Abstract Number: O-002 | ID: 3034
Long-term exposure to ambient ozone and progression of subclinical atherosclerosis: The Multi-Ethnic Study of Atherosclerosis and Air Pollution
Meng Wang*, University of Washington, United States, firstname.lastname@example.org; Lianne Sheppard, University of Washington, United States, email@example.com; Paul Sampson, University of Washington, United States, firstname.lastname@example.org; James Stein, University of Wisconsin, United States, email@example.com; Sverre Vedal, University of Washington, United States, firstname.lastname@example.org; Joel Kaufman, University of Washington, United States, email@example.com;Background: Long-term ozone (O3) exposure is associated with cardiovascular mortality, but little is known about whether O3 promotes progression of atherosclerosis. We assessed the longitudinal association of residential ambient O3 concentration with progression of atherosclerosis, characterized by intima-media thickness of common carotid artery (IMTCCA) and carotid plaque (CP) in adults.
Methods: IMTCCA and CP burden (from the CCA, bifurcation, and internal segments of both carotid arteries) were quantified longitudinally for 3640 adults ages 45-84 years in the Multi-Ethnic Study of Atherosclerosis using ultrasound at baseline and after a mean of 9 years.. Residence-specific O3 concentrations were estimated by a validated spatio-temporal prediction land use regression/kriging model spanning 1999-2012. Linear mixed model and logistic regression models evaluated relationships of long-term exposure to O3 with longitudinal change in IMTCCA, and CP formation respectively.
Results: The mean O3 concentration was 21±5 ppb. The mean IMTCCA at baseline was 760±210μm and increased on an average of 120±2μm over 10 years. An interquartile range increase of 3 ppb in long-term average O3 exposure was associated with a 5.6 μm (95%CI 1.4 to 9.7 μm) greater increase in IMTCCA over ten years among persons in the same study region. Associations were robust regardless of staged adjustment, and inclusion of co-pollutants. We also found an association of long-term average O3 with CP formation in the same population, with an odds ratio of 1.2 (95% CI, 1.1 to 1.4) for the same 3 ppb increase in O3.
Conclusion: After nearly a decade of follow-up, outdoor O3 concentrations are associated with increased carotid wall thickness and risk of plaque formation, suggesting acceleration of atherosclerosis. This is the first epidemiological study to provide evidence that O3 might accelerate atherogenesis and cardiovascular disease risk.