US EPA Confirms Air Pollution Contributes to Cause of Death

By Dr. Wayne Cascio

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

Prof Joel D Kaufman, MD, Sara D Adar, ScD, R Graham Barr, MD, Prof Matthew Budoff, MD, Prof Gregory L Burke, MD, Cynthia L Curl, PhD, Prof Martha L Daviglus, MD, Prof Ana V Diez Roux, MD, Amanda J Gassett, MS, Prof David R Jacobs Jr, PhD, Prof Richard Kronmal, PhD, Prof Timothy V Larson, PhD, Ana Navas-Acien, MD, Casey Olives, PhD, Prof Paul D Sampson, Prof Lianne Sheppard, PhD, Prof Emeritus David S Siscovick, MD, Prof James H Stein, MD, Adam A Szpiro, PhD, Prof Karol E Watson, MD

Published: 24 May 2016
DOI: http://dx.doi.org/10.1016/S0140-6736(16)00378-0

Background

Long-term exposure to fine particulate matter less than 2·5 μm in diameter (PM2·5) 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.

For more than two decades, scientific evidence has shown fine particle pollution (PM2.5) in the outside air is a cause of cardiovascular illness and death, and has justified improving the PM2.5 annual National Ambient Air Quality Standard to protect public health. Yet, MESA Air was the first U.S. research study to examine a group of people over a period of 10 years and measured directly how long-term exposure to air pollution contributes to the development of heart disease and can lead to heart attacks, abnormal heart rhythms, heart failure, and death. MESA Air did just that, and Dr. Joel Kaufman, the leader of MESA Air at the University of Washington and his colleagues should be commended for their accomplishment.

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 PM2·5/m3 and 7·2–139·2 parts per billion (ppb) NOX. For each 5 μg PM2·5/m3 increase, coronary calcium progressed by 4·1 Agatston units per year (95% CI 1·4–6·8) and for each 40 ppb NOX 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/m3 higher long-term exposure to PM2·5 in intima-media thickness was −0·9 μm per year (95% CI −3·0 to 1·3). For 40 ppb higher NOX, the estimate was 0·2 μm per year (−1·9 to 2·4).

Interpretation

Increased concentrations of PM2·5 and traffic-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.

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