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An August Bee Beard

August 13, 2014

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Blog post gets Published!

July 7, 2014

What started out as a bit of curiosity about the time-dependent toxicity of insecticides led to a blog piece I did a little over a year ago titled Time-dependent Toxicity of Imidacloprid in Bees and Ants.  I thought my results were interesting enough to get a comment from other scientists that were looking at the time-dependent toxicity question so I sent out the link to a few.  With the encouragement of especially Dr.Fransico Sanchez-Bayo at the University of Sydney in Austrailia, I went ahead expanded the research and we turned that blog post into a paper.  I am especaily grateful to my co-authors, especially Fransico Sanchez-Bayo and Nicolas Desneux, who shepparded the manuscript through the journal submission and review process.

So please take a look at the real thing.  We were published in Nature’s online publication Scientific Reports.

Delayed and time-cumulative toxicity of imidacloprid in bees, ants and termites,
Gary Rondeau, Francisco Sanchez-Bayo, Henk A. Tennekes, Axel Decourtye,
Ricardo Ramırez-Romero & Nicolas Desneux, Scientific Reports  07/2014; 4(5566):8. DOI: 10.1038/srep05566


Bumblebee Kill in Eugene Rains on Pollinator Week

June 18, 2014

[Updated 6/19/14]

It is with dismay that I must report on another bumblebee kill, this time only about a mile away from the DeadBumblesbees in my yard.  All of the details are not in yet, but the basic picture is clear.  Insecticide was sprayed early Monday morning, 6/16, on blooming linden trees in an apartment complex in northwest Eugene.  Residents reported that the sidewalks were littered with dead and dying bees.  Apparently officials from the Oregon Department of Agriculture (ODA) and Oregon State University were on the scene to collect samples and initiate an investigation.  I’m sure we will know soon what was sprayed and who did it. [We know now that the chemical sprayed was imidacloprid.]

Recall that about this time last year more than 50,000 bumblebees were killed in Wilsonville.  That prompted the ODA to issue restrictions on the neonicotinoids dinotefuran and imidacloprid, banning their use on linden trees.  It is also against label directions to spray pesticides on blooming plants when there bees present.


I went to survey the bee kill scene this evening.  The ODA and OSU investigators had gone, but the dying bees were still falling from the trees.  Walking around the complex I identified eleven blooming linden trees that had been sprayed and had dead and dying bees on the ground under the trees.  [I located two more sprayed lindens, bringing my total to 13 trees; the official report is that 17 trees were sprayed.]  Under one set of three trees I counted about 300 bees on the side-walk.  Easily there was 200 more in the grass and shrubbery.  I later learned from one of the residents that she and others had swept the bees up already once and she was dismayed to continue to see them fall from the trees.  My brief survey was apparently just the more recent victims.  The eventual body count will depend significantly on what was sprayed.  If the insecticide is one of the neonics, the chemical is designed to be taken up in the plant tissues, and the trees will be lethal to bees until after they stop blooming.  If they were sprayed with a pyrethrin, then the worst toxicity will probably be gone in about a week.

That such a thoughtless act falls in the middle of Pollinator Week just illustrates how far we still have to go.  Eugene may be the first city to ban the use of neonicotinoids on city property, but that action helps little when these chemicals are actively promoted and used by thousands of homeowners, landscapers, residential maintenance companies and pesticide applicator on private lands.

All this matters to me because my bees are in range of those trees.  EugeneBumblebeeKillRight now the blackberry honey flow is still keeping most of the bees occupied, but the blackberry flowers are beginning to dry up and the bees will be looking further afield. Bees heading west from my house that find their way across the industrial railroad yard will come upon the very attractive linden blossoms.

The residents mentioned that the trees in their neighborhood often dripped a sticky mist from aphids in the summer.  Apparently, this is not the first time that the trees have been sprayed, but this year they sprayed earlier than in previous years.

Although bee kills like this one will make headlines, it is the less dramatic impact of pesticides that are even much more troubling.  Have these trees been poisoning my bees for years at sub lethal levels?  How many pounds of these toxic pesticides are spread about in my bees’ foraging range?  Is residential beekeeping doomed by thoughtless policy and people?  The pollinators are weak this week.

