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INCREASED SUSCEPTIBILITY TO INFLUENZA INFECTION AFTER DIESEL EXHAUST EXPOSURE
Gowdy, K., J. Ciencewick, I. Jaspers, E H. Boykin, AND M I. Gilmour. INCREASED SUSCEPTIBILITY TO INFLUENZA INFECTION AFTER DIESEL EXHAUST EXPOSURE. Presented at American Thoracic Society, San Diego, CA, May 20-25, 2005.
Inhaled environmental pollutants have a possible role in modulating the susceptibility of humans to respiratory infections. Diesel exhaust (DE) is a major component of urban air pollution and their effects on pulmonary infections is of great concern. Influenza infections cause significant morbidity and mortality each year with individuals having preexisting heart and lung conditions being at the highest risk for influenza mortality. The purpose of this study was to evaluate the effects of DE exposure on the severity of an influenza infection in vivo. BALB/c mice were exposed to air, 0.5 or 2 mg/m3 of DE for 4 hours for 5 days. One hour after the final diesel exposure, mice were intratracheally instilled with 10 HA units of influenza A/Bangkok/1/79 virus. 18 hours later animals were sacrificed and bronchoalveolar lavage (BAL) fluid was collected. HA RNA, a marker of viral levels, and IFN-�, IFN-�, IFN-�, and IL-6 mRNA levels were determined by real-time RT-PCR. Lung injury was assessed by differential cell counts, and the production of LDH (U/l), microalbumin (�g/ml), and protein (�g/ml) in the BAL. Exposure to 0.5 mg/m3 DE increased influenza-induced lung injury, as indicated by enhanced levels of protein, LDH and viral HA RNA, suggesting greater viral proliferation. Enhancement of virus load was not caused by decreased interferon levels, since IFN-� and IFN-� levels were also enhanced in these mice. Differential cell counts showed higher neutrophil recruitment with the 5 day diesel exposure versus the air exposed group. We conclude that exposure to moderate levels of DE (0.5 mg/m3) may be responsible for the increased influenza levels and lung injury seen in these mice. These results indicate that exposure to DE may enhance the susceptibility to influenza virus infection. (Funded by EPA CT829470. This abstract does not reflect EPA policy).
Record Details:Record Type: DOCUMENT (PRESENTATION/ABSTRACT)
Organization:U.S. ENVIRONMENTAL PROTECTION AGENCY
OFFICE OF RESEARCH AND DEVELOPMENT
NATIONAL HEALTH AND ENVIRONMENTAL EFFECTS RESEARCH LAB
EXPERIMENTAL TOXICOLOGY DIVISION