Canadian Institutes of Health Research, Heart and Stroke Foundation of Canada, Ontario Ministry of Health and Long-Term Care, Ontario Ministry of Research, Innovation and Science, UK National Institute of Academic Anaesthesia, UK Clinical Research Collaboration, Australian and New Zealand College of Anaesthetists, and Monash University.

International audienceAssessment of the toxicity of individual pesticides to honeybees is routinely assessed. However, few data have been generated for realistic mixtures of neonicotinoid insecticides and fungicides particularly with regard to exposure levels used. Assessment of the effects of exposure of bees to predicted residues following sprayed applications of ergosterol biosynthesis inhibitor fungicides on the contact and oral toxicity of a range of neonicotinoid insecticides (thiamethoxam, clothianidin, imidacloprid and thiacloprid) showed only low levels of synergism (<3-fold maximum). Further studies showed that the scale of increase in toxicity was fungicide dose dependent with greater synergy of oral toxicity of thiamethoxam following contact dosing with propiconazole. This underlines the need for the use of realistic exposure levels and routes in studies

No abstract

This study aimed to develop an approach to evaluate potential effects of plant protection products on honeybee brood with colonies at realistic worst-case exposure rates. The approach comprised 2 stages. In the first stage, honeybee colonies were exposed to a commercial formulation of glyphosate applied to flowering Phacelia tanacetifolia with glyphosate residues quantified in relevant matrices (pollen and nectar) collected by foraging bees on days 1, 2, 3, 4, and 7 postapplication and glyphosate levels in larvae were measured on days 4 and 7. Glyphosate levels in pollen were approximately 10 times higher than in nectar and glyphosate demonstrated rapid decline in both matrices. Residue data along with foraging rates and food requirements of the colony were then used to set dose rates in the effects study. In the second stage, the toxicity of technical glyphosate to developing honeybee larvae and pupae, and residues in larvae, were then determined by feeding treated sucrose directly to honeybee colonies at dose rates that reflect worst-case exposure scenarios. There were no significant effects from glyphosate observed in brood survival, development, and mean pupal weight. Additionally, there were no biologically significant levels of adult mortality observed in any glyphosate treatment group. Significant effects were observed only in the fenoxycarb toxic reference group and included increased brood mortality and a decline in the numbers of bees and brood. Mean glyphosate residues in larvae were comparable at 4 days after spray application in the exposure study and also following dosing at a level calculated from the mean measured levels in pollen and nectar, showing the applicability and robustness of the approach for dose setting with honeybee brood studies. This study has developed a versatile and predictive approach for use in higher tier honeybee toxicity studies. It can be used to realistically quantify exposure of colonies to pesticides to allow the appropriate dose rates to be determined, based on realistic worst-case residues in pollen and nectar and estimated intake by the colony, as shown by the residue analysis. Previous studies have used the standard methodology developed primarily to identify pesticides with insect-growth disrupting properties of pesticide formulations, which are less reliant on identifying realistic exposure scenarios. However, this adaptation of the method can be used to determine dose–response effects of colony level exposure to pesticides with a wide range of properties. This approach would limit the number of replicated tunnel or field-scale studies that need to be undertaken to assess effects on honeybee brood and may be of particular benefit where residues in pollen and nectar are crop- and/or formulation-specific, such as systemic seed treatments and granular applications. Integr Environ Assess Manag 2014;10:463–470.

-Many of the reported pesticide incidents involving honeybees probably also result in mortality of bumblebees and, together with a reduction in suitable habitat, these have resulted in the decline in bumblebees in the UK over the last 20 years. Applications of sprays, e.g. pyrethroids, to flowering crops or weeds at times when honeybees are less active are likely to result in unreported bumblebee deaths. There is a need to protect foraging bumblebees from direct overspray during the early morning and late evening when pesticides which are repellent but highly toxic are applied, i.e. pyrethroids. Of particular concern are those pesticides applied when queens are emerging and establishing colonies, e.g. March/April, when colonies may be significantly impacted by the loss of a small number of workers or the queen. This is a problem which cannot readily be addressed by risk management measures due to differing foraging profiles of honeybees and bumblebees but does need to be taken into account in risk assessment and the development of more selective compounds.Bombus / pesticides / exposure / toxicity / risk assessment

This study assessed the effects of exposure to IGRs on the long-term development of the honeybee colony, viability of queens and sperm production in drones and integrated the data into a honeybee population model. Colonies treated with diflubenzuron resulted in a short-term reduction in the numbers of adult bees and brood. Colonies treated with fenoxycarb declined during the season earlier and started the season slower. The number of queens that successfully mated and laid eggs was affected in the fenoxycarb treatment group but there were no significant differences in the drone sperm counts between the colonies. An existing honeybee population model was modified to include exposure to IGRs. In the model, fenoxycarb reduced the winter size of the colony, with the greatest effects following a June or an August application. Assuming a 'larvae per nurse bee' ratio of 1.5 for brood rearing capability, the reduction in winter size of a colony following a fenoxycarb application was at its worst about 8%. However, even if only those bees reared within 2 weeks of the IGR being applied are subject to premature ageing, this might significantly reduce the size of over-wintering colonies, and increase the chance of the bee population dwindling and dying in late winter or early spring.

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The use of human and veterinary pharmaceuticals is increasing. Over the past decade, there has been a proliferation of research into potential environmental impacts of pharmaceuticals in the environment. A Royal Society-supported seminar brought together experts from diverse scientific fields to discuss the risks posed by pharmaceuticals to wildlife. Recent analytical advances have revealed that pharmaceuticals are entering habitats via water, sewage, manure and animal carcases, and dispersing through food chains. Pharmaceuticals are designed to alter physiology at low doses and so can be particularly potent contaminants. The near extinction of Asian vultures following exposure to diclofenac is the key example where exposure to a pharmaceutical caused a population-level impact on non-target wildlife. However, more subtle changes to behaviour and physiology are rarely studied and poorly understood. Grand challenges for the future include developing more realistic exposure assessments for wildlife, assessing the impacts of mixtures of pharmaceuticals in combination with other environmental stressors and estimating the risks from pharmaceutical manufacturing and usage in developing countries. We concluded that an integration of diverse approaches is required to predict ‘unexpected’ risks; specifically, ecologically relevant, often long-term and non-lethal, consequences of pharmaceuticals in the environment for wildlife and ecosystems.