Re this study, at first glance it appears to support the hypothesis that chronic exposure to field realistic doses of imidacloprid during summer and fall can lead to late winter collapse of the treated colonies.
The study got off to a good start—several colonies were fed different “field realistic” doses of imidacloprid in syrup, and colony populations and brood area were measured. If the authors would have stuck to this original design (which has already been performed numerous times in several countries) the results would have been meaningful. Indeed, after a month of feeding such syrup, the investigators did not observe any adverse effects upon the colonies due to the insecticide!
But then, since the lead investigator seemed to be eager to “prove” that CCD is caused by imidacloprid, he dreamed up the fantastic scenario that in the winter of 2006/2007 that for some inexplicable reason the nation’s supply of HFCS was contaminated with high levels of imidacloprid. My reading of the paper suggests that the author knows little about bees, little about pesticides, nothing about HFCS, had no understanding of the distribution of systemic pesticides in plants. This paper is an example of authors so bent on “proving” that imidacloprid is the cause of CCD, that they strain credulity with some of their assumptions and reasoning , and even by changing the experimental protocol midstream!
When the investigators failed to prove their case after a month of feeding spiked syrup—they changedthe protocol, and ramped up the doses of insecticide in the syrup to sky high and acutely toxic levels, and then made a series of compounding mistakes, notably by not performing the sort of necessary parasite management required for colonies to survive the winter. And then, the symptoms of the colonies when they died did not match the symptoms of CCD, yet the Harvard press agent claimed that they did!
Unfortunately, there are also a great number of factual misrepresentations and quite a bit of fuzzy thinking in the paper, which obviously was not peer reviewed by any bee biologist nor toxicologist. I realize, in retrospect, that some of my comments may sound a bit snarky, and I apologize to the authors, whom I’m sure were earnest in their quest to prove their anti-neonic agenda. Back to the paper, allow me to discuss some of the problems. The author stated in an interview:
“When other conditions cause hive collapse—such as disease or pests—many dead bees are typically found inside and outside the affected hives.”
Could someone please refresh my memory? Other than in the case of tracheal mite, which diseases or pests leave many dead bees in a hive? (Note that starvation or acute pesticide toxicity would not fall into the category of “disease or pest”). The point is, that the natural behavior of sick or old bees is to abandon the hive—one normally does not find dead bees in hives that have died from parasites, including viruses.
Let’s look at a few more sentences from the paper:
“We hypothesized that the first occurrence of CCD in 2006/2007 resulted from the presence of imidacloprid … in high-fructose corn syrup (HFCS), fed to honey bees as an alternative to sucrose-based food. There are three facts to support this hypothesis. First, since most of the suspected but creditable causes for CCD were not new to apiculture, there must have been an additional new stressor introduced to honey bee hives contemporaneous with the first occurrence of CCD during the winter months of 2006 and early 2007.”
“their beekeeping practices have been relatively unchanged during these years except for the replacement of honey or sucrose with HFCS as the supplemental sugar source for economic and convenient reasons…. Although the replacement of honey/sucrose-based feeds with HFCS among commercial beekeepers took place much earlier than 2006/2007, it was the timing of the introduction of neonicotinoid insecticides to the cornseed treatment program first occurring in 2004/2005 that coincides with CCD emergence.”
The authors give no justification for their assumption that there was any change in HFCS in 2006. And as Bob Harrison and others have pointed out, CCD actually started occurring in 2004-2005, prior to the authors’ assumption that tainted syrup hit the market beginning in 2006. Any HFCS produced from such treated corn would have necessarily have been produced following the season of harvest.
”Second, while commercial beekeepers appear to be affected by CCD at a disproportional rate…”
This is simply not true according to any of the several surveys that I’ve seen (see papers by CCD researcher Dennis van Engelsdorp). Indeed beekeepers who have never fed HFCS experienced plenty of cases of CCD.