[On a return trip Thursday afternoon, I wanted to see if more bees were finding the site during prime foraging hours.  Indeed, I saw both bumblebees and honeybees visiting the trees, though not heavily.  Curiously, there were no honeybees on the ground, just the bumblebees.  I passed several more blooming lindens along River Road on my bike trip home. These trees were abuzz with activity, sporting ample numbers of both bumblebees and honeybees. ]

The Mechanisms of Neuro-toxic Pesticides

June 15, 2014

Agricultural pesticides have become part of the chemical landscape that we all  live in.  To be able to make intelligent decision about the use and regulation of these chemicals, it’s important to understand how they work.  Almost all modern pesticides are chemicals that interfere in some way with the nervous system. The characteristics of the chemical interaction with the nervous system function can shed light on the effectiveness of the pesticide and on its physiological effects at residual levels.  We will start by looking at how some of the normal processes of the nervous system work, because it will be disruption of those processes that lead to toxic effect.  Then we will look at the mode of action for three major classes of pesticides and how they specifically interfere with normal function.  In a future article we will look at how the specific mechanisms of action can effect dose scaling relationships.

Normal Neuron Function – Neurons, action potentials, sodium and potassium voltage gated ions channels, and ion pumps

The nervous system of insects and humans share many common features, starting with the basic structure of the neuron.


There are many variations on the same theme in different parts of the organism.  Terminal branches can attach to dendrites of other neurons at synapses, or through motor synapses to muscle cells.  Individual neurons are connected in complex, interacting networks by the synaptic connections. Information processing involves summing the inputs from many neurons and generating an output.  When the summed stimulus is high enough, the neuron will generate an electrical pulse that is sent along the axon and which will, in turn, stimulate multiple downstream neurons connected through synapses to the axon branch terminals.

Neuronal signalling is accomplished by way of “action potentials”, which are short electro-chemical pulse that travel along the neuron axon.  The short pulse-like nature of the nerve signals are generated and maintained by way of “voltage-gated” ion channels and ion pumps.  Ion pumps use the cellular energy store, ATP,  to move sodium and potassium ions across the cell membrane, setting up a concentration gradient across the membrane that establishes a “resting potential” of about -70mV from the inside to the outside of the nerve cell.  Once this gradient is established, then merely opening ion channels in the cell wall allows the sodium or potassium ions to move back across the membrane and move the potential closer to zero.  Nature’s trick, that turns this process into a useful information processing network, is to open the ion channels which depolarize the neuron with a positive feedback action associated with the membrane potential.  Once the membrane potential rises from its resting potential to a “threshold” the voltage gated channels open, steepening the rising edge into the action potential nerve pulse.  The figure below is a nice schematic of the ‘anatomy’ of the action potential.

From Davies et al. 2007.  DDT, pyrethrins, pyrethroids and insect sodium channels.

From Davies et al. 2007. DDT, pyrethrins, pyrethroids and insect sodium channels.

Signaling happens by way of the action potentials, which propagate along the axons and terminate at the synapse.  There are several ways the action potential can be interact with cellular structures.  We will concentrate on the acetylcholine mediated synaptic response because this is the target of several pesticide chemicals.

Normal Synapse Function – acetylcholine-mediated transmission


Acetylcholine (ACh) is a molecular neurotransmitter that conveys information across the synapse.  In the figure above, the basic steps of the interaction are illustrated.  Action potentials, those pulses of neural activity, cause synaptic vesicles containing ACh to release the ACh molecules into the synaptic cleft, the junction region between the two cells.  The ACh quickly diffuses across the narrow junction region and is captured by acetylcholine receptors (AChRs) that are part of ion channel molecules.  The AChRs that have captured an ACh molecule open the ion channel and allow Na+ ions to enter the post-synaptic neuron.  The binding is transitory, however;  the ion channels rapidly open and close as the ACh molecules latch and unlatch from the AChR channel.  Meanwhile, another ACh receptor is also present in the synaptic junction called acetylcholinesterase (AChE).  This molecule is an enzyme which rapidly breaks apart the acetylcholine into choline and acetate, effectively ridding the synaptic cleft of the neurotransmitter almost as fast as it is made available.  The result of all of this chemical activity is that the AChRs, as an ensemble, are open only for a few milliseconds.  During this time, ions flood into the post-synaptic dendrite, depressing the potential in the down stream neuron, making it more likely to generate its own action potential.

