Accumulating studies indicate that the brain is a direct target of air pollution exposure during the fetal period. We have previously demonstrated that exposure to concentrated ambient particles (CAPs) during gestation produces ventriculomegaly, periventricular hypermyelination, and enlargement of the corpus callosum (CC) during postnatal development in mice. This study aimed to further characterize the cellular basis of the observed hypermyelination and determine if this outcome, among other effects, persisted as the brain matured. Analysis of CC-1⁺ mature oligodendrocytes in the CC at postnatal days (PNDs) 11–15 suggest a premature maturational shift in number and proportion of total cells in prenatally CAPs-exposed males and females, with no overall change in total CC cellularity. The overall number of Olig2⁺ lineage cells in the CC was not affected in either sex at the same postnatal timepoint. Assessment of myelin status at early brain maturity (PNDs 57–61) revealed persistent hypermyelination in CAPs-exposed animals of both sexes. In addition, ventriculomegaly was persistent in CAPs-treated females, with possible amelioration of ventriculomegaly in CAPs-exposed males. When oligodendrocyte precursor cell (OPC) pool status was analyzed at PNDs 57–61, there were significant CAPs-induced alterations in cycling Ki67⁺/Olig2⁺ cell number and proportion of total cells in the female CC. Total CC cellularity was slightly elevated in CAPs-exposed males at PNDs 57–61. Overall, these data support a growing body of evidence that demonstrate the vulnerability of the developing brain to environmental insults such as ambient particulate matter. The sensitivity of oligodendrocytes and myelin, in particular, to such an insult warrants further investigation into the mechanistic underpinnings of OPC and myelin disruption by constituent air pollutants.

越来越多的研究表明，大脑是胎儿时期空气污染暴露的直接目标。我们之前已经证明，妊娠期间暴露于浓缩环境颗粒（ CAP）会导致小鼠出生后发育期间脑室扩大、脑室周围髓鞘形成过度以及胼胝体（CC）增大。这项研究旨在进一步表征观察到的髓鞘形成过度的细胞基础，并确定这种结果以及其他影响是否随着大脑成熟而持续存在。对出生后第 11-15 天 (PND) 中 CC 中的 CC-1 ⁺成熟少突胶质细胞的分析表明，在产前暴露于 CAP 的男性和女性中，总细胞的数量和比例发生过早成熟转变，但总 CC 细胞结构没有总体变化。在同一出生后时间点，CC 中 Olig2 ⁺谱系细胞的总数未受到任何性别的影响。对大脑早期成熟时髓鞘质状态的评估 (PNDs 57-61) 显示，暴露于 CAPs 的两性动物均存在持续性髓鞘过度增生。此外，接受 CAP 治疗的雌性脑室扩大持续存在，而接受 CAP 治疗的雄性脑室扩大可能得到改善。当在 PND 57-61 时分析少突胶质细胞前体细胞 (OPC) 库状态时，发现 CAP 诱导的雌性 CC 中循环 Ki67 ⁺ /Olig2 ⁺细胞数量和总细胞比例发生了显着变化。在 PND 57-61 时，暴露于 CAP 的雄性中总 CC 细胞结构略有升高。总体而言，这些数据支持了越来越多的证据，证明发育中的大脑容易受到周围颗粒物等环境侵害的影响。 尤其是少突胶质细胞和髓磷脂对这种损伤的敏感性，值得进一步研究空气污染物造成的 OPC 和髓磷脂破坏的机制基础。