The relationship between persistent organic pollutants and Attention Deficit Hyperactivity Disorder phenotypes: Evidence from task-based neural activity in an observational study of a community sample of Canadian mother-child dyads.
The relationship between persistent organic pollutants and Attention Deficit Hyperactivity Disorder phenotypes: Evidence from task-based neural activity in an observational study of a community sample of Canadian mother-child dyads.
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DOI：
10.1016/j.envres.2021.112593
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发表时间：
2022-04-15
影响因子：
8.3
通讯作者：
Posner, Jonathan
中科院分区：
文献类型：
--
作者：
Sussman, Tamara J.;Baker, Brennan H.;Wakhloo, Albert J.;Gillet, Virginie;Abdelouahab, Nadia;Whittingstall, Kevin;Lepage, Jean-Francois;St-Cyr, Lindsay;Boiyin, Amelie;Gagnon, Anthony;Baccarelli, Andrea A.;Takser, Larissa;Posner, Jonathan
关键词：
产前暴露于持久性有机污染物（POP），广泛分布在北美，与注意力缺陷多动障碍（ADHD）症状增加有关，可能是ADHD表型的可改变风险。然而，中度暴露于持久性有机污染物对基于任务的抑制控制性能，相关的脑功能和ADHD相关症状的影响仍然未知，限制了我们开发针对常见暴露水平的神经影响的干预措施的能力。本研究的目的是检查产前POP暴露和抑制控制性能之间的关联，抑制控制和ADHD相关症状的神经相关性。在加拿大魁北克舍布鲁克进行的一项关于加拿大母子二人组的观察性研究中收集了前瞻性数据，这些母子二人组中度接触持久性有机污染物，包括多氯联苯和多溴联苯醚，这是盖斯特和环境队列的一部分。样本包括87名符合条件的儿童，其中46名具有母亲血浆样本，9-11岁时Simon任务表现的功能性磁共振成像（fMRI）数据，以及通过儿童行为评估系统3（BASC-3）报告的父母临床症状。西蒙任务的性能进行了探讨，通过漂移扩散模型，参数估计与持久性有机污染物暴露。西蒙任务为基础的功能磁共振成像数据进行建模，以检查差异的不一致与一致的试验中的兴趣区（ROI）确定的Meta分析。在46名有完整数据的参与者中，29名为男性，平均年龄为10.42 ± 0.55岁。持久性有机污染物暴露增加与准确性降低有关（例如，PCB摩尔和率比= 0.95; 95% CI [0.90，0.99]），漂移率（例如，PCB摩尔总和β =-0.42; 95%CI [-0.77，-0.07]），以及任务相关的大脑活动（例如，在下额叶皮质中PCB摩尔总和β = −0.35; 95% CI [−0.69，0.02]），ADHD症状增加（例如，多动PCB摩尔总和β = 2.35; 95%CI [0.17，4.53]），支持产前接触持久性有机污染物是ADHD表型的可改变风险的可能性。我们发现，暴露于持久性有机污染物与大脑区域神经活动中基于任务的变化有关，这对抑制控制很重要，这表明了先前记录的持久性有机污染物与ADHD表型中神经行为缺陷之间的相关性的生物学机制。
Prenatal exposure to persistent organic pollutants (POPs), widespread in North America, is associated with increased Attention Deficit/Hyperactivity Disorder (ADHD) symptoms and may be a modifiable risk for ADHD phenotypes. However, the effects of moderate exposure to POPs on task-based inhibitory control performance, related brain function, and ADHD-related symptoms remain unknown, limiting our ability to develop interventions targeting the neural impact of common levels of exposure. The goal of this study was to examine the association between prenatal POP exposure and inhibitory control performance, neural correlates of inhibitory control and ADHD-related symptoms. Prospective data was gathered in an observational study of Canadian mother-child dyads, with moderate exposure to POPs, including polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs), as part of the GESTation and the Environment (GESTE) cohort in Sherbrooke, Quebec, Canada. The sample included 87 eligible children, 46 with maternal plasma samples, functional magnetic resonance imaging (fMRI) data of Simon task performance at 9–11 years, and parental report of clinical symptoms via the Behavioral Assessment System for Children 3 (BASC-3). Simon task performance was probed via drift diffusion modeling, and parameter estimates were related to POP exposure. Simon task-based fMRI data was modeled to examine the difference in incongruent vs congruent trials in regions of interest (ROIs) identified by meta analysis. Of the 46 participants with complete data, 29 were male, and mean age was 10.42 ± 0.55 years. Increased POP exposure was associated with reduced accuracy (e.g. PCB molar sum rate ratio = 0.95; 95% CI [0.90, 0.99]), drift rate (e.g. for PCB molar sum β = −0.42; 95% CI [−0.77, −0.07]), and task-related brain activity (e.g. in inferior frontal cortex for PCB molar sum β = −0.35; 95% CI [−0.69, 0.02]), and increased ADHD symptoms (e.g. hyperactivity PCB molar sum β = 2.35; 95%CI [0.17, 4.53]), supporting the possibility that prenatal exposure to POPs is a modifiable risk for ADHD phenotypes. We showed that exposure to POPs is related to task-based changes in neural activity in brain regions important for inhibitory control, suggesting a biological mechanism underlying previously documented associations between POPs and neurobehavioral deficits found in ADHD phenotypes.
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