Record Display for the EPA National Library Catalog


OLS Field Name OLS Field Data
Main Title Enhance and Prolonged Pulmonary Influenza Virus Infection Following Phosgene Inhalation.
Author Ehrlich, J. P. ; Burleson, G. R. ;
CORP Author New York Univ. Medical Center, Tuxedo Park. Inst. of Environmental Medicine.;Health Effects Research Lab., Research Triangle Park, NC.
Publisher c1991
Year Published 1991
Report Number EPA-68-02-4450; EPA/600/J-91/309;
Stock Number PB92-124650
Additional Subjects Phosgene ; Toxicity ; Influenza ; Lung ; Influenza virus ; Rats ; Plaque assay ; Bronchoalveolar lavage fluid ; Virus replication ; Virulence ; Reprints ;
Library Call Number Additional Info Location Last
NTIS  PB92-124650 Most EPA libraries have a fiche copy filed under the call number shown. Check with individual libraries about paper copy. 02/24/1992
Collation 17p
Animal infectivity models have been important in the demonstration of enhanced susceptibility to viral and bacterial infection as a result of low-level toxicant exposure. The study demonstrated an enhanced and prolonged viral infection using an influenza virus infectivity model in the rat following exposure to the toxicant gas phosgene. Fischer-344 rats exposed to either air or a sublethal concentration of phosgene demonstrated peak pulmonary influenza virus titers 1 d after infection. Virus titers in rats exposed to air declined rapidly falling below detectable levels by 4 d after infection. However, a significantly enhanced and prolonged pulmonary influenza virus infection was observed on d 3 and 4 after infection in rats exposed to phosgene. Virus was cleared below detectable limits on d 5 after infection in animals exposed to phosgene. Thus, inhalation of sublethal concentrations of phosgene resulted in an increased severity of pulmonary influenza virus infection. The study provides a demonstration of the effective use of a rat viral infectivity model to detect the immunotoxicity of inhaled pollutants. The model will allow future studies to focus on the immunological mechanism(s) responsible for the enhanced and prolonged pulmonary influenza virus infection. (Copyright (c) 1991 by Hemisphere Publishing Corporation.)