Xu Yiyi, Lindh Christian H, Fletcher Tony, Jakobsson Kristina, Engström Karin
School of Public Health and Community Medicine, Institute of Medicine, University of Gothenburg, Medicinaregatan 18A, Gothenburg 413 90, Sweden.
Department of Laboratory Medicine, Division of Occupational and Environmental Medicine, Lund University, Scheelevägen 2, Lund 223 63, Sweden.
Environ Epigenet. 2022 Feb 4;8(1):dvac004. doi: 10.1093/eep/dvac004. eCollection 2022.
Perfluoroalkyl substances (PFASs) are widespread synthetic substances with various adverse health effects. A potential mechanism of toxicity for PFASs is via epigenetic changes, such as DNA methylation. Previous studies have evaluated associations between PFAS exposure and DNA methylation among newborns and adults. However, no study has evaluated how PFASs influence DNA methylation among children of school age. In this exploratory study with school-age children exposed to PFASs through drinking water highly contaminated from firefighting foams, we aimed to investigate whether exposure to PFASs was associated with alteration in DNA methylation and epigenetic age acceleration. Sixty-three children aged 7-11 years from the Ronneby Biomarker Cohort (Sweden) were included. The children were either controls with only background exposure ( = 32; perfluorooctane sulfonic acid: median 2.8 and range 1-5 ng/ml) or those exposed to very high levels of PFASs ( = 31; perfluorooctane sulfonic acid: median 295 and range 190-464 ng/ml). These two groups were matched on sex, age, and body mass index. Genome-wide methylation of whole-blood DNA was analyzed using the Infinium MethylationEPIC BeadChip kit. Epigenetic age acceleration was derived from the DNA methylation data. Twelve differentially methylated positions and seven differentially methylated regions were found when comparing the high-exposure group to the control group. There were no differences in epigenetic age acceleration between these two groups ( = 0.66). We found that PFAS exposure was associated with DNA methylation at specific genomic positions and regions in children at school age, which may indicate a possible mechanism for linking PFAS exposure to health effects.
全氟烷基物质(PFASs)是广泛存在的合成物质,具有多种不良健康影响。PFASs的一种潜在毒性机制是通过表观遗传变化,如DNA甲基化。先前的研究评估了新生儿和成年人中PFAS暴露与DNA甲基化之间的关联。然而,尚无研究评估PFASs如何影响学龄儿童的DNA甲基化。在这项探索性研究中,我们对因饮用受消防泡沫高度污染的水而接触PFASs的学龄儿童进行了研究,旨在调查PFASs暴露是否与DNA甲基化改变和表观遗传年龄加速有关。纳入了来自瑞典吕讷堡生物标志物队列的63名7至11岁儿童。这些儿童要么是仅受背景暴露的对照组(n = 32;全氟辛烷磺酸:中位数2.8,范围1 - 5 ng/ml),要么是接触非常高水平PFASs的儿童(n = 31;全氟辛烷磺酸:中位数295,范围190 - 464 ng/ml)。这两组在性别、年龄和体重指数方面进行了匹配。使用Infinium MethylationEPIC BeadChip试剂盒分析全血DNA的全基因组甲基化。表观遗传年龄加速是根据DNA甲基化数据得出的。在将高暴露组与对照组进行比较时,发现了12个差异甲基化位点和7个差异甲基化区域。这两组之间的表观遗传年龄加速没有差异(p = 0.66)。我们发现,PFAS暴露与学龄儿童特定基因组位置和区域的DNA甲基化有关,这可能表明将PFAS暴露与健康影响联系起来的一种可能机制。