The authors then cite a few studies that show that systemic insecticides are translocated, as they are intended, throughout the plants. But then they stretch by stating:
“ These study results lend credence to our hypothesis that the systemic property of imidacloprid is capable of being translocated from treated seeds to the whole plant, including corn kernels and therefore likely into HFCS.”
My gosh, this is one helluva assumption! Without taking the time to simply confirm that imidacloprid winds up in the kernels, the authors assume that it is concentrated there at high levels! And then they further go out on a limb by assuming that any such imidacloprid is then somehow concentrated when the corn is used to produce HFCS (ignoring the fact that most corn is treated with clothianidin, rather than imidacloprid):
The paper turns into farce when the author states:
“we used food-grade HFCS fortified with different levels of imidacloprid, mimicking the levels that are assumed to have been present in the older HFCS.”
Why in the world would the authors “assume” that imidacloprid was present in the older HFCS, but not present in the HFCS that he used in the current study to feed the control colonies? But then they go on to state:
“ The range of dosages used in this study from 20 to 400 μg/kg were not only environmentally relevant…”
Since when has 400 ppb ever been been considered to be “environmentally relevant”? Levels of 1-4 ppb are environmentally relevant; levels above 40 ppb are usually considered to be overtly toxic. So the 400 ppb figure is 100 – 400 times as strong as the normal measured levels in the field due to seed treatment.
As if that weren’t enough, the authors go into la-la land with some even wilder creative assumptions:
“Since there is no tolerance level for imidacloprid in HFCS, we applied a 10-fold concentrating factor, or 0.5 ppm (500 μg/kg) of imidacloprid in HFCS, by taking into account the uptake by corn plants from seeds that are treated with imidacloprid.”
They simply created this “concentrating factor” out of thin air! They give absolutely no justification for it. In the actual process of making HFCS, pesticides are largely removed. As I stated before, all that the authors had to do would have been to ask Roger Simonds at the USDA Gastonia pesticide testing lab as to the actual measured levels of imidacloprid in HFCS, and thus would not have brought embarrassment to Harvard School of Public Health by such a ludicrous assumption.
“Therefore, we are confident that the imidacloprid dosages applied in this study would be comparable, if not lower to those encountered by honey bees inside and outside of their hives.”
Unfortunately, the authors’ confidence is not supported by any actual field measurements whatsoever!
The authors state: “There are several questions that remain unanswered as a result of this study. First, the systematic loss of sealed brood in the imidacloprid-treated and control hives may indicate a common stress factor that was present across all 4 apiaries.”
Like, maybe the field investigators should have taken a few nosema or varroa counts, rather than simply assuming that these common parasites weren’t killing the colonies! For all we know, all the hives could have bee crawling with varroa or badly infected with nosema. One statement suggests that varroa was evident: “nor a large number of Varroa mites was observed in hives during the summer and fall seasons,” which suggests to me that the investigators are admitting that some something less than a “large” number of mites was indeed observed!
Let’s look at varroa: the study states that 3-lb packages were installed on March 28. Surprisingly, “By May 21st, 2010 all twenty frames in each of 20 hives were drawn out into comb and contained at least 14 frames of capped brood.” These colonies really took off, meaning that they were virtual varroa breeding grounds. By late July they averaged about 25,000 cells of sealed brood.
Strange and Calderone (2009) found Eastern package bees to contain about 3 mites per hundred bees, which would work out to about 300 mites in a 3-lb package. When colonies are rapidly expanding, mite populations double each month. So from late March through late July, we’d expect the mite populations in these hives to reach 4,800 by late July. This is a very serious mite infestation level! Yet, the researchers waited until October 5 to treat with Apistan strips (which are ineffective against mites in many areas of the U.S.)! Any experienced beekeeper would suggest that these colonies died from a varroa/Deformed Wing Virus epidemic, which leaves deadouts, as the authors observed, “remarkably empty except for stores of food and some pollen left on the frames.” Unfortunately, the authors only included a photo of a honey frame, rather than a brood frame, which might have been helpful in diagnosing the actual cause of death! The dosing with high levels of an insecticide would be expected to cause the treated colonies to suffer more from varroa than the untreated controls.
