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USA- FORBES JOURNALIST REFUTE THE BAYER EMPLOYEE ARGUMENTS ABOUT THE BAYER PRODUCTS INNOCENCE IN THE DISAPPEARANCE OF BEES

Featured Thursday, 10 May 2012 18:45 Written by Analia Manriquez

Last week I wrote a piece about the worrying phenomenon of Colony Collapse Disorder, a complicated problem that is decimating bee populations worldwide, and the theorized role of a a group of pesticides, the neonicotinoids, sold by the agrochemical giant, Bayer. In response, David L. Fischer, Director, Environmental Toxicology and Risk Assessment, from Bayer’s CropScience division in North Carolina, posted a detailed response on this blog as well as on Bayer’s Web site. My reply is below inline with his comments …

 

 

 

Mr. Fischer,

Thanks for your considered and thoughtful reply. My responses, which must all be qualified with “as I understand from my research and I’m the first to admit I am not an expert …” are inline:

DLF: As an environmental toxicologist with 25 years of experience – and current employee of Bayer CropScience – I feel it is important to share a different perspective on bee health and Colony Collapse Disorder (CCD) with you and your readers. You state that “despite a lot of research since CCD was first recognized in 2006 the causative factors have not been identified.” However, it is important to note that CCD is a symptom, not a disease.

Just as a fever is symptomatic of a many different illnesses in humans, the rapid disappearance from colonies of worker honeybees (i.e. CCD) appears to be a symptom that can occur during the end-stages of multiple bee diseases. What is clear is that the occurrence of CCD, and honeybee colony losses in general, are not correlated with exposure levels to agrochemicals (van Englesdorp et al. 2009).

“Not correlated”? From the papers you cite and others I’ve read, correlation has not been dismissed. As the conclusion of van Englesdorp et al. 2009 state: “Potentially important areas for future hypothesis-driven research … including … the role of honey bee resistance to pesticides.” That doesn’t seem to support your argument that there is no correlation.

DLF: CCD has been reported from organic beekeeping operations and in locations far away from agricultural lands. It is also important to understand that CCD is a newly coined term for a symptomology that has been observed by beekeepers for more than 100 years. In their descriptive study of CCD, van Englesdorp et al. stated “since 1869, there have been at least 18 discrete episodes of unusually high colony mortality documented internationally.

While symptomatically similar events to what we now call CCD were historically documented what, as I understand it, is new and the reason the term was coined, was that by 2006 the frequency and spread of CCD symptomatology reached previously unheard of levels (and being symptomatically similar doesn’t mean caustively identical).

DLF: In some cases, the descriptions of colony losses were similar to those described above. The idea that it all started in 2006 and coincided with the introduction of neonicotinoid insecticides is a myth.

Would it not be more accurate to say that a correlation has not been established rather than dismiss it as a myth?

DLF: Interestingly, there does seem to be a correlation between recent occurrence of CCD and the presence of residues of Varroa control chemicals. In these situations, hives with lower rates of CCD generally have higher varroacide residue levels. This suggests that beekeepers who are more vigilant in controlling Varroa are less likely to have CCD in their colonies. Varroa mites weaken bees’ immune systems and are themselves vectors of pathogens that may cause severe sickness in bees and trigger the CCD response. While I believe existing data suggest this hypothesis is true, more experiments need to be run in order to definitively test it.

I agree, the theory that Varroa mites or something connected with the mites is a factor in CCD is very interesting but what we’re discussing is the theorized connection between neonicotinoids and CCD. In fact, one could theorize that Varroa mites increase the susceptibility of bees to neonicotinoids so with the latter delivering the coup de gras the former, while a serious problem, wouldn’t by itself cause CCD.

