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TRIMELLITIC ANHYDRIDE (TMA) HYPERSENSITIVITY IN MICE AFTER MULTIPLE INTRATRACHAEL (IT) EXPOSURE
Citation:
Sailstad, D M., E H. Boykin, MDW Ward, AND MJK Selgrade. TRIMELLITIC ANHYDRIDE (TMA) HYPERSENSITIVITY IN MICE AFTER MULTIPLE INTRATRACHAEL (IT) EXPOSURE. Presented at SOT, San Francisco, CA, March 25-29, 2001.
Description:
SOT 2001 DMS214
TRIMELLITIC ANHYDRIDE (TMA) HYPERSENSITIVITY IN
MICE AFTER MULTIPLE INTRATRACHEAL (IT) EXPOSURES. D Sailstad, E Boykin, M Ward, and MJ Selgrade. NHEERL, ORD, US EPA, RTP, NC, USA.
TMA causes Th2 related respiratory hypersensitivity (RH) responses. While murine models of respiratory hypersensitivity have been effective for protein allergens, assessment of low molecular weight chemicals for respiratory sensitizing potential is difficult. We have previously demonstrated small but significant increases in specific endpoints that are indicative of RH after IT challenge of mice that were previously sensitized dermally with TMA. Our goal was to determine the effect of repeated and exclusive respiratory (IT) exposure of TMA on endpoints of RH in mice. The protocol consisted of four IT exposures of 0.25% TMA in 50 ul HBSS each over a 4-week period. Serum and bronchoalveolar lavage fluid (BALF) samples were obtained at 24 and 72 hrs following each exposure. The lungs were prepared for histopathology at 72 hrs. BALF total cell counts increased in the TMA exposed groups with each IT exposure. However, there were no changes in IgE levels, differential cell counts or cytokines (IL-4, IFN-g) that would indicate the production of respiratory hypersensitivity responses in these mice. Histopathology indicated slight non-specific inflammatory responses. While these responses were non-specific and not indicative of RH, they were only seen in mice exposed to TMA. These results along with our previous findings indicate that a murine RH model for low molecular weight chemicals may require additional IT exposures and/or exposures via a different route (dermal). Additionally, the increase in BALF total cell counts over the exposure time course and the slight changes in lung histopathology suggest that additional IT exposures may be helpful in producing a more robust murine model for respiratory hypersensitivity if exclusive respiratory exposure is desired. (This abstract does not reflect EPA policy.)