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The critical body residue (CBR), estimated from aquatic toxicity QSARs and bioconcentration‐log Kow relationships, appears to be relatively constant, at about 4 mmol L−1 of fish, for the acute toxicity of a variety of hydrophobic narcotic organic chemicals examined by the U.S. Environmental Protection Agency (Duluth, MN) in tests with the fathead minnow. However, for hydrophilic chemicals (log Kow < 1.5) the bulk of the toxicant is in the water phase rather than the organic/lipid phase of the organism, so the whole‐body residues in these cases should be similar to the LC50 water concentration. Over the log Kow range of – 1.5 to 6, acutely toxic whole‐body residues for narcotics can be approximated by the QSAR‐derived equation: CBR (mM) = 2.5 mM + 50/Kow. Estimates obtained by this method are in reasonable agreement with the limited literature data available for acutely toxic whole‐body residues of hydrophobic narcotic organic chemicals. Elimination half‐lives estimated from nonlinear curve fitting to time‐toxicity information were relatively constant for the Duluth bioassay data at approximately 3 h. Despite the relatively high variability of this type of kinetics data, the literature information for small aquatic organisms, from both toxicity‐and bioconcentration‐based tests, was in a similar range. It appears that QSARs created with raw aquatic bioassay data occur primarily as a result of the influence of chemical‐physical properties on the partitioning process. Log Kow appears to have little to do with the inherent potency of the neutral, narcotic organic chemicals examined.

Hexabromocyclododecane (HBCD) is a globally produced brominated flame retardant (BFR) used primarily as an additive FR in polystyrene and textile products and has been the subject of intensified research, monitoring and regulatory interest over the past decade. HBCD is currently being evaluated under the Stockholm Convention on Persistent Organic Pollutants. HBCD is hydrophobic (i.e., has low water solubility) and thus partitions to organic phases in the aquatic environment (e.g., lipids, suspended solids). It is ubiquitous in the global environment with monitoring data generally exhibiting the expected relationship between proximity to known sources and levels; however, temporal trends are not consistent. Estimated degradation half-lives, together with data in abiotic compartments and long-range transport potential indicate HBCD may be sufficiently persistent and distributed to be of global concern. The detection of HBCD in biota in the Arctic and in source regions and available bioaccumulation data also support the case for regulatory scrutiny. Toxicity testing has detected reproductive, developmental and behavioral effects in animals where exposures are sufficient. Recent toxicological advances include a better mechanistic understanding of how HBCD can interfere with the hypothalamic-pituitary-thyroid axis, affect normal development, and impact the central nervous system; however, levels in biota in remote locations are below known effects thresholds. For many regulatory criteria, there are substantial uncertainties that reduce confidence in evaluations and thereby confound management decision-making based on currently available information.

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