Christina wrote:

3.  Suchail points out that the metabolites are MORE toxic than the
> original IMI and are responsible for extended chronic (but not acute)
> toxicity.  This means the metabolites are also effective synaptic
> agonists.  They persist longer than the parent compound, and she doesn't
> discuss the implications beyond saying that they increase the chronic
> toxicity of IMI.  Examine figures 2 and 3.
>

Actually, in the 2004 paper

> *In vivo* distribution and metabolisation of 14C-imidacloprid in
> different compartments of *Apis mellifera* L

she says:
  The olefin derivative and 4/5-hydroxy-imidacloprid preferentially
occurred in head, thorax and abdomen, which are nicotinic acetylcholine
receptor-rich tissues. Moreover, they presented a peak value around 4 h
after imidacloprid ingestion. These results explain the prolongation of
imidacloprid action in bees, and particularly the differences between rapid
intoxication symptoms and late mortality.

Various people on this list have been claiming that the results of this
paper show that imidacloprid is COMPLETELY in metabolized in certain number
of hours (she gives figures for time in various body parts as well as in
the whole bee).  But she uses the phrase "elimination half life of
radiation in the whole bee was 25 hrs.).  So that means that the
metabolization if it is proceeding by "half life" is a curve approaching
(but never reaching) zero and the amounts remaining could be the amounts
that are bound to the receptor.

>
> She says:
> "...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." (2001) She also says "These results
> strongly suggest that 5-hydroxyimidacloprid and/or olefin contribute to
> extending the action of imidacloprid in honeybees." (2003)
>

And these were the metabolites found most strongly in receptor rich tissues.

Since  Randy has called Suchail's other work concerning the toxicity levels
of imidacloprid on bees "completely bogus",  it would probably be good to
also look at some other radioactive metabolisation studies of various
neonicotinoids.   Dick says that these are common studies the pesticide
companies have to submit for registration so would there not be several of
them on bees given that the problems with pollinators are one of the major
problems those companies are facing in continuing to use their products?

Stan

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