Ensuring the health of aquatic ecosystems and identifying species at risk from the detrimental effects of environmental contaminants can be facilitated by integrating analytical chemical analysis with carefully selected biological endpoints measured in tissues of species of concern. These biological endpoints include molecular, biochemical and physiological markers (i.e. biomarkers) that when integrated, can clarify issues of contaminant bioavailability, bioaccumulation and ecological effects while enabling a better understanding of the effects of non-chemical stressors. In the case of contaminant stressors, an understanding of chemical modes of toxicity can be incorporated with diagnostic markers of aquatic animal physiology to help understand the health status of aquatic organisms in the field. Furthermore, new approaches in functional genomics and bioinformatics can help discriminate individual chemicals, or groups of chemicals among complex mixtures that may contribute to adverse biological effects. While the use of biomarkers is not a new paradigm, such approaches have been underutilized in the context of ecological risk assessment and natural resource damage assessment. From a regulatory standpoint, these approaches can help better assess the complex effects from coastal development activities to assessing ecosystem integrity pre- and post-development or site remediation.

In aquatic environments, organisms are exposed to contaminants via direct uptake from water and by trophic transfer. However, most toxicity tests only examine uptake via the dissolved phase. We compared the response of marine and freshwater crustacean zooplankton to silver following dissolved and food exposure. Silver, like other metals, concentrates in aquatic food chains and may exert toxicity. In standard solute exposure toxicity tests, Ag is toxic to zooplankton at concentrations of 400 nM for marine copepods and 100 nM for freshwater cladocerans, concentrations far greater than those in most waters. However, if Ag is accumulated from algal food, reproductive success decreases by >50% when algae are exposed to only 1 nM Ag in copepods and 0.5 nM Ag in cladocerans. These concentrations are within an order of magnitude of those found in contaminated estuaries. Following dietary exposure, decreased egg production and viability occur when tissue Ag concentrations increase three- to fourfold to 0.3 ppm in cladocerans and 0.5 ppm in copepods. Assimilated Ag depresses egg production by reducing yolk protein deposition and ovarian development. Our results indicate that ecologically relevant toxicity tests should consider sublethal effects of contaminants obtained from food since these effects cannot be predicted from exposures to only dissolved contaminants.

In aquatic environments, organisms are exposed to contaminants via direct uptake from water and by trophic transfer. However, most toxicity tests only examine uptake via the dissolved phase. We compared the response of marine and freshwater crustacean zooplankton to silver following dissolved and food exposure. Silver, like other metals, concentrates in aquatic food chains and may exert toxicity. In standard solute exposure toxicity tests, Ag is toxic to zooplankton at concentrations of 400 nM for marine copepods and 100 nM for freshwater cladocerans, concentrations far greater than those in most waters. However, if Ag is accumulated from algal food, reproductive success decreases by >50% when algae are exposed to only 1 nM Ag in copepods and 0.5 nM Ag in cladocerans. These concentrations are within an order of magnitude of those found in contaminated estuaries. Following dietary exposure, decreased egg production and viability occur when tissue Ag concentrations increase three- to fourfold to 0.3 ppm in cladocerans and 0.5 ppm in copepods. Assimilated Ag depresses egg production by reducing yolk protein deposition and ovarian development. Our results indicate that ecologically relevant toxicity tests should consider sublethal effects of contaminants obtained from food since these effects cannot be predicted from exposures to only dissolved contaminants.

The toxicokinetics of 2,2,4,4-tetrabromodiphenyl ether (PBDE-47) was studied in the Japanese Medaka (Oryzias latipes) after a single oral exposure followed by termination at specific time points. The effects of repeated oral exposure to PBDE-47 on reproductive performance was assessed using a pair breeding experimental design with fathead minnows (Pimephales promelas) given daily PBDE-47 exposures for 25 days, during which fecundity was measured as an indicator of reproductive performance. Medaka and fathead minnows were orally exposed to PBDE-47 by bioencapsulation in brine shrimp, Artemia sp. In the medaka studies, measurable levels of PBDE-47 were detected in the carcass within 0.25 h with peak levels occurring at 8 h. The body levels of PBDE-47 slowly declined and were still 25% of peak levels at 624 h after dosing. Assimilation of the bioencapsulated dose was at least 80% and may well approach 100%. The PBDE-47 concentration-time profile was fitted to a one-compartment clearance-volume toxicokinetic model and the model-predicted value for elimination half-life was determined to be 281 h and the first-order absorption rate constant was Ka = 0.26 hr(-1). In the fathead minnow study, egg laying in the PBDE-treated breeding pairs stopped after 10 days. The condition factor of PBDE-treated males was significantly reduced (P <0.011) compared with control males, whereas no significant difference was observed in females. Histological examination revealed a greater than 50% reduction in mature sperm in PBDE-47 exposed minnows compared to controls. Collectively, these results suggest PBDE-47 is selectively toxic to sexually mature male fathead minnows.