Author + information
- Jonathan D. Newman, MD, MPH∗ (, )
- George D. Thurston, ScD,
- Kevin Cromar, PhD,
- Yu Guo, MA,
- Caron B. Rockman, MD,
- Edward A. Fisher, MD, PhD and
- Jeffrey S. Berger, MD, MS∗ ()
- ↵∗Division of Cardiology, The Center for the Prevention of Cardiovascular Disease, New York University School of Medicine, 227 East 30th Street, TRB Room 853, New York, New York 10016
Outdoor fine particulate air pollution (mass concentration of particles <2.5 μm in diameter [PM2.5]) exposure is ubiquitous and is associated with cardiovascular mortality and ischemic heart disease events (1). PM2.5 exposure also increases the risk for ischemic stroke (2). The vascular and hemodynamic effects of PM2.5 may explain some, but not all, of this increased risk (2). However, it is unknown whether PM2.5 is associated with prevalent clinical atherosclerosis, such as carotid artery stenosis (CAS), a lesion critical to the pathophysiology of ischemic stroke (3). To achieve this objective, we examined PM2.5 and prevalent CAS among more than 300,000 residents of New York, New Jersey, and Connecticut.
We selected tristate residents age 40 to 80 years participating in Life Line Vascular Screening (LLS, Independence, Ohio) without previous procedures for carotid disease (N = 307,444). The cohort consisted primarily of individuals who self-paid for vascular screening tests from 2003 to 2008 in the tristate region (4), This region was chosen because of its large, heterogeneous population and wide variation in PM2.5 exposure (6.7 to 14.7 μg/m3). Prior to vascular ultrasound, participants completed demographic, smoking, medical comorbidity, cardiovascular risk factor, and family history questionnaires (4). CAS was assessed with bilateral carotid artery duplex ultrasound. Maximal peak systolic and end diastolic velocity in the right and left internal carotid arteries (ICA) were recorded. CAS was defined as stenosis ≥50% in either ICA (or both ICAs) by duplex ultrasound (ICA peak systolic velocity ≥125 cm/s) (3,5). Each participant’s average PM2.5 exposures were estimated by zip code empirical Bayesian kriging of ambient monitoring data from the Environmental Protection Agency’s Air Quality System. PM2.5 exposures from years 2003 to 2008 were selected for analysis due to completeness of Life Line cohort screening data. Baseline characteristics and CAS prevalence by PM2.5 quartiles were examined. Multivariable logistic regression models, sequentially adjusting for age, demographics, medical history, and zip code median household income, were used to estimate the risk of CAS per 10 μg/m3 increase in PM2.5. Additional multivariable logistic regression by quartiles and medians of PM2.5 exposure on risk of CAS was performed. Sensitivity analyses of moderate and severe CAS were also conducted.
Compared with other quartiles of PM2.5 exposure, participants in quartile 4 (12.9 to 14.7 μg/m3) were younger, and were less likely to be white, have hypertension, have hyperlipidemia, or exercise regularly; however, they were more likely to have diabetes mellitus (p < 0.001 for all). In a logistic regression model adjusting for age, sex, race/ethnicity, body mass index, high cholesterol, hypertension, physical activity, family history of cardiovascular disease, household income, and smoking behaviors, we found a nearly 2-fold increase in CAS (odds ratio [OR]: 1.90, 95% confidence interval [CI]: 1.35 to 2.66) for every 10-μg/m3 increase in PM2.5. The odds of CAS increased when the highest versus lowest quartile of PM2.5 and above and below the median PM2.5 were compared (OR: 1.24, 95% CI: 1.11 to 1.37; and OR: 1.12, 95% CI: 1.04 to 1.21, respectively) (Figure 1). Results were similar by sex and race. The association between a 10-μg/m3 increase in PM2.5 and CAS was consistent when restricted to patients with moderate (OR: 1.90, 95% CI: 1.31 to 2.72) and severe (OR: 1.79, 95% CI: 1.05 to 3.07) CAS.
Our study demonstrates for the first time that PM2.5 is independently associated with CAS, an important risk factor for cerebrovascular disease and stroke. These results support the relationship between fine particle air pollution and prevalent atherosclerosis, and may suggest a pathway through which PM2.5 increases cardiovascular risk. Strengths of this study include the large sample size, validated CAS measurements, wide age range, and availability of lifestyle, medical, and household income data. Limitations include the lack of complete temporal data on PM2.5 exposure and clinical outcomes for CAS. Our assessments of cardiovascular risk factors were limited to self-report, and we lacked data on medical therapy that could modify the relationship of PM2.5 exposure to CAS. As this is a cross-sectional study, we cannot rule out exposure misclassification or the effect of copollutants on the observed PM2.5 to CAS relationship. Future studies should include source- and component-specific analyses of PM2.5 exposure to determine which PM2.5 fractions are most strongly associated with the observed increases in cerebrovascular disease and CAS.
Please note: This research was supported by National Institutes of Health R01 Grant ES019584, as well as the New York University National Institute of Environmental Health Sciences Center of Excellence (Grant ES00260). Dr. Newman was partially funded by an Empire Clinical Research Investigator Program by the New York State Department of Health to support Translational Research in Inflammation and Atherosclerotic Disease (TRIAD). Dr. Berger was partially funded by the National Heart, Lung, and Blood Institute of the National Institutes of Health (RO1HL114978) and American Heart Association Clinical Research Program (13CRP14410042). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. The authors are thankful for the participation and generosity of Life Line Screening, who provided these data free of charge for the purposes of research and with no restrictions on its use for research or resultant publications. This work has utilized computing resources at the High Performance Computing Facility of the Center for Health Informatics and Bioinformatics at New York University Langone Medical Center.
- American College of Cardiology Foundation
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