Skip to content

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.

Neonics and Bees — Political Inaction Persists Despite Mounting Evidence

October 28, 2013

Over the course of the last year, the issue of bees and the neonicotinoid pesticides has finally begun to appear in the popular press in this country.  A campaign by Friends of the Earth in the UK resulted in major garden center chains removing the neonics from their shelves in February of last year.  Early spring found US beekeepers with another year of severe winter losses, with thousands of colonies dead on arrival into the California almond orchards.  Then in April, the European Union made the decision to ban three of the most troublesome chemicals throughout the EU.  Relying on the precautionary principle and the mounting evidence implicating these chemicals, science and politics came together in Brussels and put these poisons on hold — but not without dissent.  The major chemical manufacturers, Bayer and Syngenta, predict dire consequences for European agriculture.  The UK representatives voted no to the ban being imposed upon them by the rest of Europe, despite the groundswell of popular support for a ban on the chemicals.  Meanwhile, in the US, after the disastrous bee losses during almond pollination, the EPA held a  “Pollinators Summit” to address the plight of the bees.  But the “summit” was just a love fest for the chemical companies.  The day of testimony, there were four times as many presentations justifying pesticide technology than there were talks on the plight of the bees.  Indifference at the EPA has meant that the only way to get their attention was to sue them, so that is what happened in July over the approval of yet another systemic pesticide, Suflaxofour, that was granted approval without adequate testing.

Here in Eugene, Oregon, we started our early spring fair weather with a noticeable dearth of honeybees.  I lost all of my bees over the winter, and, coming into spring, it appeared that bee numbers were down all around town.  With the handwriting on the wall in Europe, activists began to step up pressure on local retailers and the city to get rid of the neonics.  The City of Eugene has been responsive, and has ceased using neonicotinoids to maintain city plantings.  Petition campaigns and several rallies for the bees eventually persuaded two local retail establishments to include warning literature and reduce their sales efforts for the worst neonics, a small but significant victory.  During the summer, a major bumblebee kill in Wilsonville, Oregon was caused by spraying of the neonic dinotefuran on blooming linden trees.  With tens of thousands of dead bees littering the parking lot, the bee kill generated national attention and refocused local efforts to restrict use of these potent chemicals.  The Oregon Department of Agriculture (ODA) issued a six-month moratorium on the use of dinotefuran pending further investigation.

Dead bumblebees in Willsonville this summer – Xerces photo

Summer comes, the bees do better in the nice weather, and everyone gets complacent.  Last week, Mike Odenthal , pesticide investigator for the ODA was trying to make excuses for the pesticide applicator that killed the bumblebees because the spraying was done at 6 AM before bees were flying.  This begs the question of why the ODA could allow such lax rules in the first place.   Then, Beyond Toxics, having collected more than 12,000 signatures from Oregonians on a petition asking the ODA to consider further restrictions  on the neonics, received the cold shoulder from ODA.  Nothing has come from the EPA except statements that they are due to consider review of some of the neonics in 2018.

Fortunately, the bee researchers have still been at work.  The real problem with the neonicotinoids became apparent to me after reading a 2009 paper by Francisco Sanchez-Bayo which looked at the effect of toxic chemicals over time.  The lesson was simply that some compounds could have delayed toxic effects, and at least for some organisms, the neonicotinoid imidacloprid demonstrated a strong time dependence.  Earlier this year Sanchez-Bayo and Tennekes expanded on the earlier results and showed that strongly binding toxins, such as imidacloprid and other neonics, are likely to have a larger delayed toxic effect.  I looked at a compendium of published papers on imidacloprid toxicity to honeybees and found that you needed less insecticide if you wait longer for the insects to die and the lethal concentrate will vary as 1/ t2 as you wait longer for the effects to accumulate.  A very good study on bumblebees by Gill et al. showed that indeed, field realistic exposure levels (<10 ppb) of imidacloprid did effect bumblebee colony development.  Significant effects did not show up until two weeks into the experiment, which goes along with the argument the that time dependent nature of the imidacloprid toxicity is a crucial variable.

From Nigel Raine talk 8/13 - Gill et al. paper.

From Nigel Raine talk 8/13 – Gill et al. paper.

