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The Case Against Imidacloprid

March 3, 2013

Ever since French beekeepers saw their bees dying as they collected pollen from treated sunflowers back in 1996, beekeepers have been concerned that their bees are being harmed the highly toxic neonicotinoid insecticides, with imidacloprid most widely used. The use of this class of insecticide has grown steadily ever since. Bee losses have become chronic as well. However, unlike the first case in France where bees were literally falling dead while gathering pollen, the widespread colony losses today are less explainable, often associated with outbreaks of a variety of diseases, and with very high winter colony mortality. So why blame the insecticides?

To see why the bees are dying, and why these pesticides are still being sold, we must examine the toxicology of the neonicotinoid chemicals as well as the history and science of pesticide regulation.  The toxic nature of a chemical is characterized by its “LD50″ level.  This is the amount of chemical that will kill half of the test organisms in short order.  For many traditional pesticides (organophosphates), the LD50 level provides an adequate overall characterization of toxic effect.  These pesticides tend to be short-lived and generally do not bio-accumulate in the target organism.  If the dose doesn’t kill the organism, the toxic compound will be metabolized and excreted.  Since the organophospate pesticides — which for many years made up the majority of pesticides sold — could be characterized easily with the single LD50 number, the culture of pesticide regulation largely accepts the acute LD50 as determinative for all toxic effects.

The acute LD50 characterization works poorly for substances that bio-accumulate and/or have a relatively long time-to-effect characteristic.  Substances that fall into this category are heavy metals that are known to accumulate in certain tissues, and some carcinogens where an initial single exposure can give rise to cancers much later in the life of the organism.   Neonicotinoid insecticides also fit into this category.  These insecticide molecules bond strongly and irreversibly at nicotine receptor sites in the central nervous system.  There is also evidence of delayed time-to-effect of several days for exposures below the acute LD50  [Suchail et. al.(2001)].

Toxicologists attempt to model the time-dependent effects of chemicals at various dose levels [Tennekes, (2010)].  One of the simplest empirical models assumes the dose/effect relationship can be characterized by a simple “power law”  where the effect is proportional to the dose multiplied by the time-of-exposure raised to a power, b.

Effect = Dose x Timeb

Instead of a single number, now we have two numbers to characterize toxicity, the dose and the time exponent.  When a power law is plotted with logarithmic scales, one gets a straight line with slope equal to the exponent, b, and intercept equal to the Dose.  The time-independent, acute LD50 model is the special case when b=0.  For a simple bio-accumulation model, one would expect linearity in time with b=1.  Time-to-effect mechanisms require b>0.  Combinations of effects for a given organism and chemical will result in a Dose vs Effect curve with characteristic slope that includes all of the time-dependent mechanisms embedded in the value of the exponent.

Imidacloprid Toxicity

The plot above shows some published data on imidacloprid toxicity on a log-log graph.  Data for two species of small aquatic crustaceans, Daphnia magna (red squares) and Cypridopsis vidua (blue diamonds) illustrates the large range of toxicity difference between organisms, and also the large range of applicability of the model, spanning more than three orders of magnitude in concentration. [Sánchez-Bayo et. al. 2009]  Honeybees (green triangles) also have high toxicity over a wide range of concentrations [Suchail et. al.(2001)].

The best-fit power law curves are shown in the plot.  In all cases, the fit parameter, R2, is greater than 0.85. The time exponent for Daphnia, 1.3, is barely more than linear, where as for Cypridopsis and honeybees the exponent is close to 5. This means that there are strong time-dependent delayed effects from the chemical for the Cypriopsis and honeybees. The time5 dependence of the toxicity of imidacloprid for honeybees is the big problem.  Very low levels of exposure, with sufficient time, will be lethal. The power law model suggests that we should extend the time of exposure to the lifetime of the organism in order to determine the minimum dose that will have no effect. Honeybees, including the larval stage, live ~50 days in the summer and ~100 days for wintering bees. 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). This minuscule exposure level is far below the detectable limits of present technology (~1 ppb).  What we can detect are residual levels in nectar and pollen on treated plants commonly in the 1 – 10 ppb range; even these small levels are more than 10000 times the level that the power law model suggests would cause no harm to adult bees.  Looked at another way, if one bee in 10,000 returns to the colony with pollen gather from a treated plant, that would be enough toxin to begin to cause damage to the colony.

Collecting toxicity data about bees is a complex process, involving multiple trials, caged bees to limit their activity to the test sample, etc.  Aquatic crustaceans provide an easier test subject where dosage can be controlled by dilution of the water they live in.  The fact that the crustaceans conform to the power law model confirms that imidacloprid is bio-accumulative.  The same finding by Suchail et.al. for bees should not be surprising, given that both organisms have central nervous systems with nicotine receptors.

What about mammals and humans?  Very little time-dependent information is available.  There are a couple of data points on the plot above for mice.  One point was the LD50 for short time exposure and the other the threshold for immune system compromise exposed for 28 days. The data for mammals is just not available yet, but even much more modest sensitivity to the chemical could present problems for long-lived species such as humans.  There is also fear that these biologically persistent chemicals could be fueling world-wide wild life declines in many species [Mason, R. et. al. 2012].

Our regulators, (EPA) are not adequately considering the time-dependent nature of the lethal effects of the neonicotinoid class of pesticides.  The most toxic and long-lived chemicals, imidacloprid, clothanidin, and thiamethoxam should be removed from the market before more harm is done, as is happening in Europe.  Other insecticides in this class should be subject to further scrutiny as well.

