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(Circulation Research. 2008;102:589.)
© 2008 American Heart Association, Inc.

Integrative Physiology

Ambient Particulate Pollutants in the Ultrafine Range Promote Early Atherosclerosis and Systemic Oxidative Stress

Jesus A. Araujo, Berenice Barajas, Michael Kleinman, Xuping Wang, Brian J. Bennett, Ke Wei Gong, Mohamad Navab, Jack Harkema, Constantinos Sioutas, Aldons J. Lusis, Andre E. Nel

From the Department of Medicine (J.A.A., B.B., X.W., B.J.B., K.W.G., M.N., A.J.L., A.E.N.), David Geffen School of Medicine, and Department of Civil and Environmental Engineering (C.S.), University of Southern California, Los Angeles; Department of Community and Environmental Medicine (M.K.), University of California, Irvine; and Department of Pathobiology and Diagnostic Investigation (J.H.), Michigan State University, East Lansing.

Correspondence to Andre Nel, MD, PhD, Department of Medicine, David Geffen School of Medicine. 10833 Le Conte Ave, CHS 52-175, Box 951680, Los Angeles, CA 90095. E-mail ANel{at}mednet.ucla.edu

Air pollution is associated with significant adverse health effects, including increased cardiovascular morbidity and mortality. Exposure to particulate matter with an aerodynamic diameter of <2.5 µm (PM_2.5) increases ischemic cardiovascular events and promotes atherosclerosis. Moreover, there is increasing evidence that the smallest pollutant particles pose the greatest danger because of their high content of organic chemicals and prooxidative potential. To test this hypothesis, we compared the proatherogenic effects of ambient particles of <0.18 µm (ultrafine particles) with particles of <2.5 µm in genetically susceptible (apolipoprotein E–deficient) mice. These animals were exposed to concentrated ultrafine particles, concentrated particles of <2.5 µm, or filtered air in a mobile animal facility close to a Los Angeles freeway. Ultrafine particle–exposed mice exhibited significantly larger early atherosclerotic lesions than mice exposed to PM_2.5 or filtered air. Exposure to ultrafine particles also resulted in an inhibition of the antiinflammatory capacity of plasma high-density lipoprotein and greater systemic oxidative stress as evidenced by a significant increase in hepatic malondialdehyde levels and upregulation of Nrf2-regulated antioxidant genes. We conclude that ultrafine particles concentrate the proatherogenic effects of ambient PM and may constitute a significant cardiovascular risk factor.

Key Words: air pollution • ultrafine particles • atherosclerosis • oxidative stress • HDL

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