I think that bee-l would be the best forum in which to discuss the results
of the study that has been going on in Prince Edward Island, Canada about
the causes of the bee losses here and their relationship to pesticide use,
with primary emphasis (in the first year in particular) on imidacloprid.
The
study also included hives in New Brunswick. I am hopeful that perhaps the
Bayer scientists Veldon Sorenson or Robert Steffens might respond on the
list,
or that the principal researchers Jim Kemp and Dick Rogers will comment.

As a background to this post I might remind people that imidacloprid is a
systemic insecticide that goes under various trade names (Admire and Gaucho
are two major ones) that is manufactured by Bayer (Agrochemical division)
and is one of the most used pesticides in the world now.  It is highly toxic
to bees and its use in France has been restricted for several years because
of beekeeper protest.

I also would remind the beekeepers on this list that Prince Edward Island
has an unusually high percentage of its cropland (about 20%) in potatoes and
that the majority of the potatoes are either leaf treated with imidacloprid
or soil injected with imidacloprid.  I had originally complained that a few
years after the introduction of this pesticide my hives began showing signs
of doing poorly in the summer and my winter losses were increased greatly.
My first complaint was made the year BEFORE varroa came to PEI.

The first year of the study looked at the levels of imidacloprid in the soil
in the first and second years following potatoes in the normal
potato-grain-hay rotation and in goldenrod in the field margins and in the
leaves and flowers of clover (in the hay) and in the nectar of bee stomach
contents.   The soil showed significant amounts (we already knew that the
half life of the insecticide is about a year and a half in potato soil
here).
The leaves of clover showed small amounts in a few samples but the flowers
had insignificant amounts and none was found in nectar or pollen.  There
were no wax samples taken that year.  The people from Bayer said that the
chemical was hydrophilic / lipophobic (likes water/ doesn't get absorbed in
oils or waxes) and so would not be found in wax.  It was not until the end
of that year that I heard of the class action beekeeper lawsuit in the US in
which wax was said to be where the compound was found.

The second year of the study looked at a broader range of factors.  The
question was not limited to imidacloprid, but was to try and identify what
the cause of the bee decline was, and looked at many of the other compounds
commonly used in the fields here in addition to imidacloprid.

The results are now in from the sample analyses of the study.  I do not have
a copy of the exact figures, but hope that Dick or Jim or Veldon will post
them to this list for comment.  I think that what is interesting is the
results
from some hives in New Brunswick that were on seed canola following
potatoes.  These hives showed residues from imidacloprid used the previous
year.  It showed up in honey, pollen AND wax.  The amounts are in the
2 to 6 ppb range I believe, and I am sure that the company will say that
these amounts are below the NOAEC (no observed ADVERSE effect
concentration).  But they are not below the NOEC (no observed effect
concentration).  The proboscis extension test shows an effect at about 6
ppb.  There is a picture of Madame Pham-Delegue performing this test
in Bayer's own book on imidacloprid and bees.  These amounts are also from
residues that are coming from a non target crop the year after treatment,
which is problematic to say the least IMHO.

But I hope that the discussion will not be just an argument about what
levels are lethal, or sublethal, or produce damage when chronic.  To me
what has been most troubling about the study is this:  The researchers were
shown hives by beekeepers here that exhibited a very specific syndrome, that
I call "disappearing bee syndrome".   It is characterized by a hive that was
doing
well suddenly being left with a queen and a small handfull of bees.  There
are often
a half dozen or more frames of brood and the brood is usually full of
chalkbrood
and often EFB as well.  But I do not think that these diseases are the
cause,
because they could not account for an adult population plummeting from what
could
have cared for 6 big frames of brood to one or two hundred bees in such a
short
time that there are still a few living larva on the frames despite the fact
that the tiny
cluster usually abandons the now diseased and starving brood area for a
small patch
of clean comb.  One beekeeper here has taken one of these queens and put her
with fresh bees on fresh comb and she headed up a healthy colony.

The researchers have not, in my opinion, come up with any explanation for
this
despite several years of studying a huge range of factors.  I hope they will
speak
for themselves to the beekeepers on this list, but personally I do not find
that
management, nutritonal factors, queen quality, or disease can explain the
syndrome.
I know that in my case I do not have AFB, requeen a large percentage of
hives in
the spring, practice overcelling, and am a more experienced manager than I
was
before the syndrome appeared (and remember, the problem began before varroa
but after imidacloprid).

I also know that in the yards where I winter, which are composed of several
summer yards, the mortality is vastly different between groups coming from
different
summer yards (some groups show two or three times the mortality of others).

Another fact worthy of note is that the largest beekeeping operation in the
Maritimes
has kept some hives on PEI for a couple of years now, overwintering in an
indoor
facility similar to what they have in Nova Scotia with about three time the
mortality
here in PEI.

I hope this post will stimulate some informed discussion.  It would be
really useful
if the researchers would actually post some of the results here.

Regards
Stan

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