Air Pollution and Progression of Atherosclerosis in Different Vessel Beds-Results from a Prospective Cohort Study in the Ruhr Area, Germany

Abstract

Objectives: Due to inconsistent epidemiological evidence on health effects of air pollution on progression of atherosclerosis, we investigated several air pollutants and their effects on progression of atherosclerosis, using carotid intima media thickness (cIMT), coronary calcification (CAC), and thoracic aortic calcification (TAC).

Methods: We used baseline (2000-2003) and 5-y follow-up (2006-2008) data from the German Heinz Nixdorf Recall cohort study, including 4,814 middle-aged adults. Residence-based long-term air pollution exposure, including particulate matter (PM) with aerodynamic diameter $\le 2.5\mu m$ (${\mathrm{PM}}_{2.5}$), (${\mathrm{PM}}_{10}$), and nitrogen dioxide (${\mathrm{NO}}_2$) was assessed using chemistry transport and land use regression (LUR) models. cIMT was quantified as side-specific median IMT assessed from standardized ultrasound images. CAC and TAC were quantified by computed tomography using the Agatston score. Development (yes/no) and progression of atherosclerosis (change in cIMT and annual growth rate for CAC/TAC) were analyzed with logistic and linear regression models, adjusting for age, sex, lifestyle variables, socioeconomic status, and traffic noise.

Results: While no clear associations were observed in the full study sample (mean age 59.1 ($\pm 7.6$) y; 53% female), most air pollutants were marginally associated with progression of atherosclerosis in participants with no or low baseline atherosclerotic burden. Most consistently for CAC, e.g., a $1.5{\mu g/m}^3$ higher exposure to ${\mathrm{PM}}_{2.5}$ (LUR) yielded an estimated odds ratio of 1.19 [95% confidence interval (CI): 1.03, 1.39] for progression of CAC and an increased annual growth rate of 2% (95% CI: 1%, 4%).

Conclusion: Our study suggests that development and progression of subclinical atherosclerosis is associated with long-term air pollution in middle-aged participants with no or minor atherosclerotic burden at baseline, while overall no consistent associations are observed. https://doi.org/10.1289/EHP7077.

Figure 1.

Main effect estimates for the associations between different air pollutants and progression of atherosclerosis in subpopulations of the Heinz Nixdorf Recall Study based on the marker of atherosclerosis, investing all participants ($\mathrm{cIMT}\left(\text{left}\right)=\mathrm{2,116}$, $\mathrm{cIMT}\left(\text{right}\right)=\mathrm{2,197}$, $\text{CAC}=\mathrm{3,220}$, $\text{TAC}=\mathrm{3,126}$), participants with no/minor atherosclerotic burden at baseline (t0) ($\mathrm{cIMT}\left(\text{left}\right)=\mathrm{1,054}$, $\mathrm{cIMT}\left(\text{right}\right)=\mathrm{1,017}$, $\text{CAC}=\mathrm{1,527}$, $\text{TAC}=\mathrm{1,761}$), and participants with advanced atherosclerotic burden at t0 ($\mathrm{cIMT}\left(\text{left}\right)=\mathrm{1,203}$, $\mathrm{cIMT}\left(\text{right}\right)=\mathrm{1,317}$, $\text{CAC}=\mathrm{1,693}$, $\text{TAC}=\mathrm{1,469}$). Main model is adjusted for age, sex, BMI, smoking status and quantity, ETS, LDL-C/HDL-C, physical activity, education, traffic noise and for dichotomous outcomes additionally years of follow-up. (A) This panel displays OR (95% CI) for any progression in atherosclerosis based on an IQR in exposure. (B) This panel displays change in thickness ($\mathrm{\mu }\mathrm{m}$) for cIMT and change in growth rate for CAC and TAC (complementing numbers are in Tables S2 and S3). Note: BMI, body mass index; CAC, coronary artery calcification; CI, confidence interval; cIMT, carotid intima media thickness; ETS, environmental tobacco smoke; HDL-C, high-density lipoprotein cholesterol; IQR, interquartile range; LDL-C, low-density lipoprotein cholesterol; OR, odds ratio; TAC, thoracic aortic calcification.