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Evidence builds that insecticides are the main — or only — driver of bee die-offs

New Harvard research suggests that insect poisons are killing bees all by themselves — that is, without the partnership of parasites or malnutrition.

In a typical CCD scenario, a hive of commercial honeybees simply empties out over the winter, during a period when bees are taking a long break from pollinating chores or even, in cold climates, hibernating.

A new study of honeybee die-offs from the Harvard School of Public Health adds much to the case that neonicotinoid insecticides are a key cause of the problem.

Even more important, perhaps, the research suggests that these increasingly ubiquitous insect poisons are killing bees all by themselves — that is, without the partnership of parasites or malnutrition.

Published at the end of last week in the Bulletin of Insectology, the study is the Harvard team’s second look in a couple of years at how exposure to “neonics” seems to promote the baffling phenomenon known as colony collapse disorder, or CCD.

In a typical CCD scenario, a hive of commercial honeybees simply empties out over the winter, during a period when bees are taking a long break from pollinating chores or even, in cold climates, hibernating.

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Some dead bees are left behind, their numbers a small fraction of the hive’s healthy population, and in less typical incidents there may not be a large-scale abandonment. There may also be signs of other bee-killing factors, like mites, but not on a scale sufficient to explain the wholesale die-off.

The prevailing explanation for CCD since its emergence in 2005 and 2006 is that bees are overstressed by the triple burden of pesticides, parasites such as mites and intestinal fungi, and loss of foraging territory as more and more fields of wild flowering plants become lawns and parking lots.

By feeding the bees with sugar syrup and protecting from mites, the Harvard team has produced results suggesting that maybe it’s pretty much just the pesticides — and at levels far below what regulators have established as a lethal dose.

Scientific transparency

The design of this study and of its essentially identical predecessor, reported in the spring of 2012, is simplicity itself. Let’s take a minute with the details, partly because they’ve been widely misreported this time around and partly because I happen to think the research’s sheer transparency is interesting in itself.

  • In the summer of 2012, researchers led by Chengshen Lu selected six colonies of honeybees at each of three apiaries in central Massachusetts, for a total of 18; each colony consisted of a standard 10-frame hive.
  • At each site, starting at the beginning of July, bees in the six selected colonies were given sufficient sugar water, made either with sucrose or high-fructose corn syrup, to take the possibility of malnutrition out of play.
  • In each group of six, the sugar source for two colonies was treated for 13 weeks with a sublethal amount of the neonic imidacloprid; for two more, the treatment was with clothianidin; the last two were left untreated. All the colonies  consumed all the sugar water they were given each week.
  • Starting in November, with the onset of colder weather, all of the colonies got a paste form of the same sugar solution without any neonic treatment. (This would mimic real-world exposure to neonics, which typically are applied to crop seeds and then expressed throughout stems, leaves, flowers and fruit throughout the plants’ life cycle; in addition, some crops are dusted with neonics during the growing season.)
  • All the colonies were treated identically with one application of Miteaway and one of  Apistan, used by beekeepers to kill the Varroa mites that used to be the leading cause of massive bee die-offs before CCD came along. Mite counts were then taken “using the common alcohol wash method.” (But you knew that.)
  • Later on, the colonies were treated with Fumagillan-B to take care of two fungal, intestinal parasites known as Nosema apis and Nosema ceranae, also commonly big trouble for honeybees.
  • From the beginning of the test period in July 2012 through the end in April 2013, the colonies’ health was tracked with biweekly “brood assessments” and measures of “cluster size” using methods that might interest any entomologists in the house but were frankly a little opaque for me. Suffice it to say they were scientifically standard.

All’s well till winter

All of the colonies thrived about equally until winter approached, regardless of apiary location or specific sugar source or even neonic exposure. But then:

As temperatures began to decrease in late October 2012, we observed a steady decrease of bee cluster size in both control and  neonicotinoid-treated  colonies. While such decline was quickly reversed in the control colonies in January 2013, the neonicotinoid-treated hives continued to decline …

The diminishing cluster size in the neonicotinoid-treated  colonies led to the loss of six of the twelve (50%) with symptoms resembling CCD, whereas only 1 of the 6 control colonies was lost exhibiting Nosema ceranae like symptoms, although we did not perform any test to confirm Nosema infection in this control hive.

No similar Nosema-like symptoms were observed in the treated hives. Upon close examination of colonies in early April 2013, we found that the majority  of bees in all neonicotinoid-treated colonies, regardless of whether they survived or not, had abandoned  their  hives during the course of winter.

 However, we observed a complete opposite phenomenon in the control  colonies in which instead of abandonment, hives were re-populated quickly with new emerging bees. The honey bee clusters in the six surviving neonicotinoid-treated  colonies were very small, and were either without queen bees, or had no brood.

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We found no significant difference in the degree of Varroa mite infection between the control and neonicotinoid-treated colonies. …

More study needed, but…

The new study differs from its predecessor in a few ways, all of which would seem additionally damning to neonics:

  • In the earlier study, only imidacloprid was tested, with similar but worse results; the new one extends the finding to a second neonic.
  • The first study took place in a colder winter — an unavoidable, somewhat unpredictable variable that probably helped to bring the incidence of CCD-pattern mortality to 100 percent in the treated hives, even though the neonic exposure was at one-seventh the level of the newer research.

So far, critical response to the study has been both sparse and muted. Bayer CropScience, which makes neonics, says the dosages were mu’ch larger than what bees would actually encounter in the real world.

An interesting defense, considering that Bayer can neither know nor control environmental levels of exposure; they’re determined by the actions of applicators, some of which might not follow the label instructions precisely.

(The levels are also influenced, it’s becoming increasingly clear, by neonics’ unexpected and unadvertised persistence in soils and water, which can essentially reapply them in successive years without an applicator being involved at all.)

Others have dinged the study’s small sample size and its publication in a journal that doesn’t have the stature of, say, Nature, which seems to me a weird way of dissing a piece of work from, like, Harvard.

Science proceeds by disproof, as they say — or, as Holmes would have it, by eliminating all possible explanations until just one remains. And more work needs to be done on neonics and honeybees, for sure.

But with this paper, the Harvard team may well have taken Varroa mites and Nosema fungi away from center stage, where the neonics stand increasingly alone in the spotlight of discovery.

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The full paper, a mere six pages, can be read right here.