A summary of recent findings on birth outcomes and developmental effects of prenatal ETS, PAH, and pesticide exposures
A summary of recent findings on birth outcomes and developmental effects of prenatal ETS, PAH, and pesticide exposures
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DOI：
10.1016/j.neuro.2004.07.007
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发表时间：
2005-08-01
期刊：
影响因子：
3.4
通讯作者：
Kinney, PL
中科院分区：
文献类型：
--
作者：
Perera, FP;Rauh, V;Kinney, PL
城市内部的少数民族人口是不良出生结果的高风险群体，也更有可能暴露于环境污染物，包括环境烟草烟雾（ETS），苯并[a]芘B[a]P，其他环境多环芳烃（全球多环芳烃）和住宅杀虫剂。哥伦比亚儿童环境健康中心（CCCEH）正在对700名北方曼哈顿孕妇和新生儿进行前瞻性队列研究，以检查产前暴露于这些常见毒物对胎儿生长、早期神经发育和呼吸系统健康的影响。本文总结了三项已发表研究的结果，这些研究证明了产前ETS、PAH和杀虫剂对出生结果和/或神经认知发育的影响[Perera FP、Rauh V Whyatt RM、Tsai WY Bernert JT Tit YH等人，多种族人群中产前环境暴露对出生结果相互作用的分子证据。环境健康展望2004;12：630-62; Rauh VA，Whyatt RM，Garfinkel R，Andrews H，Hoepner L，Reyes A，et al.暴露于环境烟草烟雾和内城儿童物质困难的发育影响。Neurotoxicol Teratol 2004;26：373-85; Whyatt RM，Rauh V巴尔DB，Camann DE，Andrews HF Garfinkel R，et al.城市少数群体中的产前杀虫剂暴露、出生体重和身长。环境卫生展望，在新闻]。为了评估产前暴露于ETS、多环芳烃和农药的影响，研究人员分析了问卷数据、脐带血血浆（包括ETS和农药暴露的生物标志物）和B[a]P-DNA加合物（多环芳烃的分子剂量计）。自我报告的ETS与头围减小相关（P = 0.04），ETS和加合物之间存在显著的相互作用，因此在调整混杂因素后，合并暴露对出生体重（P = 0.04）和头围（P = 0.01）具有显著的倍增效应。第二项分析研究了产前ETS暴露和产后物质困难（在食物、住房和衣服方面未满足的基本需求）对2年认知发育的神经毒性影响。这两种暴露都抑制了认知发育（P < 0.05），并且存在显著的交互作用，即同时暴露于ETS和物质困难的儿童表现出最大的认知缺陷（7.1分）。第三项分析发现，毒死蜱脐带，以及毒死蜱脐带、二嗪农和残杀威代谢物的联合测量，与出生体重和/或身长呈负相关（P < 0.05）。这些结果强调了政策的重要性，减少暴露于ETS，空气污染和杀虫剂对胎儿生长和儿童神经发育的潜在不利影响。(c)2004年爱思唯尔公司All rights reserved.
Inner-city minority populations are high-risk groups for adverse birth outcomes and also more likely to be exposed to environmental contaminants, including environmental tobacco smoke (ETS), benzo[a]pyrene B[a]P, other ambient polycyclic aromatic hydrocarbons (global PAHs), and residential pesticides. The Columbia Center for Children's Environmental Health (CCCEH) is conducting a prospective cohort study of 700 northern Manhattan pregnant women and newborns to examine the effects of prenatal exposure to these common toxicants on fetal growth, early neurodevelopment, and respiratory health. This paper summarizes results of three published studies demonstrating the effects of prenatal ETS, PAH, and pesticides on birth outcomes and/or neurocognitive development [Perera FP, Rauh V Whyatt RM, Tsai WY Bernert JT Tit YH, et al. Molecular evidence of an interaction between prenatal environment exposures on birth outcomes in a multiethnic population. Environ Health Perspect 2004;12:630-62; Rauh VA, Whyatt RM, Garfinkel R, Andrews H, Hoepner L, Reyes A, et al. Developmental effects of exposure to environmental tobacco smoke and material hardship among inner-city children. Neurotoxicol Teratol 2004;26:373-85; Whyatt RM, Rauh V Barr DB, Camann DE, Andrews HF Garfinkel R, et al. Prenatal insecticide exposures, birth weight and length among an urban minority cohort. Environ Health Perspect, in press]. To evaluate the effects of prenatal exposure to ETS, PAHs, and pesticides, researchers analyzed questionnaire data, cord blood plasma (including biomarkers of ETS and pesticide exposure), and B[a]P-DNA adducts (a molecular dosimeter of PAHs). Self-reported ETS was associated with decreased head circumference (P = 0.04), and there was a significant interaction between ETS and adducts such that combined exposure had a significant multiplicative effect on birth weight (P = 0.04) and head circumference (P = 0.01) after adjusting for confounders. A second analysis examined the neurotoxic effects of prenatal ETS exposure and postpartum material hardship (unmet basic needs in the areas of food, housing, and clothing) on 2-year cognitive development. Both exposures depressed cognitive development (P < 0.05), and there was a significant interaction such that children with exposure to both ETS and material hardship exhibited the greatest cognitive deficit (7.1 points). A third analysis found that cord chlorpyrifos, and a combined measure of cord chlorpyrifos, diazinon, and propoxur-metabolite, were inversely associated with birth weight and/or length (P < 0.05). These results underscore the importance of policies that reduce exposure to ETS, air pollution, and pesticides with potentially adverse effects on fetal growth and child neurodevelopment. (c) 2004 Elsevier Inc. All rights reserved.