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DEVELOPMENT OF A DOSE-RESPONSE MODEL FOR INHALED B[A]P
Citation:
Thorslund, T. AND D. Farrar. DEVELOPMENT OF A DOSE-RESPONSE MODEL FOR INHALED B[A]P. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/R-92/135 (NTIS PB93161016), 1990.
Description:
This report analyzes the tumor data from the hamster inhalation bioassay of B[a]P conducted by Thyssen et al. (1981). etailed data on the incidence of laryngeal and pharyngeal tumors and chamber B[a]P concentration had been obtained by the authors in a previous contract (EPA 68-02-4403). wo-stage mathematical model described by Moolgavkar and Knudson (1981) was used to fit the data and to derive a low-dose linear estimate of the carcinogenic potency of inhaled B[a]P in humans. he basic approach to the two-stage model is to assume that the only effect of B[a]P is to increase each of the two relative transition rates by the same amount per unit of exposure. his model adequately fits the tumor rates in the Thyssen (1981) study, even though considerable differences in average survival existed between the exposure groups. uman unit risk estimates were derived from the low-dose linear estimate under the assumption that ppm in air is the appropriate unit of equivalent exposure between species. he unit risk for humans was estimated to be 1.36E-1 per (mg/kg)/day, which is comparable to the previous EPA estimate of 6.1 per (mg/kg)/day. This latter estimate is thought to be Inaccurate because it used inappropriate assumptions for hamster breathing rate and life span, it used incorrect exposure values, and it neglected to use the animal survival data and response data at the highest exposure level.
