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From:
randy oliver <[log in to unmask]>
Reply To:
Informed Discussion of Beekeeping Issues and Bee Biology <[log in to unmask]>
Date:
Fri, 6 Apr 2012 07:53:43 -0700
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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.
 Unfortunately, there are a great deal of factual misrepresentations and
fuzzy thinking in the paper, which obviously was not peer reviewed by
any bee biologist nor toxicologist.  For example, 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").

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.

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."

As Bob and others have pointed out, CCD actually started occurring in
2004-2005.

 "Second, while commercial beekeepers appear to be affected by CCD at a
disproportional rate"

This is not true according to any of the surveys that I've seen.

", 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 (Bonmatin et al.,
2005; Benbrook, 2008)."

It appears that the first cases of CCD preceded this time period, since any
HFCS
produced from such treated corn would have necessarily have been produced
following
the season of harvest.

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 Imd winds up in the kernels, the author *assumes* that it is
concentrated
there at high levels!  An then further goes out on a limb by "assuming"
that any
such imidacloprid is then 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. The range of dosages
used in this study from 20 to 400 ėg/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.

But then the author goes 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
ėg/kg) of imidacloprid in HFCS, by taking into account
the uptake by corn plants from seeds that are treated
with imidacloprid."

He simply created this "concentrating factor" out of thin air!  He gave
absolutely
no justification for it.  In the actual process of making HFCS, pesticides
are
largely removed.  As I stated before, all that the author had to do would
have been to
ask Roger Simonds at the USDA Gastonia pesticide testing lab as to the
actual measured levels of Imd in HFCS, and thus would
not have brought embarrassment to Harvard Medical School 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," suggesting some
something less than a "large" number of mites was indeed observed!  And
then they waited until October 5 to treat with Apistan strips, which are
ineffective against mites in many areas of the U.S.

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!

Oddly, I don't see any explanation as to why the investigators changed
treatment dosages mid trial.  To their credit, they initially treated the
colonies with "field realistic" doses of the insecticide: 0.1 - 10 ppb
(that would have actually have been a decent study).   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 support their hypothesis--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 then
feeding colonies a full half gallon of obviously toxic treated syrup weekly
for another 9 straight weeks, they still noted virtually no adverse
effects!  Note that  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.

So why did the colonies die?  Such pinsecticide exposure to hives in late
summer has been clearly 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 there was no effect of
treatment upon the colony populations, and 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
ad nauseum, I find it to be a case in which an initially fairly designed
study (the dosing of hives with a series of four field realistic doses of
Imd) 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.

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.
-- 
Randy Oliver
Grass Valley, CA
www.ScientificBeekeeping.com

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