A groundbreaking study published today in Radiology, the journal of the Radiological Society of North America (RSNA), has revealed that prolonged exposure to air pollution is linked to early signs of heart damage. Using advanced cardiac magnetic resonance imaging (MRI), researchers were able to detect increased levels of diffuse myocardial fibrosis—a subtle yet profound form of scarring in the heart muscle. This type of tissue damage is an early warning sign. It is associated with an increased risk of heart failure over time, even in individuals who do not yet show symptoms of cardiovascular disease.
Cardiovascular disease continues to be the foremost cause of death worldwide, and while numerous studies have demonstrated a correlation between poor air quality and heart-related illnesses, the exact mechanisms by which pollution affects heart tissue have mainly remained speculative. This new research adds an essential piece to the puzzle by using state-of-the-art imaging technology to visualise and quantify structural changes in the heart that may develop silently over years of exposure to air pollution.
Lead investigator Dr Kate Hanneman, from the Department of Medical Imaging at the Temerty Faculty of Medicine, University of Toronto, and the University Health Network, explained the motivation behind the study: “We know that people exposed to higher levels of air pollution are at greater risk of developing cardiovascular conditions, including myocardial infarction. What we wanted to understand was the biological mechanism behind this increased risk—what exactly is happening inside the heart tissue.” Her team utilised non-invasive MRI to precisely assess myocardial fibrosis and its association with a specific type of air pollutant, known as PM2.5.
PM2.5 refers to delicate particulate matter that measures 2.5 micrometres in diameter or less—roughly 30 times smaller than the width of a human hair. Due to their minuscule size, these particles can bypass the body’s natural defences in the respiratory tract and penetrate deep into the lungs, eventually entering the bloodstream. Familiar sources of PM2.5 include vehicle emissions, industrial output, and wildfire smoke. Long-term exposure to these particles has been associated with systemic inflammation and vascular dysfunction, but their specific role in heart tissue scarring had not been clearly defined until now.
The study population consisted of a total of 694 participants, divided into 201 healthy individuals and 493 patients diagnosed with dilated cardiomyopathy—a condition in which the heart becomes weakened and enlarged, thereby impairing its ability to pump blood effectively. This diverse sample allowed researchers to observe the effects of air pollution in both individuals with existing heart conditions and those without. Notably, the results revealed that prolonged exposure to PM2.5 was associated with higher levels of myocardial fibrosis in both groups. This suggests that fine particulate air pollution may contribute to a standard underlying pathological process regardless of baseline heart health.
Notably, the most pronounced effects were observed in women, smokers, and individuals with hypertension—groups already known to be at heightened risk of cardiovascular complications. These findings underscore the complex interplay between environmental exposures and individual susceptibility. According to Dr Hanneman, “Even modest increases in air pollution levels appear to have measurable effects on the heart. Our study suggests that environmental air quality may influence heart structure and function more significantly than previously understood.”
In addition to clarifying the biological impact of air pollution on cardiac tissue, the study also raises important implications for clinical practice and public health policy. Incorporating a patient’s history of air pollution exposure into cardiovascular risk assessments could help identify those at greater risk and ensure earlier intervention. For instance, individuals who live or work in areas with poor air quality—such as urban centres or industrial zones—may benefit from more frequent cardiovascular screening or targeted prevention strategies.
Perhaps most concerning is the fact that the levels of air pollution associated with myocardial fibrosis in the study were below many internationally accepted safety thresholds. This finding reinforces the growing consensus that there may be no truly safe level of exposure to air pollution. “Public health measures are urgently needed to further reduce air pollution, even in regions where air quality has improved in recent years,” Dr Hanneman stated. Moreover, the study highlights the expanding role of radiologists in environmental health, showing how advanced imaging can serve as a powerful tool to uncover the hidden impacts of environmental exposures on the human body.
More information: Kate Hanneman et al, Association between Long-term Exposure to Ambient Air Pollution and Myocardial Fibrosis Assessed with Cardiac MRI, Radiology. DOI: 10.1148/radiol.250331
Journal information: Radiology Provided by Radiological Society of North America
