U.S. Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Mid-Continent Ecology Division, 6201 Congdon Blvd., Duluth, MN 55804, USA.
U.S. Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Mid-Continent Ecology Division, 6201 Congdon Blvd., Duluth, MN 55804, USA.
Sci Total Environ. 2017 Apr 15;584-585:751-775. doi: 10.1016/j.scitotenv.2017.01.113. Epub 2017 Jan 24.
Ongoing honey bee (Apis mellifera) colony losses are of significant international concern because of the essential role these insects play in pollinating crops. 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 pest insects. However, mounting evidence indicates that 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. Potential for exposure was not a consideration in AOP development and therefore this effort should not be considered a risk assessment. Nonetheless, development of the AOPs described herein 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. A putative 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 toward understanding common sensitive nodes in key biological pathways and identifying where mitigation strategies may be focused to reduce colony losses.
持续的蜜蜂（Apis mellifera）蜂群损失引起了国际社会的高度关注，因为这些昆虫在为农作物授粉方面发挥着重要作用。化学和非化学应激源都被认为是导致蜂群衰竭的可能因素；然而，常用的新烟碱类杀虫剂的潜在作用尤其令人担忧。新烟碱类杀虫剂作用于中枢神经系统中的烟碱型乙酰胆碱受体（nAChRs），以消灭害虫。然而，越来越多的证据表明，新烟碱类杀虫剂也可能通过损害学习和记忆能力，以及最终的觅食成功，对有益的传粉者，如蜜蜂，产生不利影响。将 nAChR 激活与学习和记忆不良影响联系起来的具体机制尚不确定。此外，观察到的个体蜜蜂的影响与群体水平的影响之间缺乏明确的联系。本综述的目的是开发不良结局途径（AOPs），以评估激活生理靶标 nAChR 与群体水平后果之间联系的生物学合理性和经验证据。在 AOP 开发中没有考虑潜在暴露，因此，这项工作不应被视为风险评估。尽管如此，本文所描述的 AOP 的开发导致了识别研究空白，例如，在理解干扰涉及神经递质传递的途径如何会对正常的蜂群功能产生不利影响，导致蜂群不稳定和随后的蜜蜂种群衰竭方面，这些研究空白可能具有很高的优先级。开发了一个假设的 AOP 网络，为进一步了解化学和非化学应激源的组合如何影响蜜蜂种群奠定了基础。从 AOP 网络组装中获得的见解，更真实地代表了对蜜蜂群体的多应激源影响，有望深入了解关键生物途径中的共同敏感节点，并确定可以集中实施缓解策略以减少蜂群损失的地方。
