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Using an adverse outcome pathway network to describe the weight of evidence linking nicotinic acetylcholine receptor activation to honey bee colony failure
LaLone, C. Using an adverse outcome pathway network to describe the weight of evidence linking nicotinic acetylcholine receptor activation to honey bee colony failure. American Chemical Society National Meeting, Washington, DC, August 20 - 24, 2017.
This presentation provides an overview of our recent publication “Weight of evidence evaluation of a network of adverse outcome pathways linking activation of the nicotinic acetylcholine receptor in honey bees to colony death” and expands upon our knowledge of the taxonomic domain of applicability for this network beyond the honey bee.
Significant and unsustainable losses of managed honey bee (Apis mellifera) colonies have been documented over recent years, which have led to scientific investigation to determine the contributing factors. Evidence suggests that both chemical and non-chemical stressors play a role in colony failure, however there has been heightened attention for neonicotinoids due to their widespread use in pest-insect control and the growing body of literature suggesting potential toxic effects to bees. Specifically, scientists have observed individual level adverse effects to honey bees upon neonicotinoid exposure, including impacts on foraging behavior and efficiency, as well as learning and memory. Neonicotinoids are known to act as agonists via the nicotinic acetylcholine receptor (nAChR) causing neurotoxicity and death in targeted insects. Therefore, it is desirable to understand whether modulation of the nAChR could lead to the noted individual level effects and further whether those individual level effects are indicative of eventual colony death. To begin to explore the linkage between nAChR activation and the adverse outcome of regulatory concern, colony death/failure, we developed six adverse outcome pathways (AOPs) and conducted associated weight of evidence evaluations, presenting the biological plausibility and/or empirical support available for the relationships in the defined AOPs. Each AOP shared nAChR activation as the molecular initiating event (MIE) and colony death/failure as the adverse outcome, with a total of eight intermediate key events (KEs) and fourteen key event relationships (KERs) described. Overlap in the KEs and KERs in multiple AOPs allowed for the description of an AOP network. From this effort, key knowledge gaps were identified in our understanding of the biological pathway that could be used to guide future research initiatives. Overall, from the weight of evidence evaluation, it was determined that sufficient biological plausibility exists to link activation of nAChR to colony death. Additional computational evaluations, using the U.S. EPA Sequence Alignment to Predict Across Species Susceptibility tool, have been ongoing to capture the taxonomic domain of applicability for the MIE and early KEs in these pathways, as declines in non-Apis bee populations are also of concern due to their pollination services.