Benthic injury dose-response models for polychlorinated biphenyl-contaminated sediment using equilibrium partitioning.

The study goal was to develop a sediment polychlorinated biphenyl (PCB) dose-response model based on benthic invertebrate effects to PCBs. The authors used an equilibrium partitioning (EqP) approach to generate predicted PCB sediment effect concentrations (largely Aroclor 1254) associated with a gradient of toxic effects in benthic organisms from effects observed in aquatic toxicity studies. The present study differs from all other EqP collective sediment investigations in that the authors examined a common dose-response gradient of effects for PCBs rather than a single, protective value. The authors reviewed the chronic aquatic toxicity literature to identify measured aqueous PCB concentrations and associated benthic invertebrate effects. The authors control-normalized the aquatic toxic effect data and expressed results from various studies as a common metric, percent injury. Then, they calculated organic carbon-normalized sediment PCB concentrations (mg/kg organic carbon) from the aqueous PCB toxicity data set using EqP theory based on the US Environmental Protection Agency's (EPIWEB 4.1) derivation of the water-organic carbon partition coefficient (KOC ). Lastly, the authors constructed a nonlinear dose-response numerical model for these synoptic sediment PCB concentrations and biological effects: Y = 100/1 + 10([logEC50-logX] × [Hill slope]) (EC50 = median effective concentration). These models were used to generate "look-up" tables reporting percent injury in benthic biota for a range of Aroclor-specific sediment concentrations. For example, the model using the EPIWEB KOC estimate predicts mean benthic injury of 23.3%, 46.0%, 70.6%, 87.1%, and 95% for hypothetical sediment concentrations of 1 mg/kg, 2 mg/kg, 4 mg/kg, 8 mg/kg, and 16 mg/kg dry weight of Aroclor 1254, respectively (at 1% organic carbon). The authors recommend the model presented for screening but suggest, when possible, determining a site-specific KOC that, along with the tables and equations, allows users to create their own protective dose-response sediment concentration. Environ Toxicol Chem 2017;36:1311-1329. © 2016 SETAC.

A review of the tissue residue approach for organic and organometallic compounds in aquatic organisms.

This paper reviews the tissue residue approach (TRA) for toxicity assessment as it applies to organic chemicals and some organometallic compounds (Sn, Hg, and Pb) in aquatic organisms. Specific emphasis was placed on evaluating key factors that influence interpretation of critical body residue (CBR) toxicity metrics including data quality issues, lipid dynamics, choice of endpoints, processes that alter toxicokinetics and toxicodynamics, phototoxicity, species- and life stage-specific sensitivities, and biotransformation. The vast majority of data available on TRA is derived from laboratory studies of acute lethal responses to organic toxicants exhibiting baseline toxicity. Application of the TRA to various baseline toxicants as well as substances with specific modes of action via receptor-mediated processes, such as chlorinated aromatic hydrocarbons, pesticides, and organometallics is discussed, as is application of TRA concepts in field assessments of tissue residues. In contrast to media-based toxicity relationships, CBR values tend to be less variable and less influenced by factors that control bioavailability and bioaccumulation, and TRA can be used to infer mechanisms of toxic action, evaluate the toxicity of mixtures, and interpret field data on bioaccumulated toxicants. If residue-effects data are not available, body residues can be estimated, as has been done using the target lipid model for baseline toxicants, to derive critical values for risk assessment. One of the primary unresolved issues complicating TRA for organic chemicals is biotransformation. Further work on the influence of biotransformation, a better understanding of contaminant lipid interactions, and an explicit understanding of the time dependency of CBRs and receptor-mediated toxicity are all required to advance this field. Additional residue-effects data on sublethal endpoints, early life stages, and a wider range of legacy and emergent contaminants will be needed to improve the ability to use TRA for organic and organometallic compounds.

Residue-based mercury dose-response in fish: an analysis using lethality-equivalent test endpoints.

Dose-response relationships for aquatic organisms have been developed for numerous contaminants using external media exposures (water and sediment). Dose-response relationships based on internal concentrations (tissue residues) are limited. The present study reports Hg dose-response curves for early life stage and juvenile or adult fish based on published tissue-residue toxicity studies. These curves rely primarily on endpoints that can be directly related to mortality, such as survival, reproductive success, and lethal developmental abnormalities. These lethality-equivalent endpoints were linked using the common metric of injury. Uncertainties and potential applications of this mercury dose-response curve are discussed. Major uncertainties include lab to field extrapolations, biological endpoints selected by investigators, interspecific extrapolations, and the paucity of published early life stage residue (dose)-response information. To the extent this curve is based exclusively on laboratory toxicity tests and does not consider other potentially sensitive and ecologically important biological endpoints (e.g., growth and behavior), the magnitude of the adverse effects predicted by the curve may be underestimated.

Approaches for linking whole-body fish tissue residues of mercury or DDT to biological effects thresholds.

A variety of methods have been used by numerous investigators attempting to link tissue concentrations with observed adverse biological effects. This paper is the first to evaluate in a systematic way different approaches for deriving protective (i.e., unlikely to have adverse effects) tissue residue-effect concentrations in fish using the same datasets. Guidelines for screening papers and a set of decision rules were formulated to provide guidance on selecting studies and obtaining data in a consistent manner. Paired no-effect (NER) and low-effect (LER) whole-body residue concentrations in fish were identified for mercury and DDT from the published literature. Four analytical approaches of increasing complexity were evaluated for deriving protective tissue residues. The four methods were: Simple ranking, empirical percentile, tissue threshold-effect level (t-TEL), and cumulative distribution function (CDF). The CDF approach did not yield reasonable tissue residue thresholds based on comparisons to synoptic control concentrations. Of the four methods evaluated, the t-TEL approach best represented the underlying data. A whole-body mercury t-TEL of 0.2 mg/kg wet weight, based largely on sublethal endpoints (growth, reproduction, development, behavior), was calculated to be protective of juvenile and adult fish. For DDT, protective whole-body concentrations of 0.6 mg/kg wet weight in juvenile and adult fish, and 0.7 mg/kg wet weight for early life-stage fish were calculated. However, these DDT concentrations are considered provisional for reasons discussed in this paper (e.g., paucity of sublethal studies).