Is HFCS killing honeybees?

This morning, while browsing the social networks, I was linked to two different pages about a new study that is claimed to show that pesticide-laden high fructose corn syrup (HFCS) is the cause of Colony Collapse Disorder (CCD) in honeybees. One was a retweet from William Gibson linking to the Harvard press release. The other were some friends linking to a Mongobay story.

So that’s kind of worrying, right?

The study itself makes a very strong claim:

From the ecological and apicultural perspectives, the results from this study show a profound and devastating effect of low levels of imidacloprid in HFCS on honey bee colonies… It is likely that CCD was caused by feeding honey bees with low levels of imidacloprid in HFCS throughout their lifecycle in which toxicity occurred during the larval/pupal stages and was later manifested in the adult honey bees.

That should require a convincing mechanism and very strong data. The study, as written, doesn’t. The basic hypothesis is fairly believable:

  • Bee keepers use HFCS as a cheap supplement food for their bees (since humans take most of their honey).
  • Neonicotinoid pesticides in large enough doses can directly kill bees.
  • Residues from these pesticides have been found in nectar and pollen.
  • Corn crops have been increasingly treated with these pesticides.
  • HFCS likely contains these pesticides.
  • Maybe bees eating small amounts of pesticide-laden HFCS can lead to CCD.

This is the part a layman is likely to read. Isn’t it pretty believable? To make it even more believable, neonicotinoid pesticides are banned in Europe. Plus, other studies investigating CCD have show a possible link to these pesticides (certainly, bees have been outright killed by misapplication of these pesticides). I’m convinced! Aren’t you?

But the study has some major flaws, as pointed out in a Wired article and a response from Bayer (who manufactures some of these pesticides). But please read the study itself because I think some of these should jump out to a critical reader. The following are some that bothered me the most.

Pesticide Feeding Levels Unjustified

The study feeds differing levels of imidacloprid (a neonicotinoid pesticide) in HFCS to various bee colonies (as well as HFCS containing no added pesticide as a control). But there is little justification for why those levels were chosen. There’s some hand-waving about levels of pesticide residues found in pollen and nectar, but that doesn’t really tell us much about how much would be in the HFCS that beekeepers would actually feed their bees. The explanation given is:

Lastly, several earlier reports have shown that corn and sunflower plants grown from genetically engineered seeds treated with imidacloprid, one of the neonicotinoid insecticides, produce pollen with average levels of 2.1 and 3 μg/kg of imidacloprid, respectively (Suchail et al., 2001, Rortais et al., 2005). Furthermore, a recent paper published during the course of this in situ study showed elevated imidacloprid residue levels of 47 mg/L in seedling corn guttation drops germinated from seeds treated with 3 different neonicotinoid insecticides-treated (including imidacloprid) corn plants that are high enough to kill honey bees instantaneously (Girolami et al., 2009). 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.

However, the actual dosages chosen to be fed are not really explained. They varied wildly between hives — one hive was fed a range from 0.1 µg/kg (at four weeks) to 20 µg/kg (at nine weeks) while other hives were fed 10.5 µg/kg and 400 µg/kg. Why so much more after nine weeks? It’s not at all clear why this difference. I can guess — perhaps the literature indicates pesticide residues vary wildly over the season. But I shouldn’t have to guess. The only significant mention in the methods as to why the levels were chosen is:

The dosages used in this study were determined to reflect imidacloprid residue levels reported previously (Suchail et al., 2001; Bonmatin et al., 2005; Rortais et al., 2005; Girolami et al., 2009). Imidacloprid was initially fed to honey bees at 0.1, 1, 5, and 10 μg/kg in HFCS for 4 weeks starting on July 1st 2010, followed by 20, 40, 200, and 400 μg/kg for another 9 weeks, which ended on September 30th 2010.

But these are presumably just the residue levels discussed in the introduction which are residue levels in pollen, nectar and corn guttation drops1. How did the study authors calculate how much pesticide to add to mimic the amounts in commercially available HFCS?

