Elsevier

The Lancet

Volume 388, Issue 10045, 13–19 August 2016, Pages 696-704
The Lancet

Articles
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

https://doi.org/10.1016/S0140-6736(16)00378-0Get rights and content

Summary

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.

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 PM2·5 and nitrogen oxides (NOX) 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 (PM2·5, NOX, 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 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.

Funding

US Environmental Protection Agency and US National Institutes of Health.

Introduction

Particulate air pollution and traffic-related air pollutants are associated with overall mortality, cardiovascular mortality, and cardiovascular disease events. In particular, long-term exposure to high concentrations of air pollutants has been associated with risk of myocardial infarction and stroke.1 However, previous studies of cardiovascular disease and air pollution have had short follow-up duration, have often been limited by between-city exposure contrasts without precisely accounting for within-city variation, and have comprised secondary analyses of existing datasets collected to test other hypotheses. Furthermore, the underlying pathological process has not been well established, leaving the biological plausibility of these findings open to question.

To reduce uncertainties in the understanding of the potential health effects of ambient air pollutants, the US Environmental Protection Agency (EPA) supported an unprecedented effort to characterise pollutant exposures in participants of the National Heart, Lung, and Blood Institute's Multi-Ethnic Study of Atherosclerosis (MESA).2 The resultant study (the Multi-Ethnic Study of Atherosclerosis and Air Pollution, [MESA Air])3 tested a priori the associations of air pollution concentrations, specifically particulate matter of less than 2·5 μm in diameter (PM2·5), nitrogen oxides (NOX), and black carbon, with progression of subclinical arteriosclerosis. We report the association between long-term exposure to ambient air pollution and progression of coronary artery calcium and common carotid artery intima-media thickness.

Research in context

Evidence before this study

At study launch, there was no literature on progression of atherosclerosis in relation to long-term exposure to air pollution; the study was in response to the US Environmental Protection Agency's Request For Applications for a prospective observational study of cardiovascular disease initiation and progression associated with long-term exposure to ambient particulate matter and other air pollutants in a population-based sample. Although previous research has been considered to be consistent with a causal relationship between particulate matter air pollution and ischaemic heart disease events and mortality, these studies had substantial limitations and biological plausibility has continued to be questioned. Previous studies have had short follow-up durations, little attention to fine-scale variation in pollutant exposure, and comprised secondary analyses of existing datasets collected to test other hypotheses.

Added value of this study

This study provides important new information about the underlying biological processes of long-term exposure to air pollutant concentrations and their association with cardiovascular disease, through repeated assessment of coronary artery calcification by CT (a surrogate of atherosclerosis extent) in a cohort and with an unprecedented effort to characterise air pollutant exposures. The study was specifically designed to address the hypothesis that air pollutants would be associated with progression in subclinical atherosclerosis.

Exposures assessed in this study are low and relevant for understanding the health effects of ambient environments occurring nowadays in high-income, low-income, and rapidly industrialising countries.

Implications of all the available evidence

Together with accumulating observational evidence of the relationship between ambient pollutants and cardiovascular disease events, this study substantially advances the case for global efforts to reduce exposures to ambient air pollutants.

Section snippets

Study design and participants

The designs of the MESA2 and MESA Air3 studies have been described previously. Briefly, MESA recruited a cohort of 6814 participants with no history of clinical cardiovascular disease from four ethnic groups (Hispanic, black, white, and Chinese), with sex balance and uniform age distribution (range 45–84 years at recruitment) in six areas of the USA: Baltimore, MD; Chicago, IL; Los Angeles County, CA; New York City, NY; St Paul, MN; and Winston-Salem, NC. Community-based strategies that varied

Results

Of the 7060 participants initially enrolled, 5834 underwent at least two examinations and had sufficient data to be included longitudinally in the analysis of coronary artery calcium. 961 participants were included only at baseline. The mean age of the cohort at baseline was 62 years (SD 10), and 3593 (53%) of the 6795 participants assessed were women. Overall, the cohort included 2678 (39%) white, 795 (12%) Chinese, 1824 (27%) black, and 1498 (22%) Hispanic participants (table). The

Discussion

In this multi-ethnic prospectively studied population, ambient concentrations of PM2·5 and NOX were strongly associated with accelerated atherosclerosis, as shown by assessment of coronary artery calcium over a 10-year period. Air pollution was not associated with progression of intima-media thickness. This study benefited from state-of-the-art exposure estimation at the time and location of each residence during follow-up and incorporated high-quality information about potential confounding

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