The description of the dead colonies does not match the definitive signs of CCD at all—there was a dwindling of population, rather than a sudden collapse, and no abandoned brood. Rather the descriptions of the deadouts more closely matched dwindling collapse due to varroa/virus or nosema.
The authors, on a roll, simply do not know when to stop: “If imidacloprid exposure is truly the sole cause of CCD, it might also explain the scenario in which CCD occurred in honey bee hives not fed with HFCS. Considering the sensitivity of honey bees to imidacloprid as demonstrated in this study and the widespread uses of imidacloprid and other neonicotinoid insecticides, pollen, nectar, and guttation drops produced from those plants would have contained sufficient amounts of neonicotinoid insecticide residues to induce CCD.”
What are they talking about when they say “considering the sensitivity”? Even the lowest fed dosage (20 ppb) is about 5-20 times higher than that commonly found in nectar, and the other three doses were far higher–it is amazing to me that the colonies were not killed outright!
Speaking of which, I find it odd that the investigators didn’t give any explanation as to why they changed treatment dosages mid trial. To their credit, they initially treated the colonies with “field realistic” doses of the insecticide: 0.1 – 10 ppb. I suspect that after feeding the colonies for four straight weeks in July, and not noticing any adverse effects, that they then decided that they had better really hit the colonies hard if they wanted to “prove their case”–so they arbitrarily ramped up the lowest dose to 200 times stronger, and the highest dose to 40x stronger (that oughtta do it!).
I can only imagine their surprise and disappointment when after nine weekly feedings of a full half gallon of syrup intentionally spiked to widely accepted toxic levels, that they still noted virtually no adverse effects! Surprisingly, the amount of broodrearing was unaffected at the 20, 40, and 200 ppb dosages, and only slightly depressed at the clearly toxic 400 ppb dose! Note that the colonies were all still alive at midwinter, 3 months after the dosing ended. If anything, this study clearly demonstrated that colonies of bees can survive prolonged poisoning by imidacloprid at excessively high levels!
So why did the colonies die? Such insecticide exposure to hives in late summer has been previously demonstrated to greatly increase the chance of a colony later dying from nosema or varroa infection during the winter. In this study, poisoning the colonies all through late summer and early fall likely hampered the ability of the colonies to prepare a healthy population for winter.
Oddly, the investigators also took biweekly measurements of the cluster sizes of the colonies, yet chose not to include the results in the paper. This makes me wonder whether the authors simply decided to exclude any data that did not support their hypothesis.
So although this paper is surely going to be cited by anti-neonic advocates as some sort of supportive evidence, I find it to be a case in which an initially well-designed study (the dosing of hives with a series of four field realistic doses of imidacloprid) turned to farce when the investigators arbitrarily ramped up the doses, and blew it on parasite management.
In my assessment, it appears that the data from this study actually support an alternative hypothesis–that field realistic doses of imidacloprid had no measurable adverse effects upon the colonies. And even patently toxic doses had little immediate effect. I suspect that the apparent delayed effect was due to the impact of the insecticide upon late summer colony populations (which the authors inexplicably did not present), which led to later collapse due to parasite buildup.
In reality, the neonicotinoids fully appear to be “reduced risk” insecticides, which under field conditions, when properly applied (no dust issues) have never been associated with significant colony health issues. Compared to alternative insecticides, the data to date (including that of this study) support the hypothesis that neonicotinoids are an improvement over the previous classes of insecticides (there are clearly some questions about dust issues, chemigation, foliar and landscape treatments, which I will discuss in an upcoming article).
I find it unfortunate that the press, including both of our national bee journals, gave publicity to this paper without any sort of critical analysis. Such messages only confuse the public. Pesticides are a major issue to the beekeeping community. What we need are well designed and executed studies, (as well as better enforcement of pesticide law) in order to solve these problems. Sadly, this study just confuses the issues.
Republished with permission from Randy Oliver from
For the original Harvard study see the press-release with the link to the full paper: