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The Lancet Planetary Health has published a systematic review and meta-analysis of studies examining the association between air pollution and incident dementia. This review was intended to summarize all previous reviews, identify specific gaps in data, and incorporate new primary research. It included data from 32 studies and a pooled population of over 26 million people, evaluating the effect of long-term exposure (defined as one or more years) to single outdoor air pollutants on a subsequent diagnosis of dementia. It is considered the largest meta-analysis to examine this association, and includes pollutants that have not previously been considered in meta-analyses. These included studies were conducted in North America, Europe, Asia, and Australia, and meta-analyses were performed for each type of pollution when 3 or more independent studies reported an “exposure-outcome pair.”
Of all the pollutants studied, three were associated with dementia risk. One of the most commonly monitored components of air pollution, fine particulate matter (PM2.5), was evaluated in 21 studies and a pooled population of over 24 million people. Each 5 μg/m3 increase in exposure to PM2.5 was associated with an 8% higher risk for developing dementia. For nitrogen dioxide, each 10 μg/m3 increase was associated with a 3% higher risk, while for black carbon/PM2·5 absorbance every 1 μg/m3 was linked to a 13% higher risk, all significant findings. Pollutants that were not significantly associated with dementia risk included nitrogen oxides, PM10, and annual ozone. Overall certainty was rated as moderate for the included studies, with a low risk of bias.
This association between air pollution and dementia risk appears to be well-supported by plausible mechanisms. For example, air pollution may induce oxidative stress and increase neuroinflammation, and both pathways have been linked to the development of dementia. For example, in a 2025 review published in Nature Reviews Immunology, although no mention is made of the potential role of air pollution in Alzheimer’s dementia, the authors present a strong case for an inflammatory hypothesis. This includes data from genome-wide association studies (GWAS), and while 56 to 79% of Alzheimer’s risk can be attributed to inheritable genetic factors (an estimate derived from twin studies), the genes involved clearly point to immune and inflammatory pathways. The authors also consider that the many dietary and lifestyle factors that influence dementia risk, such as a Mediterranean diet, physical activity, and the gut microbiome, may modulate risk by their influence on neuroinflammation.
Another contributor to neuroinflammation is damage from reactive oxygen species (ROS), which may also contribute to neurodegeneration, as reviewed in Antioxidants. ROS can damage lipids, proteins, and DNA, and also induce epigenetic changes. The role of ROS in both Alzheimer’s disease and Parkinson’s disease is well established, occurring partly because the brain is very metabolically active, and is a low antioxidant and lipid-rich environment. Both Aβ formation and aggregation, as well as α-synuclein formation, are thought to be driven in part by ROS, with an imbalance between oxidative stress and antioxidant defenses playing a key role in neurodegeneration.
Results of a nationwide study in the U.S. published in 2023 also point to the long-term damage resulting from air pollution. PM2.5 exposure was associated with both heightened risk for Alzheimer’s disease as well as all-cause dementia, with fairly linear increases in risk at low-level exposure, suggesting that there is no safe level of exposure to these toxins. Individual components of PM2.5 also influence risk, such as black carbon (PM2.5 refers to the size of the particulates, not the individual toxicant, and can include hundreds of different types of toxins).
In 2024, Frontiers in Neuroscience published an analysis of forensic autopsies that occurred in Metropolitan Mexico City. This study (and others) concluded that the neuropathology that underlies many neurodegenerative diseases, including Alzheimer’s dementia, frontotemporal lobar degeneration, and amyotrophic lateral sclerosis is present within the first two decades of life, and that exposure to PM2.5, combustion and friction ultrafine PM (UFPM), and industrial nanoparticles are prime candidates for driving disease development. A small study conducted among adolescents in Detroit found PM2.5 exposure was associated with a variety of inflammatory markers (PGE2, 12(S)-HETE, 12(S)-HEPE, and 15(S)-HETE) as well as several types of anxiety (with some differences between the sexes). Multiple studies have also demonstrated a link between air pollution and brain development in children, so it is also a possibility that air pollution not only is a risk factor for dementia development in older adults but may initiate or amplify changes in the brain that take place much earlier in life.
Aside from filtration and pollution control measures, it’s difficult to reduce the exposure to the air we breathe. A systematic review of clinical trials published in PLoS One suggests that antioxidant supplementation may offer some benefits. For example, this review suggested that fish and olive oils may mitigate some of the cardiovascular harm associated with air pollution, via both antioxidant and anti-inflammatory mechanisms. Vitamins C and E had mixed results, with suggestive benefit for pulmonary function but lacking benefit for vitamin C (used alone) to prevent an increase in blood pressure caused by air pollution. A number of other polyphenols and antioxidants have been proposed to mitigate this harm, as well as botanicals like Melissa officinalis, but most lack controlled trials. Given the years-long deterioration leading to dementia, adequate long-term controlled trials are difficult to conduct.
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