This simplified discussion leaves out many details.  There are many more specialized molecules that are part of cell membranes.  Often molecules that are specific for one important function also are involved in unrelated functions.  Nerve cells can be specialized and synaptic details can vary.  Nevertheless, the basic picture we are painting is valid across much of the animal kingdom.  These same basic process happen in the nervous systems of humans and bees alike.  Now let us move on to discuss ways to interrupt these normal processes for insecticidal effect.

Insecticides targeting axonal voltage-gated ion channels

Two major classes of insecticides target the voltage gated ion channels shown in our cartoon.  The organochlorines (e.g. DDT, dieldrin, chlordane) and pyrethroids (e.g. deltamethrin) act by opening these voltage gated ion channels.  The molecules hold open the channels and allow ions into the axon that depolarizes the neuron.  In the depolarized state the neuron is non functional, characterized by paralysis.  In between the normal state and paralysis there is a range where the depolarization of the neuron is only partial.  Partial depolarization leaves the neuron susceptible to “false triggering”.  A small stimulus that would normally not trigger an action potential will produce one more easily as the resting potential gradually climbs to the threshold required to launch an action potential.  Organisms in this state typically exhibit twitching and uncontrolled movements as the uncontrolled nerve impulses trigger muscles to move.

Nothing is static at the molecular scale.  As organic molecules interact with one another, they can latch onto each other either very loosely or with tenacity depending upon the exact shape of the molecules involved and type of binding that happens.  Binding that occurs via the covalent sharing of electrons is usually very strong, essentially permanent and irreversible.  In contrast, many biological molecules interact through polar or Van Der Walls forces that are much weaker.  Such interactions may last for a fleeting amount of time before thermal fluctuations pull them apart.  Weak binding is reversible and can be characterized by a dissociation time, how long it takes to break the bond due to random and thermal fluctuations.

When dealing with pesticide chemicals, stronger bonds mean the insecticide is spending more time at the active site, so its potency is higher.  Frequently it is just how tenacious the binding that determine the potency of the insecticide.

Chemical scavengers known as cytochrome P450 enzymes are always on the lookout for foreign chemicals which these enzymes break down into smaller parts in the process of metabolizing and eliminating unwanted molecules.  Often, within a few hours much of a foreign chemical will be metabolized and eliminated from the organism.  Bound molecules are not as easily digested by the cytochrome P450s so once toxins are bound to their site of action, they are more immune to detoxification.

Insecticides targeting the acetylcholine pathway

There are several classes of pesticides that disrupt the acetylcholine pathway.  We will start by looking at the neonicotinoids because they have the simplest mechanism, similar to the “direct action” of the pyrethroids discussed above.

Synapse with Neonic

The neonicotinoids bind strongly to the AChRs.  Binding causes he ion channels to open so Na+ ions can flow into the neuron.  Unlike the normal acetylcholine response where the channel is only open for about a millisecond, when the neonicotinoid binds the receptors never close.  Hence, it takes only a relatively few open channels to eventually depolarize the neuron.  If the ion pumps cannot keep up with the leakage through the nicotinoid-bound AChRs the cell will depolarize. Partial depolarization will make the neuron more excitable; complete depolarization leads to paralysis.

This situation is more complicated with acetylcholinesterase inhibitors such as the organophosphate and carbaryl insecticides. For these chemicals, the insecticide does not directly bind to neuronal receptors that open ion channels. Instead the chemicals bind to the acetylcholinesterase (AChE) enzymes which rid the synaptic junction of the ACh neurotransmitter than is released with normal activity.  However, without the AChE to clear the junction, the ACh continues to bind with AChR ion channels.  The figure below shows schematically what happens with these AChE inhibitors.

AChE inhibitor action


Insecticide molecules bind to the acetylcholinesterace (AChE) sites in the synaptic junction, preventing the naturally released ACh for being removed and recycled from the junction.  The acetylcholine continues to activate receptors, keeping their channels open thereby depolarizing the post synaptic neuron.  Again, poisoning symptoms begin with an over-excitable nervous system, characterized by uncontrolled twitching, similar to the other classes of neurotoxins we have looked at.

