sharon sanders
Editor-in-Chief & President
Go Bruins!! :tiphat:
Ambient Particulate Pollutants in the Ultrafine Range Promote Early Atherosclerosis and Systemic Oxidative Stress
Jesus A. Araujo ; <wbr>Berenice Barajas ; <wbr>Michael Kleinman ; <wbr>Xuping Wang ; <wbr>Brian J. Bennett ; <wbr>Ke Wei Gong ; <wbr>Mohamad Navab ; <wbr>Jack Harkema ; <wbr>Constantinos Sioutas ; <wbr>Aldons J. Lusis ; <wbr> and Andre E. Nel <sup>*</sup> 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.
<sup>*</sup> To whom correspondence should be addressed. E-mail: ANel@mednet.ucla.edu<script type="text/javascript"><!-- var u = "ANel", d = "mednet.ucla.edu"; document.getElementById("em0").innerHTML = '<a href="mailto:' + u + '@' + d + '">' + u + '@' + d + '<\/a>'//--></script>.
<abs> </abs>
Air pollution is associated with significant adverse health<sup> </sup>effects, including increased cardiovascular morbidity and mortality.<sup> </sup>Exposure to particulate matter with an aerodynamic diameter<sup> </sup>of <2.5 ?m (PM<sub>2.5</sub>) increases ischemic cardiovascular<sup> </sup>events and promotes atherosclerosis. Moreover, there is increasing<sup> </sup>evidence that the smallest pollutant particles pose the greatest<sup> </sup>danger because of their high content of organic chemicals and<sup> </sup>prooxidative potential. To test this hypothesis, we compared<sup> </sup>the proatherogenic effects of ambient particles of <0.18<sup> </sup>?m (ultrafine particles) with particles of <2.5 ?m<sup> </sup>in genetically susceptible (apolipoprotein E?deficient)<sup> </sup>mice. These animals were exposed to concentrated ultrafine particles,<sup> </sup>concentrated particles of <2.5 ?m, or filtered air in<sup> </sup>a mobile animal facility close to a Los Angeles freeway. Ultrafine<sup> </sup>particle?exposed mice exhibited significantly larger early<sup> </sup>atherosclerotic lesions than mice exposed to PM<sub>2.5</sub> or filtered<sup> </sup>air.<sup> </sup>of the antiinflammatory capacity Exposure to ultrafine particles also resulted in an inhibition of plasma high-density lipoprotein<sup> </sup>and greater systemic oxidative stress as evidenced by a significant<sup> </sup>increase in hepatic malondialdehyde levels and upregulation<sup> </sup>of Nrf2-regulated antioxidant genes. We conclude that ultrafine<sup> </sup>particles concentrate the proatherogenic effects of ambient<sup> </sup>PM and may constitute a significant cardiovascular risk factor.
http://circres.ahajournals.org/cgi/content/abstract/CIRCRESAHA.107.164970v1
<sup> </sup>
Ambient Particulate Pollutants in the Ultrafine Range Promote Early Atherosclerosis and Systemic Oxidative Stress
Jesus A. Araujo ; <wbr>Berenice Barajas ; <wbr>Michael Kleinman ; <wbr>Xuping Wang ; <wbr>Brian J. Bennett ; <wbr>Ke Wei Gong ; <wbr>Mohamad Navab ; <wbr>Jack Harkema ; <wbr>Constantinos Sioutas ; <wbr>Aldons J. Lusis ; <wbr> and Andre E. Nel <sup>*</sup> 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.
<sup>*</sup> To whom correspondence should be addressed. E-mail: ANel@mednet.ucla.edu<script type="text/javascript"><!-- var u = "ANel", d = "mednet.ucla.edu"; document.getElementById("em0").innerHTML = '<a href="mailto:' + u + '@' + d + '">' + u + '@' + d + '<\/a>'//--></script>.
<abs> </abs>
Air pollution is associated with significant adverse health<sup> </sup>effects, including increased cardiovascular morbidity and mortality.<sup> </sup>Exposure to particulate matter with an aerodynamic diameter<sup> </sup>of <2.5 ?m (PM<sub>2.5</sub>) increases ischemic cardiovascular<sup> </sup>events and promotes atherosclerosis. Moreover, there is increasing<sup> </sup>evidence that the smallest pollutant particles pose the greatest<sup> </sup>danger because of their high content of organic chemicals and<sup> </sup>prooxidative potential. To test this hypothesis, we compared<sup> </sup>the proatherogenic effects of ambient particles of <0.18<sup> </sup>?m (ultrafine particles) with particles of <2.5 ?m<sup> </sup>in genetically susceptible (apolipoprotein E?deficient)<sup> </sup>mice. These animals were exposed to concentrated ultrafine particles,<sup> </sup>concentrated particles of <2.5 ?m, or filtered air in<sup> </sup>a mobile animal facility close to a Los Angeles freeway. Ultrafine<sup> </sup>particle?exposed mice exhibited significantly larger early<sup> </sup>atherosclerotic lesions than mice exposed to PM<sub>2.5</sub> or filtered<sup> </sup>air.<sup> </sup>of the antiinflammatory capacity Exposure to ultrafine particles also resulted in an inhibition of plasma high-density lipoprotein<sup> </sup>and greater systemic oxidative stress as evidenced by a significant<sup> </sup>increase in hepatic malondialdehyde levels and upregulation<sup> </sup>of Nrf2-regulated antioxidant genes. We conclude that ultrafine<sup> </sup>particles concentrate the proatherogenic effects of ambient<sup> </sup>PM and may constitute a significant cardiovascular risk factor.
http://circres.ahajournals.org/cgi/content/abstract/CIRCRESAHA.107.164970v1
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