Environmental Pollution, Biomarkers, and Dementia: An Evidence Review
TL;DR
Molecular evidence suggests that air pollution and environmental chemical pollutants may promote oxidative stress, neuroinflammation, metabolic dysfunction, Alzheimer’s disease pathology, and vascular damage, although evidence for epigenetic mechanisms remains more limited for environmental chemical pollutants.
Abstract
With rapid global urbanization, exposure to environmental pollutants has emerged as a potentially important determinant of cognitive health. We therefore systematically searched PubMed and Embase for epidemiological studies published between 2020 and 2026 and reviewed the associations between ambient air pollution, environmental chemical pollutants, and dementia. Evidence on potential biological mechanisms was identified to support the biological plausibility of the observed associations. Epidemiological evidence indicated that long-term exposure to particulate matter (PM2.5), nitrogen oxides (NO2), and black carbon was associated with increased dementia risk, whereas evidence for PM10 and ozone remained inconclusive. Plastic-associated chemicals, including phthalates and bisphenols, heavy metals (Lead-Pb and Cadmium-Cd), and per- and polyfluoroalkyl substances (PFOS), were linked with poorer cognitive function and dementia-related outcomes; findings for pesticides and herbicides were inconsistent. In terms of possible mechanisms, molecular evidence suggests that air pollution and environmental chemical pollutants may promote oxidative stress, neuroinflammation, metabolic dysfunction, Alzheimer’s disease pathology, and vascular damage, although evidence for epigenetic mechanisms remains more limited for environmental chemical pollutants. Overall, the evidence remains limited due to the predominance of observational studies. Future research that integrates molecular biomarkers and causal inference techniques is needed to better understand the role of environmental pollutants in dementia.