I'd suggest being wary of abstracts that contain red flags like these:

"toxicity model" [Why model?  We can directly measure and test toxicity.]
"validated for chemical carcinogens" [Carcinogens are very different from
pesticides.]
"Chemicals showing irreversible or slowly reversible binding to specific
receptors will produce cumulative effects with time of exposure" [An if-then
claim!]
"New assessment procedures are needed to evaluate the risk" [A proposed new
"risk assessment"?  Gosh, we'll need hip waders.]

One is well-advised to read the full text of papers from Tennekes with care,
as seems to be in the controversy business.

The full text is at http://bee-quick.com/reprints/Tennekes_2013.pdf

The paper posits a theoretical example for Imidacloprid at low levels being
toxic to honey bees over time.
But the math for hives foraging on only 11% "Imidacloprid contaminated"
plants (Table 6) predicts that 50% mortality should result in 7 to 12 days.
If this were true, any bloom of Imidacloprid-treated plants would result in
consistently significant and drastic worker mortality during that bloom, as
it would be easy for bees to gather 11% of their total groceries from a
single blooming plant type over two weeks.

So, this proposed mathematical model clearly does not match the experience
and observations of beekeepers and researchers.
It incorrectly predicts far more drastic outcomes than even the most
accusatory stances taken by the far fringe activists.

The model also "predicts" that a number of studies of "chronic effects" of
Imidacloprid, where bees were force-fed various levels of pesticides over
time, would have seen significant rates of mortality at very low doses, when
there was no such mortality seen at these low doses.  I recall 10-day,
30-day, and "tented" trials lasting through several complete turnovers of
entire hive populations.  In cases where a model and the tangible evidence
from actual tests disagree by wide margins, this usually means that the
experimental data has "disproven" that model.

How does Tennekes get it so wrong?  Well, he says this: "However, when a
toxicant is not eliminated or binding to specific receptors is virtually
irreversible the LC50 threshold can eventually be zero".  (I think he must
have meant to say "near zero", as then the statement would make sense.)

His error was very basic - Imidacloprid and the other neonicotinoids do not
"bind irreversibly" to the receptors at issue.  They were designed to have
reversible binding, as this is the only way to kill pests while not killing
beneficial insects.  Bees specifically metabolize neonics with the
cytochrome P450 mechanism that I mentioned in the recent "Article suggesting
a link between HFCS feeding and CCD" thread.

Tennekes goes on to say "The toxicity pattern of imidacloprid and
thiacloprid suggests that these and other neonicotinoid compounds have
irreversible binding to their nicotinic acetylcholine receptors (nAChRs) in
arthropods."  And this is where it became clear to me that our collective
legs were being pulled.  He uses the word "irreversible" 19 times in that
paper (I counted), and then he tries to slide in a coy "suggestion" that
neonicotinoids MIGHT have irreversible binding! One does not have to infer
any such thing, one looks at the molecular biology, and directly measures
the actual metabolite levels in the bees themselves.

What he did was compare lethal doses of pesticides, and find that even
higher lethal concentrations killed quicker than an LD50 level, but then
extended the line of the dose-response curve backwards to zero to
incorrectly attempt to infer that all doses were toxic, and that tiny doses
would be just as deadly over longer timeframes.  Wrong.  No, not just wrong,
he was deliberately and methodically constructing a misleading argument.  

TLDR: There are doses of neonics that bees easily metabolize.  These low
doses are, by design, intended to be the most a bee ever encounters if the
pesticide is properly used. It does not matter if the bee encounters that
same level in every meal it eats, the metabolization is still going to
protect the bee every time.  Tennekes was trying to dodge that basic fact to
create a new far-lower "acceptable level" for systemic pesticides.
Apparently "zero".

So, it is politics trying to disguise itself in a white lab coat.  
Didn't fly.
Models that were useful in the 1940s for carcinogen build-up in mammals
aren't useful to predict the metabolization of neonic pesticides by bees.
And we don't need a "new model" to replace very satisfactory direct
measurement.

So many years with varroa has turned us into experts on how insects die,
taking our focus away from better-managing live bees.







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