Joint effects of prenatal air pollutant exposure and maternal folic acid supplementation on risk of autism spectrum disorder.
Joint effects of prenatal air pollutant exposure and maternal folic acid supplementation on risk of autism spectrum disorder.
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产前空气污染物暴露和孕产妇叶酸对自闭症谱系障碍风险的关节作用。
DOI：
10.1002/aur.1885
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发表时间：
2018-01
期刊：
影响因子：
--
通讯作者：
Schmidt RJ
中科院分区：
文献类型：
--
作者：
Goodrich AJ;Volk HE;Tancredi DJ;McConnell R;Lurmann FW;Hansen RL;Schmidt RJ
独立研究报告称，围孕期叶酸 (FA) 可能会降低患自闭症谱系障碍 (ASD) 的风险，而暴露于空气污染可能会增加 ASD 风险。我们研究了妊娠期 FA 和空气污染暴露与自闭症谱系障碍 (ASD) 的联合影响。我们研究了 CHARGE 病例对照研究中的 346 个 ASD 病例和 260 个典型对照。对怀孕每个月自我报告的 FA 摄入量进行量化。根据母亲的居住史，对接近道路空气污染（NRP）的暴露程度和标准空气污染物测量值进行了评估。在怀孕第一个月内 FA 摄入量较高（>800 µg）的母亲中，在妊娠前三个月接触除臭氧外的所有空气污染物水平升高与 ASD 风险降低相关，而在 FA 摄入量较低（≤800 µg）的母亲中，相同污染物的 ASD 风险增加。对于 NO2，这种差异具有统计学意义（例如，NO2 和低 FA 摄入量：OR=1.53 (0.91, 2.56) vs NO2 和高 FA 摄入量：OR=0.74 (0.46, 1.19)，p 交互作用=0.04）。与暴露于较低水平空气污染物且报告第一个月 FA 摄入量较高的母亲相比，在怀孕前三个月暴露于较高水平（≥中位数）任何空气污染物且报告 FA 摄入量较低的母亲面临更高的 ASD 风险。联合效应显示 NRP 和 NO2 与预期相互作用存在显着 (α<0.10) 偏差。我们的结果表明，围孕期摄入 FA 可能会降低产前空气污染暴露程度高的人的自闭症谱系障碍 (ASD) 风险。需要进一步的研究来在更大的样本量中复制这些发现，并了解这种潜在关系的机制。
Independent studies report that periconceptional folic acid (FA) may decrease the risk of autism spectrum disorder (ASD) while exposure to air pollution may increase ASD risk. We examined the joint effects of gestational FA and air pollution exposures in association with ASD. We studied 346 ASD cases and 260 typically developing controls from the CHARGE case-control study. Self-reported FA intake for each month of pregnancy was quantified. Estimates of exposure to near roadway air pollution (NRP) and criteria air pollutant measures were assigned based on maternal residential history. Among mothers with high FA intake (>800 µg) in the first pregnancy month, exposure to increasing levels of all air pollutants, except ozone, during the first trimester was associated with decreased ASD risk, while increased ASD risk was observed for the same pollutant among mothers with low FA intake (≤800 µg). This difference was statistically significant for NO2 (e.g. NO2 and low FA intake: OR=1.53 (0.91, 2.56) vs NO2 and high FA intake: OR=0.74 (0.46, 1.19), p-interaction=0.04). Mothers exposed to higher levels (≥ median) of any air pollutant during the first trimester of pregnancy and who reported low FA intake were at a higher ASD risk compared to mothers exposed to lower levels of that air pollutant and who reported high first month FA intake. Joint effects showed significant (alpha<0.10) departures from expected interaction for NRP and NO2. Our results suggest that periconceptional FA intake may reduce ASD risk in those with high prenatal air pollution exposure. Further study is needed to replicate these findings in larger sample sizes and to understand mechanisms of this potential relationship.
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