Neurotoxins are among the most potent biological chemicals known.  The chemicals are targeted to interact with specific receptor molecules that are crucial for nervous system function.  This means that very few pesticide molecules are required to have a large biological effect.  Chemicals used as pesticides need to effectively poison target species while remaining benign to non-target organisms and humans.  However, much of the cellular machinery is shared across the animal kingdom, so differentiating between target and non-target organisms is a challenge.  Often only space and time are used to separate target and non-targets creatures from chemical exposure.  The environmental effects of pesticide chemicals depends upon the success of various strategies to limit harmful exposure to non-target species.  In many cases dilution is the solution, but as industrial agriculture and residential uses of potent chemicals become even more widespread, minute residual levels of toxins is inevitable.  Next time we will see why this is more likely to be a problem with some classes of chemicals more than others.

The Uke Case Music Stand

May 30, 2014

For the last few years, playing music and singing with others has become an important source of joy and connectedness in my life.  It might even be one reason this poor blog has had fewer and fewer entries as the virtual online world has taken a back seat to real life!  This all started because Ellen decided to take up the ukulele to be able to accompany herself when she sings the thousands of songs to which she seems to know all of the lyrics.Uke_Stand_3   Ellen started having such a good time, finding several groups around town to sing with, and learning her instrument, that I was drawn into the scene.  Music has always been important to me as well, but my outlet had been a rather solitary pursuit of the piano – with only moderate hard-fought success. Singing in a group with others provides a satisfaction that is hard to beat.  So I too, took up the ukulele.  Which, after all, has only four strings, the same as the number of fingers you have, so there was hope!

After a couple of years playing with our friends, the traveling paraphernalia seemed to keep growing and was becoming a burden.  The various music groups have more than half a dozen music compilation books between them; there are music stands, instrument stands, instruments, music lights, capos, and tuners, and goodies to share with friends.  The digital age came along and helped reduce the need for all of the music books with the advent of the tablet computer.   Rather than a dozen books and music sheets, now everything could be placed on the tablet, easily accessed, and read without needing a music light at night.  This appears to be standard practice with the pros these days as well.  Everybody has a tablet!  A few apps on the device complete the paraphernalia reduction. I’ve got a tuner, chord position charts, and notepad applications, eliminating the need for the physical equivalent of those items.  We seemed to be making progress, but there was still too much stuff to haul, so it was time to break out the wood working equipment and solve the problem.

Stand_Detail_3The Uke Case Music Stand was inspired by the fact that my new digital tablet just happened to fit nicely behind the instrument in the bottom of my very nice padded ukulele case.  What was still needed was a compact music stand.

Stand_Detail_2The hard instrument case provides half of the structure for the stand.  A pair of “feet” on the bottom of the case provide enough lateral stability for when the third “tripod” leg is extended to establish the base of the stand.  A wooden dovetail slide allows the music tablet to be positioned either for standing or sitting down.  When set up, the instrument case itself functions as an instrument stand when you are taking a break.  It is right in front of you and the case can open when the stand is up, so you can quickly put your instrument away before you go in search of refreshments.



Everything folds up into a small package that is easy to carry when it is time to go home.

Making music is a lot of fun – the music stand just adds to the satisfaction!

Persistent Yellow Jackets

November 29, 2013

Here we are on Thanksgiving, after a week of unseasonably cold weather for Eugene, and still the yellow jackets are pestering my bees.  Perhaps I’m just watching more carefully this year, but I’ve never noticed such a persistent problem.  YellowJacket During the summer I notice the wasps patrolling the ground in front of the hives.  I figure they are looking for stragglers that get caught in the weeds and any dead bees that are hauled out of the hive by the house bees.  They don’t really seem to be doing anybody any harm.
But as fall has closed in they have become more of a problem.  I keep an eye on the mite drop boards regularly, and they tell the tale of yellowjacket depredation with discarded wings and legs littering the witness board.  Wings&legsAs soon as I started seeing the evidence, I drastically reduced the entrance down to single file bee size, so the guards had a better chance to deal with the intruders.  This definitely helped some, but it was clear that the yellow jackets had learned where the good pickings were, and they were still taking their toll based on the evidence from the drop board.  When the cold weather hit, I thought that would be the end of the yellow jackets and my bees could have some peace, but it proved to be the opposite.   This morning, with the temperature about 40 degrees F and the sun out, the bees were not flying, but the yellow jackets were.  It was cold enough that the bees were not even close to the hive entrance so the yellow jackets could enter without challenge.

Today I completely blocked the entrance.  It is not supposed to be honeybee flying weather for the foreseeable future, so I’m just going to keep the yellow jackets out even if I have to lock the bees in.  The wasps have learned that they get easy pickings from my bee hives.  I’m hoping they will unlearn that or the snow that is predicted will finally do them in before I have to open up the entrances again.

Here is the question.  Has it always been this way?  Am I just much more aware of any little problem that could harm my bees, now that it is so difficult to get them to survive from year to year, or is this, too, a new problem?  Despite my years of keeping bees, I’ve always felt that yellow jackets were just a problem if you had very weak hives already (maybe we all do now).  Any beekeepers out there with thoughts about this?

Environmental Implications of Pesticides with Delayed Toxicity

November 17, 2013

The debate about the environmental safety, or lack there of, for the neonicotinoid insecticides begs us to ask what would be the characteristics of an environmentally safe or benign pesticide?  Despite a growing and flourishing organic agriculture movement, industrial agriculture is not going away any time soon.  Hence it is important to understand how to access the environmental risks of industrial chemicals that are deliberately spread across the landscape for agricultural purposes (EFSA 2012).

Ideally, pesticides for agriculture should effectively kill insect pest species yet have little or no effect on humans or beneficial insects that come in contact with the chemical or its residues.  This is a tall order.  All life forms share an astonishing amount of similar cellular function.  Chemicals highly toxic to insects can also be toxic to humans.  Even more difficult is finding chemicals toxic to pest insects that are not harmful to beneficial insects.  There are several strategies to solve this problem.  1) Apply insecticides only in a time and place where there is minimal contact with beneficial species. 2)  Use chemicals that are specifically toxic only to the pests you are trying to kill.  3)  Deliver the chemicals in a way that kills only the pests that come in contact with the toxin.  The degree of success at only targeting the pests while not doing harm to other creatures usually gets down to the specifics of the chemicals involved, application methods, and the consequences of residual contamination.  It is worthwhile to examine the various classes of pesticides more carefully to understand the similarities and differences in the chemicals.

The table below lists several of the most important classes of pesticides and gives specific information about representative members of the class.  I attempted to unify the example data by looking for specific properties of the chemicals for honeybees.  The chemicals are ranked in order of most toxic, (lowest LD50) first.  Also listed are soil persistence, metabolic half-life, receptor binding time, the toxicity time-scaling exponent, and the specific mode of action of the chemical.

Table 1:  Representative characteristics for several pesticide families

Pesticide Class


Oral LD50


Typical Soil half-life

Typical meta-bolic half-life

Typical binding dissociation time

Typical toxicity time-scaling exponent

Toxic Mechanism Comment



50 ng/bee

.5 – 3 yr.

4 hr.

>10 days


Synaptic nAChR agonist.Irreversible binding Often used as systemic insecticidesDirect acting on nAChRs


20 ng/bee

30-300 days

2-6 hr. (rats)





60 ng/bee

11-72 days

2 hr.

Several seconds

2 ?

Keeps open voltage gated Na+ ion channels on axon  Direct acting on Na+ channels



6190 ng/bee

2-15 yr.

6 yr.

Temperture dependant– suggests less than a second.


Keeps open voltage gated Na+ ion channels on axon Most of these chemicals have been banned by international treaty as persistent organic pollutants


133 ng/bee

5 yr.

9-12 mo. humans




370 ng/bee

15-200 days

17 hr.

16 days

1 ?

Irreversible  AChE inhibitor AChE inhibitors have inherent “threshold” action since large fraction of AChE must be bound to have toxic effectIndirect acting on ACh


720 ng/bee

1-15 days

12 hr.

? days

0.5 (fish)


Carbaryl (Sevin)

1540 ng/bee

4-30 days

8 hr.



Reversible AChE inhibitor

A quick look at the numbers for DDT and you can quickly see why this chemical was banned.  It persists for decades in the soil, and resides for years in living organisms.  The organochlorine pesticides are the most environmentally persistent and still can be found in living organism around the globe, although they have largely banned now for more than 40 years.  Curiously, one of the main reason for DDT’s removal was that it caused egg shell thinning in birds, an effect not at all predicted from its expected mode of action as a neuro-toxin.  Chemical agents often have unexpected, unpredictable effects that only extensive testing or experience after-the-fact reveal.

