Ambient air pollution and atherosclerosis in Los Angeles

Nino Künzli, Michael Jerrett, Wendy J Mack, Bernardo Beckerman, Laurie LaBree, Frank Gilliland, Duncan Thomas, John Peters, Howard N Hodis, Nino Künzli, Michael Jerrett, Wendy J Mack, Bernardo Beckerman, Laurie LaBree, Frank Gilliland, Duncan Thomas, John Peters, Howard N Hodis

Abstract

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 microm 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 PM2.5 surface derived from a geostatistical model. Individually assigned annual mean PM2.5 concentrations ranged from 5.2 to 26.9 microg/m3 (mean, 20.3). For a cross-sectional exposure contrast of 10 microg/m3 PM2.5, 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 (greater than or equal to 60 years of age), women, never smokers, and those reporting lipid-lowering treatment at baseline, the associations of PM2.5 and 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.

Figures

Figure 1. ZIP code locations of the…
Figure 1. ZIP code locations of the study population geocoded on the PM2.5 surface, modeled with 2000 PM2.5 data, and distribution of individually assigned concentrations.
Figure 2. Mean CIMT ± 1 SE…
Figure 2. Mean CIMT ± 1 SE among quartiles of the PM2.5 distribution. The y-axis shows mean CIMT levels at the population average of the adjustment covariates (age, sex, education, and income). The first quartile is the reference group.
Figure 3. Percent difference and 95% CI…
Figure 3. Percent difference and 95% CI in CIMT associated with a 10 μg/m3 contrast in ambient PM2.5 in all subjects and in subgroups. Lipid-LT, lipid-lowering therapy. All estimates are based on the cross-sectional linear model with log intima-media thickness as the dependent variable and home outdoor PM2.5 as the independent variable, adjusted for sex, age, education, and income. Numbers in parentheses are numbers of subjects per group. Data are ordered by size of point estimate; the null effect line is indicated by a dash.

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