OAK BROOK, Ill. – In one of the largest studies to date, researchers examined the relationship between long-term air pollution exposure and coronary atherosclerosis and found that even at moderate levels, long-term exposure to air pollution is associated with more advanced coronary artery disease. The research was published today in Radiology , a journal of the Radiological Society of North America ( RSNA ).
Air pollution is the leading environmental risk factor for cardiovascular disease globally, contributing to roughly 2.5 million cardiovascular deaths each year. It is one of the greatest environmental risks to health and plays a major role in causing heart attacks and stroke, according to the World Health Organization.
"This is one of the largest studies to use cardiac CT to show that air pollution is linked to more advanced coronary artery disease—going beyond calcium scoring to include total plaque burden and obstructive disease—in a population with moderate exposure levels typical of high-income countries," said senior author Kate Hanneman, M.D., M.P.H., vice chair and associate professor at the University of Toronto, Department of Medical Imaging, and deputy lead of sustainability at the University Health Network's Joint Department of Medical Imaging at Toronto General Hospital.
Previous studies have shown that short-term air pollution exposure (hours to days) is associated with increased Emergency Department visits for ischemic heart disease, hospital admissions for heart failure and greater use of medical imaging. Exposure over the longer term (months to years) is linked to increased risks of myocardial infarction, stroke and cardiovascular mortality.
Dr. Hanneman's research team analyzed data from 11,128 adults who had undergone cardiac CT exams from 2012 through 2023 across three major hospitals in Toronto. They linked patients' residential postal codes with air quality data to estimate each person's average exposure to air pollution over the 10-year period prior to CT. Three markers of coronary artery disease were assessed: calcium score, total plaque burden and obstructive stenosis (artery narrowing).
The researchers evaluated the relationship between long-term exposures to two common pollutants found in urban air, ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2). PM2.5 sources include vehicle exhaust, industrial emissions and wildfire smoke. At about 30 times smaller than a human hair, these tiny particles can penetrate deep into the lungs and bloodstream. NO2 is a harmful gas produced mainly by burning fossil fuels in vehicles, power plants and industrial processes.
For each increase in long-term PM2.5 of 1 microgram per cubic meter, there was an 11% increase in calcium build-up in the coronary arteries, 13% greater odds of more plaque and 23% greater odds of obstructive disease. Exposure to nitrogen dioxide showed similar trends, though with smaller effect sizes for every 1 part-per-billion increase.
"Medical imaging is emerging as a powerful tool for environmental health research," Dr. Hanneman said. "By directly visualizing coronary atherosclerosis, cardiac CT allows us to detect and quantify the cardiovascular effects of long-term air pollution exposure in ways that go beyond traditional risk factors."
The findings show that even levels of air pollution below or near regulatory standards and typical urban exposures are associated with early signs of heart disease—often before symptoms appear—and underscore the importance of improving air quality to reduce cardiovascular disease risk.
For individual patients, the findings may open the door to incorporating environmental exposure history into cardiovascular risk assessment, like clinicians would ask about smoking and family history.
"Even at exposure levels below current Canadian air quality standards, long-term air pollution was independently associated with more advanced coronary artery disease—suggesting current regulations may not be fully protective and that air pollution belongs alongside blood pressure, cholesterol and smoking as a modifiable cardiovascular risk factor," Dr. Hanneman said.
Dr. Hanneman notes that what makes this particularly important is the exposure context. The median 10-year PM2.5 exposure in the study group was well below the current Canadian Ambient Air Quality Standard.
"The fact that we can detect a measurable signal in coronary atherosclerosis at these levels suggests there may be no clear, safe threshold for cardiovascular harm from air pollution, and that even populations in countries with relatively clean air face meaningful cardiovascular risk from environmental exposure," she said.
The research also points out the need for prevention. Reducing air pollution exposure through policy, urban planning and personal decisions is itself a cardiovascular intervention, Dr. Hanneman added.
"It is also worth noting the connection between air pollution and climate change," she said. "Because fossil fuel combustion drives both air pollution and greenhouse gas emissions, policies that improve air quality can deliver simultaneous benefits for cardiovascular health and the planet."
This research received an RSNA Research and Education (R&E) Foundation Emerging Issues Grant.
