Mechanism for the differential toxicity of neonicotinoid insecticides in the honey bee, Apis mellifera

Abstract

Laboratory bioassays were conducted to determine the contact honey bee toxicity of commercial and candidate neonicotinoid insecticides. The nitro-substituted compounds were the most toxic to the honey bee in our laboratory studies with LD50 values of 18ng/bee for imidacloprid, 22ng for clothianidin, 30ng for thiamethoxam, 75ng for dinotefuran and 138ng for nitenpyram. The cyano-substituted neonicotinoids exhibited a much lower toxicity with LD50 values for acetamiprid and thiacloprid of 7.1 and 14.6μg/bee, respectively. Piperonyl butoxide, triflumizole and propiconazole increased honey bee toxicity of acetamiprid 6.0-, 244- and 105-fold and thiacloprid 154-, 1,141- and 559-fold, respectively, but had a minimal effect on imidacloprid (1.70, 1.85 and 1.52-fold, respectively). The acetamiprid metabolites, N-demethyl acetamiprid, 6-chloro-3-pyridylmethanol and 6-chloro-nicotinic acid when applied topically, produced no mortality at 50μg/bee. These results suggest that P450s are an important mechanism for acetamiprid and thiacloprid detoxification and their low toxicity to honey bees. When honey bees were placed in cages in forced contact with alfalfa treated with acetamiprid and the synergist, triflumizole, in combination at their maximum recommended application rates, no mortality was detected above that of the control. © 2003 Elsevier Ltd. All rights reserved.