Let's look at some studies on the combined effects of neonicotinoids and fungicides.  There are two types of outcome, depending on whether the neonic used is "cyano-substituted" (example acetamiprid) or "nitro-substituted" (example IMI):


Iwasa T, Motoyama N, Ambrose JT, Roe RM (2004) Mechanism for
the differential toxicity of neonicotinoid insecticides in the

honey bee, Apis mellifera. Crop Prot 23:371-378


Excerpt:

"To determine the importance of metabolism in honey
bee susceptibility to neonicotinoids,we measured
acetamiprid toxicity for insects pretreated with different
metabolic inhibitors and imidacloprid/thiacloprid toxicity
pretreated with PBO. The synergists used in these
studies are shown in Fig. 2. Based on a comparison of
the estimated LD50 values and their 95% confidence
intervals,no significant increase in acetamiprid toxicity
was noted for bees pretreated with 10 mg of DEF or
DEM (Table 2). However,a statistically significant
synergistic ratio of 2.96 (95% confidence interval of
1.83-4.76) was found for DEF. DEF and DEM are
inhibitors of esterase and glutathione transferase activity,
respectively. PBO,uniconazol e-P (plant growth
regulator) and especially the DMI-fungicides (triflumizole,
propiconazole, triadimefon and epoxiconazole)
had a much greater effect on acetamiprid toxicity than
either DEF or DEM. The synergistic ratios ranged from
6.04 (95% confidence interval of 4.29-8.51) for PBO to
244 (95% confidence interval of 171-347) for triflumizole
(Table 2). PBO,trifl umizole and propiconazole had
an even more dramatic effect on thiacloprid toxicity in
the honey bee with an increase in toxicity of 154-,1141-
and 559-fold,respectivel y (Table 2). In contrast,the
synergistic ratios for these same compounds for
imidacloprid were 1.70,1.85 and 1.52,respectively. No
significant differences were found in the LD50 values
between imidacloprid alone and bees pretreated with
PBO,triflumizole and propiconazole (based on comparison

of the 95% confidence intervals) (Table 2)."


In plainer English, exposure to fungicides plus cyano-substituted neonics like acetamiprid increased honeybee mortality significantly.  Fungicides plus nitro-substituted neonics like imidacloprid did not alter honeybee mortality, showing that the two neonics are differently metabolized.  In the presence of P450 inhibiting fungicides one type becomes more toxic whilst the other is unaffected.


Further, they add:


"Suchail et al. (2001) found that the metabolites of
imidacloprid in the honey bee were a hydroxy derivative
at the 50 position and an olefin derivative in the
imidazolin ring. The olefin has higher not lower
insecticidal activity than the parent (Nauen et al.,

1998). In the house fly, PBO increased imidacloprid

toxicity 10.7-fold (Liu et al.,1995 ) while O-propyl-O-(2-
propynyl) phenylphosphate (PPP) increased both imidacloprid
and acetamiprid toxicity (Yamamoto et al.,
1998). These findings suggest that metabolism and
detoxification pathways may vary between insect species
which can affect insect susceptibility to neonicotinoids.
P450 inhibitors produced only a minimal increase in
imidacloprid activity in the honey bee in our studies
(Table 2),indicating that this was not an important

detoxification pathway."


Very short summary:

1) Acetamiprid (or other cyano-substituted neonic) + fungicide = more toxic to bees than neonic alone;

2) IMI (or other nitro-substitued neonic) + fungicide = no cumulative toxic effect;

3) Bees do not metabolize all neonics the same way;

4)  Bees have different detoxification mechanisms than the target insect pests.


Now it would be helpful to know what the major seed treatment cocktails are on different crops.  Is anyone on this list knowledgeable about this?  What combined treatments are most used on canola, corn, beans, potatoes, alfalfa, others?


I notice a big difference between spring canola and winter canola.  Are both kinds foraged by bees?  Are seed treatments similar or different?


Christina

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