Most recently, a paper by Prisco et al. out of Italy demonstrated a mechanism for immune suppression by the neonicotinoids clothianidin and imidacloprid in honeybees.  They 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, while in unexposed insects the virus did not replicate in the adult bees.  This mechanism for downgrading the immune system by the neonics goes a long way to explaining the observed general bee malaise and problems with multiple pathogens that are ultimately killing colonies.

From Di Prisco et al., PNAS Oct. 2013.

From Di Prisco et al., PNAS Oct. 2013.

Despite the growing evidence against these chemicals, we face an uphill fight to get them banned.  The pesticide industry is a $45 billion giant with lobbyists in every state house and marketers filling the airwaves with greenwash.  Bayer and Syngenta have programs promoting “bee health” while churning out tons of the offending chemicals.  University Ag schools receive industry funding, which colors their decisions regarding what research is suitable if they wish to stay on the gravy train.  Politicians get campaign contributions from corporations, and are expected to fall in line.  In many places, including Oregon, government agriculture departments emphasize chemical farming.  In Oregon, the ODA is also supposed to protect us from misuse of pesticides — it’s not our department of environmental quality (DEQ) that has that role.  This inherent conflict of interest is currently showing its horns in Oregon.  How can the ODA, an agency that is part of the part of the American experiment in corporate mono-culture, manage to look itself in the mirror and question the chemicals that it normally promotes?

Next spring we will undoubtedly have another crisis in the almond orchards.  The science will increasingly point the finger at the neonicotinoids, and the popular press and the public will continue to raise the alarm.  The responsibility for the insect genocide rests with all of those that have the ability to do something about it.  Let’s start at the top with the EPA, and then our state equivalent the ODA.  But don’t stop there.  Our state legislature can mandate action, so all of our representatives are on the hook, as are all of the retail establishments that sell these products and all of the pesticide applicators who use them.  But as is often the case when power and money are involved, it will only be grass roots activism that eventually gets the job done.

Select recent papers:

Gennaro Di Prisco, Valeria Cavaliere, Desiderato Annoscia, Paola Varricchio, Emilio Caprio, Francesco Nazzi, Giuseppe Gargiulo, and Francesco Pennacchio,  Neonicotinoid clothianidin adversely affects insect immunity and promotes replication of a viral pathogen in honey beesPNAS 2013 ; published ahead of print October 21, 2013, doi:10.1073/pnas.1314923110

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

Tennekes HA, Sánchez-Bayo F. 2013. The molecular basis of simple relationships between exposure concentration and toxic effects with time. Toxicology 309:39-51.

Tomé HVV, Martins GF, Lima MAP, Campos LAO, Guedes RNC (2012) Imidacloprid-Induced Impairment of Mushroom Bodies and Behavior of the Native Stingless Bee Melipona quadrifasciata anthidioides. PLoS ONE 7(6): e38406. doi:10.1371/journal.pone.0038406

Pettis J, vanEngelsdorp D, Johnson J, Dively G. 2012. Pesticide exposure in honey bees results in increased levels of the gut pathogen Nosema. Naturwissenschaften 99:153-158.

Krupke CH, Hunt GJ, Eitzer BD, Andino G, Given K (2012) Multiple Routes of Pesticide Exposure for Honey Bees Living Near Agricultural Fields. PLoS ONE 7(1): e29268. doi:10.1371/journal.pone.0029268

DateTrike Meets Burning Man

September 29, 2013

The blog has been on summer vacation, partly because I’ve been too busy having fun to write about it.  But the seasons turn, and every year around labor day, The Man burns in the Nevada desert.

This year the DateTrike made its way to Black Rock City.  The original inspiration for the craft rose from the desert dust several years ago, so it was an event that had to happen.


Burning Man is the ultimate date and the DateTrike was the ultimate together transport on the playa.

Date on the Playa

Night on the playa needs lights. We outfitted the DateTrike with some LED strip lights and EL wire on the back canopy supports. We became part of the pretty playa party.

DateTrike Lights

Otherworldly Spaceship Man beckoned more than 60,000 visitors to Black Rock City this year.

