Even the relatively clean air typical of North American cities may damage heart arteries, especially in women.
Long-term exposure to common air pollutants from automobiles, industrial activity and fossil fuel burning is linked to advanced coronary artery disease, even at levels near or below current regulatory safety limits, researchers report in the June 2026 Radiology. Adjusting for things like high blood pressure and cholesterol weakened the association, suggesting pollution may partly work by worsening these established risk factors.
The study cannot show that air pollution causes heart disease, but adds weight to growing evidence linking the two, says cardiac surgeon Salil Deo, who was not involved in the work. “There may be no ‘floor’ at which air quality can be considered entirely safe for the human heart,” says Deo, of Case Western Reserve University School of Medicine in Cleveland.
Coronary artery disease develops when calcium deposits and plaque buildup narrow the heart’s arteries, raising the risk of heart attack. Earlier studies have associated air pollution with heart attacks and strokes, and experts estimate air pollution contributes to 4 million to 6 million of the 20 million cardiovascular deaths worldwide each year.
Instead of focusing on events like heart attacks, the new study uses heart scans to show how long-term exposure is linked to the buildup and progression of coronary artery disease, says Kate Hanneman, a cardiac radiologist at the University of Toronto.
Hanneman and colleagues tracked more than 11,000 adults in Toronto and surrounding areas who underwent heart scans from 2012 to 2023. To estimate long-term pollutant exposure, they linked each participant’s residential history to air quality data from the previous decade.
The team focused on fine particulate matter and nitrogen dioxide, or NO2. Fine particulate matter refers to tiny airborne particles small enough to be inhaled deep into the lungs, while NO2 is a gas produced mainly by vehicle traffic and fossil fuel combustion. Both can contribute to inflammation that affects the heart and blood vessels. Most participants were exposed to air pollution levels below Canada’s annual air quality standards and within levels commonly seen across North American and European cities.
The higher the exposure to fine particulate air pollution, the more signs of heart artery disease the researchers could observe on scans. As exposure increased, calcium buildup in the heart arteries was higher and plaque was more common. What’s more, the odds of serious artery narrowing were greater, especially in women. The scans showed similar, but smaller, effects for NO2.
“There was no level at which the risk clearly flattened or disappeared,” Hanneman says.
In men, the association between severe artery narrowing and higher pollutant exposure was not statistically significant, though both sexes showed more calcium and plaque as pollution increased.
“The pattern is consistent with earlier research,” Hanneman says. “It may reflect biological differences, such as breathing rates relative to body size, hormone-related inflammatory responses and higher levels of noncalcified, harder-to-detect plaque in women.”
The findings don’t mean changing daily routines for most people. But during heavy pollution episodes, such as wildfire smoke, people at higher risk of coronary artery disease, including those with heart disease, diabetes or advanced age, may benefit from staying indoors, using air filtration or wearing an N95 mask outdoors, Deo says.
“Reducing long-term exposure and moving toward stricter air quality standards could meaningfully protect cardiovascular health,” Hanneman says. “It’s an intervention that benefits both public health and the planet.”
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