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Neuroinflammation is the brain's immune response to injury or disease and can negatively impact neurological functions, ranging from mood, cognition, learning and memory, as well as promote neurodegenerative disease and even psychiatric conditions. Different environmental factors may trigger a neuroinflammatory response; the mechanisms of this activation may influence the pattern of activation, the immune subsets involved, and the persistence of the response. The duration of neuroinflammation may significantly outlast exposures, creating a potential unique vulnerability for rare or intermittent exposures. The neuroinflammatory response can be classified into acute, sub-acute and chronic phases, with sub-acute neuroinflammation representing a transient state between acute and chronic inflammation. This phase, lasting from days to weeks, is denoted by metabolic disruptions, cognitive impairments, and peripheral immune activation. Environmental exposures such as such as air pollution, pesticides, heavy metals, and social factors impact oxidative stress, glial activation, and blood-brain barrier disruption leading to neuronal injury and cognitive decline. Notably, exposures like diesel fumes and wildfire smoke have been shown to induce neuroinflammation, subsequently impacting memory and learning, and exacerbating mental health conditions such as PTSD, depression and anxiety. Triggering of reactive astrogliosis via impacts on the blood-brain barrier function may be the most common non-specific manner that environmental toxicants drive neuroinflammation, but direct outcomes from compounds that readily access the brain are also possible.