Spaceship Man

And again we were reminded of the impermanence of all things…


DateTrike Construction

May 26, 2013

Wherever we go on the DateTrike, our vehicle turns heads, gets smiles, and everyone wants one.  I’m won’t be making any more of these, but it is no harder than any other mildly complex project, so I’ll present a few of the details here for those who are up to the challenge.  If you happen to be inspired enough to build something, please post a comment – even if it is years from now.

DateBikeI started by doodling with a drawing program and came up with the basic idea shown in the plans above.  I was after moderately uniform weight distribution on the three wheels, and a design as compact as possible.  The seat spacing is snug, which allows the overall width to be under four feet, with the passengers inside of the rear wheels.  I copied the rake of the front wheel from our Sun trike. I wanted the pedals as far forward as possible, but the inside foot has to clear the frame.  The front wheel needed to be a small as possible to keep the low profile.  For the rear wheels I chose a pair 24″ wheels that are commonly used for garden carts because the hubs could be easily modified to work for the rear axle.

The Frame

A laminated frame makes possible the graceful front section curve.  Lamination also lends itself to building-in only the strength needed using less material.  The main frame is made of a box-beam construction.  Tight-grained Douglas fir is used for the core and 3/16″ birch plywood is used for the outer skins on the straight beams.  For the nose I used 1/8″ birch plywood for the laminations.

The building process begins with cutting out the conical section needed for the inside-most nose lamination.  The inside straight-frame laminations are also cut out.  Eight-to-one scarf joints are planed into the plywood, and the conical nose section and flat sides of the inside ply are glued together flat on the floor.  The basic frame takes shape by bending the pre-assembled inner ply and holding it in place with a couple of sections of 2×6 that space the two sides apart correctly.  A second 1/8″ ply is added to the nose section, and then the core spacers are glued onto the sides.  More 1/8″ ply sections are cut – but only 2″ wide sections to make up the top and bottom solid sections of the nose. Construction Regions where extra strength requires more reinforcement are filled in with core wood.  The nose-to-sides joint area is tricky and can benefit from a bit of filler that can then be planed fair.  Plywood likes to only bend in one dimension, so it is critical to keep surfaces “flat” to multi-dimensional bends.  I use an epoxy that has good gap filling properties for the lamination.  There is lots of room to hide mistakes until the very last lamination.  Then much trial and error is required to get the overall length and the scarf just right.  Once you add the glue, you are committed.

The cross-piece in the back was made as strong as possible, with gussets to increase glue joint area in the corners and lag screws in the butt joints under the final skin.  I was unsure how stiff the frame would end up, and always wanted strengthening options.  In the rear axle section, completing the box sections with glued down top and bottom ply decks would help.  For the entire frame, a fiberglass skin could be applied.  However, the frame proved to have good stiffness without those additions.

Front Wheel Mount

HeadStockThe front wheel mount took some thought because this needs to be strong and needs to hold the front wheel head stock.  I used a salvaged head stock that I cut off an old bicycle frame.  I took a couple of blocks of wood, clamped them together, and bored a hole along the split between the two boards.  I adjusted the hole by hand to fit the irregular shape, testing the fit frequently until the two board halves could be clamped together and trap the head stock.  Once epoxied together, the block was shaped to provide the desired rake  angle and carefully fit to the contour of the nose lamination   Although the part is made of cedar, a relatively soft and not particularly strong wood, I used plenty of long screws and lag bolts to fully reinforce the joint.  The block was fastened to the nose before the very last nose veneer was glued in place.  All of the screws are hidden under this last ply layer.

The Drive Train

Left Drive Each person has their own set of pedals, gears, and a drive wheel. Each axle is supported by a pair of pillow blocks. You need to use an old-fashioned “freewheel” type of gear cluster.  There are a couple of custom machined parts required for this axle.  I built them with the machines I have access to at work.  However, the most critical item, the freewheel and break disc hub, can now be purchased from the folks at Atomic Zombie.  Serious builders should browse Atomic Zombie for ideas and building suggestions.  Reviewing their Kyoto Cruiser was certainly part of the design process I went through.RightDrive I bought most of the components I needed new, including the freewheels, derailleurs, and disc brakes.  The key to using a wood frame is to add reinforcement for the attachment points for these components.  Simple blocks of aluminum, or aluminum angle extrusions can be lagged into the wooden frame and provide a very secure mount for brakes and derailleurs. Another spot that needs good strength is the crank hub installation. Bottom BracketThe threaded “bottom bracket” tube can be purchased  (or salvaged). This part of the frame was furnished with a solid core and additional support ply sections were added on each side for added joint area and strength.  A hole saw was used to create a fairly tight hole, and the metal part was epoxied in place with a gap filling epoxy designed for adhesion to metal. With the well-supported large-area joint, this will not fail.

