Department of Occupational and Environmental Medicine, Inha University Hospital, Inha University, Incheon, the Republic of Korea.
Section of Environmental Health, Department of Public Health, University of Copenhagen, Copenhagen, Denmark.
Ecotoxicol Environ Saf. 2024 Sep 15;283:116823. doi: 10.1016/j.ecoenv.2024.116823. Epub 2024 Aug 2.
This study investigated the association of prenatal and early childhood exposure to air pollution with epigenetic age acceleration (EAA) at six years of age using the Environment and Development of Children Cohort (EDC Cohort) MATERIALS & METHODS: Air pollution, including particulate matter [< 2.5 µm (PM) and < 10 µm (PM) in an aerodynamic diameter], nitrogen dioxide (NO), ozone (O), carbon monoxide (CO), and sulfur dioxide (SO) were estimated based on the residential address for two periods: 1) during the whole pregnancy, and 2) for one year before the follow-up in children at six years of age. The methylation levels in whole blood at six years of age were measured, and the methylation clocks, including Horvath's clock, Horvath's skin and blood clock, PedBE, and Wu's clock, were estimated. Multivariate linear regression models were constructed to analyze the association between EAA and air pollutants.
A total of 76 children in EDC cohort were enrolled in this study. During the whole pregnancy, interquartile range (IQR) increases in exposure to PM (4.56 μg/m) and CO (0.156 ppm) were associated with 0.406 years and 0.799 years of EAA (Horvath's clock), respectively. An IQR increase in PM (4.76 μg/m) for one year before the child was six years of age was associated with 0.509 years of EAA (Horvath's clock) and 0.289 years of EAA (Wu's clock). PM (4.30 μg/m) and O (0.003 ppm) exposure in the period were also associated with EAA in Horvath's clock (0.280 years) and EAA in Horvath's skin and blood clock (0.163 years), respectively.
We found that prenatal and childhood exposure to ambient air pollutants is associated with EAA among children. The results suggest that air pollution could induce excess biological aging even in prenatal and early life.
本研究通过环境与儿童发展队列（EDC 队列），使用 Horvath 时钟、Horvath 皮肤和血液时钟、PedBE 和 Wu 时钟等甲基化时钟，调查了产前和儿童早期暴露于空气污染与六周岁时的表观遗传年龄加速（EAA）之间的关联。
根据孕妇和儿童在六周岁时的住址，评估了两个时间段的空气污染（包括空气动力学直径小于 2.5 µm（PM）和小于 10 µm（PM）的颗粒物、二氧化氮（NO）、臭氧（O）、一氧化碳（CO）和二氧化硫（SO））：1）整个孕期，2）儿童在六周岁前一年的随访。测量了六周岁时全血的甲基化水平，并估计了甲基化时钟，包括 Horvath 时钟、Horvath 皮肤和血液时钟、PedBE 和 Wu 时钟。构建了多变量线性回归模型，以分析 EAA 与空气污染物之间的关系。
EDC 队列共纳入了 76 名儿童。整个孕期，PM（4.56 µg/m）和 CO（0.156 ppm）暴露量的四分位距（IQR）每增加 1 个单位，与 Horvath 时钟的 EAA 分别增加 0.406 年和 0.799 年。儿童六周岁前一年，PM（4.76 µg/m）的 IQR 每增加 1 个单位，与 Horvath 时钟的 EAA 增加 0.509 年，与 Wu 时钟的 EAA 增加 0.289 年。该时期 PM（4.30 µg/m）和 O（0.003 ppm）的暴露也与 Horvath 时钟的 EAA（0.280 年）和 Horvath 皮肤和血液时钟的 EAA（0.163 年）相关。
我们发现，儿童产前和儿童期暴露于环境空气污染物与 EAA 有关。结果表明，空气污染即使在产前和生命早期也可能导致过度的生物衰老。
