[Pollinator] Fwd: FW: CA Beekeeper's' rebuttal to Harvard Study

[Ladadams at aol.com]

____________________________________
 From: gludwig at almondboard.com
To: Ladadams at aol.com
Sent: 4/9/2012 5:30:36  P.M. Pacific Daylight Time
Subj: FW: CA Beekeeper's'  rebuttal to Harvard Study



 
Hi  Laurie, 
As an FYI, you may want to  attach this along with the just sent out notice 
re the study from Harvard.   
Gabriele 
 
 
Sent: Monday, April 09,  2012 1:03 PM
Subject: CA Beekeeper's' rebuttal to Harvard  Study

Randy  Oliver, a beekeeper in CA, was one of  many who posted a rebuttal to 
the Harvard paper on imidacloprid and bees. "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!" 
To  read the entire article, please see below. 
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News Items 
The Harvard Study on imidacloprid and CCD
April  2012 
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 changed the 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 ìg/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 ìg/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. 
_http://scientificbeekeeping.com/_ (http://scientificbeekeeping.com/)  
  
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