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Susceptibility of Diabetic Rats to Pulmonary and Systemic Effects of Inhaled Photochemically-Aged Atmosphere and Ozone (O3)
Citation:
Schladweiler, M., S. Snow, Todd Krantz, C. King, J. Krug, N. Modak, A. Henriquez, V. Bass, D. Miller, J. Richards, E. Boykin, R. Jaskot, Ian Gilmour, AND U. Kodavanti. Susceptibility of Diabetic Rats to Pulmonary and Systemic Effects of Inhaled Photochemically-Aged Atmosphere and Ozone (O3). Society of Toxicology Meeting, San Diego, CA, March 22 - 26, 2015.
Impact/Purpose:
Air pollutants are inhaled as a complex mixture of chemically diverse gaseous and particulate components, but most experimental studies focus on individual pollutant or pollutant sources. While high concentration O3 effects were apparent in healthy and diabetic rats, minimal effects of smog could be due to relatively low exposure concentrations.
Description:
Susceptibility of Diabetic Rats to Pulmonary and Systemic Effects of Inhaled Photochemically-Aged Atmosphere and Ozone (O3)MC Schladweiler1, SJ Snow2, QT Krantz1, C King1, JD Krug2, N Modak2, A Henriquez3, V Bass4, DJ Miller3, JE Richards1, EH Boykin1, R Jaskot1, MI Gilmour1 and UP Kodavanti11EPHD, NHEERL, ORD, U.S. EPA, Research Triangle Park, NC, USA; 2Oak Ridge Institute for Science and Education, Oak Ridge, TN, USA; 3Curriculum in Toxicology, 4SPH, UNC, Chapel Hill, NC, USAAir pollutants are inhaled as a complex mixture of chemically diverse gaseous and particulate components, but most experimental studies focus on individual pollutant or pollutant sources. The goal of this study was to assess pulmonary and metabolic impacts of a photochemically aged pollutant mixture (smog) in healthy and diabetic rats. This mixture was generated from a gasoline, alpha pinene, nitric oxide and ammonium sulfate aerosol seed solution using a photochemical reaction chamber. The concentrations of 313 µg/m3 secondary organic aerosol, 0.093 ppm O3, and 0.162 ppm NOx were achieved. Male, three month old Wistar and Goto-Kakizaki (GK) rats, a non-obese type 2 diabetic Wistar-derived model, were exposed nose-only, 4 hr/day for 1 or 5 days to filtered air or smog. Immediately following exposure, whole body plethysmography, pulmonary injury/inflammation and metabolic effects were assessed. Exposure to smog caused no changes in whole body plethysmography, bronchoalveolar lavage fluid (BALF) markers of injury and inflammation, or systemic levels of lipids, leptin, and insulin in either strain, but caused progressive hyperglycemia in GK rats over a 5 day period. In a separate study, Wistar or GK rats were exposed whole body, to filtered air or 1.0 ppm O3, 6 hr/day for 1 or 2 consecutive days. Although Wistar and GK rats produced similar glucose intolerance immediately after a single high level O3 exposure, pulmonary injury, inflammation and changes in whole body plethysmography measures were more pronounced in GK rats after 1 day exposure. GK rats also developed hyperglycemia after an O3 exposure. While 1.0 ppm O3 effects were apparent in both strains (GK>Wistar), minimal effects of smog could be due to relatively low exposure concentrations. Future studies will examine alternative mixtures of smog at higher levels to further explore the pulmonary and metabolic effects in diabetics. (This abstract does not represent U.S. EPA policy.)