Neurotoxicity of the air-borne particles: From molecular events to human diseases

Exposure to PM2.5 is associated with an increased incidence of CNS diseases in humans, as confirmed by numerous epidemiological studies. Animal models have demonstrated that PM2.5 exposure can damage brain tissue, neurodevelopmental issues and neurodegenerative diseases. Both animal and human cell models have identified oxidative stress and inflammation as the primary toxic effects of PM2.5 exposure. However, under-standing how PM2.5 modulates neurotoxicity has proven challenging due to its complex and variable composi-tion. This review aims to summarize the detrimental effects of inhaled PM2.5 on the CNS and the limited understanding of its underlying mechanism. It also highlights new frontiers in addressing these issues, such as modern laboratory and computational techniques and chemical reductionism tactics. By utilizing these approaches, we aim to fully elucidate the mechanism of PM2.5-induced neurotoxicity, treat associated diseases, and ultimately eliminate pollution.

Automated summary

Exposure to PM2.5 is linked to increased incidence of CNS diseases in humans, shown by multiple epidemiological studies. Animal models confirm that PM2.5 exposure can harm brain tissue and contribute to neurodevelopmental and neurodegenerative diseases. Both animal and human cell models indicate that oxidative stress and inflammation are the main toxic effects of PM2.5 exposure. However, understanding how PM2.5 affects neurotoxicity is challenging due to its complex and variable composition.