Bioconcentration is the process of accumulation of water-borne chemicals by fish and other aquatic animals through nondietary routes (1). A proportionality constant relating the concentration of a chemical in water to its concentration in the aquatic animal at steady-state equilibrium is the bioconcentration factor (BCF) (1). The BCF is an estimate of a chemical's propensity to accumulate in an aquatic animal. Typically fish are the targets of BCF assessments because of their importance as a human food source and the availability of standardized testing protocols.Measured or predicted BCFs are a requisite component of both human and environmental risk assessment. The most common method for estimating a chemical's BCF relies on established correlations between BCF and hydrophobicity of the chemical. The majority of these have been linear regression models of the log transformations of BCF and the chemical's partitioning be-tween octanol and water (2). The fundamental assumption of these relationships is that organic chemical hydrophobicity is the principal driving force of bioconcentration; that is, organic chemical bioconcentration is simply the thermodynamically driven partitioning between water and the lipid phase of the animal (3).The purpose of this paper is to critically evaluate the hypothesis that hydrophobicity is the principal determinant of bioconcentration in aquatic animals and examine the dependence of bioconcentration on species, body size, and envi-

Polycyclic aromatic hydrocarbons (PAHs) can cause a variety of effects in early life-stages of fish that have been chronically exposed as embryos, including mortality, deformities, and edemas. Mechanistic models of the chronic toxicity of complex mixtures of PAHs in fish have not been reported, with the exception of a previously untested model based on the lipids of fish as the site of action and toxicity caused through a narcosis mechanism. Four mechanism-based models of the chronic toxicity of embryonic exposures to complex mixtures of petrogenic PAHs in two species of fish, Pacific herring and pink salmon, were evaluated using a toxic-units approach: narcosis, aryl hydrocarbon receptor (AhR) agonism, alkyl phenanthrene toxicity, and combined toxicity. Alkyl phenanthrenes were the predominant PAH constituent determining early life-stage toxicity in both herring and salmon. The alkyl phenanthrene model had 67 to 80% accuracy in predicting the absence or presence of significant early life-stage toxicity, compared with a 40 to 50% accuracy and general underprediction of toxicity with the narcosis model. PAHs with high relative AhR affinity did not appear to contribute substantially to the observed early life-stage toxicity because of low concentrations of the most potent AhR agonists. Narcosis appeared to primarily contribute to embryo mortality and to be predominantly controlled by the concentration of naphthalenes. Except for the highest PAH exposure to herring, the primary toxic unit contribution to the combined toxicity model was alkyl phenanthrene toxicity to both herring and salmon. We recommend the continued use of total PAHs as a metric of exposure until mechanistic models have been further evaluated.

The present study describes the acute toxicity of eight commercial oil dispersants, South Louisiana sweet crude oil (LSC), and chemically dispersed LSC. The approach used consistent test methodologies within a single laboratory in assessing the relative acute toxicity of the eight dispersants, including Corexit 9500A, the predominant dispersant applied during the DeepWater Horizon spill in the Gulf of Mexico. Static acute toxicity tests were performed using two Gulf of Mexico estuarine test species, the mysid shrimp (Americamysis bahia) and the inland silversides (Menidia beryllina). Dispersant-only test solutions were prepared with high-energy mixing, whereas water-accommodated fractions of LSC and chemically dispersed LSC were prepared with moderate energy followed by settling and testing of the aqueous phase. The median lethal concentration (LC50) values for the dispersant-only tests were calculated using nominal concentrations, whereas tests conducted with LSC alone and dispersed LSC were based on measured total petroleum hydrocarbon (TPH) concentrations. For all eight dispersants in both test species, the dispersants alone were less toxic (LC50s: 2.9 to >5,600 µl/L) than the dispersant-LSC mixtures (0.4-13 mg TPH/L). Louisiana sweet crude oil alone had generally similar toxicity to A. bahia (LC50: 2.7 mg TPH/L) and M. beryllina (LC50: 3.5 mg TPH/L) as the dispersant-LSC mixtures. The results of the present study indicate that Corexit 9500A had generally similar toxicity to other available dispersants when tested alone but was generally less toxic as a mixture with LSC.

