Prenatal per- and polyfluoroalkyl substance exposures and DNA methylation among newborns in the Environmental influences on Child Health Outcomes program.

IF 4.8 Q1 GENETICS & HEREDITY
Environmental Epigenetics Pub Date : 2025-04-24 eCollection Date: 2025-01-01 DOI:10.1093/eep/dvaf010
Rose Schrott, Christine Ladd-Acosta, Vasantha Padmanabhan, Dana Boyd Barr, Carrie V Breton, Andres Cardenas, Courtney C Carignan, Dana Dabelea, Anne L Dunlop, Danielle M Fallin, Marie-France Hivert, Ellen M Howerton, Anna K Knight, Emily Oken, Alicia K Peterson, Michael C Petriello, Douglas Ruden, Rebecca J Schmidt, Alicia K Smith, Anne P Starling, Ivana V Yang, Yeyi Zhu, Jaclyn M Goodrich
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引用次数: 0

Abstract

Gestation is a vulnerable window when exposure to per- and polyfluoroalkyl substances (PFAS) may impact child development and health. Epigenetic modification, including DNA methylation (DNAm), may be one mechanism linking prenatal PFAS exposure to offspring outcomes. We tested associations between prenatal PFAS and newborn DNAm in 1017 participants from 6 cohorts in the US Environmental influences on Child Health Outcomes consortium. Concentrations of PFAS [perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorohexanesulfonic acid (PFHxS), perfluorononanoic acid (PFNA), and perfluorodecanoic acid] were measured in maternal serum or plasma. DNAm was quantified in newborn dried blood spot or umbilical cord blood leukocytes using the Infinium HumanMethylation450 (450K) or MethylationEPIC (EPIC) arrays. We tested associations between prenatal PFAS and neonatal blood DNAm on the 450K (n = 772) and EPIC (n = 245) arrays; results were meta-analysed across the platforms. Regional changes in DNAm were investigated, and findings were checked for replication in the Michigan Mother-Infant Pairs (MMIP) cohort (n = 140). Following correction for false discovery rate (q = 0.1 for meta-analyses), we identified an association between PFHxS and one cytosine-guanine (CpG) mapped to CASC3 (q = 0.065) that replicated in MMIP (P = .006). PFOS was associated with six CpG sites, of which five were mapped to the genes KIAA1841, ABR, LEP, SERPINA1, and LOXL1. One differentially methylated region (DMR) was associated with prenatal PFOA exposure, and one DMR was associated with PFOS exposure. In this multicohort analysis including a diverse group from the USA, PFOA, PFOS, PFHxS, and PFNA exposures in pregnancy were associated with offspring DNAm, and the implications for children's health merit further exploration.

产前全氟烷基和多氟烷基物质暴露和新生儿DNA甲基化对儿童健康结果的环境影响方案。
妊娠期是暴露于全氟烷基和多氟烷基物质(PFAS)可能影响儿童发育和健康的脆弱窗口期。表观遗传修饰,包括DNA甲基化(DNAm),可能是将产前PFAS暴露与后代结局联系起来的一种机制。我们测试了来自美国环境对儿童健康结果影响联盟6个队列的1017名参与者的产前PFAS和新生儿DNAm之间的关系。测定母体血清或血浆中PFAS[全氟辛烷磺酸(PFOS)、全氟辛酸(PFOA)、全氟己磺酸(PFHxS)、全氟壬酸(PFNA)、全氟癸酸]的浓度。使用Infinium HumanMethylation450 (450K)或MethylationEPIC (EPIC)阵列对新生儿干血斑或脐血白细胞进行DNAm定量。我们在450K (n = 772)和EPIC (n = 245)阵列上测试了产前PFAS与新生儿血液dna之间的关系;对各平台的结果进行meta分析。研究人员调查了DNAm的区域变化,并在密歇根母婴对(MMIP)队列(n = 140)中检查了研究结果的重复性。在校正了错误发现率(荟萃分析的q = 0.1)后,我们确定了PFHxS与一个与CASC3相关的胞嘧啶-鸟嘌呤(CpG)之间的关联(q = 0.065),该关联在MMIP中重复(P = 0.006)。PFOS与6个CpG位点相关,其中5个位点与KIAA1841、ABR、LEP、SERPINA1和LOXL1基因相关。一个差异甲基化区(DMR)与产前全氟辛烷磺酸暴露有关,一个DMR与全氟辛烷磺酸暴露有关。在这项包括来自美国的不同群体的多队列分析中,妊娠期PFOA、PFOS、PFHxS和PFNA暴露与后代dna相关,对儿童健康的影响值得进一步探讨。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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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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