One of the main problems with neonicotinoids is that they have a delayed toxic effect that renders small residual concentrations of the chemicals especially problematic for long-lived beneficial insects such as bees.  The argument is simple enough once you grasp the implications of delayed toxicity.  Allow me to digress and offer a comparison of toxic time dependence and example chemicals.

1) Threshold toxicity.  Consider CO2 – usually not a poison unless there is so much of the gas that you cannot get enough oxygen to breathe.  If the concentration of CO2 got high enough to deprive you of oxygen, it would kill you.  However, even long exposure at levels 30% of the toxic threshold are likely to have little effect.  Typical insecticides that work this way are dormant oil sprays that essentially suffocate the target insects by plugging up their tracheal breathing tubes.

2) Linear accumulation – Haber’s Rule.  Some toxins exhibit “accumulation to a threshold” behavior.  In the 1900’s Fritz Haber noticed this effect with the concentration of chlorine gas.  The concentration of the gas multiplied by the length of exposure produced the same lethal effect.  The lethal concentration varies as 1/t where t is the exposure time, or  LC50 = k/t   where LC50 is the concentration that kills half of the subjects and k is proportionality constant.  Several insecticides have this behavior, including many of the old fashion organophosphate pesticides. This all makes a certain amount of sense, because if you add up the total exposure over time, you find it takes the same total amount of toxin to kill the organism, proportionally longer if you use proportionally less concentrated toxin.

3) Delayed and Enhanced Toxicity – We can write out a scaling law as LC50 = k/tp.  When the time exponent p=0, then we have case 1) above where the toxic threshold is k.  When p=1 we have Haber’s Rule, case 2) above.  When p>1 we have a situation where the toxic concentration required to kill half of the target organisms is less if the exposure is longer, and furthermore, the total accumulated toxin required to kill the organism is less the longer you wait.  Such enhanced toxicity can come about because several conditions about how the toxin operates are met.  These included 1) strong binding for the toxic molecules to the sites of activity in the organism, 2) direct action of the toxin biologically (no threshold required to damage biological function) and 3) biological accumulated effects of the toxin.  The neonicotinoids often fit exactly these criteria.  It is not a standard requirement to evaluate the toxicity time-scaling of pesticides, although it should be.  I looked carefully at the literature and found several studies that, taken together, point to approximately a 1/t2 scaling dependence for imidacloprid with bees.

The scaling laws discussed above are just a simple way to describe the results of toxicity tests for these chemicals (Sanchez-Bayo 2009).  They are empirically derived, but such power-law scaling does a good job of describing what we see in practice.  Hence, we can plot empirically derived toxicity curves and discover the scaling exponent p for a particular chemical and organism, and have a good way to estimate the toxic effect over the life time of the organism for lower exposure levels.  See, for example, the work I have done with imidacloprid on bees and ants, and the references therein for other chemicals and organisms. One figure from that work is shown below.  The best estimate for bees is the red line that represents results from many researchers.  In all cases the toxicity scaling exponent is approximately 2 or greater, implying significant delayed toxicity for imidacloprid on bees and ants.

Imidacloprid Time Dependent Toxicity for Bees and Ants

The toxicity scaling exponent is just one of a combination of traits can lead to a prediction of trouble. The other main concern is the exposure duration and level.  This brings us to why we have a particular problem with some of the neonicotinoids.  These insecticides are designed to be used systemically, entering into the plant xylem and carried to all parts of the plant.  The chemicals need to be relatively long-lasting because they are used as preventative seed treatments before target insects are necessarily even present.

Looking at the representative numbers in Table 1 above once again, the neonicotinoids have the longest lifetime in soil of any insecticide class that hasn’t already been banned as a persistent organic pollutant.  The mode of delivery of the insecticide is systemic in the plant, so plant products collected by bees will chronically deliver some chemical to the insects.  The chemical binding at the synaptic receptor sites is irreversible, meaning the chemical can build up at the site of toxic activity in individual insects when chronically exposed.  Since the means and mechanism for chronic delivery of low level contamination is built into the way neonicotinoid insecticides are used, we must also consider the chronic time dependent toxicity scaling when assessing the likely hood of impact on pollinator populations.

This is in stark contrast to the situation with organo-phosphate and carbamate insecticides.  These classes of chemicals usually are designed to kill on contact, and have a very short lifetime in the environment. Many also bind to their receptor sites in a reversible manner so they do not build up in the organism.  Also, these are acetylcholinesterase (AChE) inhibitors which have a natural threshold requirement built into their mode of action. The toxic effect due to buildup of acetylcholine in the synapse only can happen after most of the AChE is disabled by pesticide molecules, so low levels of pesticide are likely to have little toxic effect below that threshold.  The experimental evidence suggests that these chemicals have toxicity time-dependent scaling that is either threshold-like, t0 scaling, or at most a linear dependence like Haber’s rule, t1 scaling.

However, with the neonicotinoids, we have a toxin deliberately delivered in a way that can yield chronic exposure along with  enhanced toxicity time-dependence. These are new circumstances for regulators.  The usual approach is to compare exposure just to LD50 levels and not take exposure time into consideration.  The problem with this is illustrated in Table 2 below, where we compare the level of protection necessary to avoid damage to a long-lived insect with the quantity of insecticide needed to kill target insects efficiently.

Table 2. Level of insecticide contamination compared to the application rate required to protect a long-lived pollinator (e.g. life-span 50 days) when the insect pest is targeted in 2 days (Ratio pollinator/pest = 50/2). Relative safety factors (x 3) required to protect the beneficial pollinator are indicated for each case.

Time dependence


Relative time-dependent toxicity

Include Safety Factor × 3

 t0 Threshold level only – doesn’t depend on time



 t1 Accumulate to threshold with time – Haber’s rule



 t2 Enhanced or delayed toxicity



For honeybees, the LD50 for imidacloprid is about 40ng/bee, or nectar and pollen concentrations around 800 parts per billion (ppb).  If we are trying not to kill bees that are 50 days old, then because of the t2 toxicity time dependence, we need to limit residual concentrations by a factor of almost 2000, or less than 0.4 ppb in nectar and pollen.  Honeybees live for more than 150 days when going through the winter, so we have to extend the scaling further and require less than 0.05 ppb to ensure we aren’t killing these wintering bees prematurely. These are exceedingly small quantities of pesticide, well below the level of detection of many assay measurements.  These facts demonstrate that it is impossible to effectively limit contamination levels of these chemicals to the low levels that are consistent with protecting long-lived insects while still killing target insects effectively.  The burden of proof should fall on the chemical companies to show that the scaling law is actually different that what has been observed in tests on bees with up to 60 days exposure at concentrations of 4 ppb (Dechaume-Moncharmont 2003).  The data available shows such levels are not safe chronically, and the toxicity scaling suggests that even much lower levels are problematic for long-lived winter bees.

So far we have just discussed direct toxicity of the pesticides. Pesticides can interact with other chemicals and pathogens as well.  There is recent evidence that the neonicotinoids clothianidin and imidacloprid downgrade the immune systems of bees.  This is one of those unexpected effects that is not obvious from the mode of action of the chemical, but could be responsible for some of the problems bees face with pathogens today.  A paper out of Italy demonstrated a mechanism for immune suppression by the neonicotinoids clothianidin and imidacloprid in honeybees (Di Prisco 2013).  The authors went on to show that for one of the common known bee viruses, deformed wing virus (DWV), bees exposed to the neonicotinoids had further replication of the virus in their bodies, whereas in unexposed insects the virus did not replicate in the adult bees.  They showed that the effect was both proportional to dose and time.  This mechanism, downgrading the immune system by the neonicotinoids, goes a long way to explaining the observed general bee malaise and problems with multiple pathogens that are ultimately killing our colonies (Cornman 2012).  The Di Prisco paper looked at modest doses and time span of a just a few days.  It seems likely the immune deficiency might scale with time much like the mortality effects we see.  In fact it could be the immune system downgrade that is the reason for the observed scaling we see.  More studies would be needed to understand this fully.

The face of chronic neonicotinoid poisoning looks quite different from the type of pesticide poisoning that beekeepers have become accustomed to dealing with.  Delayed toxicity implies early death for older bees.  The consequences are likely to include: 1) smaller honey crops because forgers are older bees, 2) poorer wintering and higher winter losses because winter bees need to live for several months, 3) more queen failures because queens live for several years, need to consume large quantities of food,  and hence would be subject to longer and higher residual toxic exposure.

