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Health Effects Associated with Inhalation Exposure to Diesel Emission Generated with and without CeO2 Nano Fuel Additive
Citation:
Snow, S., M. Schladweiler, J. Mcgee, V. Bass, D. Nash, J. Weinstein, R. Willis, Bill Linak, C. Wood, S. Elmore, J. Morrison, C. Johnson, R. Thomas, D. Miller, Todd Krantz, C. King, Ian Gilmour, A. Ledbetter, J. Richards, AND U. Kodavanti. Health Effects Associated with Inhalation Exposure to Diesel Emission Generated with and without CeO2 Nano Fuel Additive. Presented at Society of Toxicology, Phoenix, AZ, March 23 - 27, 2014.
Impact/Purpose:
Addition of nano cerium oxide additive to diesel fuel increases fuel burning efficiency resulting in altered emission characteristics and potentially altered health effects. Our data show that exposure to diesel exhaust generated after addiing cerium, induces adverse pulmonary effects that on a mass basis, causes greater injury than echaust from diesel without added cerium, and that cerium accumulates in the lung during exposure to exhaust from cerium doped diesel.
Description:
Diesel exhaust (DE) exposure induces adverse cardiopulmonary effects. Addition of nano cerium (Ce) oxide additive to diesel fuel (DECe) increases fuel burning efficiency resulting in altered emission characteristics and potentially altered health effects. We hypothesized that inhalation of DECe will cause greater adverse pulmonary health effects in rats than DE. Male Sprague-Dawley rats (8 wks old) were exposed to either DE or DECe (1000 μg/m3) 5 hrs/day for 2 days. We observed an increase in lung lavage fluid N-acetyl glucosaminidase in rats exposed to DECe as compared to air group. There was also a minor but nonsignificant trend for increases in several lung injury biomarkers in both exposure groups (DECe>DE). To further characterize DECe toxicity, we exposed rats to DECe (100 or 1000 μg/m3) or the gas-phase components of DECe (1000 μg/m3) 5 hrs/day for either 2 days or 4 wks (5 days/wk) with one group allowed a 14 day recovery. Ce lung burden levels indicated a time- and concentration-dependent accumulation with the 14 day recovery leading to a 35% clearance of Ce from the lung. The high dose of DECe increased lung inflammation at the 2 day time point that was reduced at 4 wks except for the sustained lavage fluid activity of γ-glutamyl transferase. Increased alveolar septae thickness due to edema and increased presence of pigmented macrophages after DECe exposure was illustrated by histology and TEM illustrated. Lung effects were also evident after exposure to gas-phase of DECe, suggesting the effects of whole exhaust may be driven by gas-phase components and/or particulate effects may be modified by gas-phase components. These data indicate that exposure to DECe induces adverse pulmonary effects that on a mass basis, causes greater injury than DE alone. (Does not reflect the US EPA policy)