DLF: Ultimately, there is no credible scientific evidence demonstrating a link between the use of neonicotinoid insecticides and the occurrence of widespread honey bee colony losses, including CCD. Imidacloprid, and neonicotinoid insecticides generally, remain safe and effective management tools to control a wide range of destructive insect pests. There have been a few incidents of acute poisoning of honey bees from the use of neonicotinoids, though far fewer compared to other major classes of insecticides. Still, in these cases, the affected colony typically recovers to normal health and population levels within a few weeks.

Many of the papers you cite don’t definitively refute a correlation between CCD  and neonicotinoids moreover most papers suggesting that further research is needed (see below). Also, the effects of long-term sub-lethal exposure to neonicotinoids particularly in concert with other factors such as Varroa infection appear to be unknown so it would seem at this point somewhat optimistic to say that neonicotinoids are definitely not implicated.

DLF: It is not just my opinion that neonicotioinds are generally safe for bees, when used properly.

Ah! “when used properly” … proper use is a real concern with all sophisticated agrochemicals. The 2008 incident in Germany was a great example of how usage can go wrong and the fact that the EPA still doesn’t make the use of “stickers” to ensure pesticides adhere to seeds is surprising.

DLF: This has been the conclusion of many recent peer-reviewed scientific publications where the authors have either reviewed all of the pertinent evidence (see, for example, Cresswell et al. 2011) or conducted multifactorial studies of bee health in various regions of the world (see, for example, Chauzat et al., 2009; Nguyen et al., 2009; Generisch et al., 2010; van Englesdorp et al., 2009, 2010).

As I mentioned earlier; the majority of the studies you cite aren’t as definitive as you imply:

Cresswell et al. 2011:”It is concluded that dietary neonicotinoids cannot be implicated in honey bee declines, but this position is provisional because important gaps remain in current knowledge. Avenues for further investigations to resolve this longstanding uncertainty are therefore identified.

Chauzat et al., 2009: ”No statistical relationship was found between colony mortality and pesticide residues. … although certain pesticide residues were detected in apicultural matrices and occasionally with another pesticide residual, more work is needed to determine the role these residues play in affecting colony health.

Nguyen et al., 2009: ”Moreover, a very large number of our samples contained acaricides either prohibited or ineffective against Varroa destructor (Anderson & Trueman) (Acari: Varroidae), suggesting that the treatment methods used by the beekeepers to be inadequate for mite control. Our results support the hypothesis that imidacloprid seed-treated maize has no negative impact on honey bees.”

van Englesdorp et al., 2009: ”This is the first comprehensive survey of CCD-affected bee populations that suggests CCD involves an interaction between pathogens and other stress factors. We present evidence that this condition is contagious or the result of exposure to a common risk factor. Potentially important areas for future hypothesis-driven research, including the possible legacy effect of mite parasitism and the role of honey bee resistance to pesticides, are highlighted.

van Englesdorp et al., 2010:”Our CART analysis provides evidence that CCD is probably the result of several factors acting in concert, making afflicted colonies more susceptible to disease. This analysis highlights several areas that warrant further attention, including the effect of sublethal pesticide exposure on pathogen prevalence and the role of variability in bee tolerance to pesticides on colony survivorship.

The conclusions of the 2011 Purdue study (Krupke CH, Hunt GJ, Eitzer BD, Andino G, Given K (2012) Multiple Routes of Pesticide Exposure for Honey Bees Living Near Agricultural Fields. PLoS ONE 7(1): e29268. doi:10.1371/journal.pone.0029268) are also significant:

