Sitting in traffic every day ups the risk of Alzheimer’s

There's a link between exposure to traffic pollution and brain-gumming amyloid plaques.

There's a link between exposure to traffic pollution and brain-gumming amyloid plaques. Photo: Getty

Traffic pollution impairs human brain function in just a few hours, we reported last year.

Participants were exposed for a short time to diesel exhaust in a controlled experiment.

Disruptions to the ability of different areas of the brain to communicate with each other were watched by scientists in real time. This was a first-time discovery.

Notably, the changes in the brain were temporary and participants’ connectivity returned to normal after the exposure. (Read our full report here.)

Now, new research shows repeated exposure to traffic exhaust has a longer, potentially devastating outcome.

Higher rates of amyloid plaques

In a new study, Emory University researchers found a link between traffic pollution and Alzheimer’s.

Namely, people with higher exposure to traffic pollution were more likely to have high amounts of amyloid plaques in their brains after death.

Amyloid plaques are misfolded proteins that form in the spaces between nerve cells. They’re thought to play a central role in Alzheimer’s disease. They first develop in the areas of the brain concerned with memory and other cognitive functions.

The new study

The American Academy of Neurology stated the researchers examined the brain tissue of 224 people who agreed to donate their brains at death to advance research on dementia. They had died at an average age of 76.

Researchers looked at the exposure to traffic-related air pollution based on their home address in the Atlanta area at the time of death.

Specifically, they looked at fine particulate matter, PM2.5. These consist of pollutant particles of less than 2.5 microns in diameter suspended in air.

These are a major source of ambient pollution in urban areas where most donors lived.

The average level of exposure in the year before death, and in the three years before death, were calculated.

Researchers then compared these pollution exposures to the signs of Alzheimer’s disease in the brain. That is, the amount of amyloid plaques and tau tangles.

People with higher PM2.5 exposure in the year before death were nearly twice as likely to have higher levels of plaques.

Those with higher exposure in the three years before death were 87 per cent more likely to have higher levels of plaques.

The gene variant

Researchers also looked at “whether having the main gene variant associated with Alzheimer’s disease, APOE e4, had any effect on the relationship between air pollution and signs of Alzheimer’s in the brain”.

They found that “the strongest relationship between air pollution and signs of Alzheimer’s was among those without the gene variant”.

This was significant. It suggests 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”.

Caveats and previous research

The study does not prove that air pollution causes more amyloid plaques in the brain. It only shows an association.

“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, PhD, of Emory University in Atlanta.

“More research is needed to investigate the mechanisms behind this link.”

A limitation of the study is that researchers only had the home address of people at the time of their death for measuring air pollution, so it’s possible that pollution exposure may have been misclassified.

However, a 2023 study from the University of British Columbia and University of Victoria, found that higher levels of PM2.5 air pollution are linked to a higher number of dementia cases developing over time.

The Canadian researchers said their study was the first of its kind in the world. They said it “provides fresh evidence supporting a connection between air pollution and cognition”.

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