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While studies on the sublethal effects of chemical residues in beeswax on adult honey bees are increasing, the study protocols assessing the impacts on honey bee brood in realistic conditions still need to be investigated. Moreover, little is known about the residue’s effect on gene expression in honey bee brood. This study reports the effects of chlorpyriphos-ethyl, acrinathrin and stearin worker pupae exposure through contaminated or adulterated beeswax on the gene expression of some key health indicators, using a novel in vivo realistic model. Larvae were reared in acrinathrin (12.5, 25, 10 and 100 ppb) and chlorpyriphos-ethyl (5, 10, 500 and 5000 ppb) contaminated or stearin adulterated beeswax (3, 4, 5, 6 and 9%) in newly formed colonies to reduce the influence of external factors. On day 11, mortality rates were assessed. Honey bee pupae were extracted from the comb after 19 days of rearing and were analysed for the gene expression profile of four genes involved in the immune response to pathogens and environmental stress factors ( Imd , dorsal , domeless and defensin ), and two genes involved in detoxifications mechanisms (CYP6AS14 and CYP9Q3). We found no linear relation between the increase in the pesticide concentrations and the brood mortality rates, unlike stearin where an increase in stearin percentage led to an exponential increase in brood mortality. The immune system of pupae raised in acrinathrin contaminated wax was triggered and the expression of CYP6AS14 was significantly upregulated (exposure to 12.5 and 25 ppb). Almost all expression levels of the tested immune and detoxification genes were down-regulated when pupae were exposed to chlorpyrifos-contaminated wax. The exposure to stearin triggered the immune system and detoxification system of the pupae. The identification of substance-specific response factors might ultimately serve to identify molecules that are safer for bees and the ecosystem’s health.

Abstract Because nontarget, beneficials, like insect pollinators, may be exposed unintentionally to insecticides, it is important to evaluate the impact of chemical controls on the behaviors performed by insect pollinators in field trials. Here we examine the impact of a portable mosquito repeller, which emits prallethrin, a pyrethroid insecticide, on honey bee foraging and recruitment using a blinded, randomized, paired, parallel group trial. We found no significant effect of the volatilized insecticide on foraging frequency (our primary outcome), waggle dance propensity, waggle dance frequency, and feeder persistency (our secondary outcomes), even though an additional deposition study confirmed that the treatment device was performing appropriately. These results may be useful to consumers that are interested in repelling mosquitos, but also concerned about potential consequences to beneficial insects, such as honey bees.

Global concern over widely documented declines in pollinators 1 – 3 has led to the identification of anthropogenic stressors that, individually, are detrimental to bee populations 4 – 7 . Synergistic interactions between these stressors could substantially amplify the environmental effect of these stressors and could therefore have important implications for policy decisions that aim to improve the health of pollinators 3 , 8 , 9 . Here, to quantitatively assess the scale of this threat, we conducted a meta-analysis of 356 interaction effect sizes from 90 studies in which bees were exposed to combinations of agrochemicals, nutritional stressors and/or parasites. We found an overall synergistic effect between multiple stressors on bee mortality. Subgroup analysis of bee mortality revealed strong evidence for synergy when bees were exposed to multiple agrochemicals at field-realistic levels, but interactions were not greater than additive expectations when bees were exposed to parasites and/or nutritional stressors. All interactive effects on proxies of fitness, behaviour, parasite load and immune responses were either additive or antagonistic; therefore, the potential mechanisms that drive the observed synergistic interactions for bee mortality remain unclear. Environmental risk assessment schemes that assume additive effects of the risk of agrochemical exposure may underestimate the interactive effect of anthropogenic stressors on bee mortality and will fail to protect the pollinators that provide a key ecosystem service that underpins sustainable agriculture. A meta-analysis of studies in which bees were exposed to combinations of agrochemicals, nutritional stressors and/or parasites revealed evidence for synergistic effects on mortality when bees were exposed to multiple agrochemicals at field-realistic levels.

