> [Are you] Sure?
Sure I'm sure! But you don't have to take my word for it. You could read
each of the publications I'll list below. Fair warning, it took me several
years to get up to speed on this issue, and even then, I am only at a mere
"conversational level" of comprehension.
All of these papers are far more applicable to the problems of bees than the
abstract you found that may have matched a few keywords, but discussed
Barnflies, which are clearly NOT killed by the Imidacloprid in field
application, thereby refuting the implication you inferred from the keyword
"irreversible":
http://www.merckmanuals.com/vet/integumentary_system/flies/stable_flies.html
"A combination of two compounds, imidacloprid and permethrin, works together
to repel Stomoxys calcitrans. Monthly application of this product repels
these flies and prevents their blood feeding on dogs, but the product does
not kill this type of biting fly." (In my barn, I used simple flypaper to
trap them.)
Looking at the entire body of evidence as it has developed over time, one
sees that essentially all of it flatly refutes, rather than supports
Tennekes.
On the one hand, you have Tennekes, self-publishing his own book and
comparing himself to Rachel Carson(!) on the website promoting that book,
making flat statements like "In my view, neonicotinoids are destroying the
web of life and should be banned".
Tennekes, H.A., 2010. "The Systemic Insecticides: A Disaster in the Making"
http://www.disasterinthemaking.com/
And Tennekes often cites Suchail's study which famously and hilariously
claimed chronic "low-level" effects when using concentrations of
Imidacloprid that were above the known acute lethal dose in:
Suchail, S., Guez, D., Belzunces, L.P., 2001. Discrepancy between acute and
chronic toxicity induced by imidacloprid and its metabolites in Apis
mellifera. Environ. Toxicol. Chem. 20, 2482-2486.
And on the other hand, you have everyone else, who not only disagree with
Tennekes, but have data that back up descriptions of specific mechanisms,
and have formed a consistent and cohesive view that make sense from several
angles. They also do not indulge in flat statements or take political
stances:
Here are the specific voltage clamp studies on single insect neurons,
showing rapidly reversible binding:
Nauen, R., Ebbinghaus-Kintscher, U., Elbert, A., Jeschke, P., Tietjen, K.,
2001. Acetylcholine receptors as sites for developing neonicotinoid
insecticides. In: Ishaava, I. (Ed.), Biochemical Sites of Insecticide Action
and Resistance. Springer, Berlin, Heidelberg, pp. 77-105.
Tomizawa, M., Casida, J.E., 2003. Selective toxicity of neonicotinoids
attributable to specificity of insect and mammalian nicotinic receptors.
Annu. Rev. Entomol. 48, 339-364
Jeschke, P., Nauen, R., 2005. Neonicotinoid insecticides. In: Gilbert, L.I.,
Iatrou, K.,Gill, S.S. (Eds.), Comprehensive Molecular Insect Science.
Elsevier B.V., Oxford,
pp. 53-105.
Here you have Radioligand binding studies, which also showed reversible
binding. (When I can see similar results using two different technologies,
this gives me very high confidence that what is being measured is real.)
Liu, M.Y., Casida, J.E., 1993. High-affinity binding of [3H] Imidacloprid in
the insect acetylcholine receptor. Pestic. Biochem. Physiol. 46, 40-46
Here we have even Aphids, the most common target pest for neonics,
recovering from Imidacloprid under on-and-off exposure conditions, showing
that even their much more primitive metabolisms are not overwhelmed if they
feed for an short period on a treated plant, and then feed on an untreated
plant. This shows that the binding is reversible even for the target
insect.
Nauen, R., 1995. Behaviour modifying effects of low systemic concentrations
of imidacloprid on Myzus persicae with special reference to an antifeeding
response. Pestic. Sci. 44, 145-153
And here you have a neat summary of the long-term exposure tests, the ones
that give one hard numbers, rather than the straight-line extrapolation from
one or two data points that Tennekes proposes from data gathered in shorter
studies.
Schmuck, R., 2004. Effects of a chronic dietary exposure of the honeybee
Apis mellifera (Hymenoptera: Apidae) to imidacloprid. Arch. Environ. Contam.
Toxicol. 47, 471-478.
To give an example of the need to actually measure both "acute" and
"chronic" exposure limits, I could take your 100-meter sprint time as a
valid measurement of your ability to run short distances, but to extrapolate
from that to predict your 5K, 10K, or 26-mile marathon times would be
laughable, as your performance would not be "linear". But this is exactly
the sort of thing Tennekes proposes. Measuring each actual finishing time
would be far more valid than trying to infer all running performance from a
single sprint time. When we can measure actuals, why would anyone stand for
mere extrapolation?
Last, here are some studies where actual bees where fed actual "realistic
field doses" of Imidacloprid under both lab and field conditions over longer
periods of time. The results did not show the massive mortality predicted
by Tennekes in his Table 6 in the paper you cited. (Tennekes has made prior
attempts to promote this same idea, dating back to 2010.) The results did
not even show SLIGHTLY increased mortality with longer exposures.
Schmuck, R., 2004. Effects of a chronic dietary exposure of the honeybee
Apis mellifera (Hymenoptera: Apidae) to imidacloprid. Arch. Environ. Contam.
Toxicol. 47, 471-478.
Faucon, J.P., Aurieres, C., Drajnudel, P., Ribiere, M., Martel, A.C.,
Zeggance, S., Chauzat, M.P., Aubert, M., 2004. Experimental study of the
toxicity of imidacloprid distributed in feeder syrup to bee colonies (Apis
mellifera). AFSSA, Laboratory for studies and research into the pathology of
small ruminants and bees, Sophia Antipolis, 32 pp.
Schmuck, R., 1999. No causal relationship between Gaucho seed dressing in
sunflowers and the French bee syndrome. Pflanzenschutz-Nachrichten Bayer 52,
257-299.
Cure, G., Schmidt, H.W., Schmuck, R., 2001. Results of a comprehensive field
research programme with the systemic insecticide imidacloprid (Gaucho). In:
Proceedings of the Symposium Hazard of Pesticides to Bees, vol. 98, Avignon
(France), September 7-9, 1999, INRA (Paris) (Les Colloques), pp. 49-59.
Schmuck, R., Schoning, R., Sur, R., 2005. Studies on the effects of plant
protection products containing imidacloprid on the honeybee,Apis mellifera
L. In: Forster, R., Bode, E., Brasse, D. (Eds.), Das "Bienensterben" im
Winter 2002/2003 in Deutschland - Zum Stand der wissenschaftlichen
Erkenntnisse. Bundesamt für Verbraucherschutz und Lebensmittelsicherheit
(BVL), Braunschweig, pp. 68-92.
This makes a pretty convincing case that low levels of Imidacloprid do NOT
"accumulate" over time in the way that a carcinogen would.
There's also this textbook, as the papers published in this area are far
less than self-explanatory:
Yu, S. J., 2008. The Toxicology and Biochemistry of Insecticides. CRC Press,
Taylor & Francis Group, Boca Raton, pp. 115-142.
But that's a lot of very hard reading to overcome the confirmation bias
resulting from simple searching for keywords. That's why I try to provide
the full text to papers being touted by those who read only the abstracts,
and why I detail my critiques with specifics. Abstracts are like bumper
stickers or headlines. Often misleading.
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