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Particulate matter, the newborn methylome, and cardio-respiratory health outcomes in childhood

机译：儿童微粒物质，新生儿甲基化组和心脏呼吸健康结果

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Ambient air pollution is associated with adverse health outcomes including cardio-respiratory diseases. Epigenetic mechanisms such as DNA methylation may play a role in driving such associations. We investigated the effects of prenatal particulate matter (PM) exposure on DNA methylation of 178,309 promoter regions in 240 newborns using the Infinium HumanMethylation450 BeadChip, using a generalized linear regression model with a quasi-binomial link family, adjusted for gender, plate, and cell types. PM-associated CpG loci were then investigated for their associations with childhood asthma, carotid intima-media thickness (CIMT), and blood pressure (BP) using logistic or linear regression. Thirty-one loci were associated with either PM10 or PM2.5 using FDR-corrected p-values of less than 0.15. Two loci were evaluated for replication in a separate population of 280 Children’s Health Study (CHS) subjects using Pyrosequencing, of which one successfully replicated (COLEC11 cg03579365). Three of the 31 loci were also associated with physician-diagnosed asthma at 6 years old, two were associated with CIMT and one with systolic BP at 10 years old. A higher methylation level in TM9SF2 (cg02015529) and UBE2S (cg00035623), respectively, was associated with a 2SD increase in prenatal PM and was also associated with 36% and 98% increased odds of asthma; whereas methylation of TDRD6 (cg22329831) was negatively associated with PM and a 24% decreased odds of asthma. Prenatal PM exposure was associated with altered DNA methylation in newborn blood in a small number of gene promoters, some of which were also associated with cardio-respiratory health outcomes later in childhood. Keywords : methylation, particulate matter, air pollution, asthma, cardiovascular.
机译：环境空气污染与包括心脏呼吸系统疾病在内的不良健康后果相关。表观遗传机制（例如DNA甲基化）可能在驱动此类关联中发挥作用。我们使用Infinium HumanMethylation450 BeadChip研究了产前颗粒物质（PM）暴露对240例新生儿中178,309个启动子区域DNA甲基化的影响，使用具有准二项式链接族的广义线性回归模型，并针对性别，平板和细胞进行调整类型。然后使用逻辑回归或线性回归研究与PM相关的CpG基因座与儿童哮喘，颈动脉内膜中层厚度（CIMT）和血压（BP）的关系。使用小于0.15的FDR校正的p值，将31个基因座与PM 10 或PM 2.5 关联。使用焦磷酸测序法评估了两个基因座，分别在280名儿童健康研究（CHS）受试者中进行复制，其中一个成功复制（COLEC11 cg03579365）。 31个位点中的三个也与6岁时经医生诊断的哮喘有关，两个与CIMT相关，一个在10岁时与收缩压有关。分别在TM9SF2（cg02015529）和UBE2S（cg00035623）中较高的甲基化水平与产前PM升高2SD有关，也与哮喘几率增加36％和98％有关;而TDRD6（cg22329831）的甲基化与PM呈负相关，哮喘几率降低24％。产前PM暴露与少数基因启动子中新生儿血液中DNA甲基化的改变有关，其中一些基因启动子还与儿童后期的心脏呼吸健康结果有关。关键词：甲基化，颗粒物，空气污染，哮喘，心血管疾病。

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