> As for clear proof that IMI or other neonics have cumulative effects, I
don't think there is clear proof, just as (in my opinion) 
> there isn't clear proof that they do no harm to bees.   

This is why this issue is so complex for us poor beekeepers, we are forced
to do all the work of slogging through these papers, and we end up with mere
inferences, but yet PhDs in biology aren't yet satisfied with anyone's
claims.  

I'm not sure how one could provide clear proof that they "do no harm".
Isn't that the basis for the "precautionary principle"?

> Still, the fact that bees end up with an LD50 dose either by drinking lots
of a dilute solution, or less of a more concentrated one is pretty
interesting. 
> It does mean the stuff builds up over the time they are accessing it.  It
was the Bayer science that pointed this out, by the way.

I'll have to go back and read that Nauen 2001 paper again, as I did not come
away with that understanding of the results. 

I understand that a high acute dose makes the feed unpalatable to the bees,
even though they still eat enough to get a fatal dose.  But that paper
compared acute oral doses with acute contact doses, and that no data was
offered on chronic doses.  (My post of late last night mislabeled the oral
doses as "chonic" rather than "acute")  

So, what you took away from the paper about (chronic) "build up" is from
commentary attempting to explain the metabolism in acute oral scenarios?  Is
that fair, given that the authors were speaking only about acute doses? 

And if it did build up, why didn't anyone see high mortality in the
lower-dose long-term chronic feeding studies?  This is the essential point
that I keep coming back to, there are lots of hives on crops like Canola in
Canada getting significant volumes of Imidacloprid in the diets at the low
levels claimed to be "safe" by the pesticide companies, and they didn't see
bees dying, nor did they see behavioral impact.  That to me is a pretty
powerful demo.

But for a pesticide with absolutely no "build up" at all, why wouldn't the
chronic oral LD50 have to be nearly the same as the acute oral LD50?  I'm
not offering an argument here, I'm asking for an explanation of the
mechanisms.




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