Recent epidemiological studies indicate early-life exposure to pollution particulate is associated with adverse neurodevelopmental outcomes. The need is arising to evaluate the risks conferred by individual components and sources of air pollution to provide a framework for the regulation of the most relevant components for public health protection. Previous studies in rodent models have shown diesel particulate matter has neurotoxic potential and could be a health concern for neurodevelopment. The present study shows an evaluation of pathological and protracted behavioral alterations following neonatal exposure to aerosolized diesel exhaust particles (NIST SRM 1650b). The particular behavioral focus was on temporal control learning, a broad and fundamental cognitive domain in which reward delivery is contingent on a fixed interval schedule. For this purpose, C57BL/6 J mice were exposed to aerosolized NIST SRM 1650b, a well-characterized diesel particulate material, from postnatal days 4–7 and 10–13, for four hours per day. Pathological features, including glial fibrillary-acidic protein, myelin basic protein expression in the corpus callosum, and ventriculomegaly, as well as learning alterations were measured to determine the extent to which NIST SRM 1650b would induce developmental neurotoxicity. Twenty-four hours following exposure significant increases in glial-fibrillary acidic protein (GFAP) in the corpus callosum and cortex of exposed male mice were present. Additionally, the body weights of juvenile and early adult diesel particle exposed males were lower than controls, although the difference was not statistically significant. No treatment-related differences in males or females on overall locomotor activity or temporal learning during adulthood were observed in response to diesel particulate exposure. While some sex and regional-specific pathological alterations in GFAP immunoreactivity suggestive of an inflammatory reaction to SRM 1650b were observed, the lack of protracted behavioral and pathological deficits suggests further clarity is needed on the developmental effects of diesel emissions prior to enacting regulatory guidelines.

中文翻译：

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新生儿吸入C57BL / 6小鼠的柴油机排气颗粒后产生的有限发育神经毒性

最近的流行病学研究表明，生命早期接触污染颗粒与不良的神经发育结果有关。迫切需要评估由各个组成部分和空气污染源所带来的风险，从而为监管最相关的组成部分提供框架，以保护公共卫生。先前在啮齿动物模型中的研究表明，柴油颗粒物具有神经毒性的潜力，并且可能是神经发育的健康问题。本研究显示了新生儿暴露于雾化柴油机废气颗粒后的病理和长期行为改变的评估（NIST SRM 1650b）。特定的行为重点是时间控制学习，这是一个广泛而基础的认知领域，在该领域中，奖励的交付取决于固定的时间间隔。为此，从出生后第4-7天和第10-13天起，每天将C57BL / 6 J小鼠暴露于气溶胶​​化的NIST SRM 1650b（一种特性良好的柴油颗粒物质）中，每天暴露四个小时。测量病理特征，包括神经胶质纤维酸性蛋白，my体中髓鞘碱性蛋白表达，脑室肥大以及学习改变，以确定NIST SRM 1650b诱导发育神经毒性的程度。暴露后二十四小时，暴露的雄性小鼠的call体和皮层中的胶质原纤维酸性蛋白（GFAP）显着增加。此外，暴露于青少年和早期成年柴油颗粒的男性的体重低于对照组，尽管差异在统计学上并不显着。未观察到对柴油微粒暴露的反应，男性或女性在总体运动能力或成年期的时间学习方面与治疗相关的差异。尽管观察到了GFAP免疫反应性中的某些性别和区域特定病理学改变，表明对SRM 1650b会发生炎症反应，但缺乏持久的行为和病理学缺陷表明在制定监管指南之前，需要进一步明确柴油机排放物的发展影响。