Steering and Brakes

It took having the frame and drive train together and staring at the trike for a week or two to finally come up with the cable under-seat steering design.  Steering Tiller I wanted either passenger to be able to steer, and I liked the under-seat operation because it is a natural position for your hands. But how to do the linkage?  Looking for inspiration, I came upon the pedal and crank from my salvage bike and realized that this could be the basis for the steering lever with the chain linkage to the steering cable.  Another “bottom bracket” tube is glued into the seat support cross member to hold the steering arm bearing.  The cable system works well on the trike because the framework lends itself to the cable circuit.  To turn the wheel Steering PulleyI had to make a special steering pulley that  I could fasten to the front fork through the fender bolt hole.  The “half pulley” was built with a groove for the cable and a clamp to fix the cable position.  There was a certain amount of trial and error to get the right fit.  For one-to-one steering angle motion, the pulley diameter and the crank chain diameter should be the same.  Four cable pulleys were fastened to the frame as required to route the cable close to the frame and out of the way of the pedals.  A turn-buckle is used to adjust the tension.

The steering is responsive, and allows a tight turning radius.  On tight turns the steering lever slips under your legs.  The steering tiller also has the brake lever for the dual disk rear brakes.  The dual acting lever powers both brakes.


SeatsWhen I came to the seats, once again the project sat on hold while I considered various options, none of which were adequate.  I went so far as to purchase a boat seat, but Ellen quickly nixed that idea!  It was hard to beat the nice foam seat on Ellen’s single person Sun trike for comfort, so I finally decided that those seat cushions were the place to start.  Then, in keeping with the wood work, I decided on simple woven seat backs, similar to classic Shaker tape-back chair weaving.  I went for weather resistant polyester webbing on oak frames.
For simplicity, and because this project is mostly for Ellen and myself, I opted for just fixed seat positions.  A piece of 3/4″ plywood was attached to the bottom of the seat cushions, with thread inserts so it could be bolted to the frame seat cross member from the bottom.  The seat  backs were attached to the plywood piece with a pair of hinges so the back angle is adjustable.   Back braces are attached to the seat-back frame and fastened to the rear member of the frame.  You can give a strong pedal push and securely transfer the force into the seat without concern.  It took several stages of adjustment, added holes, and trial and error to get the final seat position.  Making the seats adjustable is an improvement that the next builder might want to design in.

Do It

If you have read this far, perhaps you should start sharpening your plane blade and get started on building one.  Working with wood epoxy construction takes on a pace that is hard to hurry.  Each lamination needs to cure before the next is applied.  You will become ingenious inventing clamps and jigs to hold things in place while the epoxy cures.  You don’t need many special tools.  The only additional tools I acquired for the project was a saber saw for cutting the conical sections from the plywood, and the correct size hole saw for mounting the bottom bracket parts.  So, its time to get started.  Add your creativity to the process, and let us advance the technology and comfort of the bicycle built for two.

Time-dependent Toxicity of Imidacloprid in Bees and Ants

May 7, 2013
Imidacloprid Time Dependent Toxicity for Bees and Ants

Honeybee colony losses continue to be unacceptably high.  In the US this spring, colonies brought in to California to pollinate almonds from throughout the country, about half of the colonies were lost (New York Times, March 29, 2013).  It is generally accepted that multiple pathogens ultimately bring down stressed colonies (Cornman 2012).  However the role of pesticide stress on colonies remains controversial.  Chronic exposure studies are often poorly constructed and frequently do not follow the exposed insects long enough for effects of the toxin to become evident.  The best studies look at mortality, or behavioral effects, over a substantial fraction of the insect’s lifespan while varying the toxin concentration or dose.  Time-to-effect studies lend themselves to a simple time dependent “power law” empirical model which can guide expectations for field toxicity effects (Tennekes 2011, Sánchez-Bayo 2009).  Other reviews of the toxicity of imidacloprid (Cresswell 2011) attempt to establish specific “acute” or “chronic” levels, but this seems useless if the time of exposure is not explicitly included.

