Mice were exposed to ambient PM particles 8 h per day, 6 days per week, for twenty-four weeks in enrichment chambers, with real-time mass concentration of PM_2.5 around 70 µg/m³, and the number of PM_0.1 about 10,000-20,000/m³. The component analysis of PM particles by inductive coupled plasma emission spectrometer detected low concentrations of species associated with crustal materials, metalloid, transition metals, and heavy metals originating from industrial emission. High-performance liquid chromatography (HPLC) detected 22 polycyclic aromatic hydrocarbons originating from traffic exhausts. We found that PM particles from dirty air entered mouse brain which were visualized by field emission scanning electron microscopy (FE-SEM) and were counted by femtosecond pulsed laser illumination microscopy. FE-SEM of brain tissues from dirty air (n=8), and filtered air (control) (n=8) revealed ultrastructural hallmarks of neuroinflammation, enlarged perivascular space, and the attachment of inflammatory cells to the endothelium of blood vessels in brain. Exposure to dirty air containing ambient PM particles resulted in amyloid deposits and formation of neurofibrillary tangles and plaques. Desorption electrospray ionization mass spectrometry imaging enabled label-free elucidation of the spatial distribution of metabolites and lipids in brain tissue samples without any pretreatment. Ceramide Cer(t18:0/34:0(34OH)), m/z 822.54, and sulfatides, ST18:0, m/z 806.54; ST(d18:1/h22:0), m/z 878.60; ST(24:1), m/z 888.62, and ST(d18:1/h24:0), m/z 906.62 showed upregulation with significant differences in brain tissue from mice exposed to dirty air as compared to filtered air (control). The upregulation of ceramide resulted in formation of neurofibrillary tangles and plaques. Moreover, upregulation of sulfatides might enhance the leakiness of the blood brain barrier by weakening myelin sheaths. Although limited by sample number, our results strongly suggest that prolonged exposure to dirty air contributes to the observed increase in the incidence of cognitive decline and dementia, such as Alzheimer's disease.

将小鼠每天8小时，每周6天，每天8h在浓缩室中暴露于周围的PM颗粒中，持续24周，其中PM _2.5的实时质量浓度约为70 µg / m ³，PM _0.1的数量约为10,000 -20,000 /米³。通过电感耦合等离子体发射光谱仪对PM颗粒进行成分分析，发现与工业产生的地壳材料，准金属，过渡金属和重金属有关的低浓度物种。高效液相色谱（HPLC）检测到22种源自交通尾气的多环芳烃。我们发现，来自脏空气的PM颗粒进入小鼠大脑，并通过场发射扫描电子显微镜（FE-SEM）进行了可视化，并通过飞秒脉冲激光照明显微镜进行了计数。脏空气（n = 8）和过滤空气（对照）（n = 8）对脑组织的FE-SEM显示出神经炎症的超微结构特征，扩大的血管周围空间以及炎症细胞附着于脑血管内皮。暴露于含有环境PM颗粒的脏空气中会导致淀粉样蛋白沉积并形成神经原纤维缠结和斑块。解吸电喷雾电离质谱成像无需任何预处理，即可无标记地阐明脑组织样品中代谢物和脂质的空间分布。神经酰胺Cer（t18：0/34：0（34OH）），m / z 822.54，和硫化物，ST18：0，m / z 806.54；ST（d18：1 / h22：0），m / z 878.60；ST（24：1），m / z 888.62和ST（d18：1 / h24：0），m / z 906.62显示了上调，与过滤空气相比，暴露于脏空气的小鼠的脑组织有显着差异。神经酰胺的上调导致神经原纤维缠结和斑块的形成。此外，硫化物的上调可能通过削弱髓鞘而增强血脑屏障的泄漏。尽管受样本数量的限制，但我们的结果强烈表明，长时间暴露在肮脏的空气中会导致观察到的认知能力下降和痴呆症（例如阿尔茨海默氏病）的发生率增加。