Molecular Biosciences, UC Davis School of Veterinary Medicine, Davis, CA, USA.
Psychiatry, UC Davis School of Medicine, Sacramento, CA, USA.
Transl Psychiatry. 2020 May 27;10(1):166. doi: 10.1038/s41398-020-0845-3.
Epidemiological studies link traffic-related air pollution (TRAP) to increased risk for various neurodevelopmental disorders (NDDs); however, there are limited preclinical data demonstrating a causal relationship between TRAP and adverse neurodevelopmental outcomes. Moreover, much of the preclinical literature reports effects of concentrated ambient particles or diesel exhaust that do not recapitulate the complexity of real-world TRAP exposures. To assess the developmental neurotoxicity of more realistic TRAP exposures, we exposed male and female rats during gestation and early postnatal development to TRAP drawn directly from a traffic tunnel in Northern California and delivered to animals in real-time. We compared NDD-relevant neuropathological outcomes at postnatal days 51-55 in TRAP-exposed animals versus control subjects exposed to filtered air. As indicated by immunohistochemical analyses, TRAP significantly increased microglial infiltration in the CA1 hippocampus, but decreased astrogliosis in the dentate gyrus. TRAP exposure had no persistent effect on pro-inflammatory cytokine levels in the male or female brain, but did significantly elevate the anti-inflammatory cytokine IL-10 in females. In male rats, TRAP significantly increased hippocampal neurogenesis, while in females, TRAP increased granule cell layer width. TRAP had no effect on apoptosis in either sex. Magnetic resonance imaging revealed that TRAP-exposed females, but not males, also exhibited decreased lateral ventricular volume, which was correlated with increased granule cell layer width in the hippocampus in females. Collectively, these data indicate that exposure to real-world levels of TRAP during gestation and early postnatal development modulate neurodevelopment, corroborating epidemiological evidence of an association between TRAP exposure and increased risk of NDDs.
流行病学研究将与交通相关的空气污染(TRAP)与各种神经发育障碍(NDD)的风险增加联系起来;然而,目前仅有有限的临床前数据证明 TRAP 与不良神经发育结果之间存在因果关系。此外,许多临床前文献报道的集中环境颗粒或柴油废气的影响并不能再现真实世界 TRAP 暴露的复杂性。为了评估更现实的 TRAP 暴露对发育的神经毒性,我们在妊娠和新生后早期发育期间将雄性和雌性大鼠暴露于直接从加利福尼亚北部的交通隧道中提取的 TRAP,并实时递送至动物。我们比较了暴露于 TRAP 的动物与暴露于过滤空气的对照动物在新生后第 51-55 天的与 NDD 相关的神经病理学结果。如免疫组织化学分析所示,TRAP 显著增加了 CA1 海马中的小胶质细胞浸润,但减少了齿状回中的星形胶质细胞增生。TRAP 暴露对雄性或雌性大脑中的促炎细胞因子水平没有持续影响,但显著增加了雌性的抗炎细胞因子 IL-10。在雄性大鼠中,TRAP 显著增加了海马神经发生,而在雌性大鼠中,TRAP 增加了颗粒细胞层宽度。TRAP 对两性的细胞凋亡均无影响。磁共振成像显示,暴露于 TRAP 的雌性大鼠,而不是雄性大鼠,还表现出侧脑室体积减小,这与雌性大鼠海马中颗粒细胞层宽度增加相关。总的来说,这些数据表明,在妊娠和新生后早期发育期间暴露于真实世界水平的 TRAP 会调节神经发育,与 TRAP 暴露与 NDD 风险增加之间的关联的流行病学证据相符。