You are here:
Weight of evidence evaluation of a network of adverse outcome pathways linking activation of the nicotinic acetylcholine receptor in honey bees to colony death
Citation:
LaLone, C., Dan Villeneuve, J. Wu-Smart, R. Milsk, K. Sappington, K. Garber, J. Housenger, AND G. Ankley. Weight of evidence evaluation of a network of adverse outcome pathways linking activation of the nicotinic acetylcholine receptor in honey bees to colony death. SCIENCE OF THE TOTAL ENVIRONMENT. Elsevier BV, AMSTERDAM, Netherlands, 584:751–775, (2017).
Impact/Purpose:
From adverse outcome pathway (AOP) development focused on chemical perturbation of the honey bee nicotinic acetylcholine receptor (nAChR), AOP network construction, and weight of evidence evaluation, sufficient evidence indicates that a connection is plausible to link activation of nAChR to colony loss/failure. However, quantitative linkages involving a variety of modulating factors and uncertainties (i.e., subunits that make up an insect nAChR, presence of nAChR in invertebrate mitochondria, etc.) make it difficult to define exactly what concentration, duration, and/or timing of neonicotinoid exposure and interaction with nAChR will lead to adverse colony outcomes. Therefore, the AOP framework and overall network can be used to guide future research to quantitatively assess such relationships.
Description:
Ongoing honey bee colony losses are of significant international concern because of the essential role these insects play in pollinating many high nutrient crops, such as fruits, vegetables, and nuts. Both chemical and non-chemical stressors have been implicated as possible contributors to colony failure, however, the potential role(s) of commonly-used neonicotinoid insecticides has emerged as particularly concerning. Neonicotinoids act on the nicotinic acetylcholine receptors (nAChRs) in the central nervous system to eliminate target pest insects. However, mounting evidence indicates that these neonicotinoids also may adversely affect beneficial pollinators, such as the honey bee, via impairments on learning and memory, and ultimately foraging success. The specific mechanisms linking activation of the nAChR to adverse effects on learning and memory are uncertain. Additionally, clear connections between observed impacts on individual bees and colony level effects are lacking. The objective of this review was to develop adverse outcome pathways (AOPs) as a means to evaluate the biological plausibility and empirical evidence supporting (or refuting) the linkage between activation of the physiological target site, the nAChR, and colony level consequences. Development of AOPs has led to the identification of research gaps which, for example, may be of high priority in understanding how perturbation of pathways involved in neurotransmission can adversely affect normal colony functions, causing colony instability and subsequent bee population failure. An AOP network was developed, laying the foundation for further insights as to the role of combined chemical and non-chemical stressors in impacting bee populations. Insights gained from the AOP network assembly, which more realistically represents multi-stressor impacts on honey bee colonies, are promising aids for understanding common sensitive nodes in key biological pathways and identifying where mitigation strategies may be focused to reduce colony losses.