No abstract

Ecological risks to aquatic organisms are typically assessed using acute toxicity data for relatively few species and with limited understanding of relative species sensitivity. We developed a comprehensive set of interspecies correlation estimation (ICE) models based on acute toxicity data for aquatic organisms and evaluated three key sources of model uncertainty: taxonomic relatedness, chemical mode of action (MOA), and model parameters. Models are least-squares regressions of acute toxicity of surrogate and predicted species. A total of 780 models were derived from acute values for 77 species of aquatic organisms and over 550 chemicals. Cross-validation of models showed that accurate model prediction was greatest for models with surrogate and predicted taxa within the same family (91% of predictions within 5-fold of measured values). Recursive partitioning provided user guidance for selection of robust models using model mean square error and taxonomic relatedness. Models built with a single MOA were more robust than models built using toxicity values with multiple MOAs, and improve predictions among species pairs with large taxonomic distance (e.g., within phylum). These results indicate that between-species toxicity extrapolation can be improved using MOA-based models for less related taxa pairs and for those specific MOAs.

The Deepwater Horizon (DWH) oil spill was the largest environmental disaster and response effort in U.S. history, with nearly 800 million liters of crude oil spilled. Vast areas of the Gulf of Mexico were contaminated with oil, including deep-ocean communities and over 1,600 kilometers of shoreline. Multiple species of pelagic, tidal, and estuarine organisms; sea turtles; marine mammals; and birds were affected, and over 20 million hectares of the Gulf of Mexico were closed to fishing. Several large-scale field efforts were performed, including assessments of shoreline and wildlife oiling and of coastal waters and sediments. The assessment of injuries, damages, and restoration options for the DWH spill is ongoing. Although petroleum and the polycyclic aromatic hydrocarbon component of oils are known to affect the immune systems of aquatic organisms and wildlife, immunotoxicity is not typically assessed during oil spills and has not been a focus of the DHW assessment. The effects of oil spill contaminants on immune responses are variable and often exposure dependent, but immunotoxic effects seem likely from the DHW spill based on the reported effects of a variety of oils on both aquatic and wildlife species.

No abstract

The photoenhanced toxicity of weathered Alaska North Slope crude oil (ANS) was investigated in the eggs and larvae of Pacific herring (Clupea pallasi) with and without the chemical dispersant Corexit 9527. Oil alone was acutely toxic to larvae at aqueous concentrations below 50 microg/L total polycyclic aromatic hydrocarbons (tPAH), and median lethal (LC50s) and effective concentrations (EC50s) decreased with time after initial oil exposure. Brief exposure to sunlight (approximately 2.5 h/d for 2 d) significantly increased toxicity 1.5- to 48-fold over control lighting. Photoenhanced toxicity only occurred when oil was present in larval tissue and increased with increasing tPAH concentration in tissue. Ultraviolet radiation A (UVA) treatments were less potent than natural sunlight, and UVA + sunlight caused greater toxicity than sunlight alone. The toxicity of chemically dispersed oil was similar to oil alone in control and UVA treatments, but oil + dispersant was significantly more toxic in the sunlight treatments. The chemical dispersant appeared to accelerate PAH dissolution into the aqueous phase, resulting in more rapid toxicity. In oil + dispersant exposures, the 96-h no-observed-effect concentrations in the UVA + sunlight treatment were 0.2 microg/L tPAH and 0.01 microg/g tPAH. Exposure of herring eggs to oil caused yolk sac edema, but eggs were not exposed to sun and UVA treatment did not cause phototoxicity. These results are consistent with the hypothesis that weathered ANS is phototoxic and that UV can be a significant and causative factor in the mortality of early life stages of herring exposed to oil and chemically dispersed oil.