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  1. #1
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    Default The Case Against Imidicloprid

    Please bee folk, I did a little playing with graphs and looked at various toxicity data on Imidacloprid and plotted on log-log graph to find the power law. It's disturbing to say the least. If you are wondering why we don't see residue in collapsed colonies, the answer is that the effects happen at unobservably small chronic doses.

    The post is here: http://squashpractice.wordpress.com/...-imidacloprid/

    We've got to follow the Europeans and get rid of this stuff!

  2. #2
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    Default Re: The Case Against Imidicloprid

    An excellent article, thank you for posting it!

    The link at the bottom to the work of Rosemary Mason should be followed up as well.
    I was lucky to have Rosemary visit our farm last year, to see a prime habitat of the endangered Great Yellow Bumblebee.

  3. #3
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    Default Re: The Case Against Imidicloprid

    Very interesting, will follow the links at the bottom of the article to find out more.

  4. #4
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    Default Re: The Case Against Imidicloprid

    This is an interesting theory and may well have some validity. It does, though, also seem to be a convenient means for keeping alive the theory that what cannot be detected is actually the problem. It would also seem to suggest that there would only be a single narrow window for neonic exposure. Is that plausible? Maybe, maybe not. I would suggest that if someone is to actually prove such a theory that they need actual data proving this rapid rate of metabolization and excretion.
    "People will generally accept facts as truth only if the facts agree with what they already believe."- Andy Rooney

  5. #5
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    Default Re: The Case Against Imidicloprid

    Quote Originally Posted by jim lyon View Post
    This is an interesting theory and may well have some validity. It does, though, also seem to be a convenient means for keeping alive the theory that what cannot be detected is actually the problem. It would also seem to suggest that there would only be a single narrow window for neonic exposure. Is that plausible? Maybe, maybe not. I would suggest that if someone is to actually prove such a theory that they need actual data proving this rapid rate of metabolization and excretion.
    This is not a theory. All I was doing is fitting existing data to a convenient toxicity model and extrapolating to the age that bees normally live. The fact the the model works well with the neonics with other species, and fits published bee toxicity data, suggest that actually the chemical is NOT metabolized and excreted, but rather bio-accumulates and continues to produce toxic effects well after exposure.

  6. #6
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    Default Re: The Case Against Imidicloprid

    Quote Originally Posted by grondeau View Post
    This is not a theory. All I was doing is fitting existing data to a convenient toxicity model and extrapolating to the age that bees normally live. The fact the the model works well with the neonics with other species, and fits published bee toxicity data, suggest that actually the chemical is NOT metabolized and excreted, but rather bio-accumulates and continues to produce toxic effects well after exposure.
    Then wouldnt you agree that a lack of residue could, among other things, mean either that there never was any residue? How could you differentiate without some sort of data? Again, I am not saying its not a viable theory just trying to understand how showing that something is possible may not be an indication of anything other than that it is, in fact, possible. Please clarify.
    "People will generally accept facts as truth only if the facts agree with what they already believe."- Andy Rooney

  7. #7
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    Default Re: The Case Against Imidicloprid

    Hi Jim,
    We CAN detect residue in pollen in plants grown from treated seed. Typical levels are in the 1-10 ppb range. Problem is, the bees dilute this since they bring in pollen from other sources as well. Plus the stuff does degrade. Our detection limit is around 1 ppb, so we are starting from a point close to the detecion limit anyway. By the time you dilute, you not expect to be able to detect it. This is not a mystery. Nor would you expect that toxins in the sub ppb range would kill bees immediately. There is not a lot of data on how low doses of neonics kill bees. Best paper is Suchiel 2001. There is nice data on how very low doses of neonics kill other arthropods (the other paper I ref.). Both sets of data fit the power law toxicity model very well. The model (and Suchiel's data) show individual bee mortality at sub ppb dose levels when given enough time. (7-10 dyas for Suchiel).

