Effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3 years of life among inner-city children.
Effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on neurodevelopment in the first 3 years of life among inner-city children.
复制标题
在城市内部儿童生命的前三年中，产前暴露于空气中多环芳烃对神经发育的影响。
DOI：
10.1289/ehp.9084
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发表时间：
2006-08
影响因子：
10.4
通讯作者：
Kinney, Patrick
中科院分区：
文献类型：
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作者：
Perera, Frederica P;Rauh, Virginia;Whyatt, Robin M;Tsai, Wei-Yann;Tang, Deliang;Diaz, Diurka;Hoepner, Lori;Barr, Dana;Tu, Yi-Hsuan;Camann, David;Kinney, Patrick
我们对纽约市不吸烟的非洲裔美国人和多米尼加母亲和儿童进行的前瞻性队列研究正在评估产前接触城市污染物（包括多环芳烃 (PAH)、环境烟草烟雾 (ETS) 和杀虫剂）在神经行为障碍发病机制中的作用。我们使用贝利婴儿发育量表来评估怀孕期间通过个人空气采样监测的产前接触空气中多环芳烃对儿童智力和精神运动发育的影响。行为发展通过儿童行为检查表进行评估。我们调整了潜在的混杂因素，包括社会人口因素和产前接触 ETS 和毒死蜱。产前接触多环芳烃与精神运动发育指数或行为问题无关。然而，产前大量接触 PAH（上四分位）与 3 岁时智力发育指数较低相关 [β= –5.69； 95% 置信区间 (CI)，–9.05 至 –2.33； p < 0.01]。对于产前接触量高的儿童，认知发育迟缓的几率也显着更高（优势比 = 2.89；95% CI，1.33 至 6.25；p = 0.01）。一般估计方程分析显示年龄 × PAH 对智力发育有显着影响 (p = 0.01)，证实了年龄特异性回归结果。对领先地位的进一步调整并没有改变这种关系。不同种族的效应大小没有差异。结果需要确认，但表明纽约市空气中最近遇到的环境多环芳烃水平可能会对 3 岁时儿童的认知发展产生不利影响，从而影响学校表现。
Our prospective cohort study of nonsmoking African-American and Dominican mothers and children in New York City is evaluating the role of prenatal exposure to urban pollutants, including polycyclic aromatic hydrocarbons (PAHs), environmental tobacco smoke (ETS), and pesticides, in the pathogenesis of neurobehavioral disorders. We used the Bayley Scales of Infant Development to evaluate the effects on child mental and psychomotor development of prenatal exposure to airborne PAHs monitored during pregnancy by personal air sampling. Behavioral development was assessed by the Child Behavior Checklist. We adjusted for potential confounders including sociodemographic factors and prenatal exposure to ETS and chlorpyrifos. Prenatal exposure to PAHs was not associated with psychomotor development index or behavioral problems. However, high prenatal exposure to PAHs (upper quartile) was associated with lower mental development index at age 3 [β= –5.69; 95% confidence interval (CI), –9.05 to –2.33; p < 0.01]. The odds of cognitive developmental delay were also significantly greater for children with high prenatal exposure (odds ratio = 2.89; 95% CI, 1.33 to 6.25; p = 0.01). General estimated equation analysis showed a significant age × PAH effect on mental development (p = 0.01), confirming the age-specific regression findings. Further adjustment for lead did not alter the relationships. There were no differences in effect sizes by ethnicity. The results require confirmation but suggest that environmental PAHs at levels recently encountered in New York City air may adversely affect children’s cognitive development at 3 years of age, with implications for school performance.