Changes in juvenile coho salmon electro‐olfactogram during and after short‐term exposure to current‐use pesticides

Abstract

For anadromous salmonids, olfaction is a critical sense, enabling return migration. In recent years, several pesticides have been identified that interfere with salmonid olfaction at concentrations in the microg/L range; thus, they may pose a risk to species longevity. In the present study, we investigated the acute effects of five agricultural pesticides on juvenile coho salmon (Oncorhynchus kisutch) olfaction using the electro-olfactogram (EOG), a measure of odorant-evoked field potentials. Electro-olfactogram responses to the odorant L-serine were measured during and following a 30-min exposure of the left olfactory rosette to chlorothalonil, endosulfan, glyphosate acid, iodocarb (IPBC), trifluralin, and 2,4-dichlorophenoxyacetic acid. With the relatively insoluble pesticides endosulfan and trifluralin, decreases in EOG amplitude were only apparent at relatively high concentrations (100 and 300 microg/L, respectively) following 20 min of exposure and were absent for chlorothalonil (1 mg/L). With the water-soluble herbicide glyphosate, significant EOG reductions occurred within 10 min of exposure to 1 mg/L and more rapidly with higher concentrations. Recovery of EOG post-glyphosate exposure was concentration-dependent, and complete recovery was not observed with some concentrations at 60 min postexposure. Dichlorophenoxyacetic acid only affected EOG at high concentration (100 mg/L), where it eliminated EOG within 2 min of exposure. With IPBC, EOG was decreased at 25 min of exposure to 1 microg/L; higher concentrations caused decreases to occur more rapidly. Excluding IPBC and glyphosate, all EOG reductions occurred at concentrations greater than the current Canadian water-quality guidelines and reported 96-h lethality values. Our results show that olfactory neurons can be impaired rapidly by some current-use pesticides, even at exposures in the low-microg/L range.

Sub-lethal effects of Roundup™ on tadpole anti-predator responses

“…Can we be sure that the lack of a response is not due to the Roundup™ impairing the olfactory epithelium? Tierney et al (2006) showed that it takes approximately 10 min of exposure for 1.0 mg/L of Roundup™ to impair the olfactory system, and an increase in concentration increases the speed of the impairment. In our experiment, we mixed the 5 ml of 0.5 mg/L Roundup™ solution with 5 ml of alarm cue and introduced it to a container with 0.5 L of water giving a final concentration of 0.05 ml a.e./L.…”

“…Clearly, understanding how prey respond to risk in the presence of Roundup™ and other pesticides deserves further attention. In a study on Coho salmon (Oncorhynchus kisutch), Tierney et al (2006) established that Roundup™ blocks olfaction in fish exposed to 1 mg a.e./L glyphosate acid. There was a significant reduction in electro-olfactogram (EOG) readings 10 min after the exposure started.…”

Evidence for behavioral preference toward environmental concentrations of urban‐use herbicides in a model adult fish

“…For example, rainbow trout were attracted to 6 mg/L of NiCl 2 but avoided 24 mg/L [29]. Alternately, the combination of the four herbicides, two of which are known to evoke olfactory sensory neuron responses (2,4-D and glyphosate; [13]), may have created an interesting odor bouquet. Whether the attraction was a concentration and/or mixture effect, fish chose to expose themselves to herbicide mixtures.…”

Linuron and carbaryl differentially impair baseline amino acid and bile salt olfactory responses in three salmonids

“…The omnipresence of AChE across the animal kingdom provides ample opportunity for nontarget species effects. Furthermore, carbamates have previously been shown to alter both EOG responses (Jarrard et al, 2004;Tierney et al, 2006a) and olfactorymediated behaviors in coho salmon (Tierney et al, 2006b). The method in which carbamates impair olfaction remains unknown, as AChE impairment does not obviously translate to impaired olfaction.…”