>Randy says: “Again, if the binding were truly irreversible, wouldn't we
expect to see every forager on seed-treated canola to drop dead after a day
or so?”
>No. As you and many others have pointed out, the bees are getting
“sub-lethal” doses, unless they bring home dust. There are lots of AChR
receptors in each synapse...thousands of them in fact. If just a small
number are blocked, the rest can continue to work.
I'm surprised at your answer, Christina. It is not a question of whether
the others continue to work--the question is about the number that are
opening the sodium channel. The mode of action of neonics are as agonists
(causing an opening of channels), not as antagonists (blocking nerve
transmission).
If such opening of the channels were irreversible, then the sodium channels
would remain open, and be cumulative, as you suggested when you started
this discussion, citing Haber's Law. Now you appear to be taking the
reverse argument.
What we are interested in here are *effects* upon the bee--not the
chemistry of the binding mechanism. If a bee were to be exposed
chronically to the neonic, and if the *effects* of the binding (as opposed
to the molecular binding itself) were indeed irreversible, then after some
period of time, then such irreversible binding would indeed cause the death
of the bee, even at field-realistic doses. This doesn't happen in real
life.
>
> >Sub-lethal means impaired. This could explain behavior problems. It
> also means delayed mortality. This could explain shortened lifespans. To
> the neuron, being chronically depolarized by leaky membranes is
> life-threatening.
Thank you for your list of potential mechanisms for reversing the effects
of exposure to neonics!
Christina, you may be reading me wrong. I am indeed concerned about sub
lethal effects, upon bees, and upon other wildlife. That is why I go to
the length of following up on reports of such effects!
What surprises me is that everyone is focusing upon the sublethal effects
of the neonics alone. As the Fraziers point out:
" Indeed, if a relative hazard to honey bees is calculated as the product
of mean residue times frequency detected divided by the LD50, the hazard
due to pyrethroid residues is three-times greater than that of
neonicotinoids detected in pollen samples."
http://www.extension.org/pages/60318/pesticides-and-their-involvement-in-colony-collapse-disorder
So why your focus solely upon the neonics? It would appear to me that you
would be far more interested in investigating the sublethal effects of the
neurotoxic pyrethroids, to which bees are far more commonly exposed.
Note also that the exposure of bees to pyrethroids jumped suddenly in North
America around 1990, and ramped up each year from then on, perhaps peaking
a few years ago as the use of Mavrik finally dropped off.
--
Randy Oliver
Grass Valley, CA
www.ScientificBeekeeping.com
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