Acute poisoning by any neurotoxin usually produces tremors and twitching in the dying insect.  Often the twitching is followed by paralysis as the toxin goes from over-stimulating nerves to killing neurons.  The much slower onset of chronic poisoning will likely cause lethargy, behavioral changes and susceptibility to disease.  Bee deaths will be spread out geographically, as affected individuals cannot navigate back to the hive.  Low level poisoning may not produce any bee deaths near the source of the contaminated nectar or pollen.

The incidents with bumblebees in Wilsonville and Hillsborough provide two cases in point.  In Wilsonville, the bees were attracted to flowers that had recently been sprayed with the neonicotinoid dinotefuran.  The exposure levels were high and bees died en masse on the spot with typical insecticide poisoning symptoms.  In Hillsborough, the trees had been sprayed several months earlier.  The insecticide had translocated into the plant tissue and moved into nectar and pollen, where it could be ingested by bees.  Dinotefuran is expected to photolyze and degrade in less than 2 days in direct sunlight. Hence it is unlikely that contact exposure from residue on leaves was the cause of the bumblebee deaths reported in Hillsborough.  Although the concentration of bee deaths in the Hillsborough case were not nearly as large massive number of bees found under the trees in Wilsonville, the implications of the Hillsborough bee deaths are much worse.  First, there is little reason to think that bees visiting the linden trees in Hillsborough died immediately.  Most of the bees likely succumbed to the toxin after delivering many loads back to the nest.  They probably died throughout their foraging range, perhaps several days after working the contaminated linden trees, so the hundreds of dead bees found at the tree site is likely just the tip of iceberg in that case.  The trees were sprayed months before the trees bloomed, so we have direct evidence in this case, that even when applied according to label directions, this insecticide is lethal to bees.  The contaminated nectar and pollen brought back to the colony will be consumed by developing larvae and house bees, so not only is the loss of foragers a problem, but entire colony is put in jeopardy by the contaminated food supply (Gill 2012).

Even worse than spraying pesticide is the practice of direct injection of the neonicotinoids into trees.  This method of insect control is becoming more common, and is potentially deadly to bees.  Flowering trees are especially attractive to bees because a tree represents a concentrated food source.  Bees recruit additional foragers to attractive sources, so a single tree in bloom can be more important to the bees than a myriad of scattered flowers.

In light of the growing evidence against these chemicals, Oregon should follow the lead to regulators in the European Union and ban the use of imidacloprid, clothianidin, thiamethoxam, and also dinotefuran from use on plants visited by bees.  Residential use of these chemicals is inappropriate considering their extraordinary toxicity to a wide variety of arthropods (Mason 2013).  These insecticides should also be restricted so they cannot be used on trees that produce flowers or are otherwise visited by pollinators.

Selected References:

Cornman RS, Tarpy DR, Chen Y, Jeffreys L, Lopez D, Pettis JS, vanEngelsdorp D, Evans JD. 2012. Pathogen webs in collapsing honey bee colonies. PLoS One 7:e43562.

Dechaume-Moncharmont F-X, Decourtye A, Hennequet-Hantier C, Pons O, Pham-Delegue M-H. 2003. Statistical analysis of honeybee survival after chronic exposure to insecticides. Environ Toxicol Chem 22:3088-3094.

Di Prisco G, Cavaliere V, Annoscia D, Varricchio P, Caprio E, Nazzi F, Gargiulo G, Pennacchio F. 2013. Neonicotinoid clothianidin adversely affects insect immunity and promotes replication of a viral pathogen in honey bees. PNAS in press. 10.1073/pnas.1314923110.

EFSA. 2013. Conclusion on the peer review of the pesticide risk assessment for bees for the active substance imidacloprid. EFSA J 11:3068.

Gill RJ, Ramos-Rodriguez O, Raine NE. 2012. Combined pesticide exposure severely affects individual- and colony-level traits in bees. Nature 491:105-108.

Mason R, Tennekes H, Sánchez-Bayo F, Jepsen PU. 2013. Immune suppression by neonicotinoid insecticides at the root of global wildlife declines. Journal of Environmental Immunology and Toxicology 1:3-12.

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


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