Neurotoxic effects of airborne inhaled particulate matters
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Abstract
Cumulated epidemiological and experimental studies have demonstrated that exposure to airborne particulate matters (PM) contributes to induction of neuroinflammation, disruption of neurosynaptic physiology, reduced expression of neurotransmitters, and cerebrovascular damage, and is associated with the risk of neurodegenerative diseases including Alzheimer's and Parkinson's diseases. The review briefly described how inhaled PM are transported into the brain:through the nasal mucosa-olfactory nerve axon-olfactory bulb pathway or the systemic circulation-blood brain barrier (BBB) pathway. Human and animal studies have documented that that the particle size and chemical composition of transported PM contribute to neurotoxicity. Moreover, the mechanisms of PM affecting the central nervous system can be ascribed to increased neuroinflammation, BBB damage, and oxidative stress. Especially, microglia and astroglia have been identified as prominent sources of cytokines and reactive oxygen species to trigger neurodegenerative diseases in response to PM exposure. Therefore, future research is required to reveal the critical mechanism of PM uptake by nerve and underlying molecular mechanism of chemical components.
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