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      Association between air pollution and coronary artery calcification within six metropolitan areas in the USA (the Multi-Ethnic Study of Atherosclerosis and Air Pollution): a longitudinal cohort study

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          Summary

          Background

          Long-term exposure to fine particulate matter less than 2·5 μm in diameter (PM 2·5) and traffic-related air pollutant concentrations are associated with cardiovascular risk. The disease process underlying these associations remains uncertain. We aim to assess association between long-term exposure to ambient air pollution and progression of coronary artery calcium and common carotid artery intima-media thickness.

          Methods

          In this prospective 10-year cohort study, we repeatedly measured coronary artery calcium by CT in 6795 participants aged 45–84 years enrolled in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air) in six metropolitan areas in the USA. Repeated scans were done for nearly all participants between 2002 and 2005, for a subset of participants between 2005 and 2007, and for half of all participants between 2010 and 2012. Common carotid artery intima-media thickness was measured by ultrasound in all participants at baseline and in 2010–12 for 3459 participants. Residence-specific spatio-temporal pollution concentration models, incorporating community-specific measurements, agency monitoring data, and geographical predictors, estimated concentrations of PM 2·5 and nitrogen oxides (NO X) between 1999 and 2012. The primary aim was to examine the association between both progression of coronary artery calcium and mean carotid artery intima-media thickness and long-term exposure to ambient air pollutant concentrations (PM 2·5, NO X, and black carbon) between examinations and within the six metropolitan areas, adjusting for baseline age, sex, ethnicity, socioeconomic characteristics, cardiovascular risk factors, site, and CT scanner technology.

          Findings

          In this population, coronary calcium increased on average by 24 Agatston units per year (SD 58), and intima-media thickness by 12 μm per year (10), before adjusting for risk factors or air pollutant exposures. Participant-specific pollutant concentrations averaged over the years 2000–10 ranged from 9·2–22·6 μg PM 2·5/m 3 and 7·2–139·2 parts per billion (ppb) NO X. For each 5 μg PM 2·5/m 3 increase, coronary calcium progressed by 4·1 Agatston units per year (95% CI 1·4–6·8) and for each 40 ppb NO X coronary calcium progressed by 4·8 Agatston units per year (0·9–8·7). Pollutant exposures were not associated with intima-media thickness change. The estimate for the effect of a 5 μg/m 3 higher long-term exposure to PM 2·5 in intima-media thickness was −0·9 μm per year (95% CI −3·0 to 1·3). For 40 ppb higher NO X, the estimate was 0·2 μm per year (−1·9 to 2·4).

          Interpretation

          Increased concentrations of PM 2·5 and traffc-related air pollution within metropolitan areas, in ranges commonly encountered worldwide, are associated with progression in coronary calcification, consistent with acceleration of atherosclerosis. This study supports the case for global efforts of pollution reduction in prevention of cardiovascular diseases.

          Funding

          US Environmental Protection Agency and US National Institutes of Health.

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          Author and article information

          Journal
          2985213R
          5470
          Lancet
          Lancet
          Lancet (London, England)
          0140-6736
          1474-547X
          30 August 2016
          24 May 2016
          13 August 2016
          13 August 2017
          : 388
          : 10045
          : 696-704
          Affiliations
          Department of Environmental and Occupational Health Sciences (Prof J D Kaufman MD, A J Gassett MS, C Olives PhD, Prof L Sheppard PhD), Department of Epidemiology (Prof J D Kaufman), Department of Medicine (Prof J D Kaufman, Prof Emeritus D S Siscovick MD), Department of Biostatistics (Prof R Kronmal PhD, Prof L Sheppard PhD, A A Szpiro PhD), Department of Civil and Environmental Engineering (Prof T V Larson PhD), and Department of Statistics (Prof P D Sampson), University of Washington, Seattle, WA, USA; Department of Epidemiology, University of Michigan, Ann Arbor, MI, USA (S D Adar ScD); Department of Medicine and Department of Epidemiology, Columbia University, New York, NY, USA (R G Barr MD); Los Angeles Biomedical Research Institute at Harbor, UCLA Medical Center, Torrance, CA, USA (Prof M Budoff MD); Division of Public Health Sciences, Wake Forest University, Winston-Salem, NC, USA (Prof G L Burke MD); Department of Community and Environmental Health, Boise State University, Boise, ID, USA (C L Curl PhD); Feinberg School of Medicine, Northwestern University, Evanston, IL, USA (Prof M L Daviglus MD); Institute for Minority Health Research, University of Illinois at Chicago, Chicago, IL, USA (Prof M L Daviglus); School of Public Health, Drexel University, Philadelphia, PA, USA (Prof A V Diez Roux MD); School of Public Health, Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, MN, USA (Prof D R Jacobs PhD); Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, MD, USA (A Navas-Acien MD); New York Academy of Medicine, New York, NY, USA (Prof D S Siscovick Emeritus); Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA (Prof J H Stein MD); and Department of Medicine, Division of Cardiology, University of California Los Angeles, Los Angeles, CA, USA (Prof K E Watson MD)
          Author notes
          Correspondence to: Prof Joel D Kaufman, University of Washington, Seattle, WA 98105, USA joelk@ 123456u.washington.edu
          Article
          PMC5019949 PMC5019949 5019949 nihpa792610
          10.1016/S0140-6736(16)00378-0
          5019949
          27233746
          51e9dfdc-be54-454d-8fea-f2b170bd2ba6
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