Van Dang Kristina, Choi Eun Young, Crimmins Eileen, Finch Caleb, Ailshire Jennifer
Leonard Davis School of Gerontology, University of Southern California, Los Angeles, California, USA.
J Gerontol A Biol Sci Med Sci. 2025 Jun 10;80(7). doi: 10.1093/gerona/glaf092.
Prior research has examined associations of exposure to air pollution and heat with epigenetic alterations separately; however, these 2 exposures commonly used to measure climate change typically co-occur. We examine joint effects of exposure to elevated PM2.5 and heat on DNA methylation. Data come from the 2016 Health and Retirement Study DNA Methylation Sample (N = 3 947) and census tract level annual ambient PM2.5 concentrations and daily heat index data averaged 7 days before blood collection. We used 5 epigenetic aging measures: Horvath, Hannum, PhenoAge, GrimAge, and DunedinPACE. Four categories of joint PM2.5 and heat were analyzed: (a = reference) low PM2.5 (<9.2 µg/m3) and low heat (<80 on heat index); (b) low PM2.5 and high heat; (c) high PM2.5 and low heat; and (d) high PM2.5 and high heat. Linear regression models were adjusted for age, gender, race/ethnicity, education, neighborhood poverty, and cell type. Compared to the reference of low PM2.5 and heat, we found associations of short-term (7-day) high heat and long-term (annual) low PM2.5 with accelerated DNA methylation aging for Horvath (β = 0.74, 95% CI: 0.04, 1.15), Hannum (β = 0.74, 95% CI: 0.20, 1.28), and PhenoAge (β = 0.93, 95% CI: 0.33, 1.52). High PM2.5 and low heat had weaker associations (Horvath β = -0.001, 95% CI: -0.68, 0.68, Hannum β = 0.36, 95% CI: -034, 1.05; PhenoAge β = 0.18, 95% CI: -0.56, 0.92), as did joint effects of high PM2.5 and high heat (Horvath β = 0.11, 95% CI: -0.68, 0.89; Hannum β = 0.42, 95% CI: -0.46, 1.20; PhenoAge β = 0.56, 95% CI: -0.30, 1.42). Exposure to short-term high heat and low air pollution may accelerate epigenetic aging.
先前的研究分别考察了空气污染暴露和高温暴露与表观遗传改变之间的关联；然而，这两种常用于衡量气候变化的暴露通常同时发生。我们研究了暴露于高浓度细颗粒物（PM2.5）和高温对DNA甲基化的联合影响。数据来自2016年健康与退休研究DNA甲基化样本（N = 3947），以及人口普查区层面的年度环境PM2.5浓度和采血前7天的每日热指数数据平均值。我们使用了5种表观遗传衰老指标：霍瓦斯（Horvath）、汉纳姆（Hannum）、表型年龄（PhenoAge）、格里姆年龄（GrimAge）和达尼丁PACE（DunedinPACE）。分析了PM2.5和高温的四类联合情况：（a = 参考）低PM2.5（<9.2微克/立方米）和低热（热指数<80）；（b）低PM2.5和高热；（c）高PM2.5和低热；以及（d）高PM2.5和高热。线性回归模型针对年龄、性别、种族/族裔、教育程度、邻里贫困程度和细胞类型进行了调整。与低PM2.5和低热的参考组相比，我们发现短期（7天）高热和长期（年度）低PM2.5与霍瓦斯（β = 0.74，95%置信区间：0.04，1.15）、汉纳姆（β = 0.74，95%置信区间：0.20，1.28）和表型年龄（β = 0.93，95%置信区间：0.33，1.52）的DNA甲基化加速衰老存在关联。高PM2.5和低热的关联较弱（霍瓦斯β = -0.001，95%置信区间：-0.68，0.68；汉纳姆β = 0.36，95%置信区间：-0.34，1.05；表型年龄β = 0.18，95%置信区间：-0.56，0.92），高PM2.5和高热的联合影响也是如此（霍瓦斯β = 0.11，95%置信区间：-0.68，0.89；汉纳姆β = 0.42，95%置信区间：-0.46，1.20；表型年龄β = 0.56，95%置信区间：-0.30，1.42）。暴露于短期高热和低空气污染可能会加速表观遗传衰老。
