Perfluoroalkyl substances influence DNA methylation in school-age children highly exposed through drinking water contaminated from firefighting foam: a cohort study in Ronneby, Sweden

IF 4.8 Q1 GENETICS & HEREDITY
Yiyi Xu, C. Lindh, T. Fletcher, K. Jakobsson, Karin Engström
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引用次数: 9

Abstract

Abstract 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 (n = 32; perfluorooctane sulfonic acid: median 2.8 and range 1–5 ng/ml) or those exposed to very high levels of PFASs (n = 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 (P = 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.
瑞典Ronneby的一项队列研究表明,全氟烷基物质对高度接触消防泡沫污染饮用水的学龄儿童DNA甲基化的影响
摘要全氟烷基物质是一种广泛存在的合成物质,对健康有各种不良影响。PFASs毒性的一个潜在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人PFAS暴露与DNA甲基化之间的关系。然而,没有研究评估PFAS如何影响学龄儿童的DNA甲基化。在这项针对学龄儿童的探索性研究中,我们旨在调查接触全氟辛烷磺酸是否与DNA甲基化和表观遗传学年龄加速的改变有关。来自Ronneby生物标志物队列(瑞典)的63名7-11岁的儿童被纳入研究。这些儿童要么是仅有背景暴露的对照组(n = 32;全氟辛烷磺酸:中位数2.8,范围1-5 ng/ml)或暴露于非常高水平PFASs(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。表观遗传学年龄加速来自DNA甲基化数据。当将高暴露组与对照组进行比较时,发现12个差异甲基化位置和7个不同甲基化区域。表观遗传学年龄加速在两组间无差异(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PFAS暴露对健康影响的可能机制。
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来源期刊
Environmental Epigenetics
Environmental Epigenetics GENETICS & HEREDITY-
CiteScore
6.50
自引率
5.30%
发文量
0
审稿时长
17 weeks
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