Bioaccumulation Model 
Much progress has been made in the last decade toward providing a reliable bioaccumulation 
prediction capability for aquatic organisms through complementaiy use of empirical BAFs and 
more mechanistic food chain models. Site-specific variations in bioavailabilhy have been largely 
reduced through lipid and organic carbon normalization and tropic level determination. Besides 
the chemical’s hydrophobicity and potential for metabolism in the food chain, we now recognize 
the distribution between water and sediments and the relative benthic versus pelagic food web 
composition as critical determinants of bioaccumulation. The following important gaps need to 
be filled: 
1. Rates of metabolism are needed for many PBTs in order to allow accurate predictions of 
bioaccumulation with food chain models. These rates are best determined from field data in 
order to fit the risk assessment needs. 
2. The metabolism rate gap extends to bioaccumulation of PBTs like the PAHs in embryo-larval 
stages of fi^ with potential vulnerability to photo-induced toxicity. 
3. Very few bioaccumulation data sets are of sufficient quality to validate the uses of BAFs and 
BSAFs, especially when extrapolated across species and/or ecosystems. 
4. Existing BAFs, BSAFs, and food chain models are based on whole adult organisms and thus 
may not be sufficient when dose to early life stages (ELSs) and/or specific tissues must be 
evaluated. Early life stage dosimetry-based bioaccumulation factors and PB-TK models are 
needed to fill this gap. 
5. Comprehensive and compatible BAFs, BSAFs, and food chain models are needed to meet the 
requirements of joint action toxicity models such as for TCDD toxicity equivalence or photo- 
induced PAH toxicity. 
Toxicity Model 
As would be expected, existing toxicity data vary greatly in amount and applicability for different 
PBTs. The risk assessment paradigm (Figure 8) and the conceptual model for PBTs (Figure 11) 
provide contexts for determining toxicological research needs for PBTs. Chemical residue-based 
dosimetry is an essential requirement. Ideally, residue dose-response models should relate to the 
most sensitive end points, species, and life stages which may result in population declines. 
Often, however, the toxicity data available are obtained prior to establishment of specific risk 
assessment requirements. This increases the need for development of tools for extrapolation of 
effects across species and end points. It also increases the need to plan future toxicology research 
so that the data fit into an ecological risk assessment profile for the particular class of PBT. Such 
a profile might be based on the mechanism of toxicity, ecological and exposure vulnerability of 
species, and expectations for differences in species sensitivity. A trivial example would be the 
low benefit to be expected from investigation of a specific receptor mediated toxicity in a class of 
aquatic organisms which is known to not possess the receptor. Most PBTs fall in groups based 
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