Neurodevelopmental toxicity induced by PM2.5 Exposure and its possible role in Neurodegenerative and mental disorders

• Published in: Human & experimental toxicology Vol. 42; p. 9603271231191436
• Main Authors: Liu, Xin-qi, Huang, Jia, Song, Chao, Zhang, Tian-liang, Liu, Yong-ping, Yu, Li
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.01.2023; Sage Publications Ltd
• Subjects: Alzheimer's disease; Antibiotics; Autism; Bipolar disorder; Blood-brain barrier; Brain damage; Brain-derived neurotrophic factor; Central nervous system; Cyclic AMP response element-binding protein; Deoxyribonucleic acid; DNA; Dysbacteriosis; Epigenetics; Exposure; Flora; Inflammation; Intestinal microflora; Mental disorders; Microglia; Movement disorders; Neurodegenerative diseases; Neurodevelopmental disorders; Neurotoxicity; Olfactory system; Oxidative stress; Parkinson's disease; Particulate matter; Pathogenesis; Schizophrenia; Wnt protein; β-Catenin; neurodegenerative diseases; autism; PM2.5; mental disorders
• ISSN: 0960-3271; 1477-0903
• DOI: 10.1177/09603271231191436

Recent extensive evidence suggests that ambient fine particulate matter (PM2.5, with an aerodynamic diameter ≤2.5 μm) may be neurotoxic to the brain and cause central nervous system damage, contributing to neurodevelopmental disorders, such as autism spectrum disorders, neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, and mental disorders, such as schizophrenia, depression, and bipolar disorder. PM2.5 can enter the brain via various pathways, including the blood–brain barrier, olfactory system, and gut-brain axis, leading to adverse effects on the CNS. Studies in humans and animals have revealed that PM2.5-mediated mechanisms, including neuroinflammation, oxidative stress, systemic inflammation, and gut flora dysbiosis, play a crucial role in CNS damage. Additionally, PM2.5 exposure can induce epigenetic alterations, such as hypomethylation of DNA, which may contribute to the pathogenesis of some CNS damage. Through literature analysis, we suggest that promising therapeutic targets for alleviating PM2.5-induced neurological damage include inhibiting microglia overactivation, regulating gut microbiota with antibiotics, and targeting signaling pathways, such as PKA/CREB/BDNF and WNT/β-catenin. Additionally, several studies have observed an association between PM2.5 exposure and epigenetic changes in neuropsychiatric disorders. This review summarizes and discusses the association between PM2.5 exposure and CNS damage, including the possible mechanisms by which PM2.5 causes neurotoxicity.