Abstract
The toxicity of pesticides used in agriculture towards non-targeted organisms and especially pollinators has recently drawn the attention from a broad scientific community. Increased honeybee mortality observed worldwide certainly contributes to this interest. The potential role of several neurotoxic insecticides in triggering or potentiating honeybee mortality was considered, in particular phenylpyrazoles and neonicotinoids, given that they are widely used and highly toxic for insects. Along with their ability to kill insects at lethal doses, they can compromise survival at sublethal doses by producing subtle deleterious effects. In this study, we compared the bee’s locomotor ability, which is crucial for many tasks within the hive (e.g. cleaning brood cells, feeding larvae…), before and after an acute sublethal exposure to one insecticide belonging to the two insecticide classes, fipronil and thiamethoxam. Additionally, we examined the locomotor ability after exposure to pyrethroids, an older chemical insecticide class still widely used and known to be highly toxic to bees as well. Our study focused on young bees (day 1 after emergence) since (i) few studies are available on locomotion at this stage and (ii) in recent years, pesticides have been reported to accumulate in different hive matrices, where young bees undergo their early development. At sublethal doses (SLD48h, i.e. causing no mortality at 48h), three pyrethroids, namely cypermethrin (2.5 ng/bee), tetramethrin (70 ng/bee), tau-fluvalinate (33 ng/bee) and the neonicotinoid thiamethoxam (3.8 ng/bee) caused a locomotor deficit in honeybees. While the SLD48h of fipronil (a phenylpyrazole, 0.5 ng/bee) had no measurable effect on locomotion, we observed high mortality several days after exposure, an effect that was not observed with the other insecticides. Although locomotor deficits observed in the sublethal range of pyrethroids and thiamethoxam would suggest deleterious effects in the field, the case of fipronil demonstrates that toxicity evaluation requires information on multiple endpoints (e.g. long term survival) to fully address pesticides risks for honeybees. Pyrethroid-induced locomotor deficits are discussed in light of recent advances regarding their mode of action on honeybee ion channels and current structure-function studies.
Highlights
Pollinators play a crucial role in maintaining vegetal biodiversity and participate in improving agricultural production
Two criteria were mandatory in our experiments to select experimental SLD48h: i) a dose producing a mortality level not statistically different from the control was considered as a SLD48h and ii) twice the chosen dose (SLD48h) had to produce a mortality level significantly higher than the control
SLD48h for each insecticide are given in S1 Table, with results of the statistical analysis on mortality assays (p-values from exact Fisher tests)
Summary
Pollinators play a crucial role in maintaining vegetal biodiversity and participate in improving agricultural production. In the last few decades, an increase in honeybee colony mortalities has been reported around the world and focused the attention of a broad scientific community on the potential consequences of pesticide misuse on pollinator survival [3,4,5]. These studies have been especially focused on two families of insecticides, neonicotinoids and phenylpyrazoles, owing to their use as systemic insecticides in seed treatment [6]. These insecticides all target ion channels involved in the function of a variety of tissues (including the nervous and the muscular systems), and it is known that their primary mode of action is to interfere with the normal function of voltage-gated sodium channels (for pyrethroids), nicotinic acetylcholine receptors (for neonicotinoids) and glutamate and GABA receptors (for phenylpyrazoles)
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