Since 1985, the United States Environmental Protection Agency (USEPA) has classified 2,3,7,8-tetrachloro-p-dioxin (TCDD) as a probable human carcinogen; subsequently, sources of TCDD in the environment have been regulated on the basis of animal cancer rates extrapolated to doses associated with human exposures. Two major activities have prompted the decision to reassess this approach for evaluating TCDD toxicity and its associated risks. First, an epidemiological study of cancer mortality in U.S. chemical workers by the National Institute of Occupational Safety and Health provided evidence of TCDD-mediated human carcinogenicity (Fingerhut et al. 1991 ). Second, at a 1990 Banbury conference a consensus was reached that TCDD's mode of action involves the activation of a TCDD-receptor complex in susceptible species as a necessary, but not sufficient, prerequisite for any TCDD-related effects (Scheuplein et al. 1991 ). Based on these findings, USEPA identified a need for biologically based dose-response models for TCDD, and related chemicals, to establish a scientific base for more credible risk assessments. As a consequence, USEPA has designed and implemented a TCDD reassessment research plan. Because of an increasing body of knowledge concerning TCDD exposure to and effects on aquatic life and wildlife, this plan includes a component that addresses ecological risk (USEPA 1993).