BACKGROUND Air pollution exposure during fetal life has been related to impaired child neurodevelopment, but it is unclear if brain structural alterations underlie this association. The authors assessed whether air pollution exposure during fetal life alters brain morphology and whether these alterations mediate the association between air pollution exposure during fetal life and cognitive function in school-age children. METHODS We used data from a population-based birth cohort set up in Rotterdam, The Netherlands (2002-2006). Residential levels of air pollution during the entire fetal period were calculated using land-use regression models. Structural neuroimaging and cognitive function were performed at 6 to 10 years of age (n = 783). Models were adjusted for several socioeconomic and lifestyle characteristics. RESULTS Mean fine particle levels were 20.2 μg/m3 (range, 16.8-28.1 μg/m3). Children exposed to higher particulate matter levels during fetal life had thinner cortex in several brain regions of both hemispheres (e.g., cerebral cortex of the precuneus region in the right hemisphere was 0.045 mm thinner (95% confidence interval, 0.028-0.062) for each 5-μg/m3 increase in fine particles). The reduced cerebral cortex in precuneus and rostral middle frontal regions partially mediated the association between exposure to fine particles and impaired inhibitory control. Air pollution exposure was not associated with global brain volumes. CONCLUSIONS Exposure to fine particles during fetal life was related to child brain structural alterations of the cerebral cortex, and these alterations partially mediated the association between exposure to fine particles during fetal life and impaired child inhibitory control. Such cognitive impairment at early ages could have significant long-term consequences.

中文翻译：

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学龄儿童胎儿生命期间的空气污染暴露、脑形态和认知功能

背景 胎儿生命期间的空气污染暴露与儿童神经发育受损有关，但尚不清楚大脑结构改变是否是这种关联的基础。作者评估了胎儿生命期间空气污染暴露是否会改变大脑形态，以及这些改变是否介导了胎儿生命期间空气污染暴露与学龄儿童认知功能之间的关联。方法 我们使用来自荷兰鹿特丹（2002-2006）的基于人口的出生队列的数据。使用土地利用回归模型计算整个胎儿时期的住宅空气污染水平。结构神经影像学和认知功能在 6 至 10 岁时进行（n = 783）。模型针对几个社会经济和生活方式特征进行了调整。结果平均细颗粒水平为 20.2 μg/m3（范围，16.8-28.1 μg/m3）。在胎儿生命期间暴露于较高颗粒物水平的儿童，每 5 个大脑半球的几个大脑区域的皮质较薄（例如，右半球楔前叶区域的大脑皮质薄 0.045 毫米（95% 置信区间，0.028-0.062） -μg/m3 增加细颗粒）。楔前叶和前额中部区域的大脑皮层减少部分介导了暴露于细颗粒与抑制控制受损之间的关联。空气污染暴露与全球脑容量无关。结论 胎儿期接触细颗粒物与儿童大脑皮层结构改变有关，这些变化部分介导了胎儿生命期间接触细颗粒与儿童抑制控制受损之间的关联。这种早期的认知障碍可能会产生重大的长期后果。