Growth and survival of pacific coho salmon smolts exposed as juveniles to pesticides within urban streams in western Washington, USA.

Pesticides are frequently detected in urban streams, with concentrations often exceeding those reported in surface waters within agricultural areas. The authors studied growth, survival, and return rates of coho salmon (Oncorhynchus kisutch) smolts exposed to a pesticide mixture ("cocktail") representative of the pesticides most frequently reported within urban streams in western Washington State, USA, in fall through early spring. Exposure concentrations were selected to represent a reasonable worst-case scenario based on field monitoring data. Smolts were continuously exposed to pulses of the cocktail either from fertilization through swim-up (2007-2008) or from fertilization through smoltification (2007-2008 and 2008-2009), coded wire tagged, and released in 2008 and 2009. Pre-release endpoints (growth, survival, sex ratio, brain acetylcholinesterase activity, and gonado- and hepatosomatic indices) were not affected. However, the number of returning adults exposed to the cocktail to swim-up (0.90%, n = 42) was more than double that of unexposed controls (0.38%, n = 26) in 2008, whereas in 2009, fish exposed through smoltification returned in lower numbers (0.15%, n = 18) than controls (0.37%, n = 30). Variability in return rates among treatments between years was comparable to that observed in previous whole life cycle studies with Pacific salmon and other contaminants. Results suggest that exposure to pesticides in urban streams does not directly impair early life stages of coho salmon, and that additional studies incorporating releases of larger numbers of smolts across several years are necessary to adequately quantify effects on return rates.

Brain acetylcholinesterase activity in shiner perch (Cymatogaster aggregata) and juvenile chinook salmon (Oncorhynchus tshawytscha) after application of carbaryl to control burrowing shrimp within Willapa Bay, Washington.

Carbaryl has been applied in Willapa Bay, Washington, for five decades to control burrowing shrimp (Neotrypaea californiensis and Upogebia pugettensis) on commercial oyster (Crassostrea gigas) beds. Concerns about effects on nontarget species, including fishes, have led to restrictions in use despite a lack of data on in situ exposure. We measured brain acetylcholinesterase (AChE) activity in adult Shiner perch (Cymatogaster aggregata) and juvenile Chinook salmon (Oncorhynchus tshawytscha) after operational applications. We hypothesized that exposure in Shiner perch would be greater than in juvenile Chinook salmon because of their greater site fidelity and benthic foraging. However, Shiner perch exhibited no statistically significant AChE inhibition. Enzyme activity was statistically decreased (≤14 %) in juvenile Chinook salmon after a second spray event; however, inhibition was less than that associated with overt effects and was similar to controls by 48 h after the spray. Diet analyses confirmed that Shiner perch were primarily feeding on benthic invertebrates and that juvenile Chinook salmon were feeding primarily within the water column. Composition of Shiner perch diets and amount of food consumed varied little among channels and time periods; however, Shiner perch on beds consumed more food 6 h after application than those at other time points and locations. There were no consistent differences in the diets of juvenile Chinook salmon within channels among time periods. Results suggest (1) that carbaryl applications pose little hazard to fish in the bay having habitat and dietary preferences similar to those of Shiner perch and juvenile Chinook salmon and (2) that quantification of direct exposure in the field is essential to adequately assess risk.

Pesticides in urban streams and prespawn mortality of Pacific coho salmon.

The listing of several runs of Pacific salmon as threatened or endangered and associated federal, state, and local efforts to restore/enhance salmon habitat in the Pacific Northwest make it imperative that the factors associated with these population declines are understood. Prespawn mortality (PSM) has been documented in coho salmon (Oncorhynchus kisutch) within urban streams in western Washington since the late 1990s and is characterized by a suite of neurological and respiratory symptoms with mortality occurring shortly thereafter. Mortality rates in returning adults have ranged between 17 and 100%. The cause of PSM is not known, but the presence of pesticide residues within urban streams led to a hypothesis that PSM in coho salmon and pesticides in urban streams were linked. We exposed pairs of "green" (unripe) prespawn male and female coho salmon to a pesticide mixture ("cocktail") reported in urban streams in western Washington State, USA. Longevity, ripening in female salmon, and brain acetylcholinesterase were not significantly affected by continuous exposure to the maximum reported concentrations of the pesticides. Fertilization, hatching success, and growth of fry were also not affected when green adults were exposed to these concentrations for 96 h. The absence of effects suggests it is unlikely that pesticides within stormwater are singularly responsible for PSM in coho salmon or that they impair the reproductive capability of exposed adults.

Pesticides in urban streams and early life stages of Pacific coho salmon.

Pesticides are frequently detected in urban streams and are believed to be primarily the result of homeowner use. Although concentrations in most cases are low (<1 µg/L), there is concern that pesticide inputs threaten efforts to restore and enhance salmon habitat. The authors exposed early life stages of coho salmon (Oncorhynchus kisutch) to a pesticide mixture ("cocktail") representative of those pesticides most frequently reported in urban streams in western Washington State, USA. Life stages were continuously exposed to pulses of the cocktail simulating those in urban streams in fall and winter when coho salmon eggs and sac fry are present. Nominal concentrations of eight herbicides, two insecticides, a fungicide, and a breakdown product were the maximum detected. Fertilization, hatching success, survival, deformities, and growth of fry were not significantly affected. A reduction in fertilization success (19-25%) was not reproducible even when gametes were exposed to 100 times the maximum concentrations detected. Based on the end points examined in the present study, the results suggest that direct exposure to the pesticides most frequently detected in urban streams in western Washington does not impair early life stages of coho salmon and is not a major factor governing the recovery of salmon populations. The extent to which pesticide exposure would affect smoltification, outmigration, and ocean survival needs to be determined.

Defining and modeling known adverse outcome pathways: Domoic acid and neuronal signaling as a case study.

An adverse outcome pathway (AOP) is a sequence of key events from a molecular-level initiating event and an ensuing cascade of steps to an adverse outcome with population-level significance. To implement a predictive strategy for ecotoxicology, the multiscale nature of an AOP requires computational models to link salient processes (e.g., in chemical uptake, toxicokinetics, toxicodynamics, and population dynamics). A case study with domoic acid was used to demonstrate strategies and enable generic recommendations for developing computational models in an effort to move toward a toxicity testing paradigm focused on toxicity pathway perturbations applicable to ecological risk assessment. Domoic acid, an algal toxin with adverse effects on both wildlife and humans, is a potent agonist for kainate receptors (ionotropic glutamate receptors whose activation leads to the influx of Na(+) and Ca²(+)). Increased Ca²(+) concentrations result in neuronal excitotoxicity and cell death, primarily in the hippocampus, which produces seizures, impairs learning and memory, and alters behavior in some species. Altered neuronal Ca²(+) is a key process in domoic acid toxicity, which can be evaluated in vitro. Furthermore, results of these assays would be amenable to mechanistic modeling for identifying domoic acid concentrations and Ca²(+) perturbations that are normal, adaptive, or clearly toxic. In vitro assays with outputs amenable to measurement in exposed populations can link in vitro to in vivo conditions, and toxicokinetic information will aid in linking in vitro results to the individual organism. Development of an AOP required an iterative process with three important outcomes: a critically reviewed, stressor-specific AOP; identification of key processes suitable for evaluation with in vitro assays; and strategies for model development.