based criteria development and application, including use in TMDLs designed to protect 
populations of sensitive fish and wildlife species. The association of the historical lake trout 
population decline in Lake Ontario with exposure of embryos to AhR agonists such as 2,3,7,8- 
TCDD (Cook et al. 1997) will be used as a device to examine the applicability of population 
models when used in tandem with residue based toxicity data. The extent to which extrapolation 
of lake trout risks to other species involves more than species sensitivity to TCDD and degree of 
exposure/bioaccumulation will be examined in the context of toxicokinetic, toxicodynamic, 
biochemical, and life history factors. 
Data gaps and modeling limitations will be identified and further described as research needs for 
development of a general risk assessment capability for all PBTs. This analysis will include an 
initial conceptual evaluation of the degree to which similarities and differences in PBT properties 
and mechanisms of action will define a balance between generic and diemical ^cific PBT risk 
assessment approaches and models. For example, do the properties of persistence and 
bioaccumulation, in combination with principles of population dynamics, indicate that effects on 
ELS development and survival are invariably risk detemiining for PBTs in general? If so, what 
are the basic PBT toxicity and exposure data and modeling requirements for ecological risk 
assessments? Population matrix modeling will be a primary tool for evaluating vulnerability 
differences between species based on differences in life stage sensitivities, exposure profiles, and 
reproductive strategies. 
Other aquatic stressors research projects involving PBTs are expected to contribute periodically 
new or improved risk assessment capabilities which can then be integrated into the PBT 
framework under this project. Although the continuing development of the framework will 
include incorporation of all relevant new data and models, many new capabilities are expected to 
become available as the result of completions of APMs. Examples of expected risk assessment 
capability advances, listed in association with the APGs and projects, are: 
Methods for developing WQC based on characterization of population-level risks of toxic 
chemicals to aquatic life and aquatic-dependent wildlife (APG 3): 
• Rates of metabolism and improved food chain bioaccumulation models for metabolizable 
PBTs (project B2). 
• Models for assessing relative risks of multiple stressors to avian populations with large 
geographic ranges (project B3). 
• Improved understanding of fish early life stage dosimetry including appearance and 
extent of metabolism during development (project B2). 
Models for extrapolating chemical toxicity data across exposure conditions, endpoints, life 
stages, and species (APG 4): 
• Methods for inter-site extrapolation of BAFs based on site-specific food chains and 
bioavailability conditions (project B2). 
Ill 
