PM2.5 induced neurotoxicity and depression unveiling exposure risks and mechanistic insights.

Fine particulate matter PM2.5 is increasingly linked to neuropsychiatric burden beyond its established cardiopulmonary effects. This narrative review integrates epidemiological, animal, and mechanistic evidence connecting PM2.5 exposure with depression and depression-related phenotypes. Human studies across different populations generally associate long-term PM2.5 exposure with elevated depression risk or symptom severity, with vulnerable windows including prenatal development and late life. Animal studies support biological plausibility by showing depression-like behaviors, electrophysiological changes, and neural injury after PM2.5 exposure. Component-focused evidence implicates metals, black carbon, organic compounds, and other constituents in oxidative stress, neuroinflammation, blood-brain barrier disruption, synaptic dysfunction, HPA axis dysregulation, neurotransmitter imbalance, and alterations in the kynurenine pathway. These findings support PM2.5 as a potential environmental risk factor for depression and highlight the need for component-resolved exposure assessment and mechanism-guided prevention strategies.