Skip Navigation

University of Washington

Superfund Research Program

Biochemical Mechanisms of Metal Olfactory Injury

Project Leader: Evan P. Gallagher
Grant Number: P42ES004696
Funding Period: 2009-2023
View this project in the NIH Research Portfolio Online Reporting Tools (RePORT)

Project-Specific Links

Connect with the Grant Recipients

Visit the grantee's eNewsletter page Visit the grantee's eNewsletter page Visit the grantee's Facebook page Visit the grantee's Video page

Project Summary (2015-2017)

Exposure to environmental concentrations of pesticides and metals can cause neurobehavioral changes that influence survival of Pacific salmon. These neurological impacts that arise from central and peripheral nervous system deficits, including inhibition of peripheral olfactory function, may block the ability to detect predators and prey, alter reproductive timing, and interfere with homing to natal streams. The fish peripheral olfactory system is highly vulnerable to the toxic effects of dissolved contaminants due to its direct contact with the aquatic environment. Olfactory injury is now documented in other aquatic species exposed to environmental pollutants, suggesting far-reaching ecological ramifications of this phenomenon.

This research project is working to understand the mechanisms of chemical-induced olfactory injury in Pacific salmon, and based upon findings, generate biomarkers of olfactory injury to evaluate the ecological health and remediation outcomes at Superfund sites. The studies also use zebrafish, a well-defined genetic model, to better understand the mechanisms of olfactory injury that are relevant to salmon. In this project, the researchers continue to integrate molecular, biochemical, physiological, and behavioral endpoints using model metal olfactory toxicants that are relevant to Superfund exposures. This novel approach allows a thorough understanding of mechanisms of chemical-induced olfactory injury in fish.

The research team is identifying olfactory receptor neuron populations that are targets of cadmium (Cd) and addressing impaired olfactory signaling and neuron regeneration (neurogenesis) as mechanisms of Cd-mediated olfactory injury. The researchers are also investigating transcriptional control of olfaction during metal exposures. They are developing olfactory biomarkers generated from their work for field studies at Superfund sites. They are also verifying and testing glutathione S-transferase (GST) isoforms as biomarkers of olfactory injury.

Back
to Top