A quick review of the recent paper on pesticide analysis of U.S. beehives.  All
the following are quotes from the paper [with my comments in brackets].

From Mullin CA, Frazier M, Frazier JL, Ashcraft S, Simonds R, et al. 2010 High
Levels of Miticides and Agrochemicals in North American Apiaries:
Implications for Honey Bee Health. PLoS ONE 5(3): e9754  [I have removed
some citations for ease of reading]

No neonicotinoid residues were found in bees, [although they were rarely
found in] pollen and wax. Overall, pyrethroids and organophosphates
dominated total wax and bee residues followed by fungicides, systemics,
carbamates and herbicides, whereas fungicides prevailed in pollen followed
by organophosphates, systemics, pyrethroids, carbamates and herbicides.  [The
fungicide of most concern is the commonly detected chlorothalanil (Bravo®,
Headline®), which has been associated with “entombed pollen.”]

Beeswax remains the ultimate sink from the long-term use of the miticides
fluvalinate, coumaphos, amitraz and bromopropylate [this is an interesting
finding, since this chemical is not registered for use in the U.S.]…. Colony
residue levels of these miticides, after their in-hive application, have
been shown to increase from honey to pollen to beeswax. Beeswax is the
resource of the hive that is least renewable and is thus where persistent
pesticides can provide a “toxic-house” syndrome for the bees. The uniform
high levels of these miticides present in foundation is particularly
disturbing, since replacement of comb is currently recommended to reduce
pesticide contaminants. The broad contamination of European foundation with
especially miticides has been reviewed previously. Fluvalinate residues in
beeswax best correlated with the French bee winter kill of 1999–2000,
although disease factors were more emphasized in the report.

Almost all wax and pollen samples (98.4%) contained two or more pesticide
residues, of which greater than 83% were fluvalinate and coumaphos. Clearly,
substantial residues of these bee-toxic pyrethroid and organophosphate
compounds prevailed together in most beehives sampled. Chronic exposures to
high levels of these persistent neurotoxicants elicits both acute and
sublethal reductions in honey bee fitness, especially queens, and they can
interact synergistically on bee mortality. Our work does not directly
associate these miticides with CCD, although higher coumaphos levels may
actually benefit the colony, possibly via mite control

Externally-derived, highly-toxic pyrethroids, up to 9 in addition to
fluvalinate per sample, were the most frequent and dominant class of
insecticides in our samples. Pyrethroids are frequently associated with bee
kills. A sample of dead bees, obtained after a community-wide tree
application of permethrin according to label instructions, contained 19.6
ppm, 18-times the established bee LD50. Pollen and wax levels of more toxic
pyrethroids including bifenthrin, cyfluthrin, cyhalothrin, deltamethrin, and
fenpropathrin ranged up to 613 ppb, which is above the bee LD50 for
deltamethrin. This level can be lethal depending on pollen consumption rates
by differing castes, or wax transfer rates to brood or indirectly to pollen.
Moreover, some bee residues of deltamethrin, fenpropathrin and cypermethrin
are above levels shown to disorient foragers  and cause CCD-like symptoms
(see above). It is important to note that pyrethroids are rarely found
alone, and in 50% of our pollen and wax samples co-occur with
chlorothalonil, a fungicide known to increase bee toxicity of cypermethrin
by greater than 5-fold. Bee toxicity of the pyrethroid bifenthrin doubles
after Apistan (fluvalinate) treatment, which frequently coincides in our
samples. Potential for interactions among multiple pyrethroids and
fungicides seems highly likely to impact bee health in ways yet to be
determined.

Pyrethroids other than fluvalinate have been reported to impact the foraging
capabilities of honey bees. After topical application with 0.009 µg
permethrin/bee … none of the foraging workers returned to the hive at days
end, and only 43% of these bees returned even once to the hive because of
disorientation due to the treatment. vanDame et al.  found a similar effect
on foragers with deltamethrin at 0.0025 µg/bee (25 ppb), a dose 27 time
lower than the LD50, which disoriented 91% of return bee flights to the
hive. These symptoms are reminiscent of those reported for CCD.

Our results do not support sufficient amounts and frequency in pollen of
imidacloprid (mean of 3.1 ppb in less than 3% of pollen samples) or the less
toxic neonicotinoids thiacloprid and acetamiprid to account for impacts on
bee health…

[It is surprising to me that the authors bring up the neonicotinoid
insecticides some twelve times in the paper, when the most notable chemical
in this class, imidacloprid (mentioned thirteen times), was only found in
1.7% of the samples!  Note also that there were zero detections of
clothianidin, a widely-used neonicotinoid, which has frequently been blamed
for colony collapses!  For example, the authors state:]

Systemic neonicotinoid use has greatly increased recently for treating seeds
of many major crops, particularly those genetically-engineered, and
considerable impact to non-target species may occur. Neonicotinoids and
systemic fungicides are often combined as pest control inputs, and many of
the latter synergize the already high bee toxicity of neonicotinoids [Iwasa
2004].  A recent landscape-level study of imidacloprid seed treatments on
maize in Belgium demonstrated no impacts on honey bees; however, their high
prevalence with EBI and other fungicides including myclobutanil, although
refuted by some field results [Schmuck 2003], may have more direct impacts
on bee health through synergistic combinations.

[I find it of interest here to quote from the papers cited.  Iwasa states
that three tested synergists had “minimal effect on imidicloprid
[toxicity].”  He also states that “When honey bees were placed in cages in
forced contact with alfalfa treated with acetamiprid and the
synergist,triflumizole,in combination at their maximum recommended
application rates,no mortality was detected above that of the control.“ The
Schmuck paper concludes that “Our results suggest that, at the recommended
use rates, thiacloprid poses a negligible lethal risk to honeybees when
applied either alone or in tank mixes with fungicides of various chemical
classes.”]



[As far as the beekeeper-applied miticides are concerned, the authors state
that] High levels of fluvalinate and coumaphos are co-occuring with lower
but significant levels of 98 other insecticides, fungicides and herbicides
in pollen…. Foundation wax is uniformly contaminated with miticides….
Twenty-one
wax samples from six different commercial and two private foundation sources
were uniformly contaminated with up to 10.1 ppm fluvalinate …and up to 14.3
ppm coumaphos.

Extraordinary enhancement of toxicity has been found with addition of
commercial synergists to fluvalinate, where a topical LD50 of 0.00964
µg/bee, a 980-fold increase to their reported 9.45 µg/bee without the
additive, occurred if 100 µg of piperonyl butoxide [a common pesticide
synergist] was applied 1 hr prior to the pyrethroid.

[My take on these results is that attention to the neonicotinoid pesticides
is largely displaced, whereas we should be focusing on the in-hive
miticides, the agricultural pyrethroids, and the fungicides.]

Randy Oliver

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