Gestational exposure to PM_2.5 is associated with adverse postnatal outcomes. PM_2.5 can enter alveoli by using intratracheal instillation, even penetrate through lung cells into the blood circulation. Subsequently, they are transferred across the placenta and fetal blood brain barrier, causing the adverse birth outcomes of offspring. This study demonstrated that the gestational exposure resulted in cognitive and emotional disorders in female offspring although the offspring were not exposed to PM_2.5. Placental metabolic pathways modulated fetal brain development and played a pivotal role for maternal-placental-fetal interactions in the fetal programming of adult behavioral and mental disorders. Samples of fetus, offspring hippocampus and placenta from the mice exposed to PM_2.5 were investigated using a comprehensive approach including mass spectrometry-based lipidomics and three-dimensional imaging. The exposure induced the neuro-degeneration in hippocampus, impairment of placental cytoarchitecture, and reprogramming of lipidome, which might affect the modulation of maternal-fetal cross-talk and result in the behavior disorders of offspring. The variation of spatial distribution of lipids was profoundly affected in dorsal pallium and hippocampal formation regions of fetal brain, offspring hippocampus, as well as labyrinth and junctional zones of placenta. The abundance alteration of lipid markers associated with neurodegenerative diseases was validated in transgenic mouse model with Alzheimer’s disease and human cerebrospinal fluid from patients with Parkinson’s disease. The finding could help with the selection of more suitable heterogeneous-related substructures targeting PM_2.5 exposure and the exploration of PM_2.5-induced toxicological effects on neurodegenerative diseases.

妊娠期暴露于 PM _2.5与不良的产后结局有关。PM _2.5可通过气管内滴注进入肺泡，甚至穿透肺细胞进入血液循环。随后，它们被转移穿过胎盘和胎儿血脑屏障，导致后代的不良出生结果。_{这项研究表明，尽管后代没有暴露于 PM 2.5}，但妊娠期暴露会导致女性后代出现认知和情绪障碍. 胎盘代谢途径调节胎儿大脑发育，并在成人行为和精神障碍的胎儿编程中对母体-胎盘-胎儿相互作用发挥关键作用。_{暴露于 PM 2.5}的小鼠的胎儿、后代海马体和胎盘样本使用包括基于质谱的脂质组学和三维成像在内的综合方法进行了研究。暴露导致海马神经退化、胎盘细胞结构受损和脂质组重编程，这可能影响母胎串扰的调节并导致后代行为障碍。脂质空间分布的变化在胎儿大脑的背侧大脑皮层和海马体形成区域、后代海马体以及胎盘的迷路和交界区受到深刻影响。与神经退行性疾病相关的脂质标志物的丰度变化在患有阿尔茨海默病的转基因小鼠模型和来自帕金森病患者的人脑脊液中得到验证。_2.5暴露和探索PM _2.5对神经退行性疾病的毒理作用。