Long-term air pollution exposure raises risk of dementia

Exposure to outdoor air pollutants such as fine particulate matter (PM_2.5) and nitrogen dioxide (NO₂), among others, for at least a year can put people at increased risk of dementia.

In a recent meta-analysis led by researchers from the University of Cambridge, Cambridge, UK, pooled data from 32 studies showed that the risk of dementia increased by 8 percent for every 5-μg/m³ of PM_2·5 (21 studies, n=24,030,527; adjusted hazard ratio (aHR), 1.08, 95 percent confidence interval [CI], 1.02–1.14; I²=95 percent) and by 3 percent for every 10-μg/m³ of NO₂ (16 studies, n=17,228,429; aHR, 1.03, 95 percent CI, 1.01–1.05; I²=84 percent). [Lancet Planet Health 2025;doi:10.1016/S2542-5196(25)00118-4]

Black carbon/PM_{2.5 absorbance} or soot was also associated with dementia, with each 1-μg/m³ raising the risk by 13 percent (six studies, n=19,421,865; aHR, 1.13, 95 percent CI, 1.01–1.27; I²=97 percent).

In subgroup analyses, the point estimates of effect size for PM_2.5, BC/PM_{2.5 absorbance}, and NO₂ were higher for vascular dementia than for Alzheimer’s disease, although the differences were not statistically significant. Similarly, numerically higher point estimates for PM_2.5 and NO₂ were seen in Europe than in North America, with the difference not reaching significance.

“These findings suggest that efforts to reduce exposure to these key pollutants are likely to help reduce the burden of dementia on society,” said Clare Rogowski who is the co-first author of the study with Dr Christiaan Bredell.

“Stricter limits for several pollutants are likely to be necessary targeting major contributors such as the transport and industry sectors. Given the extent of air pollution, there is an urgent need for regional, national, and international policy interventions to combat air pollution equitably,” Rogowski said.

Air pollution is thought to contribute to dementia development through various direct and indirect mechanisms, often involving neuroinflammation and oxidative stress. Early evidence for direct effects comes from studies in dogs living in highly polluted cities, wherein metals had been found to be accumulating from the olfactory mucosa to the frontal cortex, suggesting the olfactory nerve as a direct entry point for air pollution into the brain. Brain samples from these dogs revealed pathologies consistent with human Alzheimer’s disease. [Trends Neurosci 2009;32:506-516; Toxicol Pathol 2002;30:373-389]

“Future research should aim to better represent low-income and middle-income countries and include diverse populations spanning different racial and ethnic groups, levels of urbanization, and socioeconomic backgrounds. Such efforts would ultimately inform a truly global and equitable approach to reduce the burden of dementia, and yield long-term health, social, and economic benefits,” according to Rogowski, Bredell, and colleagues.

Of the 32 studies included in the meta-analysis, three had a probably high risk of bias in one of seven domains. All other studies had probably to definitely low risk of bias. The overall certainty of evidence was moderate.

The studies were conducted in countries across Europe, North America, Asia, and Oceania. The minimum age of participants was 55, 60, or 65 years, and the proportion of female participants ranged between 43 percent and 72 percent. An exposure duration of at least 1 year was classified as long term.