
Air Pollution Exposure May Influence Cardiac Outcomes in Patients With Breast Cancer
Key Takeaways
- Fine particulate matter, ozone, NO₂, and PM₁₀ promote oxidative stress and inflammation, overlapping mechanistically with pathways that drive cardiotoxicity and adverse remodeling during breast cancer therapy.
- Higher PM2.5 and O₃ exposure correlated with measurable declines in LVEF and myocardial strain, alongside increased LV mass, suggesting subclinical injury progressing toward structural remodeling.
Air pollution exposure, particularly fine particulate matter and ozone, may worsen cardiac outcomes in patients with breast cancer receiving cardiotoxic therapies.
As survival outcomes for patients with breast cancer continue to improve, attention has increasingly shifted toward long-term treatment-related complications. Among these, cardiovascular toxicity remains a leading concern, particularly for patients receiving anthracyclines or HER2-targeted therapies. Emerging evidence now suggests that air pollution exposure may play an important role in modifying cardiac outcomes in this population, highlighting a new dimension of risk in breast cancer care.
Environmental Exposures in Breast Cancer
Air pollution has been extensively linked to adverse health outcomes, including cardiovascular disease and cancer. Breast cancer is no exception, with air pollutants such as fine particulate matter (PM2.5) and other pollutants linked to both cancer cases and their development.1 Patients with breast cancer can be biologically affected by environmental toxins even before they start treatment.
Certain air pollutants, such as PM2.5, ozone (O₃), nitrogen dioxide (NO₂), and particulate matter (PM₁₀), can trigger systemic inflammation and oxidative stress—the mechanisms also responsible for cancer biology.2 When undergoing treatments, patients with cancer may be subjected to these exposures that can interact with therapy-related toxicities, causing them to alter the outcomes further.
New Evidence Linking Pollution to Cardiac Changes
According to new research published in JAMA Network Open, researchers evaluated 580 women with breast cancer who were treated with anthracyclines and/or trastuzumab (Herceptin; Genentech). The study tracked the duration of patients’ exposure to pollution and assessed changes in their hearts over time.
The researchers observed that greater exposure to PM2.5 and O3 was associated with declines in cardiac function, including decreases in left ventricular ejection fraction and worsening myocardial strain. Additionally, increased pollutant exposure was associated with muscle changes, including increased left ventricular mass, a sign of early adverse cardiac remodeling.3
Importantly, patients who were exposed to the highest levels of pollutants had a significantly higher risk of therapy-related cardiac dysfunction than those who were exposed to lower levels.3 Therefore, these results indicate that environmental factors may affect how patients with breast cancer respond to cardiotoxic therapies.
Why Patients With Breast Cancer May Be at Higher Risk
Additionally, breast cancer survivors often require long-term monitoring, making them particularly susceptible to cumulative environmental exposures over time.
Patients with breast cancer frequently undergo treatment that places the cardiovascular system under a lot of stress. Myocardial injury is a known adverse effect of anthracycline chemotherapy, especially at high doses. In contrast, cardiac dysfunction brought about by HER2-targeted agents such as trastuzumab is often reversible.4
If these risks are combined with environmental exposures such as air pollution, they may become even greater. Fine particulate matter can reach the blood, leading to activation of inflammatory signaling, production of oxidative substances, and weakening of cardiac tissue.2 In patients already experiencing treatment-related stress on the myocardium, this additional burden may accelerate the development of cardiac dysfunction.
Additionally, breast cancer survivors often require long-term monitoring, making them particularly susceptible to cumulative environmental exposures over time.
Clinical Considerations for Pharmacists
For oncology pharmacists, these findings highlight the importance of considering environmental exposures as part of a comprehensive risk assessment. While traditional counseling focuses on medication-related adverse effects, incorporating guidance on air quality may provide additional benefit.
Patients may be advised to monitor local air quality, reduce outdoor activity during high-pollution periods, and consider environmental mitigation strategies when feasible. These interventions, while simple, may help reduce cumulative cardiovascular risk.
From a broader perspective, recognizing environmental factors as modifiers of treatment outcomes supports a more personalized approach to breast cancer care. Integrating these considerations into survivorship planning may improve long-term outcomes.
Conclusion
Air pollution exposure represents an emerging, modifiable factor that may influence cardiac outcomes in patients with breast cancer undergoing treatment. As oncology continues to prioritize survivorship and quality of life, incorporating environmental risk factors into patient care may help optimize both cancer and cardiovascular outcomes.
REFERENCES
White AJ, Bradshaw PT, Hamra GB. Air pollution and breast cancer: a review. Curr Epidemiol Rep. 2018;5(2):92-100. doi:10.1007/s40471-018-0143-2
Liu Y, Goodson JM, Zhang B, Chin MT. Air pollution and adverse cardiac remodeling: clinical effects and basic mechanisms. Front Physiol. 2015;6:162. doi:10.3389/fphys.2015.00162
Jung W, Ko K, Smith AM, et al. Air pollution and cardiac remodeling and function in patients with breast cancer. JAMA Netw Open. 2026;9(1):e2552323. doi:10.1001/jamanetworkopen.2025.52323
Zamorano JL, Lancellotti P, Rodriguez Muñoz D, et al. 2016 ESC position paper on cancer treatments and cardiovascular toxicity developed under the auspices of the ESC Committee for Practice Guidelines: the task force for cancer treatments and cardiovascular toxicity of the European Society of Cardiology (ESC). Eur Heart J. 2016;37(36):2768-2801. doi:10.1093/eurheartj/ehw211








































































































































