone. https://doi.org/10.1289/EHP14291.
揭示基因-环境相互作用可以为疾病的早期预防提供新的见解。然而，目前对于遗传易感性与空气污染在心肌梗死（MI）风险中的相互作用的理解仍然有限。此外，空气污染物对 MI 发病率风险的潜在长期影响在社区人群中需要更确凿的证据。
我们研究了遗传易感性与暴露于空气污染物之间的相互作用对 MI 发病的影响。
本研究纳入了英国生物库的 456354 名参与者和英国环境、食品和农村事务部（2006-2021 年）提供的年度平均空气污染物（、、、和）。采用 Cox 比例风险模型探讨慢性空气污染物暴露后 MI 的发病情况。通过计算多基因风险评分（PRS）来量化遗传风险，本研究进一步在加性和乘法尺度上研究了遗传风险与空气污染物暴露在 MI 发展中的相互作用。
在 456354 名参与者中，中位随访 12.08 年期间观察到 9114 例 MI 事件。慢性空气污染物暴露与 MI 发生风险增加相关。具体而言，每四分位距（IQR）的危险比（95%CI）分别为 1.12（95%CI：1.10，1.13）、1.20（95%CI：1.19，1.22）、1.13（95%CI：1.12，1.15）和 1.12（95%CI：1.11，1.13）。就联合效应而言，在所有研究参与者中，PRS 较高且空气污染暴露水平较高的参与者 MI 风险最高（增加 10%至 324%）。值得注意的是，在 MI 发病中，环境空气污染物暴露和遗传风险之间存在乘法和加法相互作用。
环境空气污染物暴露与遗传易感性之间存在相互作用，影响 MI 的发病风险。此外，这两种暴露的联合效应大于每种因素单独的效应。https://doi.org/10.1289/EHP14291.
