Short-Term Exposure of PM2.5 and Epigenetic Aging: A Quasi-Experimental Study,Environmental Science & Technology

当前位置： X-MOL 学术 › Environ. Sci. Technol. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

Short-Term Exposure of PM2.5 and Epigenetic Aging: A Quasi-Experimental Study
Environmental Science & Technology ( IF 10.8 ) Pub Date : 2022-10-05 , DOI: 10.1021/acs.est.2c05534
Xu Gao ₁ , Jing Huang ₁ , Andres Cardenas ₂ , Yan Zhao ₁ , Yanyan Sun ₃ , Jiawei Wang ₁ , Lijun Xue ₁ , Andrea A Baccarelli ₄ , Xinbiao Guo ₁ , Ling Zhang ₃ , Shaowei Wu _{5,

6,

7}

Affiliation

Epigenetic age (EA) is an emerging DNA methylation-based biomarker of biological aging, but whether EA is causally associated with short-term PM_2.5 exposure remains unknown. We conducted a quasi-experimental study of 26 healthy adults to test whether short-term PM_2.5 exposure accelerates seven EAs with three health examinations performed before, during, and after multiple PM_2.5 pollution waves. Seven EAs were derived from the DNA methylation profiles of the Illumina HumanMethylationEPIC BeadChip from CD4+ T-helper cells. We found that an increase of 10 μg/m³ in the 0–24 h personal PM_2.5 exposure prior to health examinations was associated with a 0.035, 0.035, 0.050, 0.055, 0.052, and 0.037-unit increase in the changes of z-scored DNA methylation age acceleration (AA,Horvath), AA (Hannum), AA (GrimAge), DunedinPoAm, mortality risk score (MS), and epiTOC, respectively (p-values < 0.05). The same increase in the 24–48 h average personal PM_2.5 exposure yielded smaller effects but was still robustly associated with the changes in AA (GrimAge), DunedinPoAm, and MS. Such acute aging effects of PM_2.5 were mediated by the changes in several circulating biomarkers, including EC-SOD and sCD40L, with up to ∼28% mediated proportions. Our findings demonstrated that short-term PM_2.5 exposure could accelerate aging reflected by DNA methylation profiles via blood coagulation, oxidative stress, and systematic inflammation.

中文翻译：

PM2.5 的短期暴露与表观遗传老化：一项准实验研究

表观遗传年龄 (EA) 是一种新兴的基于 DNA 甲基化的生物衰老生物标志物，但 EA 是否与短期 PM _2.5暴露有因果关系仍然未知。我们对 26 名健康成年人进行了一项准实验研究，以测试短期 PM _{2.5暴露是否会加速七个 EA，并在多次 PM}_2.5污染波之前、期间和之后进行了三项健康检查。七个 EA 来自 CD4+ T 辅助细胞的 Illumina HumanMethylationEPIC BeadChip 的 DNA 甲基化谱。我们发现0-24 小时个人 PM _{2.5增加了 10 μg/m}³健康检查前的暴露与 z 评分 DNA 甲基化年龄加速 (AA,Horvath)、AA (Hannum)、AA (GrimAge) 的变化增加 0.035、0.035、0.050、0.055、0.052 和 0.037 个单位相关、但尼丁PoAm、死亡风险评分（MS）和epiTOC，分别为（p值<0.05）。_{24-48 小时平均个人 PM 2.5}暴露的同样增加产生了较小的影响，但仍与 AA (GrimAge)、DunedinPoAm 和 MS 的变化密切相关。PM _2.5的这种急性老化效应是由几种循环生物标志物的变化介导的，包括 EC-SOD 和 sCD40L，介导比例高达 28%。我们的研究结果表明，短期 PM _2.5暴露可以通过血液凝固、氧化应激和系统性炎症加速 DNA 甲基化谱反映的衰老。

更新日期：2022-10-05

点击分享查看原文

点击收藏

阅读更多本刊最新论文本刊介绍/投稿指南11