Prenatal exposure to air pollution is associated with altered brain structure, function, and metabolism in childhood.
Prenatal exposure to air pollution is associated with altered brain structure, function, and metabolism in childhood.
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DOI：
10.1111/jcpp.13578
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发表时间：
2022-02
期刊：
影响因子：
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通讯作者：
Brad Peterson;R. Bansal;Siddhant Sawardekar;Carlo Nati;Eman R Elgabalawy;Lori A. Hoepner;Wanda E Garcia;Xuejun Hao;A. Margolis;F. Perera;V. Rauh
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文献类型：
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作者：
Brad Peterson;R. Bansal;Siddhant Sawardekar;Carlo Nati;Eman R Elgabalawy;Lori A. Hoepner;Wanda E Garcia;Xuejun Hao;A. Margolis;F. Perera;V. Rauh
出生前暴露于空气污染会干扰认知、情感和行为发育。与产前空气污染有关的大脑紊乱在很大程度上是未知的。方法：在这项前瞻性队列研究中，我们估计了332名6-14岁青年的产前细颗粒物（PM2.5）和多环芳烃（PAH）暴露，然后评估了其与脑解剖结构，组织显微结构，神经代谢物和血流测量的相关性。然后，我们评估了这些大脑紊乱与智力、ADHD和焦虑症状以及社会化的相关性。结果两种暴露均伴有背顶叶皮质变薄，后下壁和近中壁皮质增厚。它们与较小的白色物质体积、内囊和额叶的白色物质组织减少、额叶皮质代谢物浓度较高、皮质血流量减少以及皮质下灰质核团的显微结构组织增加有关。男孩的PM2.5和女孩的PAH的关联性更强。低暴露量的青少年在多动症、焦虑、社交和智力测量与皮质厚度和白色物质体积之间的关系中占了最重要的地位，而高暴露量似乎通常会破坏这些神经典型的大脑行为关联，这可能是因为强烈的与焦虑相关的影响增加了这些大脑测量的差异。结论：暴露影响的共性表明PM2.5和PAH通过一种或多种常见的分子途径（如炎症或氧化应激）破坏大脑发育。逐渐升高的暴露量与局部体积、组织结构、代谢物浓度和整个皮质和皮质下脑区的血流以及互连它们的白色物质通路的更大破坏相关。这些受影响的区域共同组成了皮质-纹状体-丘脑-皮质回路，这些回路支持思想，情绪和行为的调节。
BACKGROUND Prenatal exposure to air pollution disrupts cognitive, emotional, and behavioral development. The brain disturbances associated with prenatal air pollution are largely unknown. METHODS In this prospective cohort study, we estimated prenatal exposures to fine particulate matter (PM2.5 ) and polycyclic aromatic hydrocarbons (PAH), and then assessed their associations with measures of brain anatomy, tissue microstructure, neurometabolites, and blood flow in 332 youth, 6-14 years old. We then assessed how those brain disturbances were associated with measures of intelligence, ADHD and anxiety symptoms, and socialization. RESULTS Both exposures were associated with thinning of dorsal parietal cortices and thickening of postero-inferior and mesial wall cortices. They were associated with smaller white matter volumes, reduced organization in white matter of the internal capsule and frontal lobe, higher metabolite concentrations in frontal cortex, reduced cortical blood flow, and greater microstructural organization in subcortical gray matter nuclei. Associations were stronger for PM2.5 in boys and PAH in girls. Youth with low exposure accounted for most significant associations of ADHD, anxiety, socialization, and intelligence measures with cortical thickness and white matter volumes, whereas it appears that high exposures generally disrupted these neurotypical brain-behavior associations, likely because strong exposure-related effects increased the variances of these brain measures. CONCLUSIONS The commonality of effects across exposures suggests PM2.5 and PAH disrupt brain development through one or more common molecular pathways, such as inflammation or oxidative stress. Progressively higher exposures were associated with greater disruptions in local volumes, tissue organization, metabolite concentrations, and blood flow throughout cortical and subcortical brain regions and the white matter pathways interconnecting them. Together these affected regions comprise cortico-striato-thalamo-cortical circuits, which support the regulation of thought, emotion, and behavior.