Ambient Air Pollution and Atherosclerosis in Los Angeles

• Published in: Environmental health perspectives 2005-02, Vol.113 (2), p.201-206
• Main Authors: Künzli, Nino, Jerrett, Michael, Mack, Wendy J., Beckerman, Bernardo, LaBree, Laurie, Gilliland, Frank, Thomas, Duncan, Peters, John, Hodis, Howard N.
• Format: Article
• Language: English
• Subjects: Adult; Air pollution; Air Pollution - adverse effects; Arteriosclerosis - epidemiology; Arteriosclerosis - etiology; Arteriosclerosis - pathology; Atherosclerosis; Cardiovascular diseases; Carotid Arteries - diagnostic imaging; Carotid Arteries - pathology; Cohort studies; Computer software industry; Cross-Sectional Studies; Environmental health; Environmental Monitoring; Epidemiological Monitoring; Female; Geographic Information Systems; Humans; Los Angeles - epidemiology; Male; Middle Aged; Mortality; Particle Size; Particulate matter; Risk Factors; Secondhand smoke; Smoke; Tobacco smoking; Tunica Intima - diagnostic imaging; Tunica Intima - pathology; Tunica Media - diagnostic imaging; Tunica Media - pathology; Ultrasonography; Workers' compensation
• ISSN: 0091-6765; 1552-9924
• DOI: 10.1289/ehp.7523

Associations have been found between long-term exposure to ambient air pollution and cardiovascular morbidity and mortality. The contribution of air pollution to atherosclerosis that underlies many cardiovascular diseases has not been investigated. Animal data suggest that ambient particulate matter (PM) may contribute to atherogenesis. We used data on 798 participants from two clinical trials to investigate the association between atherosclerosis and long-term exposure to ambient PM up to 2.5 μm in aerodynamic diameter ( PM2.5). Baseline data included assessment of the carotid intima-media thickness (CIMT), a measure of subclinical atherosclerosis. We geocoded subjects' residential areas to assign annual mean concentrations of ambient PM2.5. Exposure values were assigned from a PM2.5surface derived from a geostatistical model. Individually assigned annual mean PM2.5concentrations ranged from 5.2 to 26.9 μ g/ m3(mean, 20.3). For a cross-sectional exposure contrast of 10 μ g/ m3PM2.5, CIMT increased by 5.9% (95% confidence interval, 1-11%). Adjustment for age reduced the coefficients, but further adjustment for covariates indicated robust estimates in the range of 3.9-4.3% (p-values, 0.05-0.1). Among older subjects (≥ 60 years of age), women, never smokers, and those reporting lipid-lowering treatment at baseline, the associations of PM2.5and CIMT were larger with the strongest associations in women ≥ 60 years of age (15.7%, 5.7-26.6%). These results represent the first epidemiologic evidence of an association between atherosclerosis and ambient air pollution. Given the leading role of cardiovascular disease as a cause of death and the large populations exposed to ambient PM2.5, these findings may be important and need further confirmation.