Air pollution is a major environmental factor contributing to neuroinflammation and central nervous system (CNS) diseases. It induces chronic inflammation, oxidative stress, and neuropathology, linking it to conditions such as stroke, Alzheimer's disease, and Parkinson's disease. Air pollution components, including particulate matter (PM) and ground-level ozone, can reach the brain through various pathways, including systemic inflammation, translocation of nanoparticles via the olfactory pathway, and direct entry through the blood-brain barrier. PM, especially PM2.5 and ultrafine particles (UFPM), are particularly harmful, causing damage to the brain and contributing to neurodegenerative diseases. Microglia, astrocytes, and brain capillaries are key players in the inflammatory response to air pollution, leading to chronic inflammation, oxidative stress, and neurotoxicity. Air pollution also disrupts the blood-brain barrier, increasing the entry of harmful substances into the CNS. The mechanisms of air pollution-induced CNS damage involve systemic inflammation, particle effects, adsorbed compounds, and ozone-induced oxidative stress. These processes contribute to neuroinflammation, neuronal damage, and the accumulation of pathological proteins such as amyloid-beta and alpha-synuclein. The study highlights the need for further research into the mechanisms and epidemiological links between air pollution and CNS diseases, emphasizing the importance of addressing this environmental toxin to mitigate its impact on human health.Air pollution is a major environmental factor contributing to neuroinflammation and central nervous system (CNS) diseases. It induces chronic inflammation, oxidative stress, and neuropathology, linking it to conditions such as stroke, Alzheimer's disease, and Parkinson's disease. Air pollution components, including particulate matter (PM) and ground-level ozone, can reach the brain through various pathways, including systemic inflammation, translocation of nanoparticles via the olfactory pathway, and direct entry through the blood-brain barrier. PM, especially PM2.5 and ultrafine particles (UFPM), are particularly harmful, causing damage to the brain and contributing to neurodegenerative diseases. Microglia, astrocytes, and brain capillaries are key players in the inflammatory response to air pollution, leading to chronic inflammation, oxidative stress, and neurotoxicity. Air pollution also disrupts the blood-brain barrier, increasing the entry of harmful substances into the CNS. The mechanisms of air pollution-induced CNS damage involve systemic inflammation, particle effects, adsorbed compounds, and ozone-induced oxidative stress. These processes contribute to neuroinflammation, neuronal damage, and the accumulation of pathological proteins such as amyloid-beta and alpha-synuclein. The study highlights the need for further research into the mechanisms and epidemiological links between air pollution and CNS diseases, emphasizing the importance of addressing this environmental toxin to mitigate its impact on human health.