Insecticide Synergists: Good or Bad for Honey Bees?

An increasing global population (estimated at over 9 billion by the year 2050) brings the problem of maintaining a sustainable agricultural system, with the constraints on land-use and environmental protection that such a process incurs. One acute problem is that of arthropod pests, chemical control of which remains the foundation of pest control for growers today, and for the foreseeable future. Insecticide resistance continues both to increase and broaden; a situation that will be exacerbated by the withdrawal of some older insecticidal actives under the EU's Pesticide Framework Directive. One possible solution that has been advocated is the use of synergists, especially if coupled with 'temporal synergism', a concept reported previously in Outlooks on Pest Management, whereby a synergist contacts a pest some hours before the insecticide component of the treatment. For example, when crop pests were exposed to piperonyl butoxide (PBO) several hours before pyrethroid, carbamate or neonicotinoid insecticides, inhibition of the metabolic enzymes (P450s and esterases) that would normally degrade these insecticides occurred, leaving the insect pests in a hypersensitive state before exposure to the insecticide. However, it may be that not just the target insects would be exposed to both synergists and insecticides, beneficial insects such as bees would potentially also be at risk. The honey bee (Apis mellifera) (Hymenoptera: Apidae) is a global pollinator of many crop plants, encountering various challenges such as disease, parasites and both intended and unintended insecticide exposure. Although, as mentioned earlier, chemical control is currently an indispensable input for global agriculture, pesticides have been suspected by some to be involved in the disappearance of honey bees since the first report of colony collapse disorder in 2006. As with other insects, honey bees use their metabolic enzymes to detoxify insecticides and although their genome contains a smaller number of genes encoding detoxification enzymes (as judged by comparison with the published genomes of other insects), the literature indicates that a lower number of detoxification genes does not necessarily correspond to a lower detoxification activity. So, will a regime to control insect pests by inhibition of their detoxifying enzymes also penalise honey bees in the same way? Before advocating widespread use of synergists such as PBO, it is essential that studies are performed to characterise their effects against the defence enzymes of the honey bee, both in terms of potency and to identify which defence enzymes (P450s and /or esterases) are inhibited. The synthetic pyrethroid, tau-fluvalinate, is used widely as an acaricide treatment against the bee parasite Varroa destructor in apiculture. It has been reported that the reason for tau-fluvalinate's lower toxicity to the bees themselves is due to rapid metabolism by their P450s. If this is correct, and PBO inhibits this honey bee defence system, it could be expected that exposure to this pyrethroid would result in high mortality, rendering this insecticide of no value impotent for parasite control.