on a common mechanism of toxicity and thus joint toxicity models are an important facet of this 
path. The following important gaps need to be filled: 
1. Residue-based toxicity data bases need to be advanced and evaluated for applicability to 
aquatic ecological risk assessment requirements for PBTs. 
2. Is absence of overt mortality, even for early life stages, an adequate effects end point for 
preventing population declines caused by PBTs? If not, how do we determine what is adequate? 
3. Commonly measured biochemical effect indicators, such as P450 enzyme induction, have 
uncertain relationships to organismal, much less population-level, risks. 
4. Complex, multi-stressor models, such as required for photo-induced PAH toxicity to fish 
during embryo-larval stage of development, need to be developed and applied to determine the 
magnitude of ecological risks which are presently highly uncertain. 
5. Virtually unexplored are the toxicokinetic and toxicodynamic determinants for interspecies 
and inter-effect extrapolations of potency ratios required for PBT mixture toxicity risk 
assessment using a toxic units model approach, such as the additive TCDD toxicity equivalence 
model. 
Population Model 
Population models are used to translate organismal responses to toxicity into population changes 
which may reflect risk to the population. Thus, life stage specific mortality or chronic effects 
which reduce survival may lead to a reduced population or extinction. While population models, 
such as the Leslie matrix age-class or individually based models, have been developed, relatively 
few applications in retrospective risk assessments for aquatic organisms exposed to PBTs have 
been reported. Examples of prospective use of population models for protection of aquatic life 
from PBT toxicity are fewer. This is unfortunate because WQC and other forms of risk 
assessment for protection of aquatic life from PBT toxicity should have a problem formulation 
based on the levels of population protection required. Clearly, the population model path is 
important for relating toxicity-induced mortality of individual organisms to population level 
changes in an ecosystem. However, a potentially equally important use is for the systematic 
definition of species characteristics, life stages, and toxicity effects that are most likely to 
determine risks to populations associated with PBTs having a particular mechanism of action. 
The following important gaps need to be filled: 
1. Population models need to be developed and applied through case studies to explicitly 
demonstrate risk assessment requirements for prediction of adverse population impacts, as a 
result of PBT toxicity caused reductions in survival of aquatic organisms. 
2. Complex mixtures of PBTs are the norm, so interspecies differences in potency, as well as in 
bioaccumulation, for individual chemicals in the mixture must be factored into population level 
risk predictions. 
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