    Please tell me how bees that gather pollen from sources which have ~1ppb residue - could NOT have some residue more than 0.0001 ppb in their bee food. We can't see that, but it would be folly to assume that just those molecules jumped off the pollen load on the way back to the hive.

  8. #8
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    Default Re: The Case Against Imidicloprid

    ... suggest that actually the chemical is NOT metabolized and excreted, but rather bio-accumulates and continues to produce toxic effects well after exposure. -grondeau
    Fascinating stuff. Do you have any sources that suggest that such bioaccumulation can occur? The chemicals that tend to bioaccumulate are often not as water-soluble as the neonicotinoids are. If it does bioaccumulate, it should be easy to demonstrate. Older bees should have increased levels of neonicotinoids in their systems.

    Our detection limit is around 1 ppb, so we are starting from a point close to the detecion limit anyway. -grondeau
    I don't know about this one. I've talked to some researchers who work on these sorts of things, and they have all been confident that they could detect presence at the "ppt" level or maybe less. However, most of them caution that such low limits of detection mean that virtually all samples will show up as positive results.

    ...some residue more than 0.0001 ppb in their bee food. -grondeau
    This sort of level is 0.1 ppt, or less than one molecule per bee. PPT is likely less than one molecule per bee. If you have one molecule of neonicotinoid per several bees, I doubt that that single molecule could affect more than one bee, if that.

  9. #9
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    Default Re: The Case Against Imidicloprid

    This is an interesting theory. I'm not as likely to accept a graph that happens to fit a specific hypothesis.

    I find the bigger question to be why are many commercial beekeepers successful in maintaining healthy colonies in areas with widespread neonic useage?

    I think neonic poisoning is a 'sexy' cause for hive death/CCD. Most people claiming CCD don't regularly monitor varroa mite levels. I think in many cases it is easier to blame a pesticide for the lose of hives than to take the time to monitor and control mites.

    Tom

  10. #10
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    Default Re: The Case Against Imidicloprid

    Today monitoring and treating for mites might be enough to keep colonies healthy enough to overcome bee losses due to pesticides - sometimes. That used to be the case where I live. Seems less so today. Usual CCD losses are associated with any number of diseases. Varroa is a bad one - but not the only culprit. They are visible and easy to blame, however!
    Last edited by Barry; 03-05-2013 at 07:02 AM. Reason: quoting

  11. #11
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    Default Re: The Case Against Imidicloprid

    Taken from your report "Extrapolating the green dashed line trying to reach 50 to 100 days would require reducing continuous exposure to less than 0.0001 parts per billion (ppb). "

    You've got one data point 3 orders of magnitude larger than your 0.0001 ppb assertion. You can't expect us to take this seriously? Such simple models (at best) can perhaps describe "local" phenomenon within your data set, gross extrapolation is simply folly. One of my former professors liked the phrase: "Models have limitations, stupidity does not", Michael Athans, MIT
    Horseshoe Point Honey -- http://localvahoney.com/

  12. #12
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    Default Re: The Case Against Imidicloprid

    grondeau just use already published scientific data (proper references has been provided) and use logarithmic coordinates to plot EXISTING SCIENTIFIC data. Sometime, the way of data presentation helps to understand the trends. Plotting in different coordinates does not change the data.

    There is acute (one single shot, very high dose) and chronic toxicity. It is misconception that in chronic toxicity the "poison" is accumulated and may be detected. It is damage from slow poisoning accumulates and eventually kill. "Poison" has been spent on poisoning, it did not accumulate itself... In case of neonics, it irreversibly bind to Nicotinic acetylcholine receptors and thus disappears from the scene - bind neonic is not detectable anymore by standard technique. Neonics are evil because they are using normal biological pathways.
    Серёжа, Sergey

  13. #13
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    Default Re: The Case Against Imidicloprid

    What justification do you use to rely on the suchal data? No other study has been able to replicate those results. If you are going to use data that is clearly anomolous from everything else done in the 12 years since, there should be a reason other than it is the most convenient to fit a hypothesis.