Neonicotinoid insecticides, which are widely used and highly toxic to honey bees, have been found in previous analyses of honey bee pollen and comb material. However, the routes of exposure have remained largely undefined. We used LC/MS-MS to analyze samples of honey bees, pollen stored in the hive and several potential exposure routes associated with plantings of neonicotinoid treated maize. Our results demonstrate that bees are exposed to these compounds and several other agricultural pesticides in several ways throughout the foraging period. During spring, extremely high levels of clothianidin and thiamethoxam were found in planter exhaust material produced during the planting of treated maize seed. We also found neonicotinoids in the soil of each field we sampled, including unplanted fields. Plants visited by foraging bees (dandelions) growing near these fields were found to contain neonicotinoids as well. This indicates deposition of neonicotinoids on the flowers, uptake by the root system, or both. Dead bees collected near hive entrances during the spring sampling period were found to contain clothianidin as well, although whether exposure was oral (consuming pollen) or by contact (soil/planter dust) is unclear. We also detected the insecticide clothianidin in pollen collected by bees and stored in the hive. When maize plants in our field reached anthesis, maize pollen from treated seed was found to contain clothianidin and other pesticides; and honey bees in our study readily collected maize pollen. These findings clarify some of the mechanisms by which honey bees may be exposed to agricultural pesticides throughout the growing season. These results have implications for a wide range of large-scale annual cropping systems that utilize neonicotinoid seed treatments.”

DLF: This is also the conclusion of the EPA, whose position is based on their review of hundreds of research studies conducted by independent researchers as well as chemical manufacturers.

Alas, the EPA’s handling of the approval process for neonicotinoids was a mess and doesn’t make them look like a completely reliable authority. The EPA first granted a “conditional registration” for Clothianidin (a neonicotinoid developed by Takeda Chemical Industries and Bayer AG) in 2003 and required a field study to be delivered in 2006. When the study was delivered a year after the deadline the EPA accepted it but three years later took another look and realized that it was flawed.  In an internal EPA memo from 2010, seven years after the EPA first granted a “conditional registration” for neonicotinoids products the agency states:

“Clothianidin’s major risk concern is to nontarget insects (that is, honey bees).  Clothianidin is a neonicotinoid insecticide that is both persistent and systemic.  Acute toxicity studies to honey bees show that clothianidin is highly toxic on both  a contact and an oral basis. … information from standard tests and field studies, as well as incident reports involving other neonicotinoids insecticides (e.g., imidacloprid) suggest the potential for long term toxic risk  to honey bees and other beneficial insects. An incident in Germany already illustrated the toxicity of clothianidin to honeybees when allowed to drift off-site from treated seed during planting. A previous field study (MRID 46907801/46907802) investigated the effects of clothianidin on whole hive parameters and was classified as acceptable.  However, after another review of this field study in light of additional information, deficiencies were identified that render the study supplemental.  It does not satisfy the guideline 850.3040, and another field study is needed to evaluate the effects of clothianidin on bees through contaminated pollen and nectar.  Exposure through contaminated pollen and nectar  and potential toxic effects therefore remain an uncertainty for pollinators.

This memo was cited in a 2010 article on the Grist web site that paints a very poor picture of both the EPA and Bayer. There is also a timeline of this sagaon the Grist site.

Grist recently published an article that discusses recent CCD research that further implicate neonicotinoids.

DLF: Bayer has been actively involved in finding solutions to improve bee health for more than 25 years. As a company, we also are committed to environmental stewardship and sustainable agricultural practices, including the conservation of beneficial insects such as honey bees.

While I appreciate your response I don’t think you’ve proved your assertion that neonicotinoids are not a factor in CCD. Indeed, the majority of the papers you cite (a small subset of the relevant research) don’t definitively dismiss neonicotinoids as blameless as a factor in CCD.

The most worrying aspect of your defense of the company you work for is that Bayer did not behave responsibly in the process of getting approval for neonicotinoid products.

What I don’t understand is how, in the face of significant environmental, scientific, and public concern you, an experienced scientist, would not opt for a “better safe than sorry” policy.

Given that there appears to be a some non-trivial level of doubt that neonicotinoids are safe where bees are concerned do you really want to roll the dice? If we were to substitute “your children” for “bees” would you still take the chance? And, finally, do you want to be one of the people who we might point at in a few years time and say “yep, he’s one of the people who killed off the bees”?

Yours sincerely,
Mark Gibbs.

 

 

 

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