Health & Environmental Research Online (HERO)


Print Feedback Export to File
2617342 
Journal Article 
Abstract 
Gas-particle interactions in driving vascular lipid peroxidation following inhalation of traffic-related air pollutants 
Campen, MJ; Lund, A; Seagrave, J; Lucero, J; Mathews, N; Mauderly, JL; Mcdonald, J 
2010 
Yes 
American Journal of Respiratory and Critical Care Medicine
ISSN: 1073-449X
EISSN: 1535-4970 
181 
A1164 
English 
WOS:000208771000165 
is part of a larger document 3452678 Proceedings of the American Thoracic Society 2010 International Conference, May 14-19, 2010, New Orleans
Traffic-related air pollutants (TRAPs) have recently been associated with progressive vascular disease. To explore the biological plausibility of complex TRAPs in driving systemic vascular toxicity, we have designed a model of combined vehicular emissions to test with and without background PM from other sources. Diesel and gasoline engine emissions, therefore, are combined in a mixing chamber to generate the basic TRAP atmosphere. We then can filter vehicular particulate matter (PM) and replace with modeled background PM (secondary sulfate or nitrate PM). These various atmospheres, at 100 or 300 μg PM/m , are then administered to apolipoprotein E-null 3 (apoE ) mice for 6 h/d x 7 or 50 days by whole boy inhalation. As a primary endpoint, we have isolated aortic tissue and serum and -/- performed measurements of lipid peroxidation (thiobarbituric acid-reactive substances or TBARS). Oxidized low density lipoprotein (LDL) was modestly elevated in combined TRAP emissions, but filtration of PM significantly reduced his effect. A more robust increase in lipid peroxidation was noted in the aorta, potentially related to the accumulative nature of the lipid byproducts in the atheromatous vessel. Interestingly, the combined diesel and gasoline engine emissions were synergistically toxic compared to either engine emission alone, and these effects could be completely abrogated by filtration of the vehicular PM. While sulfate and nitrate PM alone caused no increase in vascular lipid peroxidation, addition of either PM subtype to the gaseous portion of the combined vehicular emissions caused significant increases in vascular TBARS. Lastly, to test the potential for a scavenger receptor, LOX-1, to drive vascular lipid peroxidation, we co-treated a cohort of mice with LOX-1 antibodies. Significant increases in vascular LOX-1 mRNA were noted following exposure to combined gasoline and diesel engine emissions. The LOX-1 antibody cotreatment completely abolished the increase in LOX-1 mRNA and furthermore blocked the increase in vascular lipid peroxidation. CONCLUSIONS: Thus, it appears that gas-particle interactions have synergistic effects on driving vascular lipid peroxidation, potentially through oxidized lipid scavenger receptors. These findings offer new mechanistic insights into the potential relationship between TRAPs and human health effects. 
American Thoracic Society 2010 International Conference 
New Orleans, LA 
May 14-19, 2010