Why does 2005/2006 HFCS matter?

The authors are very concerned about replicating HFCS used in 2005/2006 (when CCD supposedly began):

We hypothesized that the first occurrence of CCD in 2006/2007 resulted from the presence of imidacloprid (1-((6chloro-3-pyridinyl) methyl)-N-nitro-2-imidazolidinimine, CAS# 138261-41-3), 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. Second, while commercial beekeepers appear to be affected by CCD at a disproportional rate, 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. This is because many of the commercial beekeepers leave very little honey in their hives to sustain honey bees through the winter months, and therefore require the least expensive alternative for honey. 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 (Bonmatin et al., 2005; Benbrook, 2008).

Later in the discussion:

One apparent deficiency, in addition to the small number of honey bee hives used in this study, is that we were not able to obtain HFCS manufactured in 2005/2006 for use in this experiment. Instead, 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.

Colony collapses are still occurring. If this is the cause of CCD, why should it matter that they replicate levels that may have existed (again, entirely unproven) in the past, when the problem supposedly began? If this is the cause of CCD (or even a major one) then surely levels of pesticide residues in HFCS should be an ongoing concern.

Why not just measure pesticide concentrations directly?

The biggest problem that bothers me about this study is that it claims that HFCS contains low-level pesticide residues, then attempts to demonstrate what levels of them will kill a colony, but never actually talks about measuring pesticide concentrations directly! This seems just completely obvious to me. If for some reason that’s hard to measure (the Wired article talks a bit about that), then don’t the authors need to provide a clear discussion as to why they chose the pesticide residue levels they used? As it is, I’m left to assume they chose these levels because it got them results.

A Minor Point

In the introduction, the authors mention genetically modified crops:

The wide-spread planting of genetically engineered corn seeds treated with elevated levels of neonicotinoid insecticides, such as imidacloprid since 2004 (Van Duyn, 2004), and their acute toxicity to honey bees led us to hypothesize a link between CCD and feeding of HFCS containing neonicotinoid insecticides.

This is mentioned again in the discussion:

We have validated the study hypothesis in which the initial emergence of CCD in 2006/2007 coincided with the introduction of genetically engineered corn seeds treated with imidacloprid and other neonicotinoid insecticides.

Corn grown in the US today is commonly a GE variety, so pretty much any new pesticide applied to corn crops will be applied specifically to GE corn crops. So why mention it except to invoke fear of genetic engineering? The problem, the authors claim, is the use of an insecticide, not genetically engineered crops. It strikes me as manipulative to mention “GE corn” in a context where any corn would likely be GE because to uncritical readers2 it implies that the “GE” part had something to do with it. It is likely an inadvertent inclusion. However, given the degree of fearful reporting related to agricultural sciences, it is unfortunate.

The aforementioned Wired article and a response from Bayer make some further critical points that I find credible:

  • The pesticide used in this study isn’t even one commonly applied in the United States.
  • The studied failed to gather enough data (enough bee hives) to achieve statistical significance.
  • Given other research showing many other possible triggers for CCD (fungi, mites, virii, bacteria, etc), a study claiming a very particular cause should at least give a nod to why these other causes aren’t as likely.

Given that the lead author, Chensheng Lu, is quoted in Wired saying:

“The hives were dead silent,” he said. “I kind of ask myself: Is this the repeat of Silent Spring? What else do we need to prove that it’s the pesticides causing colony collapse disorder?”

I think it pretty clear the author truly believes that pesticides are causing bee hive collapses. Unfortunately, this study isn’t very convincing to me, even if I think it likely pesticides are somehow involved with CCD.

  1. “Corn guttation drops” are drops of xylem from corn plants.

  2. Specifically, the mainstream media tends to take quotes from science reports and attribute more meaning to irrelevant parts than is warranted. Obviously we should expect more competence in science journalism, but scientists can help avoid some of the worst of it by not writing confusing papers.