A pair of recent papers indicted neonicotinoids, a widely used class of insecticides, for contributing to a catastrophic decline of honeybees, especially since 2006. Hives across North America have been hammered, many by a particularly mysterious syndrome known as colony collapse disorder, or CCD. Now an additional field trial strengthens even more the case arguing that these pollinators have been poisoned by these chemicals.
This latest research also points to a potentially novel source of the chemicals: corn syrup.
CCD tends to occur in winter or early spring, often when bees begin their first foraging trips of the year. In affected colonies, bees leave but fail to come home, despite their hives having adequate food. One suspicion, which is supported by studies released March 29, is that pesticides or some other poison might impair a forager's memory or behavior.
But Chensheng Lu, an environmental scientist at the Harvard School of Public Health in Boston, was puzzled as to when and where the critical exposures occured. After all, affected bees were disappearing after months without exposure to toxic agents outside the hive. Lu now argues that bees can undergo a chronic poisoning if their hives' honey was tainted by insecticides that the pollinators encountered months earlier.
During winter, he charges, what looks just like colony collapse disorder largely emptied 15 of his team's 16 test hives in central Massachusetts. Each had been exposed experimentally for 13 weeks during the summer to low doses of imidacloprid. Growers rely on this and related neonicotinoid insecticides to protect their crops.
How long a hive’s colony survived after treatment diminished with increasing exposure of its bees to the insecticide the previous summer, Lu and his colleagues reported online April 5 in the Bulletin of Insectology.
Among four untreated hives, three survived. The other perished, but from dysentery — an intestinal infection — not CCD.
Fast food for bees
For their experiments, Lu and his colleagues set out groups of five hives, each consisting of healthy commercially purchased honeybees. The experiments were carried out in quadruplicate, with each grouping of five hives sited at least 12 kilometers from another. Insects at each site could forage throughout the wilds.
The researchers also provided each hive with the equivalent of its own on-site fast-food restaurant: a plastic feeder containing high fructose corn syrup.
Bees apparently love the sugary drink. Indeed, Lu says, many apiarists regularly feed this inexpensive beverage to their colonies in late winter to compensate for any overharvesting of honey (wintertime grub for bees).
One hive at each test site got corn syrup free of imidacloprid. The rest each got access to syrup containing small additions of the pesticide. Depending on the hive, syrup concentrations of the chemical ranged from 20 to 400 parts per billion. These values were all below federal limits for the pesticide in corn, Lu explains.
Offering hives corn syrup allowed the scientists to precisely doctor each batch with known quantities of the test chemical. It also allowed Lu to explore a hypothesis: that bees might be seriously impacted if even small quantities of neonicotinoid chemicals find their way into corn syrup.
And they might, he argues. Commercial beekeepers have been disproportionately affected by hive losses. One of the few changes they’ve made to insect husbandry in recent years has been to supplement hives with corn syrup during winter months. Although that began prior to 2006, what did almost precisely coincide with the initial outbreaks of CCD was the emergence of widespread commercial treatment of corn seed with neonicotinoid insecticides.
Seed treatments questioned
In North America and parts of Europe, many seeds now are coated with neonicotinoid insecticides before planting. As seeds germinate, the chemical enters the plant and circulates throughout its tissues, protecting vulnerable roots.
This systemic circulation of the pesticide bolsters concern by Lu’s team that imidacloprid can move into corn kernels. If it does, then the chemical could end up tainting corn syrup.
Today, imidacloprid or one of its neonicotinoid cousins coats most conventional and virtually all genetically modified corn seed, notes Charles Benbrook, chief scientist at the Organic Center in Troy, Ore.
That’s troubling, he argues, because in terms of their impact on bees, neonicotinoids “are the most acutely toxic pesticides ever registered.” They are also moderately persistent in soil, he says. And in recent years, insecticide-based seed coatings have tended to use a controlled release formulation. This extends crop protection benefits, Benbrook says, “but it also extends the time during which residues from seed treatments are likely to persist in treated plants.”
Like Lu, he suspects these insecticides can get into corn kernels — and the corn syrup now frequently fed to bees (something Benbrook’s organization has attempted to assay, unsuccessfully). But there are plenty of other routes by which bees can become exposed to these chemicals, Benbrook notes.
He points to data showing that plants from treated seeds can “sweat out” minute quantities of the insecticide into morning dew, a beverage popular with bees. Detectable quantities of imidacloprid have also been measured in the pollen of corn and sunflower plants whose seeds had been treated with the chemical. And European researchers have documented some seed planting equipment that roughs up seeds, generating an airborne exhaust cloud containing insecticide-laced residues.
In light of such data, including Lu’s new paper, Benbrook concludes that “there’s strong evidence that [neonicotinoid] seed treatments are putting pollinators at risk around the world.”
But treated seed is hardly bees' only possible source of exposure to these chemicals. Even five to seven years ago, Benbrook points out, 70 percent of U.S. apples, 79 of pears and 40 to 50 percent of broccoli and cauliflower were treated with these insecticides.
Some doubts remain
Not everyone is convinced by the Massachusetts field trials. Louisa Hooven, a beekeeper and scientist at Oregon State University in Corvallis, says that based on the sketchy observations described in the new paper, she finds it hard to be sure that the authors have indeed replicated CCD. For instance, "the presence of dead bees in front of the hives [reported by Lu's team] does not resemble CCD," she says. "In CCD, no bees are found." And certain characteristic symptoms of the syndrome went unmentioned in Lu's report. She says this includes whether the queen and some of her attendants remained behind even after most adult bees had fled the hive, as often occurs with CCD. Or whether there were signs of sealed pollen, which has also been associated with a hive's collapse.
At the Society of Toxicology meeting in March, Hooven presented some of her own data from preliminary experiments in which she exposed bees to pesticides. She administered low-dose concentrations of three chemicals to clean hives. All three pesticides are among those that have been measured tainting North American honeybee hives. After a few weeks of living with the chemicals,Hoover saw no deaths But the queens' egglaying behavior was perturbed and the maturation of nurse bees exhibited a delay.
Such subtle but potentially important changes also highlight one problem facing any environmental scientist sleuthing the putative mechanisms for CCD: Most bees simply aren't exposed to just one toxic chemical. A 2010 study by scientists from around the United States quantified 121 different pesticides and their breakdown products that they had isolated from bees, pollen, wax and other hive materials. The average number of pesticides identified in wax: eight. Among 350 pollen samples retrieved from hives, each harbored an average of seven such chemicals — but at times up to 31 pesticides (or their breakdown products, some of which are more toxic to bees than the parent chemical).
C. Lu, K.M. Warchol and R.A. Callahan. In situ replication of honey bee colony collapse disorder. Bulletin of Insectology, Vol. 65, June 2012.
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