/knowledge-vault:ingest Air pollution is increasingly recognized as a major environmental risk factor for neurodegenerative disease. Epidemiological studies spanning multiple continents have demonstrated consistent associations between long-term exposure to ambient particulate matter, particularly PM2.5, and increased risk of dementia and cognitive decline. The biological mechanisms underlying these associations involve multiple pathways including neuroinflammation, oxidative stress, blood-brain barrier disruption, and cerebrovascular damage. Animal models have shown that inhaled ultrafine particles can translocate directly to the brain via the olfactory nerve, triggering microglial activation and neuronal damage. Human neuroimaging studies have documented associations between PM2.5 exposure and reduced hippocampal volume, white matter hyperintensities, and accelerated brain aging. The dose-response relationship appears to extend below current regulatory thresholds, suggesting no safe level of exposure. Vulnerable populations include the elderly, individuals with genetic predisposition such as APOE4 carriers, and those with pre-existing cardiovascular conditions. The 2020 Lancet Commission on dementia prevention formally recognized air pollution as one of twelve modifiable risk factors, attributing a 2% population attributable fraction to this exposure. Traffic-related air pollution, which includes a complex mixture of particulate matter, nitrogen dioxide, and volatile organic compounds, has shown particularly strong associations with cognitive outcomes in studies using land-use regression models for exposure assessment. Recent cohort studies have begun to explore mediation pathways, with evidence suggesting that hypertension and cerebrovascular disease partially mediate the relationship between air pollution exposure and incident dementia. Policy interventions targeting air quality standards could potentially reduce the global burden of dementia, though the latency period between exposure reduction and cognitive benefit remains uncertain. Future research priorities include improved exposure characterization using personal monitoring devices, investigation of critical exposure windows across the life course, and identification of gene-environment interactions that modify susceptibility to pollution-related neurodegeneration. The convergence of evidence from epidemiology, toxicology, and neuroimaging provides a compelling case for urgent public health action to reduce ambient air pollution levels worldwide as part of a comprehensive dementia prevention strategy that addresses all modifiable risk factors throughout the life course including education in early life, hearing loss and traumatic brain injury in midlife, and smoking, depression, physical inactivity, social isolation, diabetes, excessive alcohol consumption, and air pollution in later life.