Review Article | Published:

Adverse cardiovascular effects of air pollution

Nature Clinical Practice Cardiovascular Medicine volume 6, pages 3644 (2009) | Download Citation

Subjects

Abstract

Air pollution is increasingly recognized as an important and modifiable determinant of cardiovascular disease in urban communities. Acute exposure has been linked to a range of adverse cardiovascular events including hospital admissions with angina, myocardial infarction, and heart failure. Long-term exposure increases an individual's lifetime risk of death from coronary heart disease. The main arbiter of these adverse health effects seems to be combustion-derived nanoparticles that incorporate reactive organic and transition metal components. Inhalation of this particulate matter leads to pulmonary inflammation with secondary systemic effects or, after translocation from the lung into the circulation, to direct toxic cardiovascular effects. Through the induction of cellular oxidative stress and proinflammatory pathways, particulate matter augments the development and progression of atherosclerosis via detrimental effects on platelets, vascular tissue, and the myocardium. These effects seem to underpin the atherothrombotic consequences of acute and chronic exposure to air pollution. An increased understanding of the mediators and mechanisms of these processes is necessary if we are to develop strategies to protect individuals at risk and reduce the effect of air pollution on cardiovascular disease.

Key points

  • Exposure to air pollution is associated with increased cardiovascular morbidity and deaths from myocardial ischemia, arrhythmia, and heart failure

  • Fine particulate matter derived from the combustion of fossil fuels is thought to be the most potent component of the air pollution cocktail

  • Particulate matter upregulates systemic proinflammatory and oxidative pathways, either through direct translocation into the circulation or via secondary pulmonary-derived mediators

  • Exposure to particulate matter has the potential to impair vascular reactivity, accelerate atherogenesis, and precipitate acute adverse thrombotic events

  • In patients with coronary heart disease, exposure to combustion-derived particulate can exacerbate exercise-induced myocardial ischemia

  • Improving air quality standards, reducing personal exposures, and the redesign of engine and fuel technologies could all have a role in reducing air pollution and its consequences for cardiovascular morbidity and mortality

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Acknowledgements

NL Mills is supported by a Michael Davies Research Fellowship from the British Cardiovascular Society. This work was supported by a British Heart Foundation Programme Grant (RG/05/003) and the Swedish Heart Lung Foundation.

Charles P Vega, University of California, Irvine, CA, is the author of and is solely responsible for the content of the learning objectives, questions and answers of the Medscape-accredited continuing medical education activity associated with this article.

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Affiliations

  1. NL Mills is a Clinical Lecturer in Cardiology, PW Hadoke is a Senior Academic Fellow in Pharmacology, NA Boon is a Consultant Cardiologist, and DE Newby is a British Heart Foundation funded Professor of Cardiology at the Centre for Cardiovascular Science, Edinburgh University, Edinburgh, UK.

    • Nicholas L Mills
    • , Ken Donaldson
    • , Paddy W Hadoke
    • , Nicholas A Boon
    •  & David E Newby
  2. W MacNee is Chair of Respiratory and Environmental Medicine and K Donaldson is Scientific Director of the ELEGI Colt Laboratory, Edinburgh University. FR Cassee is Head of the Department of Inhalation Toxicology at the National Institute for Public Health and the Environment, Bilthoven, The Netherlands.

    • William MacNee
    •  & Flemming R Cassee
  3. T Sandström is Professor of Respiratory Medicine and A Blomberg is Associate Professor at the Department of Respiratory Medicine and Allergy, Umeå University, Sweden.

    • Thomas Sandström
    •  & Anders Blomberg

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The authors declare no competing financial interests.

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Correspondence to Nicholas L Mills.

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DOI

https://doi.org/10.1038/ncpcardio1399