Hence, I’ve made an effort to identify relevant time-to-effect studies in the literature  most specifically for imidacloprid with insects of order hymenoptera, which includes bees and ants.  As it turns out, there is an interest in concocting ant baits that proffer sub-lethal doses of toxin to forager ants.  A study done by Rust, 2004, has time-dependent toxicity measurements for imidacloprid on Argentine ants.

For the honeybee data, we have the paper by Suchail 2001 that I discussed previously. However, there is general concern in the research community that there is something wrong with the Suchail results.  Many other studies do not show such a  high sensitivity to the toxin.  So I looked for other experiments that also include time-to-effect measurements.  There is a study by DEFRA (2007) that has time-to-effect figures, and also a compilation to many researchers’ LD50 numbers for 24, 48, 72, and 96 hr. periods (FERA 2013).    To be able to plot both chronic and acute data on the same graph, I take the acute LD50 numbers and divide by the time interval for the measurement to obtain daily dose rates.Dechaume-Imidicloprid_chronic data  At higher concentrations there is an anti-feedant  effect that reduces the consumption rate, so I’ve plotted the reported consumption of toxin (ng/day) versus the time of exposure until half the bees have died (LT50).

Many studies only follow the bees for 10 days or less.  At lower concentrations, the LT50 time is never reached in the experiments.  However, there is a paper by Dechaume-Moncharmont, et al. 2003, which contains a couple of data points with time-to-effect numbers for relatively low sub-lethal concentrations.  The data show  that 4-8 ppb samples eventually kills bees in  about 30 days.   All of these data are plotted in the chart below.  I had to estimate the consumption rate for the ants in order to plot it with the other data, but an incorrect estimate would shift the curve left or right, but not change its slope.  I show the power law best-fit line for each data set, where the Dechaume-Moncharmont points (blue squares) are included with LD50 averages from the FERA 2013 paper.

Imidacloprid Time Dependent Toxicity for Bees and Ants

First notice that the LT50 times for the Argentine ants do a remarkably good job of following a simple power law with roughly t1.7 dependence.  This adds confidence to the utility of the empirical power law model for imidacloprid.  Recall that simple accumulation to a toxic threshold would appear as directly proportional to time ( t1.0 ). An exponent larger than one can be interpreted as coming from damaging secondary physiological effects that take time to develop.

The DEFRA data stands out as not falling with the averages of other researchers.  In general, there appears to be a wide variation between experiments, and hence individual colonies or strains of bees, to the sensitivity of this insecticide.  The DEFRA study has time-to-effect numbers and consumption data, so it provides a good data set for looking at time scaling, even if the DEFRA bees are not particularly representative of most other bees tested.  Again we see the data taken can be very well explained by the power law formulation, this time with about t1.6 dependence.  We might expect that healthy individuals of similar species would exhibit similar temporal effects to the same toxin, and this seems to be the case.  Finally, the average LD50 numbers from many researchers also fits the power law model.  I also included the Dechaume-Moncharmont data in the power law fit, here about t2 .  The Dechaume-Moncharmont data extends the  model into the high field-realistic exposure range when approaching the lifespan of summer bees.   If we extrapolate the curve to the lifespan of winter bees, we are well into the range of field-realistic exposure (0.01 ng/day).  Hence, even with healthy bees, exposure to modest field-realistic levels of imidacloprid will compromise the longevity of winter bees, and could easily cause problems getting the bees through the winter.

It is known that imidacloprid is relatively quickly metabolized in the honeybee.  The metabolic half-life is about 5 hours (Suchail 2004). Yet the effects of the poison are cumulative and long-lasting.  This seeming paradox is explained by the fact that when the imidacloprid molecule binds to the nAChR receptor sites in the nervous system of the insect, it binds strongly and essentially irreversibly.  So while free circulating imidacloprid may decay away, the damaging bound molecules remain, continuously compromising the nervous system.

