Maternal exposure to atmospheric PM2.5 and fetal brain development: Associations with BAI1 methylation and thyroid hormones
Maternal exposure to atmospheric PM2.5 and fetal brain development: Associations with BAI1 methylation and thyroid hormones
复制标题
母亲暴露于大气 PM2.5 和胎儿大脑发育：与 BAI1 甲基化和甲状腺激素的关联
DOI：
10.1016/j.envpol.2022.119665
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发表时间：
2022
影响因子：
8.9
通讯作者：
Huo Xia
中科院分区：
文献类型：
--
作者：
Zeng Zhijun;Xu Xijin;Wang Qihua;Zhang Zhuxia;Meng Peipei;Huo Xia
孕妇在怀孕期间暴露于大气细颗粒物（PM2.5）与胎儿发育不良有关，包括大脑发育异常。然而，潜在的机制和影响因素仍不确定。本研究探讨了母亲接触电子垃圾PM2.5后，涉及神经发育和甲状腺激素（THs）的基因DNA甲基化在胎儿大脑发育中的作用。在2011年6月至2012年9月招募的939名健康孕妇中，包括101对电子废物暴露者和103对参考母婴对（共204对）。通过估算得到2011年和2012年电子垃圾暴露区域（116.38°E, 23.29°N）和参考区域（116.67°E, 23.34°N）的年地面PM2.5浓度，并通过计算个体慢性每日PM2.5摄入量（cdi）来评估孕产妇暴露情况。测定分娩后不久采集的脐带血中促甲状腺激素（TSH）、游离三碘甲状腺原氨酸（FT3）和游离甲状腺素（FT4）的甲基化水平和甲状腺素（THs）水平。我们发现，地面PM2.5浓度越高，接触电子垃圾的孕妇的PM2.5个体CDI就越高。在调整性别和出生体重指数后，发现脑特异性血管生成抑制剂1 （BAI1）基因+13和+ 32位点甲基化（分别为9.8%和5.3%,P < 0.05和P < 0.01）对母亲PM2.5暴露与出生头围的不利关联有显著的中介作用，而连环蛋白钙粘蛋白相关蛋白α 2 （CTNNA2）基因的甲基化没有中介作用。BAI1（位置+13）甲基化也与FT3水平显著相关（rs = -0.156, P = 0.032），尽管PM2.5的母体CDI与TSH水平异常的几率较高呈正相关（OR = 5.03, 95% CI: 1.00, 25.20, P = 0.05），而不是FT3水平。我们的研究结果表明，新生儿的甲基化（可能与三氯甲烷有关）可能在母亲暴露于电子垃圾产生的大气PM2.5导致的大脑发育异常风险中发挥中介作用。
Maternal exposure to atmospheric fine particulate matter (PM2.5) during pregnancy is associated with adverse fetal development, including abnormal brain development. However, the underlying mechanisms and influencing factors remain uncertain. This study investigated the roles of DNA methylation in genes involving neurodevelopment and thyroid hormones (THs) in fetal brain development after maternal exposure to PM2.5 from e-waste. Among 939 healthy pregnant women recruited from June 2011 to September 2012, 101 e-waste-exposed and 103 reference mother-infant pairs (204 pairs totally) were included. Annual ground-level PM2.5 concentrations over e-waste-exposed area (116.38°E, 23.29°N) and reference area (116.67°E, 23.34°N) in 2011, 2012 were obtained by estimates and maternal exposure was evaluated by calculating individual chronic daily intakes (CDIs) of PM2.5. Methylation and THs including thyroid-stimulating hormone (TSH), free triiodothyronine (FT3) and free thyroxine (FT4) level were measured in umbilical cord blood collected shortly after delivery. We found higher ground-level PM2.5 concentrations led to greater individual CDI of PM2.5 in e-waste-exposed pregnant women. After adjustment for gender and birth BMI, significant mediation effects on the adverse associations of maternal PM2.5 exposure with birth head circumference were observed for methylations at positions +13 and + 32 (respectively mediated proportion of 9.8% and 5.3%, P < 0.05 and P < 0.01) in the brain-specific angiogenesis inhibitor 1 (BAI1) gene, but not for methylations in the catenin cadherin-associated protein, alpha 2 (CTNNA2) gene. BAI1 (position +13) methylation was also significantly correlated with FT3 levels (rs = -0.156, P = 0.032), although maternal CDI of PM2.5 was positively associated with higher odds of abnormal TSH levels (OR = 5.03, 95% CI: 1.00, 25.20, P = 0.05) rather than FT3 levels. Our findings suggest that methylation (likely linked to THs) in neonates may play mediation roles associated with abnormal brain development risk due to maternal exposure to atmospheric PM2.5 from e-waste.