Superfund Research Program
Mechanisms and Biomarkers of Metal Olfactory Injury in Salmon
Final Progress Reports
Year: 2016 2014
This project addresses how metal exposures cause olfactory injury, a phenomenon linked to loss of fish survival and relevant for human smell disorders. A significant highlight was a study that demonstrated that low exposures to cadmium occurring in some Superfund sites can cause long-lasting olfactory deficits in coho salmon. Furthermore, using laser ablation ICP mass spectrometry analysis, the researchers showed that a component of the long-lasting olfactory deficits in salmon were due to bioaccumulation of cadmium within the salmon olfactory system. A novel olfactory sensory neuron array was developed to identify neurons in the salmon olfactory system that are particularly sensitive targets of cadmium, and continued the characterization of molecular antioxidant olfactory biomarker genes that they believe protect against metal-induced olfactory injury. The researchers continued the development of transgenic zebrafish lines that help the research team understand how a molecular transcription factor provides protection in this process, and they used other transgenics to visualize the impacts of chemicals in real-time and to monitor the recovery of the zebrafish olfactory system from toxic injury. Their results in zebrafish are applicable to understanding how Superfund chemicals impact wild salmon and other fish. The researchers extended their studies in a new initiative to examine the effects of emerging contaminants, and showed a marked bioaccumulation of certain pharmaceuticals and personal care products released through wastewater treatment plants in juvenile Puget Sound salmon. Collectively, their approaches are developing biomarkers that can be used to assess remediation outcomes and the health of ecologically sensitive fish in aquatic Superfund sites.