Imidacloprid is a systemic
insecticide which acts as an
insect neurotoxin and belongs to a class of chemicals called the
neonicotinoids which act on the
central nervous system of insects with much lower toxicity to mammals. The chemical works by interfering with the transmission of stimuli in the insect nervous system. Specifically, it causes a blockage in a type of neuronal pathway (nicotinergic) that is abundant in insects and not in warm-blooded animals (making the chemical selectively toxic to insects and not warm-blooded animals). This blockage leads to the accumulation of acetylcholine, an important insect neurotransmitter, resulting in the insect's paralysis, and eventually death. It is effective on contact and via stomach action.[SUP]
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Although it is now off patent, the primary manufacturer of this chemical is Bayer CropScience, (part of
Bayer AG). It is sold under many names for many uses. Imidacloprid is one of the most widely used insecticides and can be applied by soil injection, tree injection, application to the skin, broadcast foliar, ground application as a granular or liquid formulation, or as a pesticide-coated
seed treatment.[SUP]
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Bees and other insects
Main article:
Imidacloprid effects on bees
Imidacloprid is one of the most highly toxic insecticides to honey bees with a contact acute LD50 = 0.078 ug a.i./bee and an acute oral LD50 = 0.0039 ug a.i./bee.[SUP]
[26][/SUP] In 2006, U.S. commercial migratory beekeepers reported sharp declines in their honey bee colonies. Unlike previous losses, adult bees were abandoning their hives. Scientists named this phenomenon
colony collapse disorder (CCD). Reports show that beekeepers in most states have been affected by CCD.[SUP]
[27][/SUP] Although no single factor has been identified as causing CCD, the United States Department of Agriculture (USDA) in their progress report on CCD stated that CCD may be "a syndrome caused by many different factors, working in combination or synergistically." [SUP]
[28][/SUP] Recently, USDA researcher Jeff Pettis published the results of his study, which showed that bees treated with sub-lethal or low levels of imidacloprid had higher rates of infection with the pathogen
Nosema than untreated bees.[SUP]
[29][/SUP] His research was confirmed by Alaux (2010) and Vidau (2011) who found that interactions between
Nosema and neonicotinoids weakened bees and led to increased mortality.[SUP]
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Researchers Kreutzweiser and Thompson (2009) from the Canadian Forest Service showed that imidacloprid at realistic field concentrations inhibits non-target terrestrial invertebrates that decompose leaf litter. In their study, there was no significant indication that invertebrates detected or avoided imidacloprid-treated leaves.[SUP]
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David Goulson (2012) from the University of Sterling was able to show that trivial effects due to imidacloprid in lab and greenhouse experiments can translate into large effects in the field. The research found that bees consuming the pesticide suffered an 85% loss in the number of queens their nests produced, and a doubling of the number of bees who failed to return from food foraging trips.[SUP]
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