Fine particulate matter (PM2.5) pollution remains a prominent environmental problem worldwide, posing great threats to human health. The adverse effects of PM2.5 on the respiratory and cardiovascular systems have been extensively studied, while its detrimental effects on the central nervous system (CNS), specifically neurodegenerative disorders, are less investigated. Neurodegenerative disorders are characterized by reduced neurogenesis, activated microglia, and neuroinflammation. A variety of studies involving postmortem examinations, epidemiological investigations, animal experiments, and in vitro cell models have shown that PM2.5 exposure results in neuroinflammation, oxidative stress, mitochondrial dysfunction, neuronal apoptosis, and ultimately neurodegenerative disorders, which are strongly associated with the activation of microglia. Microglia are the major innate immune cells of the brain, surveilling and maintaining the homeostasis of CNS. Upon activation by environmental and endogenous insults, such as PM exposure, microglia can enter an overactivated state that is featured by amoeboid morphology, the over-production of reactive oxygen species, and pro-inflammatory mediators. This review summarizes the evidence of microglial activation and oxidative stress and neurodegenerative disorders following PM2.5 exposure. Moreover, the possible mechanisms underlying PM2.5-induced microglial activation and neurodegenerative disorders are discussed. This knowledge provides certain clues for the development of therapies that may slow or halt the progression of neurodegenerative disorders induced by ambient PM.

Exposure to fine particulate matter (PM 2.5 ) is associated with various adverse health effects, such as respiratory and cardiovascular diseases. This study aimed to evaluate the association of PM 2.5 with neural damage biomarkers. A total of 34 healthy retirees were recruited from Xinxiang Medical University from December 2018 to April 2019. Concentrations of PM 2.5 constituents including 24 metals and nonmetallic elements and 6 ions, and 5 biomarkers of neural damage including brainderived neurotrophic factor (BDNF), neurofilament light chain (NfL), neuronspecific enolase (NSE), protein gene product 9.5 (PGP9.5), and S100 calciumbinding protein B (S100B) in serum were measured. A linear mixed-effect model was employed to estimate the association of PM 2.5 and its constituents with neural damage biomarkers. Modification effects of glutathione S-transferase theta 1 gene (GSTT1) polymorphism, sex, education, and physical activity on PM 2.5 exposure with neural damage were explored. PM 2.5 and its key constituents were significantly associated with neural damage biomarkers. A 10 μg/m 3 increase in PM 2.5 concentration was associated with 2.

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