Letter | Published:

The contribution of outdoor air pollution sources to premature mortality on a global scale

Nature volume 525, pages 367371 (17 September 2015) | Download Citation

Abstract

Assessment of the global burden of disease is based on epidemiological cohort studies that connect premature mortality to a wide range of causes1,2,3,4,5, including the long-term health impacts of ozone and fine particulate matter with a diameter smaller than 2.5 micrometres (PM2.5)3,4,5,6,7,8,9. It has proved difficult to quantify premature mortality related to air pollution, notably in regions where air quality is not monitored, and also because the toxicity of particles from various sources may vary10. Here we use a global atmospheric chemistry model to investigate the link between premature mortality and seven emission source categories in urban and rural environments. In accord with the global burden of disease for 2010 (ref. 5), we calculate that outdoor air pollution, mostly by PM2.5, leads to 3.3 (95 per cent confidence interval 1.61–4.81) million premature deaths per year worldwide, predominantly in Asia. We primarily assume that all particles are equally toxic5, but also include a sensitivity study that accounts for differential toxicity. We find that emissions from residential energy use such as heating and cooking, prevalent in India and China, have the largest impact on premature mortality globally, being even more dominant if carbonaceous particles are assumed to be most toxic. Whereas in much of the USA and in a few other countries emissions from traffic and power generation are important, in eastern USA, Europe, Russia and East Asia agricultural emissions make the largest relative contribution to PM2.5, with the estimate of overall health impact depending on assumptions regarding particle toxicity. Model projections based on a business-as-usual emission scenario indicate that the contribution of outdoor air pollution to premature mortality could double by 2050.

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Acknowledgements

We are grateful to the EDGAR team of the Joint Research Centre in Ispra, Italy, for the emission data. We acknowledge support from the Distinguished Scientist Fellowship Program at the King Saud University, Riyadh. The research leading to these results has received funding from the European Research Council under the European Union’s Seventh Framework Programme (FP7/2007-2013)/ERC grant agreement no. 226144.

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Affiliations

  1. Max Planck Institute for Chemistry, Atmospheric Chemistry Department, 55128 Mainz, Germany

    • J. Lelieveld
    •  & A. Pozzer
  2. The Cyprus Institute, Energy, Environment and Water Research Center, 1645 Nicosia, Cyprus

    • J. Lelieveld
    •  & D. Giannadaki
  3. Harvard School of Public Health, Boston, Massachusetts 02215, USA

    • J. S. Evans
  4. Cyprus International Institute for Environment and Public Health, Cyprus University of Technology, 3041 Limassol, Cyprus

    • J. S. Evans
  5. King Saud University, College of Science, Riyadh 11451, Saudi Arabia

    • M. Fnais

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Contributions

J.L., A.P. and M.F. planned the research, A.P. performed the model calculations, J.L., A.P., D.G. and J.S.E. analysed the results, and J.L. and J.S.E. wrote the paper. All authors contributed to the manuscript.

Competing interests

The authors declare no competing financial interests.

Corresponding author

Correspondence to J. Lelieveld.

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https://doi.org/10.1038/nature15371

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