The environmental exposome in heart failure risk and progression
January 25, 2026
Abstract
Environmental exposures have a crucial role in the incidence and progression of heart failure (HF) by exacerbating genetic predisposition and other pathophysiological mechanisms. The exposome — encompassing pollution, climate and the urban environment — and the biological responses to these factors shape cardiovascular health in complex ways. Air, noise and light pollution, exposure to toxic metals, and extremes of temperature adversely affect HF outcomes. Social determinants of health, including socioeconomic status, amplify these environmental risks, disproportionately affecting vulnerable populations. Conversely, green spaces and walkable neighbourhoods are linked to a reduced risk of HF, improved vascular health and medication adherence. Emerging evidence suggests that environmental stressors influence HF outcomes from early life by altering gene expression through epigenetic mechanisms. Despite these insights, research gaps remain. Future studies must integrate environmental, genetic and multiomics data to refine risk prediction and guide targeted public health interventions. A comprehensive understanding of the exposome in the aetiology of HF is essential for developing prevention strategies that address both biological and social determinants of cardiovascular health.
Key points
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The environmental exposome encompasses the cumulative effects of external and internal factors influencing the risk and progression of heart failure (HF).
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Air pollution, particularly particulate matter with an aerodynamic diameter <2.5 µm, significantly elevates the risk of HF through inflammatory and oxidative pathways.
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Chronic noise exposure disrupts autonomic balance, increasing the risk of HF and adverse cardiovascular events.
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Toxic metals, such as cadmium and lead, exacerbate oxidative stress, contributing to myocardial damage and the progression of HF.
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Climate conditions, artificial light and socioeconomic disparities further compound the risk of HF, necessitating comprehensive public health interventions.
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Acknowledgements
O.H. is a Young Scientist of the DZHK (German Center for Cardiovascular Research), Partner Site Rhine-Main, Mainz, Germany, and Guest Scientist at the Max Planck Institute for Chemistry, Mainz, Germany. The work was supported by the environmental network EXPOHEALTH funded by the Science Initiative of the state Rhineland-Palatinate, Germany, and by the environmental research consortium MARKOPOLO, which is funded by the European Union (Grant Agreement Number 101156161) and the Swiss State Secretariat for Education, Research and Innovation (SERI). S.R. is supported by National Institutes of Health Grant R35 ES031702. The views and opinions expressed are those of the authors only and do not necessarily reflect those of the European Union, the European Health and Digital Executive Agency (HADEA) or the SERI. Neither the European Union nor the granting authorities can be held responsible for them.
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O.H., S.W. and S.A.-K. researched data for the article. O.H., S.W., S.R. and S.A.-K. discussed the content of the manuscript. O.H., S.W. and S.A.-K. wrote the article. All the authors reviewed and edited the manuscript before submission.
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Hahad, O., Wass, S., Rajagopalan, S. et al. The environmental exposome in heart failure risk and progression.
Nat Rev Cardiol (2026). https://doi.org/10.1038/s41569-026-01247-1
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DOI: https://doi.org/10.1038/s41569-026-01247-1
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