Just so that everyone can evaluate this for themselves, and not just take my word for it, here are a few quotes followed by my interpretation of what is being said in the Suchail et al paper entitled:

SÉVERINE  SUCHAIL , DAVID  GUEZ , and LUC  P. BELZUNCES Discrepancy between acute and chronic toxicity induced by imidacloprid and its metabolites in Apis mellifera. Environmental Toxicology and Chemistry, Vol. 20, No. 11, pp. 2482–2486, 2001

Materials and Methods:  “Bees were fed a 50% sucrose solution ad libitum.”

“The honeybees were deprived of food for 2 h before administration of the active substance. For acute toxicity, each bee received 10 µl of 50% sucrose solution (vehicle) containing graded doses of imidacloprid or its metabolites or the dosing vehicle alone (control). After consuming this solution, bees were fed 50% straight sucrose solution ad libitum. Mortality was recorded at 2, 4, 6, 10, 14, 20, 24 30, 48, 72, and 96 h.”

“For chronic toxicity studies, bees were continuously fed 50% (w/v) sucrose solution containing or not the tested substances during 10 d. During the experiments, feeders were changed daily with fresh sucrose solutions containing the products tested.  To avoid photodecomposition, opaque feeders were used.  The individual daily consumption of the sucrose solution was determined by weighing the feeders and was corrected by the surviving bees. Cumulated doses were calculated directly from sucrose solution consumption, the concentration of the products tested, and the density of the sucrose solution.”

Results:

“After acute intoxication by imidacloprid or its metabolites, early symptoms of neurotoxicity were observed. They include hyperresponsiveness, hyperactivity, and trembling. After several hours, these symptoms gradually disappeared, and the worker bees became hyporesponsive and hypoactive.”

“Chronic toxicity was studied during a 10-d period. For all products tested, mortality in the control group was under 15% in all experiments, as recommended in European and Mediterranean Plant Protection Organization guidelines. Results obtained revealed some particular unexpected characteristics (Fig. 2). Surprisingly, the chronic oral test showed that imidacloprid and all studied metabolites were toxic. Bee mortality was induced only 72 h after the onset of intoxication. Imidacloprid and its metabolites exhibited similar long-term toxicity.  For imidacloprid, toxicity was similar with concentrations of 1 and 10 µg/L, whereas with 0.1 µg/L of imidacloprid, the mortality rate was lower. With 5-hydroxyimidacloprid, mortality increased with the concentration. With the other metabolites, olefin, 4,5-dihydroxyimidacloprid, desnitroimidacloprid, 6-chloronicotinic acid, and urea, mortality evolution was similar during 10 d for all concentrations tested.  In chronic experiments, each honeybee ingested approximately 12 µl of contaminated sucrose solution per day. Therefore, for the concentration of the toxic compounds of 0.1, 1, and 10 µg/L, each honeybee ingested 0.010, 0.1, and 1 ng of compound per day, respectively.”

I am assuming that someone misunderstood the methods here.  They state that the bees were fed 10µl of the test solution (containing the toxin) after 2 hr. starvation during the acute trials.  When they had consumed this amount, they were given a 50% sucrose solution ad libitum….that means “continuously”.   In the chronic trials they were fed continuously, with 50% sucrose solutions containing one of the toxins, and this solution was refreshed daily.  I don’t think they were starved if this protocol was followed because they had continuous access to sucrose except in the acute trials where food was withheld for two hours prior to administering the dose with the toxin in it.  Then they were returned to ad libitum sucrose solution.

The conclusions did surprise the researchers because the mortality curves were the same for all metabolites and mortality began in earnest after 72 h following exposure.

This is interesting, how do we explain it?  The authors state in their discussion that “Although imidacloprid LD50
of about 5 (worse case) or 60 ng/bee (usual case) (50 or 600 µg/kg) are found, LD50 values may vary from colony to colony and can range from 5 to 500 ng/bee (50–5,000 µg/kg).”

More interesting!  How can there be such variability in mortality after IMI exposure among individual colonies?  The study that Jim Fischer recently sent us regarding the variable susceptibility of barn flies to IMI comes to mind.

The Suchail paper authors continue on this topic, saying that “This difference of imidacloprid sensitivity from colony to colony can be due to a variation in detoxification capacity in honeybee colonies.  Schonbrod et al. [19] studied the relationship between acute toxicity and mono-oxygenase levels in preselected strains of houseflies. They concluded that no clear relationship existed between mono-oxygenase activity and insecticide resistance in this insect. On the other hand, in the honeybee, Smirle et al. [20] showed that a significant linear relationship existed between the acute toxicity of an organophosphorus insecticide, the diazinon, and colony polysubstrate mono-oxygenase activity.  The variation in detoxification capacity in honeybee colonies was a significant factor in determining resistance to diazinon. Thus, intracolony variations of imidacloprid sensitivity can be explained by the difference in oxidative metabolisms between honeybee colonies.”

So this study doesn’t show bees were starved, IMO.  It does show that IMI and its metabolites cause a delayed mortality when the IMI is administered in very low doses and also when the IMI is administered in an acute, higher dose.  Either way, it takes some time...a delay of 72 hours....before the bees die.

It also presents us with a possible explanation for the differences observed in the field among colonies exposed to IMI.

Unless the methods section does not accurately reflect what the researchers actually did, the bees were not starved.  Was something else at fault in the methods?

Christina

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