Kusters Michelle S W, López-Vicente Mónica, Muetzel Ryan L, Binter Anne-Claire, Petricola Sami, Tiemeier Henning, Guxens Mònica
ISGlobal, Barcelona, Spain; Universitat Pompeu Fabra, Barcelona, Spain; Department of Child and Adolescent Psychiatry/Psychology, Erasmus University Medical Centre, Rotterdam, the Netherlands.
ISGlobal, Barcelona, Spain; Universitat Pompeu Fabra, Barcelona, Spain; Department of Child and Adolescent Psychiatry/Psychology, Erasmus University Medical Centre, Rotterdam, the Netherlands; Spanish Consortium for Research on Epidemiology and Public Health (CIBERESP), Instituto de Salud Carlos III, Madrid, Spain.
Environ Res. 2024 Dec 1;262(Pt 2):119828. doi: 10.1016/j.envres.2024.119828. Epub 2024 Aug 23.
Recent evidence suggests an association of air pollution exposure with brain development, but evidence on white matter microstructure in children is scarce. We investigated how air pollution exposure during pregnancy and childhood impacts longitudinal development of white matter microstructure throughout adolescence.
Our study population consisted of 4108 participants of Generation R, a large population-based birth cohort from Rotterdam, the Netherlands. Residential air pollution exposure to 14 air pollutants during pregnancy and childhood was estimated with land-use regression models. Diffusion tensor images were obtained around age 10 and 14, resulting in a total of 5422 useable scans (n = 3082 for wave 1 and n = 2340 for wave 2; n = 1314 for participants with data on both waves). We calculated whole-brain fractional anisotropy (FA) and mean diffusivity (MD) and performed single- and multi-pollutant analyses using mixed effects models adjusted for life-style and socioeconomic status variables.
Higher exposure to PM during pregnancy, and PM, PM, PM, and NO during childhood was associated with a consistently lower whole-brain FA throughout adolescence (e.g. - 0.07 × 10 FA [95%CI -0.12; -0.02] per 1 standard deviation higher PM exposure during pregnancy). Higher exposure to silicon (Si) in PM and oxidative potential of PM during pregnancy, and PM during childhood was associated with an initial higher MD followed by a faster decrease in MD throughout adolescence (e.g. - 0.02 × 10 mm/s MD [95%CI -0.03; -0.00] per year of age per 1 standard deviation higher Si exposure during pregnancy). Results were comparable when performing the analysis in children with complete data on the outcome for both neuroimaging assessments.
Exposure to several pollutants was associated with a consistently lower whole-brain FA throughout adolescence. The association of few pollutants with whole-brain MD at baseline attenuated throughout adolescence. These findings suggest both persistent and age-limited associations of air pollution exposure with white matter microstructure.
最近的证据表明空气污染暴露与大脑发育有关，但关于儿童白质微观结构的证据很少。我们研究了孕期和儿童期的空气污染暴露如何影响整个青春期白质微观结构的纵向发育。
我们的研究人群包括来自荷兰鹿特丹的基于人群的大型出生队列“R世代”的4108名参与者。使用土地利用回归模型估计孕期和儿童期住宅空气污染暴露于14种空气污染物的情况。在10岁和14岁左右获取扩散张量图像，共得到5422次可用扫描（第1波n = 3082，第2波n = 2340；两波均有数据的参与者n = 1314）。我们计算了全脑分数各向异性（FA）和平均扩散率（MD），并使用针对生活方式和社会经济地位变量进行调整的混合效应模型进行单污染物和多污染物分析。
孕期暴露于较高水平的PM，以及儿童期暴露于PM、PM、PM和NO，与整个青春期全脑FA持续降低有关（例如，孕期PM暴露每增加1个标准差，全脑FA降低 - 0.07×10 FA [95%CI -0.12；-0.02]）。孕期暴露于PM中的硅（Si）和PM的氧化潜能，以及儿童期暴露于PM，与MD最初升高随后在整个青春期更快下降有关（例如，孕期Si暴露每增加1个标准差，每年MD降低 - 0.02×10 mm/s MD [95%CI -0.03；-0.00]）。在对两种神经影像学评估结果均有完整数据的儿童中进行分析时，结果具有可比性。
暴露于几种污染物与整个青春期全脑FA持续降低有关。少数污染物与基线时全脑MD的关联在整个青春期减弱。这些发现表明空气污染暴露与白质微观结构存在持续和年龄受限的关联。