The social nature of bees naturally draws one to a human analogy. Imagine that a toxic chemical is slowly poisoning our brains. (Think lead pipes and the Romans.) Instead of healthy people living into their 70′s, the toxic effects are bringing on Alzheimer’s-like symptoms to folks in their 40′s and 50′s. The younger healthier part of the population has its hands full, providing for themselves and those that no longer support their own livelihood. Everyone is hungry. Now introduce a bad case of the flu, or the plague, and the already weakened population is devastated.  That is what our bees are facing today. The levels of poison are rising as more and more of these pesticides are being used, building up in our soil and in treated plants.  The bees are dying younger, and we are gradually eliminating a host of insects and creatures we don’t even know we are poisoning.

Mason, R., H A Tennekes, F Sánchez-Bayo, P U Epsen (2012) Immune suppression by neonicotinoid insecticides at the root of global wildlife declines. J Environ Immunol Toxicol 1: (in press)

Sánchez-Bayo, F.,2009. From simple toxicological models to prediction of toxic
effects in time. Ecotoxicology 18,343–354.

Suchail, S.,Guez,D.,Belzunces,2001. Discrepancy between acute and chronic toxicity induced by imidacloprid and its metabolites in Apis mellifera. Environ.Toxicol.Chem. 20,2482–2486.

Tennekes, H, A. The significance of the Druckrey-Kupfmuller equation for the risk assessment — the toxciity of neonicotinoid insecticides to arthropods is reinforced by exposure time.  Toxicology. 2010 Sep 30;276(1):1-4

12 Comments leave one →
  1. March 24, 2013 9:24 am

    I’ve been studying the neonicotinoid issue for 3 years now and this is the best explaination I’ve ever seen. Excellent contribution to our beekeeping community. Thank you! … Donald P. Studinski, Broomfield, Colorado

  2. March 25, 2013 7:36 am

    Is there a petition we can sign?

  3. April 11, 2013 9:49 am

    Hi all

    Actually, you can make almost exactly the same case using the research on CO2 effects on honey bees. Sub-lethal doses of CO2 produce the same responses as the various pesticides: premature foraging, impaired responses, memory loss.

    In fact, if you compare a graph of the increase in atmospheric CO2, it corresponds neatly to the increase in bee mortality. Could increased levels of atmospheric CO2 cause honey bee mortality? Quite possibly. Do they? Well, no. That’s because the levels in the real world are much lower than those used in the lab.

    Same goes with neonics. Real world concentrations are generally lower than the LOD (limit of detection). Meanwhile, bees have been thriving on neonic treated crops such as Canola. More honey is produced in Canada from Canola than any other crop. It’s a good honey plant in the UK, as well.

    Pete

    • April 11, 2013 3:44 pm

      Undetectable doses show increased nosema … thus, showing the damage to the immune system which is exactly what neonics target along with the nervous system.

    • Bill permalink
      April 13, 2013 5:19 pm

      Lower concentrations mean nothing when the bees are consuming it 24/7, there is no such thing as a safe dose with these neurotoxins, it’s a slow poisoning.

  4. April 11, 2013 2:30 pm

    Hi Pete,
    I can’t argue with you completely! There certainly are cases where there appears to be no ill effects on honeybees that have been in contact with neonic treated crops. However, with the neonics, the damaging effects are cumulative and permanent to individual bees (unlike CO2). With sub lethal exposure, barring secondary stresses, the colony could indeed flourish. It is exactly this uneven response to neonic assaults that that I address here:

    http://squashpractice.wordpress.com/2013/04/01/resolving-the-imidacloprid-paradox-and-the-ccd-connection/

    • April 11, 2013 3:57 pm

      Gary, I enjoyed reading your work. Thank you for the link.
      I would like to add that the cumulative effect of neonics may be a significant factor. A colony may do very will indeed for a time until some unknown threshold is reached. We also need to be mindful of the half-life of the neonics which is measured in hundreds of days always and thousands of days in some dense soils. Cumulative effects combined with long half life may result in colony illness after a study has completed.

      • April 11, 2013 11:03 pm

        Indeed, some of my concerns as well. In the case of fields or treated canola that Pete mentioned, you can imagine that early in the year the benefits of an abundant floral source might be more than the detriment of small amounts of insecticide. Maybe it only reduces the summer life of a bee by a week, yet allows the colony to put away lots of stores. CCD colonies often have plenty of stored honey on hand when they go down. A healthy queen can overcome the bee losses and you would be hardly aware of a problem. Come late fall and the issues are different. The bees need to live longer to go through the winter. The queen is not making as many replacements. Pesticide in stored honey and pollen now gets ingested by long lived bees and becomes their legacy as they try to hang on until spring. If all they need to do is be warm bodies, maybe the colony with weakened bees can last till the queen turns on Spring production. If any kind of stress hits, the colony goes down rapidly.

  5. April 23, 2013 11:53 pm

    Gary, You may not be aware of it, but I published a paper in 2010 in the journal Toxicology (Toxicology. 2010 Sep 30;276(1):1-4) that demonstrated that the effects of neonicotinoid insecticides in arthropods are reinforced by exposure time, an pointed to the similarities in dose:response characteristics of neonicotinoids and genotoxic carcinogens. I am somewhat surprised that you did not cite this paper, but, as I said, you may not be aware of it.

    • April 24, 2013 6:57 am

      Henk, Thank you for your comment. In fact your 2010 article was instrumental in my understanding of this issue and should have been included. I just added it.

  6. May 9, 2013 7:02 pm

    Gary, I’m referring to your work in my current post to BCBA and NCBA. I wanted to copy you, but I can’t find an email address for you. If you wish to connect, please find me on honeybeekeep.com … dons
    CSBA Pesticide Committee Chairman

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