Randy told me:

"Christina,  May I suggest that you review Suchail 2003 Metabolism of imidacloprid in Apis mellifera?  They found that IMD and its metabolites were rapidly cleared from the bees' bodies."

OK.  I did.  In the introduction, they point out that:

“…in 10-day chronic toxicity studies, all imidacloprid metabolites revealed equal toxicity to bees, but the total dose ingested by the bees was about 3000–100 000 times lower than the doses needed to produce the same effect after acute intoxication.”

This information was referenced from another paper of theirs, it’s this one:

Suchail S, Guez D and Belzunces LP, Discrepancy between acute and chronic toxicity induced by imidacloprid and its metabolites in Apis mellifera. Environ Toxicol Chem 20:2482–2486 (2001).

It means that chronic toxicity occurs at 3,000 to 100,000 times less IMI than required for acute toxicity.  (In other words, chronic = ‘sublethal’, bees can bring the stuff home, share it around, and die later.)

They also say in their introduction:

“At 48 h, oral and contact LD50  values are 5 and 25 ng per bee, respectively.  Studies on the acute toxicity of imidacloprid have revealed important characteristics.  (1) After oral exposure, the dose-mortality relation presents a multi-phase profile with ascending and descending phases. (2) The kinetics of mortality are delayed as doses increase. These features suggest that metabolic pathways might be involved in imidacloprid toxicity. (3) Neurotoxicity symptoms appear rapidly, whereas mortality occurs 4 h after acute imidacloprid intoxication and is prolonged during more than 96 h.”

The reason they say “more than 96 hours” is because they didn’t follow up after that so they don’t know what the limit of prolonged mortality is.

A quote from the discussion:

“The present study showed that honeybees are able to rapidly metabolise imidacloprid through a process that reduces exposure to the parent compound and, in most of cases, its toxicity. However, the appearance of 5-hydroxyimidacloprid and olefin, two metabolites toxic at low doses in chronic exposure and at higher doses in acute exposure, coincides with the appearance of mortality induced after acute oral intoxication by imidacloprid. These results strongly suggest that 5-hydroxyimidacloprid and/or olefin contribute to extending the action of imidacloprid in honeybees. Moreover, this study also suggests the existence of other imidacloprid metabolites. It would be interesting to characterise all imidacloprid metabolites in honeybees after oral intoxication by imidacloprid to obtain the whole metabolic profile. Furthermore, locating all the residues in different compartments of honeybees could help us to understand the mode of action of imidacloprid by correlating the pharmacokinetics and the pharmacodynamics of imidacloprid in honeybees.”


So…Randy…I am unclear why you wanted me to read this?  Suchail et al are quite explicit about the presence of prolonged mortality due to IMI.  Why do you use this paper to support the idea that there is no prolonged mortality due to IMI when the authors themselves acknowledge that they can’t account for 30% of the dose the bees ingested, and the bees continue to die of chronic effects “during more than 96 h”?


Well, bees on Canadian canola do just fine.  Whatever IMI does to bees, in some situations they obviously can cope.


Christina

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