AAAR 31st Annual Conference
October 8-12, 2012
Hyatt Regency Minneapolis
Minneapolis, Minnesota, USA
Abstract View
Oxidative Stress and the Acceleration of Atherosclerosis in Susceptible Mice After Exposure to Semi-Volatile Components of Ultrafine Particulate Matter
ANDREW KEEBAUGH, Payam Pakbin, Loyda Mendez, Zhi Ning, Glenn Gookin, Constantinos Sioutas, Michael Kleinman, University of California, Irvine
Abstract Number: 706 Working Group: Health Related Aerosols
Abstract Exposure to ultrafine particulate matter (UF-PM) has been associated with adverse cardiovascular health effects. UF-PM contains semi-volatile organics (SVOCs) that are bound to particles but can partition to the vapor phase after emission. SVOCs contain species such as polycyclic aromatic hydrocarbons and quinones that can induce oxidative stress and may be responsible for the exacerbation of cardiovascular disease by UF-PM. Therefore, we hypothesized that the removal of SVOCs from an aerosol should decrease the ability of the particle to cause oxidative damage and consequently the acceleration of atherosclerotic plaque formation. ApoE -/- mice, which are prone to developing atherosclerosis, were exposed to UF concentrated ambient particles (CAPs), CAPs with the SVOC components removed, or SVOC components without the particle core. A control group was exposed to purified, filtered air. Particles were concentrated using a VACES, and SVOCs were separated from the particle core using a thermal denuder. The exposures took place 5 hours/day, 4 days/week for 8 weeks in downtown Los Angeles, 100m downwind of a major freeway. Plaque formation in the aortic arch and total and LDL cholesterol in the serum were measured to evaluate the progression of atherosclerosis. Serum concentrations of lipid peroxidation, protein carbonyl content, and glutathione were assessed to determine systemic oxidative stress. Aortic plaque formation in mice exposed to unmodified CAPs was higher than in those exposed to CAPs with no SVOCs. Similarly, higher levels of lipid peroxidation were measured in mice exposed to unmodified CAPs and SVOC components of CAPs compared to those exposed to CAPs without SVOCs. The corresponding trends in plaque formation and lipid peroxidation support the notion that exposure to SVOCs may contribute to the acceleration of atherosclerosis via an oxidative stress pathway.