March 6, 2024
People who live in areas with lots of vehicle traffic and who breath in pollutants from diesel exhaust and other sources have brain changes that are tied to an increased risk of Alzheimer’s disease. These findings, detailed in a recent study, add to growing evidence linking air pollution to brain decline.
For the new study, published in the journal Neurology, researchers at Emory University looked for signs of Alzheimer’s disease in the brains of 224 deceased men and women in the Atlanta area who had donated their brains to science. Their average age at death was 76.
The researchers also looked at the home addresses of the donors at the time of death, and determined traffic-related air pollution levels near their homes in the years preceding their deaths. They focused on levels of PM2.5, the tiny pollutant particles smaller than 2.5 micrometers in diameter that can be particularly damaging to health. This fine particulate matter can enter the bloodstream where high levels are linked to an increased risk of heart attacks, stroke, respiratory problems and lung disease. These tiny particles may also enter the brain, and a growing body of research has linked them to an increased risk of dementia.
The investigators found that those people who lived in areas with high levels of traffic-related air pollution had higher amounts of amyloid plaques in their brains. The presence of amyloid plaques, which are formed by the clumping together of toxic beta-amyloid in the brain, is a hallmark of Alzheimer’s disease. People with the highest exposure to fine particulate matter in the year before their death were nearly twice as likely to have higher levels of plaques, while those with higher exposure in the three years before death were 87 percent more likely to have higher levels of plaques.
Researchers also looked at whether study participants carried the APOE-E4 gene variant, which increases the risk of developing Alzheimer’s disease. They found that the strongest relationship between air pollution and signs of Alzheimer’s was among those without the gene variant.
“These results add to the evidence that fine particulate matter from traffic-related air pollution affects the amount of amyloid plaque in the brain,” said study author Anke Huels of the Emory University School of Public Health. The findings further suggest that “environmental factors such as air pollution could be a contributing factor to Alzheimer’s in patients in which the disease cannot be explained by genetics,” she said.
The study does not prove that air pollution causes more amyloid plaques in the brain. It only shows an association. But other studies indicate that air pollution may play a role in the onset of Alzheimer’s disease. Earlier studies have shown, for example, that women who live in areas with the worst quality air scored lower on tests of memory and thinking than those who lived in cleaner areas. Even over the course of a few weeks, breathing in air pollutants may lead to declines in memory and thinking skills. Other studies have shown that living in areas with heavily polluted air, whether from car emissions, power plants, factories or forest fires, can accelerate the onset of Alzheimer’s in people who may already be vulnerable to developing the disease.
Experts say that the best way to mitigate exposure to airborne pollutants is to limit time outdoors when air pollution concentrations are high and wearing a mask when appropriate. Other changes such as driving an electric vehicle or taking public transportation can contribute to reducing pollution levels. And government efforts to tighten air pollution exposure standards in the future may further help reduce the risk of Alzheimer’s disease.
By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by Eric Schmidt, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.
Source: Grace M. Christensen, PhD; Zhenjiang Li, PhD; Donghai Liang, PhD; et al: “Association of PM2.5 Exposure and Alzheimer Disease Pathology in Brain Bank Donors — Effect Modification by APOE Genotype.” Neurology, February 21, 2024
