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      Estimates and 25-year trends of the global burden of disease attributable to ambient air pollution: an analysis of data from the Global Burden of Diseases Study 2015

      research-article
      , Dr, DSc a , * , * , , Prof, ScD b , * , , PhD c , , Prof, MD d , , MPH e , , MPA e , , Prof, PhD f , , Prof, PhD g , , Prof, MD e , h , , PhD h , , Prof, PhD i , , MPH e , , PhD j , , PhD k , , Prof, MD l , , PhD m , , PhD n , , Prof, PhD o , , PhD p , , Prof, PhD q , , PhD c , , PhD r , , Prof, PhD k , , PhD k , , PhD s , , PhD o , , Prof, PhD e , , Prof, DPhil e , , PhD , e
      Lancet (London, England)
      Elsevier

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          Summary

          Background

          Exposure to ambient air pollution increases morbidity and mortality, and is a leading contributor to global disease burden. We explored spatial and temporal trends in mortality and burden of disease attributable to ambient air pollution from 1990 to 2015 at global, regional, and country levels.

          Methods

          We estimated global population-weighted mean concentrations of particle mass with aerodynamic diameter less than 2·5 μm (PM 2·5) and ozone at an approximate 11 km × 11 km resolution with satellite-based estimates, chemical transport models, and ground-level measurements. Using integrated exposure–response functions for each cause of death, we estimated the relative risk of mortality from ischaemic heart disease, cerebrovascular disease, chronic obstructive pulmonary disease, lung cancer, and lower respiratory infections from epidemiological studies using non-linear exposure–response functions spanning the global range of exposure.

          Findings

          Ambient PM 2·5 was the fifth-ranking mortality risk factor in 2015. Exposure to PM 2·5 caused 4·2 million (95% uncertainty interval [UI] 3·7 million to 4·8 million) deaths and 103·1 million (90·8 million 115·1 million) disability-adjusted life-years (DALYs) in 2015, representing 7·6% of total global deaths and 4·2% of global DALYs, 59% of these in east and south Asia. Deaths attributable to ambient PM 2·5 increased from 3·5 million (95% UI 3·0 million to 4·0 million) in 1990 to 4·2 million (3·7 million to 4·8 million) in 2015. Exposure to ozone caused an additional 254 000 (95% UI 97 000–422 000) deaths and a loss of 4·1 million (1·6 million to 6·8 million) DALYs from chronic obstructive pulmonary disease in 2015.

          Interpretation

          Ambient air pollution contributed substantially to the global burden of disease in 2015, which increased over the past 25 years, due to population ageing, changes in non-communicable disease rates, and increasing air pollution in low-income and middle-income countries. Modest reductions in burden will occur in the most polluted countries unless PM 2·5 values are decreased substantially, but there is potential for substantial health benefits from exposure reduction.

          Funding

          Bill & Melinda Gates Foundation and Health Effects Institute.

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          Most cited references21

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          A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010

          The Lancet, 380(9859), 2224-2260
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            Long-term ozone exposure and mortality.

            Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect of long-term exposure to ozone on air pollution-related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes. Data from the study cohort of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,850 subjects, with 118,777 deaths in an 18-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are < or = 2.5 microm in aerodynamic diameter [PM(2.5)]) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models. In single-pollutant models, increased concentrations of either PM(2.5) or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM(2.5) was associated with the risk of death from cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration of 10 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used. In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM(2.5) was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration. 2009 Massachusetts Medical Society
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              Ambient air pollution, birth weight and preterm birth: a systematic review and meta-analysis.

              Low birth weight and preterm birth have a substantial public health impact. Studies examining their association with outdoor air pollution were identified using searches of bibliographic databases and reference lists of relevant papers. Pooled estimates of effect were calculated, heterogeneity was quantified, meta-regression was conducted and publication bias was examined. Sixty-two studies met the inclusion criteria. The majority of studies reported reduced birth weight and increased odds of low birth weight in relation to exposure to carbon monoxide (CO), nitrogen dioxide (NO(2)) and particulate matter less than 10 and 2.5 microns (PM(10) and PM(2.5)). Effect estimates based on entire pregnancy exposure were generally largest. Pooled estimates of decrease in birth weight ranged from 11.4 g (95% confidence interval -6.9-29.7) per 1 ppm CO to 28.1g (11.5-44.8) per 20 ppb NO(2), and pooled odds ratios for low birth weight ranged from 1.05 (0.99-1.12) per 10 μg/m(3) PM(2.5) to 1.10 (1.05-1.15) per 20 μg/m(3) PM(10) based on entire pregnancy exposure. Fewer effect estimates were available for preterm birth and results were mixed. Pooled odds ratios based on 3rd trimester exposures were generally most precise, ranging from 1.04 (1.02-1.06) per 1 ppm CO to 1.06 (1.03-1.11) per 20 μg/m(3) PM(10). Results were less consistent for ozone and sulfur dioxide for all outcomes. Heterogeneity between studies varied widely between pollutants and outcomes, and meta-regression suggested that heterogeneity could be partially explained by methodological differences between studies. While there is a large evidence base which is indicative of associations between CO, NO(2), PM and pregnancy outcome, variation in effects by exposure period and sources of heterogeneity between studies should be further explored. Crown Copyright © 2012. Published by Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Journal
                Lancet
                Lancet
                Lancet (London, England)
                Elsevier
                0140-6736
                1474-547X
                13 May 2017
                13 May 2017
                : 389
                : 10082
                : 1907-1918
                Affiliations
                [a ]Health Effects Institute, Boston, MA, USA
                [b ]University of British Columbia, Vancouver, BC, Canada
                [c ]Health Canada, Ottawa, ON, Canada
                [d ]St George's, University of London, London, UK
                [e ]Institute for Health Metrics and Evaluation, Seattle, WA, USA
                [f ]Sri Ramachandra University, Chennai, Tamil Nadu, India
                [g ]University of Utrecht, Utrecht, Netherlands
                [h ]Public Health Foundation of India, New Delhi, India
                [i ]Auckland University of Technology, Auckland, New Zealand
                [j ]United States Environmental Protection Agency, Washington, DC, USA
                [k ]University of Bath, Bath, UK
                [l ]Fudan University, Yangpu Qu, Shanghai, China
                [m ]University of Queensland, St Lucia, QLD, Australia
                [n ]Emory University, Atlanta, GA, USA
                [o ]Dalhousie University, Halifax, NS, Canada
                [p ]Queensland University of Technology, Brisbane, QLD, Australia
                [q ]Brigham Young University, Provo, UT, USA
                [r ]International Agency for Research on Cancer, Lyon, France
                [s ]European Commission, Brussels, Belgium
                Author notes
                [* ]Correspondence to: Dr Aaron J Cohen, Health Effects Institute, Boston, MA 02110-1817, USACorrespondence to: Dr Aaron J CohenHealth Effects InstituteBostonMA02110-1817USA acohen@ 123456healtheffects.org
                [*]

                Joint first authors

                [†]

                Senior author

                Article
                S0140-6736(17)30505-6
                10.1016/S0140-6736(17)30505-6
                5439030
                28408086
                b7db7ca4-d4b4-4220-a9f4-9218f9a27e60
                © 2017 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

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