Abstract

Background:Long-term ozone () exposure is associated with cardiovascular mortality, but little is known about the associations between and subclinical arterial disease.Objectives:We studied the longitudinal association of exposure to and progression of key subclinical arterial markers in adults: intima-media thickness of common carotid artery (), carotid plaque (CP) burden, and coronary artery calcification (CAC).Methods:CAC was measured one to four times at baseline and at follow-up exams (1999–2012) by computed tomography (CT) in 6,619 healthy adults, recruited at age 45–84 y without cardiovascular disease (CVD), over a mean of 6.5 y (standard deviation: 3.5 y). and CP burden were quantified in 3,392 participants using carotid artery ultrasound imaging acquired over a mean of 9 y (1.7 y). Over 91% and 89% participants had at least one follow-up and CAC measurement, respectively. Residence-specific concentrations were estimated by a validated spatiotemporal model spanning from 1999 to 2012. This model relied on comprehensive monitoring data and geographical variables to predict individualized long-term average concentrations since baseline. Linear mixed models and logistic regression model were used to evaluate relationships of long-term average exposure to with longitudinal change in , CAC, and CP formation, respectively.Results:Mean progression rates of and CAC were and . CP formation was identified in 55% of the subjects. A increase in long-term average exposure was associated with a [95% confidence interval (CI): 1.4, 9.7] greater increase in over 10 y. A increase in was also associated with new CP formation [odds ratio (OR): 1.2 (95% CI: 1.1, 1.4)] but not CAC progression [ (95% CI: , 2)]. Associations were robust in the analysis with extended covariate adjustment, including copollutants, i.e., nitrogen oxides () and particulate matter with diameter ().Conclusion:Over almost a decade of follow-up, outdoor concentrations were associated with increased rate of carotid wall thickness progression and risk of new plaque formation, suggesting arterial injury in this cohort. https://doi.org/10.1289/EHP3325

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