AMBIENT air pollution, particularly fine particulate matter (PM2.5), has long been associated with cardiovascular disease, yet the specific pathways linking exposure to heart damage remain insufficiently understood. A new retrospective study sought to explore this relationship by evaluating the extent of diffuse myocardial fibrosis in individuals exposed to varying levels of PM2.5. The analysis, conducted using cardiac MRI native T1 mapping, included both patients diagnosed with dilated cardiomyopathy (DCM) and healthy controls. A key finding was that higher long-term exposure to PM2.5 was significantly associated with increased markers of myocardial fibrosis, even in individuals without overt heart disease.
The study assessed 694 individuals who underwent cardiac MRI between 2018 and 2022 at a single UK centre. This cohort included 493 patients with DCM and 201 control participants with normal imaging. Myocardial fibrosis was quantified using native T1 mapping z scores, adjusted for scanner strength (1.5T or 3T). Ambient PM2.5 exposure was estimated using daily concentration data from the monitoring station nearest to each participant’s residence, averaged over the year prior to imaging. The models were adjusted for known cardiovascular risk factors to isolate the effect of air pollution.
Results demonstrated that for every 1 µg/m³ increase in annual PM2.5 exposure, native T1 z scores increased by 0.30 in DCM patients (95% CI: 0.13–0.47; p<0.001) and by 0.27 in controls (95% CI: 0.04–0.51; p=0.02). When considering scanner-specific native T1 times, this equated to increases of 9.1 ms at 1.5T (P=0.01) and 12.1 ms at 3T (p<0.001). Subgroup analyses revealed that the strongest associations were observed in women (β=0.49), smokers (β=0.43), and individuals with hypertension (β=0.48), suggesting a potential vulnerability in these populations.
These findings underscore the potential of fine particulate pollution to contribute to myocardial fibrosis even in individuals without diagnosed heart disease. While the retrospective and observational design limits causal inference, and single-centre data may restrict generalisability, the consistency of results across subgroups highlights a clinically important risk factor. Clinicians should consider environmental exposure as part of holistic cardiovascular risk assessment, especially in vulnerable patient groups.
Reference
Du Plessis J et al. Association between Long-term Exposure to Ambient Air Pollution and Myocardial Fibrosis Assessed with Cardiac MRI. Radiology. 2025;316(1):e250331.