The imidacloprid toxicity graph tells us that we need to be careful not to expose bees to more than a very few parts per billion (ppb) of toxin if we wish there to be no effect over the lifespan of the bees.  Reports of levels of neonicotinoids from treated agricultural crops are frequently in the 1 to 5 ppb range.  Typical honeybee consumption is about 20 µl/d, so at 5 ppb, the ingested toxin would be 0.1 ng/day which is the upper end of the yellow zone in the figure.

The Suchail (2001) results show a much higher sensitivity to imidacloprid than would fit the trends we see with the other data sets. Rather than the  t2  dependence, lethal effect seems to scale as toxic concentration times t5.  It is tempting to disregard the Suchail results, however one test site in trials by Shmuck (2004) also showed very high sensitivity to imidacloprid as well.  Hence it is worth considering a secondary stressors that could result in a higher sensitivity to the toxin.  The logical culprits would be pathogens, bacterial, viral or the microsporidian nosema.

Pathogen interactions with a host could lead to several time-dependent processes. First, damage to the host immune system has to occur for a pathogen to get a foothold. Then, before the host succumbs to the pathogen, the infectious organism must grow and multiply to lethal levels. Damage from the pathogen itself may take time to manifest in the host organism. Several of these time-dependent processes happening simultaneously would lead to a higher order time dependence.

The interaction between nosema and imidacloprid was studied by Alaux, et. al. (2010).  The study fed bees 200,000 nosema spores to initiate infection and subject the bees to various doses of imidacloprid.  There was some interaction between the pesticide and the pathogen, but the study only followed the bees for ten days so it is hard to draw conclusions at field-realistic doses, and the nosema infection dominated the experiment.  Two data points from the study are plotted on our graph (blue diamonds).

A very good study, Aufauvre (2012), looks at the interaction of the systemic insecticide fipronil and nosema infection, and finds a strong synergy between the pesticide and the pathogen.  The figure from that paper, below, shows what happens when sub lethal infection levels are combined with sub lethal insecticide exposure.

Aufauvre, 2012

The curves (purple) show what happens with both the pathogen and the toxin combined.  Neither nosema alone (red) nor fipronil alone (green) are very different from the control (blue), since  low doses were used.  However, the combination, given enough time, is especially lethal.  The study examines the effects of the relative timing of the exposure and infection, but finds synergistic interaction between the pathogen and the toxin in all cases.  The study followed the bees for twenty-two days, significantly longer than the typical ten-day chronic studies.  The added time is crucial for the delayed toxic and synergistic effects to show up.  The same is true with the Dechaume-Moncharmont experiment, where there were no deaths in either the control or exposed bees at the ten-day point, yet the toxic effect was clearly evident by day 30.

The choice of nosema as the pathogen for this study is convenient because the infection is easily accomplished with a spore solution, and the progress of the infection can be followed with microscopic examination of the bees.  Curiously, the level of the nosema infection as measured by spore counts,  was not much different with or without the pesticide exposure. Viruses are much more difficult to use as the infectious agent because of the difficulty of diagnosing their presence and quantifying the infectious dose and infection progress.  However, viruses are more ubiquitous in honeybee colonies than nosema, and could easily have a similar synergistic interaction with pesticides on the bee’s health.

Cornman et al. (2012) found that CCD (colony collapse disorder) colonies were more likely to have higher levels of a wide variety of pathogens than weak, but non-CCD, colonies.  Not only were the levels of pathogens higher, but multiple agents were frequently found in combinations not typical of non-CCD colonies.  The figure below from that paper does a great job of graphically illustrating the situation.

Pathogen Webs

It looks like the immune system has gone awry.  Could it be a few parts per billion of insecticide that makes the difference?  More research is still needed here, perhaps looking at pesticide interaction with KBV or AMPV virus, since these viruses show up in CCD colonies.

Extrapolating LD50 numbers or 10-day chronic LC50 values to the lifetime of bees wintering in the honeybee colony requires some understanding of the time-dependent nature of the toxin.  We have shown that the published LD50 and LC50 data can be empirically modeled using a simple power law.  For imidacloprid with healthy honeybees, the time dependence is approximately t2 , indicating that not only is the exposure cumulative, but also that there are delayed toxic effects.