    Deknow
    The perils of benefactors; The blessings of parasites; Blindness blindness and sight -Joni Mitchell 'Shadows and Light'

  14. #14
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    Default Re: The Case Against Imidicloprid

    Quote Originally Posted by AstroBee View Post
    Taken from your report "Extrapolating the green dashed line trying to reach 50 to 100 days would require reducing continuous exposure to less than 0.0001 parts per billion (ppb). "

    You've got one data point 3 orders of magnitude larger than your 0.0001 ppb assertion. You can't expect us to take this seriously? Such simple models (at best) can perhaps describe "local" phenomenon within your data set, gross extrapolation is simply folly. One of my former professors liked the phrase: "Models have limitations, stupidity does not", Michael Athans, MIT
    I actually stand corrected on this. Frankly I was so amazed that the data could be so well modeled by a simple power law that I couldn't resist the extrapolation. Nevertheless, I want my bees living longer than 10 days (0.1 ppb) and I see little reason to expect a sudden turn upward to the curve. What will change the toxicological dynamics? Who's job is it to find where the curve finally turns up? I'd be happy if someone did it in the water crustaceans since it is so much easier than with bees. With those critters, the authors of the study took them out to about 7-8 days with the critter's normal life span ~ 30-35 days and still showing power law behavior. It certainly would be curious to see how many more orders of magnitude you can take this before it breaks down. You want to do it!

  15. #15
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    Default Re: The Case Against Imidicloprid

    Quote Originally Posted by deknow View Post
    What justification do you use to rely on the suchal data? No other study has been able to replicate those results. If you are going to use data that is clearly anomolous from everything else done in the 12 years since, there should be a reason other than it is the most convenient to fit a hypothesis.

    Deknow
    I know of one other study of low-level extended-time experiments. That was Shmuck. Of his four trials one showed similar results to Suchiel, the others did not. Shmuck was a Bayer scientist and chose to disregard the data he didn't really want to have be the truth. Not saying he was wrong, but his data would not fit a power law like that reported by Sanchez-Bayo on crustaceans either. If you can point me to other studies that looked at low levels out to 10 days, I would be grateful.

  16. #16
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    Default Re: The Case Against Imidicloprid

    Hi grondeau

    I would be interested in your opinion on this theory:

    Quote Originally Posted by Stromnessbees View Post

    Some studies have reported that summer bees rather than winter bees were found in colonies going into the winter. The difference is in the smaller fat reserves, leaving summer bees with much shorter lifespans.
    When the fat reserve is used up, a bee leaves the colony to die away from the hive.
    Lots of bees leaving at the same time leave behind an empty hive, the beekeeper calls it CCD or Marie Celeste or dwindling disease.

    The trigger for winter bee production in a healthy colony is the shortening of daylength after the summer solstice, June 21st.
    Depending on your type of bee, winter bee production should commence soon or slightly later after that.


    If the colony is under the influence of neurotoxins, like neonicotinoids, the bees might not be able to perceive the change of daylight and continue production of summer bees.

    It has already been proven that neonicotinoids reduce the memory of bees in field studies (reutrn rate of foragers) and in the lab (training experiments).

    A compromised memory would make perception of daylight changes impossible, and as many colonies are exposed to neonics at the critical time of year for winter bee procuction, we should look into this possibility more closely.
    ...

    It would explain why no or very little residue of neonics can be found in CCD hives.

  17. #17
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    Default Re: The Case Against Imidicloprid

    It would explain why no or very little residue of neonics can be found in CCD hives. -Stromnessbees
    How so? Are you suggesting that the bees are carrying all of the residual pesticides out of the hives with them in their bodies?

  18. #18
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    Default Re: The Case Against Imidicloprid

    Quote Originally Posted by Kieck View Post
    This sort of level is 0.1 ppt, or less than one molecule per bee. PPT is likely less than one molecule per bee. If you have one molecule of neonicotinoid per several bees, I doubt that that single molecule could affect more than one bee, if that.
    Not true. NA=6x10^23 molecules/mole. Assume bees are mostly water --> molecular weight = ~20; lets use 60 so more numbers cancel... bee weighs 0.1 g --> N = 6e23 * .1 / 60 = 10^21 molecules in a bee. 0.1ppt --> 10^8 toxin molecules. there is along way to go before we get to the single molecule per bee range - and the bee is long dead from natural causes on the toxicity graph.

  19. #19
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    Default Re: The Case Against Imidicloprid

    Quote Originally Posted by Kieck View Post
    How so? Are you suggesting that the bees are carrying all of the residual pesticides out of the hives with them in their bodies?
    In a way, yes!


    The bees that collect the neonic contaminated pollen & nectar don't 'consume' it, they just transport it.
    It's the nurse bees that ingest the pollen and some of that nectar, the rest of the nectar will be converted to winter food and stored.

    The case where I saw the clearest connection between neonics and CCD was a valley in Austria, where all apiaries near Clothianidin treated maize collapsed from CCD in late autumn and winter.

    This maize/corn would have supplied mostly contaminated pollen, as well as maybe some contaminated guttation droplets earlier in the season.

    This pollen would have been consumed by the young bees that emerged in late August and September. Most of those should have done a lot of extra eating in order to build up fat reserves which would turn them into long lived winter bees. The trigger for that is the shortening daylength.

    But maybe they failed to register the shortening daylength whilst under the influence of the neonics and didn't gorge themselves enough.

    The toxins themselves would mostly be metabolized by the time winter arrives
    , and all the short lived bees leave the hive to die. - Which is unfortunately the bulk of the bees, as no proper winterbees have developed, creating the appearance of CCD - an empty hive with just a small cluster and possibly the queen and some remaining brood left behind.

  20. #20
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    Default Re: The Case Against Imidicloprid

    Not true. NA=6x10^23 molecules/mole. -grondeau
    I was considering it from the standpoint of the number of cells in a bee, not the number of molecules. You're right.

    Of course, that all assumes perfect solubility, perfect transfer of molecules across cellular membranes, perfect retention within the cells after permeating the membrane, and ability to affect the organism if the molecules are locked in cells throughout the body.

    This maize/corn would have supplied mostly contaminated pollen, ... -Stromnessbees
    I'm not rejecting or denying what you say, but I will reiterate: I'm convinced that bees do not collect much corn pollen under normal conditions. I've spent thousands of hours counting various insects in corn throughout the season. Honeybees are largely absent from cornfields at most times. I suspect that bees only collect corn pollen when other sources of pollen are very scarce or have failed. Teasing out the pesticide effect from the effects that might induce bees to collect corn pollen would be difficult, I think.

    ... as well as maybe some contaminated guttation droplets earlier in the season. -Stromnessbees
    That one keeps coming up as a possible source of poisoning. I've never observed honeybees collecting guttation droplets from corn. Guttation occurs only occasionally here, typically in the early morning hours. Most bees that I've observed are not seeking sources of water at the time of day that guttation tends to occur, and guttation in corn tends to occur in conditions that cause guttation in any number of other plants. I've read that droplets collected from corn guttation can contain amounts of neonicotinoids that could cause bees problems. The difficulty I see is how infrequently honeybees are likely to collect guttation from corn.

    The toxins themselves would mostly be metabolized by the time winter arrives, and all the short lived bees leave the hive to die. -Stromnessbees
    Makes some sense to me. What about the stores left behind in hives that have died from CCD? My understanding is that leaving behind adequate to large amounts of stores is a symptom of CCD. In fact, I've read and heard that new bees put into a hive that collapsed from CCD are also likely to suffer the same fate rapidly (if they can even be enticed to take up residence in the hive). What would cause such a symptom if the pesticide residues are all gone?

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