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Firefighting involves repeated exposure to combustion products, heat, physical exertion, and sleep disturbances. However, the long-term effects of such exposure on brain health and cognition remain unknown. This narrative review examined the neurotoxic burden associated with firefighting and explored how fireground exposures and stressors may link to neuroinflammation and neurodegenerative diseases. Primary epidemiological, in vivo, and in vitro evidence was synthesized; secondary and contextual literature was used for background. A narrative review with a systematic, PRISMA-informed search was performed. PubMed, ScienceDirect, Scopus, Cochrane Library, and EBSCOhost databases were searched for literature published between 1960 and June 2026. The search terms included combinations of firefighter exposure, fire smoke, particulate matter (PM), carbon monoxide (CO), hydrogen cyanide (HCN), polycyclic aromatic hydrocarbons (PAHs), neurotoxicity, neuroinflammation, cognitive outcomes, and neurodegenerative diseases. No meta-analysis or formal risk-of-bias assessment was performed. Firefighters are exposed to combustion products via inhalation and dermal contact. CO and HCN can cause hypoxia, leading to ATP depletion and acute neuropsychiatric effects. Fine PM and PAHs may reach the brain, activate glia through NLRP3, and promote ferroptosis and brain aging. Heat stress, fatigue, and sleep disruption may amplify these processes, contributing to cognitive decline and neurodegenerative disorders. Current evidence suggests potential neurological and neurocognitive effects associated with occupational firefighting exposure. However, the available firefighter literature is predominantly cross-sectional, and mechanistic evidence is substantially informed by experimental studies outside firefighter populations. Therefore, causal relationships between occupational exposure and neurodegeneration or brain aging remain uncertain.
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Kumar et al. (2026) studied this question.
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