Behavioral impairment and increased predation mortality in cutthroat trout exposed to carbaryl

Willapa Bay is a coastal estuary in Washington State that provides seasonal rearing habitat for anadromous cutthroat trout Oncorhynchus clarki clarki. Cutthroat trout forage throughout the estuary in the summer months when carbaryl, a carbamate insecticide, is applied to oyster beds via aerial spraying and other application methods to control burrowing shrimp populations. The insecticide interferes with normal nervous system function in trout via the inhibition of acetylcholinesterase, an enzyme that regulates neurotransmitter-mediated signaling at synapses. In the present study, we show that the olfactory system of trout is unresponsive to carbaryl, and that trout do not avoid seawater containing the pesticide at environmentally representative concentrations. Short-term (6 h) carbaryl exposures significantly reduced acetylcholinesterase activity in both brain and muscle in a dose-dependent manner. Enzyme activity gradually recovered over 42 h following carbaryl exposure (6 h at 500 mu g l(-1)). In tests of swimming performance, trout were unable to orient to directional flow and swim effectively at exposure concentrations >= 750 mu g l(-1). Finally, we determined rates of predation by lingcod Ophiodon elongatus on carbaryl-exposed and unexposed trout. Exposed animals were consumed by predators at significantly higher rates at concentrations >= 500 mu g l(-1). We conclude that cutthroat trout are unlikely to avoid carbaryl-contaminated seawater, and that estuarine applications are likely to cause neurobehavioral impairments in trout that may increase individual mortality due to predation.