Air Pollution and Cardiac Remodeling and Function in Patients With Breast Cancer

The relationship between air pollution and cardiac remodeling in patients with cancer treated with cardiotoxic therapy is undefined.

To assess the associations between air pollutants and changes in cardiac function, structure, and remodeling in patients with breast cancer treated with anthracyclines and/or trastuzumab therapy.

This longitudinal prospective cohort study included patients with breast cancer enrolled at multiple sites of a quaternary health care system from July 1, 2010, to November 1, 2018. All participants were initiating anthracyclines and/or trastuzumab. Data were analyzed from December 1, 2024, to April 30, 2025.

Three-year average census tract-level concentrations of fine particulate matter with diameter of 2.5 µm or less (PM2.5), particulate matter with diameter of 10 µm or less (PM10), nitrogen dioxide (NO2), and ozone (O3).

Core laboratory-quantified, echocardiography-derived measures of cardiac remodeling and function and incidence of cardiac dysfunction, defined as a left ventricular ejection fraction (LVEF) decline of 10% or more from baseline to less than 50%. Multivariable linear regression and generalized estimating equations defined the cross-sectional and longitudinal associations between air pollution and measures of cardiac remodeling and function. Cause-specific hazard models defined the adjusted associations between air pollution and cardiac dysfunction.

Across 580 female patients (median age, 50 years [IQR, 42-58 years]), 3642 echocardiograms were obtained at standardized time intervals over a median of 3.1 years (IQR, 2.3-3.6 years) and centrally quantified. Cardiac dysfunction was observed in 98 of 574 participants (17.1%). Concentrations of PM2.5 (median, 9.26 μg/m3 [IQR, 8.49-10.17 μg/m3]) and O3 (median, 47.00 parts per billion [ppb] [IQR, 45.50-48.19 ppb]) were each associated with cardiac dysfunction and adverse remodeling, cross-sectionally and longitudinally. Over time, each IQR-increment increase in PM2.5 (1.68 μg/m3) and O3 (2.69 ppb) was associated with a mean LVEF change of -1.3% (95% CI, -1.8% to -0.8%) and -1.4% (95% CI, -1.8% to -1.0%), respectively; worse longitudinal strain (-1.0% [95% CI, -1.3% to -0.7%] and -1.1% [95% CI, -1.3% to -0.8%], respectively); and left ventricular mass increase of 4.8 g/m2 (95% CI, 3.1-6.5 g/m2) and 3.2 g/m2 (95% CI, 2.1-4.3 g/m2), respectively. Patients in the highest tertiles of PM2.5 (adjusted hazard ratio [AHR], 2.03; 95% CI, 1.17-3.52) and O3 (AHR, 2.15; 95% CI, 1.23-3.78) exposure were at a significantly higher risk of cardiac dysfunction compared with those in the lowest tertile. Neither PM10 (AHR, 0.84; 95% CI, 0.49-1.44) nor NO2 (AHR, 0.92; 95% CI, 0.50-1.70) showed significant associations with cardiac dysfunction.

In this cohort study, PM2.5 and O3 exposure was independently associated with worse cardiac remodeling and function in patients with breast cancer treated with cardiotoxic therapy. These findings highlight the importance of modifying environmental exposures to mitigate cardiovascular disease risk.