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Abstract：
Per- and polyfluoroalkyl substances (PFAS) are shown to have neurotoxic effects on animals, but epidemiological evidence for associations between childhood PFAS exposure and neurodevelopment is inconclusive. We examined if childhood PFAS concentrations are associated with a diagnosis of autism spectrum disorder (ASD), developmental delay (DD), and other early concerns (OEC) in development.
We included 551 children 2-5 years old from the CHildhood Autism Risks from Genetics and Environment (CHARGE) case-control study. Children were clinically diagnosed and classified as having ASD, DD, OEC, and typical development (TD). Fourteen PFAS were quantified in child serum samples collected when diagnostic assessments were performed. We used multinomial logistic regression models to investigate the cross-sectional associations of individual PFAS concentrations with neurodevelopmental outcomes and weighted quantile sum (WQS) regression models with repeated holdout validation to investigate the associations with PFAS mixtures.
Childhood perfluorooctanoic acid (PFOA) was associated with increased odds of ASD (odds ratio [OR] per ln ng/mL increase: 1.99, 95% confidence interval [CI]: 1.20, 3.29) and DD (OR: 2.16, 95% CI: 1.21, 3.84) versus TD. Perfluoroheptanoic acid (PFHpA) was associated with increased odds of ASD (OR: 1.61, 95% CI: 1.21, 2.13). However, perfluroundecanoic acid (PFUnDA) was associated with decreased odds of ASD (OR: 0.43, 95% CI: 0.26, 0.69). From mixture analyses, the WQS index was associated with increased odds of ASD (average OR: 1.57, 5th and 95th percentile: 1.16, 2.13). Child\'s sex and homeownership modified associations of perfluorodecanoic acid (PFDA) with DD and ASD, respectively.
In this case-control study, childhood PFOA, PFHpA, and a PFAS mixture was associated with increased odds of ASD, while PFUnDA was associated with decreased odds of ASD. Because we used concurrent measurements of PFAS, our results do not imply causal relationships and thus need to be interpreted with caution.
We included 551 children 2-5 years old from the CHildhood Autism Risks from Genetics and Environment (CHARGE) case-control study. Children were clinically diagnosed and classified as having ASD, DD, OEC, and typical development (TD). Fourteen PFAS were quantified in child serum samples collected when diagnostic assessments were performed. We used multinomial logistic regression models to investigate the cross-sectional associations of individual PFAS concentrations with neurodevelopmental outcomes and weighted quantile sum (WQS) regression models with repeated holdout validation to investigate the associations with PFAS mixtures.
Childhood perfluorooctanoic acid (PFOA) was associated with increased odds of ASD (odds ratio [OR] per ln ng/mL increase: 1.99, 95% confidence interval [CI]: 1.20, 3.29) and DD (OR: 2.16, 95% CI: 1.21, 3.84) versus TD. Perfluoroheptanoic acid (PFHpA) was associated with increased odds of ASD (OR: 1.61, 95% CI: 1.21, 2.13). However, perfluroundecanoic acid (PFUnDA) was associated with decreased odds of ASD (OR: 0.43, 95% CI: 0.26, 0.69). From mixture analyses, the WQS index was associated with increased odds of ASD (average OR: 1.57, 5th and 95th percentile: 1.16, 2.13). Child\'s sex and homeownership modified associations of perfluorodecanoic acid (PFDA) with DD and ASD, respectively.
In this case-control study, childhood PFOA, PFHpA, and a PFAS mixture was associated with increased odds of ASD, while PFUnDA was associated with decreased odds of ASD. Because we used concurrent measurements of PFAS, our results do not imply causal relationships and thus need to be interpreted with caution.
摘要：
全氟烷基和多氟烷基物质（PFAS）被证明对动物有神经毒性作用，但儿童PFAS暴露与神经发育之间关联的流行病学证据尚无定论.我们检查了儿童PFAS浓度是否与自闭症谱系障碍（ASD）的诊断有关，发育迟缓（DD），以及开发中的其他早期问题(OEC)。
我们纳入了551名2-5岁儿童的遗传和环境自闭症风险（CHARGE）病例对照研究。儿童被临床诊断为患有ASD，DD,OEC,和典型发展(TD)。在进行诊断评估时收集的儿童血清样品中定量了14个PFAS。我们使用多项逻辑回归模型来研究个体PFAS浓度与神经发育结果的横截面关联，并使用加权分位数和（WQS）回归模型进行重复保持验证来研究与PFAS混合物的关联。
儿童全氟辛酸（PFOA）与ASD的几率增加相关（优势比[OR]每lnng/mL增加：1.99，95％置信区间[CI]：1.20，3.29）和DD（OR：2.16，95％CI：1.21，3.84）与TD相比。全氟庚酸（PFHpA）与ASD的几率增加相关（OR：1.61，95％CI：1.21，2.13）。然而,全氟十二烷酸(PFUnDA)与ASD发生几率降低相关(OR:0.43,95%CI:0.26,0.69).从混合物分析，WQS指数与ASD几率增加相关(平均OR:1.57,第5和第95百分位数:1.16,2.13).儿童性别和房屋所有权修改后的全氟癸酸（PFDA）与DD和ASD的关联，分别。
在本病例对照研究中，童年PFOA,PFHpA,PFAS混合物与ASD的几率增加有关，而PFUnDA与ASD几率降低相关。因为我们使用了同时测量PFAS，我们的结果并不意味着因果关系,因此需要谨慎解释.
我们纳入了551名2-5岁儿童的遗传和环境自闭症风险（CHARGE）病例对照研究。儿童被临床诊断为患有ASD，DD,OEC,和典型发展(TD)。在进行诊断评估时收集的儿童血清样品中定量了14个PFAS。我们使用多项逻辑回归模型来研究个体PFAS浓度与神经发育结果的横截面关联，并使用加权分位数和（WQS）回归模型进行重复保持验证来研究与PFAS混合物的关联。
儿童全氟辛酸（PFOA）与ASD的几率增加相关（优势比[OR]每lnng/mL增加：1.99，95％置信区间[CI]：1.20，3.29）和DD（OR：2.16，95％CI：1.21，3.84）与TD相比。全氟庚酸（PFHpA）与ASD的几率增加相关（OR：1.61，95％CI：1.21，2.13）。然而,全氟十二烷酸(PFUnDA)与ASD发生几率降低相关(OR:0.43,95%CI:0.26,0.69).从混合物分析，WQS指数与ASD几率增加相关(平均OR:1.57,第5和第95百分位数:1.16,2.13).儿童性别和房屋所有权修改后的全氟癸酸（PFDA）与DD和ASD的关联，分别。
在本病例对照研究中，童年PFOA,PFHpA,PFAS混合物与ASD的几率增加有关，而PFUnDA与ASD几率降低相关。因为我们使用了同时测量PFAS，我们的结果并不意味着因果关系,因此需要谨慎解释.