Neonicotinoid seed coating is associated with reduced density of wild bees, as well as reduced nesting of solitary bees and reduced colony growth and reproduction of bumblebees, but appears not to affect honeybees. Bees' responses to neonicotinoids examined Reports that neonicotinoid insecticides have adverse effects on bee populations remain controversial. Some studies have been criticized as using unrealistically high insecticide dosages or conditions far removed from those in the field, and it has been suggested that bees might be able to detect the insecticides and avoid treated crops. Two papers in this issue of Nature present results that fill some of the gaps in our knowledge. In laboratory experiments Sébastien Kessler et al . use field-level doses of three commonly used neonicotinoids — clothianidin, imidacloprid and thiamethoxam — to show that both honeybees and bumblebees are able to detect their presence. However, the bees do not avoid neonicotinoid-treated food and may even prefer it. Maj Rundlöf et al . sowed oilseed rape with and without a clothianidin seed coating in matched and replicated agricultural landscapes. They found the seed coating to be associated with reduced density of wild bees, as well as reduced nesting of solitary bees and reduced colony growth of bumblebees, but they did not detect an effect on honeybees. Understanding the effects of neonicotinoid insecticides on bees is vital because of reported declines in bee diversity and distribution 1 , 2 , 3 and the crucial role bees have as pollinators in ecosystems and agriculture 4 . Neonicotinoids are suspected to pose an unacceptable risk to bees, partly because of their systemic uptake in plants 5 , and the European Union has therefore introduced a moratorium on three neonicotinoids as seed coatings in flowering crops that attract bees 6 . The moratorium has been criticized for being based on weak evidence 7 , particularly because effects have mostly been measured on bees that have been artificially fed neonicotinoids 8 , 9 , 10 , 11 . Thus, the key question is how neonicotinoids influence bees, and wild bees in particular, in real-world agricultural landscapes 11 , 12 , 13 . Here we show that a commonly used insecticide seed coating in a flowering crop can have serious consequences for wild bees. In a study with replicated and matched landscapes, we found that seed coating with Elado, an insecticide containing a combination of the neonicotinoid clothianidin and the non-systemic pyrethroid β-cyfluthrin, applied to oilseed rape seeds, reduced wild bee density, solitary bee nesting, and bumblebee colony growth and reproduction under field conditions. Hence, such insecticidal use can pose a substantial risk to wild bees in agricultural landscapes, and the contribution of pesticides to the global decline of wild bees 1 , 2 , 3 may have been underestimated. The lack of a significant response in honeybee colonies suggests that reported pesticide effects on honeybees cannot always be extrapolated to wild bees.

Neonicotinoid pesticides cause mortality and decline in insect pollinators. One repeatedly noted effect is a reduction in bee colony size. However, the mechanism behind this reduction is unclear. Crall et al. performed complex real-time monitoring of bumblebee behavior within their nests (see the Perspective by Raine). Neonicotinoid exposure reduced nurse and caretaking behaviors, which affected productivity and harmed colony thermoregulation. These changes in behavior acted together to decrease colony viability, even when exposure was nonlethal. Science , this issue p. 683 ; see also p. 643 Neonicotinoid insecticides disrupt worker-bee caretaking behavior within bumblebee colonies. Neonicotinoid pesticides can negatively affect bee colonies, but the behavioral mechanisms by which these compounds impair colony growth remain unclear. Here, we investigate imidacloprid’s effects on bumblebee worker behavior within the nest, using an automated, robotic platform for continuous, multicolony monitoring of uniquely identified workers. We find that exposure to field-realistic levels of imidacloprid impairs nursing and alters social and spatial dynamics within nests, but that these effects vary substantially with time of day. In the field, imidacloprid impairs colony thermoregulation, including the construction of an insulating wax canopy. Our results show that neonicotinoids induce widespread disruption of within-nest worker behavior that may contribute to impaired growth, highlighting the potential of automated techniques for characterizing the multifaceted, dynamic impacts of stressors on behavior in bee colonies.

Growing evidence for declines in bee populations has caused great concern because of the valuable ecosystem services they provide. Neonicotinoid insecticides have been implicated in these declines because they occur at trace levels in the nectar and pollen of crop plants. We exposed colonies of the bumble bee Bombus terrestris in the laboratory to field-realistic levels of the neonicotinoid imidacloprid, then allowed them to develop naturally under field conditions. Treated colonies had a significantly reduced growth rate and suffered an 85% reduction in production of new queens compared with control colonies. Given the scale of use of neonicotinoids, we suggest that they may be having a considerable negative impact on wild bumble bee populations across the developed world.

The honeybee ( Apis mellifera ) forms two female castes: the queen and the worker. This dimorphism depends not on genetic differences, but on ingestion of royal jelly, although the mechanism through which royal jelly regulates caste differentiation has long remained unknown. Here I show that a 57-kDa protein in royal jelly, previously designated as royalactin, induces the differentiation of honeybee larvae into queens. Royalactin increased body size and ovary development and shortened developmental time in honeybees. Surprisingly, it also showed similar effects in the fruitfly ( Drosophila melanogaster ). Mechanistic studies revealed that royalactin activated p70 S6 kinase, which was responsible for the increase of body size, increased the activity of mitogen-activated protein kinase, which was involved in the decreased developmental time, and increased the titre of juvenile hormone, an essential hormone for ovary development. Knockdown of epidermal growth factor receptor (Egfr) expression in the fat body of honeybees and fruitflies resulted in a defect of all phenotypes induced by royalactin, showing that Egfr mediates these actions. These findings indicate that a specific factor in royal jelly, royalactin, drives queen development through an Egfr-mediated signalling pathway. A queen among fruitflies The difference between the queen in a honeybee colony and the workers is not a matter of genetics but of nutrition: larvae that consume royal jelly become queens. The active royal-jelly ingredient has long remained elusive, but is now identified as royalactin, a previously known protein that exhibits epidermal growth factor (EGFR)-like effects on rat hepatocytes. Surprisingly, royalactin also induces queen-like phenotypes in the fruitfly Drosophila melanogaster , increasing body size and ovary development through an EGFR-mediated signalling pathway.