Queen bees can live for several years.  Queen bees also need to consume large amounts of food in order to churn out the thousands of eggs they lay every day.  This make queen bees especially susceptible to such a toxin. Queen failure was one of the precursors to colony mortality found by vanEngelsdorp et al. (2013).  Queen failure, even if the bees succeed in raising a new one, will leave the colony without a fresh supply of young bees.  A colony with pesticide stress may be relying on young bees to make up for those that disappear before their time.

I only looked at studies that addressed bee mortality.  Bees affected by pesticide may not immediately die, but they may be practically useless to the colony, or may be unable to forage or navigate, and hence become lost and perish outside the hive.  Quantifying behavioral effects is more difficult than counting dead bees, but one might expect that the time-to-effect scaling would be similar to the mortality data.


Alaux, C., Brunet, J.-L., Dussaubat, C., Mondet, F., Tchamitchan, S., Cousin, M., Brillard, J., Baldy, A., Belzunces, L. P. and Le Conte, Y. (2010), Interactions between Nosema microspores and a neonicotinoid weaken honeybees (Apis mellifera). Environmental Microbiology, 12: 774–782. doi: 10.1111/j.1462-2920.2009.02123.x

Aufauvre, J., D.G. Biron, et al. (2012). Parasite-insecticide interactions: a case study of Nosema ceranae and fipronil synergy on honeybee. Scientific Reports 2: 326. doi:10.1038/srep00326

Cornman RS, Tarpy DR, Chen Y, Jeffreys L, Lopez D, et al. (2012) Pathogen Webs in Collapsing Honey Bee Colonies. PLoS ONE 7(8): e43562. doi:10.1371/journal.pone.0043562

Cresswell, J.E. (2011). A meta-analysis of experiments testing the effects of a neonicotinoid insecticide (imidacloprid) on honey bees. Ecotoxicology,20(1), 149-157.

DEFRA – Department for Environment, Food and Rural Affairs (20o7): Assessment of the risk posed to honeybees by systemic pesticides. March 2007.

vanEngelsdorp D,  Tarpy DR, Lengerich EJ, Pettis JS, Idiopathic brood disease syndrome and queen events as precursors of colony mortality in migratory beekeeping operations in the eastern United States.  Preventive Veterinary Medicine, 108,  2–3, February 2013, Pages 225–233.

FERA – Food and Environment Research Agency, Neonicotinoid Pesticides and Bees,Report to Syngenta Ltd.
January 2013.

New York Times, March 29, 2013. Mystery Malady Kills More Bees, Heightening Worry on Farms

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.

Suchail, S., Debrauwer, L. and Belzunces, L. P. (2004), Metabolism of imidacloprid in Apis mellifera. Pest. Manag. Sci., 60: 291–296. doi: 10.1002/ps.772

Tennekes HA, Sánchez-Bayo F (2011) Time-Dependent Toxicity of Neonicotinoids and Other Toxicants: Implications for a New Approach to Risk Assessment. J Environment Analytic Toxicol S4:001. doi:10.4172/2161-0525.S4-001

DateTrike Complete

April 22, 2013

The DateTrike made its debut last summer.  Since them there have been a few refinements, and finishing details that have given the craft a more finished look and some added features.

DateTrike Complete
The fenders are a big appearance boost, and also keep arms and sleeves off the rear tires. Tubing chain guards keep your pants clean.

DateTrike Deck

I finished the rear deck which includes a storage area under a sliding door for a place to carry travel essentials.  Lighting was also added.  A front hub generator provides ready power for both a nice bright headlight and the pair of LED tail lights.  Good lighting makes for a pleasurable ride home from the theatre late a t night.

Ellen and Sammy

Sammy the dog is always ready to go for a run with the trike, and so is Ellen!

Even though the trike is now officially complete, there is one more accessory that is still to come, and that is the canopy.  If all goes well, the DateTrike will be coming to Black Rock City later this year and we will need the shade.


Get every new post delivered to your Inbox.

Join 101 other followers

%d bloggers like this: