>https://docs.google.com/file/d/0B7FCgF0BwlDGZXZVWFFqUUtRTGl5Uzdyb21VRV9Bdw/edit?pli=1
>
>...full study.
Thanks for this, Dean.
I've had a chance to look it over, and give it all the consideration it
seems to deserve, and unless I am missing something, and as much as I would
love to think that the problem is now solved and the hanging can proceed,
it seems that all that was accomplished was to simulate some CCD symptoms
by spiking HFCS with imidacloprid.
That imidacloplid cause bees to fly out and die was AFAIK not at all in doubt,
even among those of us who have reservations about the existence of a single,
unique CCD or uncertain of imidacloprid's exact role in current and past bee
losses.
Moreover, they never proved or even suggested there was any proof
that an commercial HFCS had EVER been shown to contain detectable
imidacloprid.
We have all wondered, especially since we are now imagining, with some justification,
imidacloprid everywhere.
I started wondering over ten years ago, but as much as I wonder, I need evidence.
When I consult people I respect and who would know about such things if anyone
would, they say they wonder too, but there is no evidence.
This group extrapolated theoretically possible levels in HFCS
from maximum permissible levels, in corn, but never showed if and
how it might be present in manufactures HFCS, or if the processing
might affect the transfer to the finished product.
Nor did they show that these levels -- or any detectable levels -- had ever
been approached in HFCS practice! It is not as if nobody had ever thought
of that before, or investigated it. The control hives were fed HFCS after all.
Quoting from the paper:
> ...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...
Sorry, I don't see how one speculation proves another speculation. I have
little doubt that this is possible, but the present study does nothing to
quantify that effect or show that it is observed in the real world.
Further, it seems to me that any such mechanisms should be common knowledge
in the chemical and processing industry and the regulators, and not a matter
of speculation.
There are a number of processes and although some aspects are probably
'secret', the general processes are widely known. I'm sure many people
think about these things and have actual numbers. If they were in the
detecable range, we'd be hearing about it. After all, HFCS has caused bee
problems before (not insecticide-related) and been closely scrutinized.
Quoting from the paper:
> It should be noted here that the residue levels of imidacloprid, or other
neonicotinoid insecticides, have not been routinely monitored in HFCS.
Routinely, perhaps, but I have doubts that monitoring was not done before
setting MRLs and after. This information should be available through FDA or
EPA and at least an effort should have been made to reference it. I see
some loosely related studies cited, but not what I would expect from a
serious study looking for contaminatiuon in HFCS.
They knew the cause of HFCS bee problems. They cited this:
>LEBLANC B. W., EGGLESTON G., SAMMATARO D., CORNETT C.,
DUFAULT R., DEEBY T., CYR E. St., 2009.- Formation of hy-
droxymethylfurfural in domestic high-fructose corn syrup
and its toxicity to the honey bee (Apis mellifera). Journal of
Agricultural and Food Chemistry, 57: 7369-7376.
Quoting again from "In situ replication of honey bee colony collapse
disorder:
>Each apiary consisted of 4 different
imidacloprid-treated hives and a control hive, which
was managed identically to the treated hives except no
imidacloprid was added to its HFCS.
> Sample type Imidacloprid (µg/kg) Sample size Recovery (%)
> Blank HFCS5 n.a. 6 n.a.
> Contained imidacloprid levels below the limit of detection at 0.1 µg/kg.
There was no detectable in the HFCS they used and no indication that they
had to hunt around to find HFCS that was not apparently free of the insecticide.
Further,
> Data from this in situ study provide convincing evi-
dence that exposure to sub-lethal levels of imidacloprid
causes honey bees to exhibit symptoms consistent to
CCD months after imidacloprid exposure. Should stres-
sor factors other than feeding honey bees with HFCS
containing imidacloprid cause CCD, the loss of honey
bees would not occur disproportionally on those imida-
cloprid-treated hives. The survival of the control hives
unequivocally augments this conclusion.
OK. I think everyone already knew that poisoned hives
don't do as well as hives fed a good, insecticide-free bee feed.
> The range of dosages used in this study from 20 to 400 µg/kg were not
only environmentally relevant to those reported imida-
cloprid levels by studies that are cited previous, but also
lie within legally allowable levels, set by the US Envi-
ronmental Protection Agency (EPA) as the tolerance of
0.05 ppm (50 µg/kg) for corn (US CFR, 2010). Since
there is no tolerance level for imidacloprid in HFCS, we
applied a 10-fold concentrating factor, or 0.5 ppm (500
µg/kg) of imidacloprid in HFCS, by taking into account
the uptake by corn plants from seeds that are treated
with imidacloprid. The 10-fold concentrating factor is
very conservative compared to the reported average
level of 47 mg/L of imidacloprid measured in guttation
drops collected from corn seedlings germinated from
commercial seeds obtained in 2008 coated with 0.5
mg/seed of imidacloprid (Girolami et al., 2009).
The title is: "In situ replication of honey bee colony collapse disorder"
Did they replicate CCD or just kill bees?
You decide
I'm going to bite my tongue now.
***********************************************
The BEE-L mailing list is powered by L-Soft's renowned
LISTSERV(R) list management software. For more information, go to:
http://www.lsoft.com/LISTSERV-powered.html
Guidelines for posting to BEE-L can be found at:
http://honeybeeworld.com/bee-l/guidelines.htm
|