The honey bee is a major pollinator whose health is of global concern. Declines in bee health are related to multiple factors, including resource quality and pesticide contamination. Intensive agricultural areas with crop monocultures potentially reduce the quality and quantity of available nutrients and expose bee foragers to pesticides. However, there is, to date, no evidence for synergistic effects between pesticides and nutritional stress in animals. The neonicotinoids clothianidin (CLO) and thiamethoxam (TMX) are common systemic pesticides that are used worldwide and found in nectar and pollen. We therefore tested if nutritional stress (limited access to nectar and access to nectar with low-sugar concentrations) and sublethal, field-realistic acute exposures to two neonicotinoids (CLO and TMX at 1/5 and 1/25 of LD50) could alter bee survival, food consumption and haemolymph sugar levels. Bee survival was synergistically reduced by the combination of poor nutrition and pesticide exposure (−50%). Nutritional and pesticide stressors reduced also food consumption (−48%) and haemolymph levels of glucose (−60%) and trehalose (−27%). Our results provide the first demonstration that field-realistic nutritional stress and pesticide exposure can synergistically interact and cause significant harm to animal survival. These findings have implications for current pesticide risk assessment and pollinator protection.

It has been suggested that the negative effects on bees of neonicotinoid pesticides could be averted in field conditions if they chose not to forage on treated nectar; here field-level neonicotinoid doses are used in laboratory experiments to show that honeybees and bumblebees do not avoid neonicotinoid-treated food and instead actually prefer it. Bees' responses to neonicotinoids examined Reports that neonicotinoid insecticides have adverse effects on bee populations remain controversial. Some studies have been criticized as using unrealistically high insecticide dosages or conditions far removed from those in the field, and it has been suggested that bees might be able to detect the insecticides and avoid treated crops. Two papers in this issue of Nature present results that fill some of the gaps in our knowledge. In laboratory experiments Sébastien Kessler et al . use field-level doses of three commonly used neonicotinoids — clothianidin, imidacloprid and thiamethoxam — to show that both honeybees and bumblebees are able to detect their presence. However, the bees do not avoid neonicotinoid-treated food and may even prefer it. Maj Rundlöf et al . sowed oilseed rape with and without a clothianidin seed coating in matched and replicated agricultural landscapes. They found the seed coating to be associated with reduced density of wild bees, as well as reduced nesting of solitary bees and reduced colony growth of bumblebees, but they did not detect an effect on honeybees. The impact of neonicotinoid insecticides on insect pollinators is highly controversial. Sublethal concentrations alter the behaviour of social bees and reduce survival of entire colonies 1 , 2 , 3 . However, critics argue that the reported negative effects only arise from neonicotinoid concentrations that are greater than those found in the nectar and pollen of pesticide-treated plants 4 . Furthermore, it has been suggested that bees could choose to forage on other available flowers and hence avoid or dilute exposure 4 , 5 . Here, using a two-choice feeding assay, we show that the honeybee, Apis mellifera , and the buff-tailed bumblebee, Bombus terrestris , do not avoid nectar-relevant concentrations of three of the most commonly used neonicotinoids, imidacloprid (IMD), thiamethoxam (TMX), and clothianidin (CLO), in food. Moreover, bees of both species prefer to eat more of sucrose solutions laced with IMD or TMX than sucrose alone. Stimulation with IMD, TMX and CLO neither elicited spiking responses from gustatory neurons in the bees’ mouthparts, nor inhibited the responses of sucrose-sensitive neurons. Our data indicate that bees cannot taste neonicotinoids and are not repelled by them. Instead, bees preferred solutions containing IMD or TMX, even though the consumption of these pesticides caused them to eat less food overall. This work shows that bees cannot control their exposure to neonicotinoids in food and implies that treating flowering crops with IMD and TMX presents a sizeable hazard to foraging bees.

Large-scale losses of honey bee colonies represent a poorly understood problem of global importance. Both biotic and abiotic factors are involved in this phenomenon that is often associated with high loads of parasites and pathogens. A stronger impact of pathogens in honey bees exposed to neonicotinoid insecticides has been reported, but the causal link between insecticide exposure and the possible immune alteration of honey bees remains elusive. Here, we demonstrate that the neonicotinoid insecticide clothianidin negatively modulates NF-κB immune signaling in insects and adversely affects honey bee antiviral defenses controlled by this transcription factor. We have identified in insects a negative modulator of NF-κB activation, which is a leucine-rich repeat protein. Exposure to clothianidin, by enhancing the transcription of the gene encoding this inhibitor, reduces immune defenses and promotes the replication of the deformed wing virus in honey bees bearing covert infections. This honey bee immunosuppression is similarly induced by a different neonicotinoid, imidacloprid, but not by the organophosphate chlorpyriphos, which does not affect NF-κB signaling. The occurrence at sublethal doses of this insecticide-induced viral proliferation suggests that the studied neonicotinoids might have a negative effect at the field level. Our experiments uncover a further level of regulation of the immune response in insects and set the stage for studies on neural modulation of immunity in animals. Furthermore, this study has implications for the conservation of bees, as it will contribute to the definition of more appropriate guidelines for testing chronic or sublethal effects of pesticides used in agriculture.