The death of bees can be a warning that something is wrong with our agricultural practices, just as the death of a caged canary used to be a warning to underground miners. We need bees to pollinate plants so that we can produce food for consumption and with less bees, or even worse no bees, we seriously risk our food production systems.
Bees are dying and colonies collapsing and many believe that the finger of blame points at the toxicity of pesticides and the way that we use them.
Of particular concern is a group of pesticides called neonicotinoids that are sprayed or used as systemic pesticides (1).These pesticides are used to coat seeds before planting (2) or they are sprayed on crops, for example on apples to protect them from woolly aphids and codling moths.
They are absorbed into the plant and attack insects when they land on the plant to feed off it. In apple orchards, to continue our example, they can be transmitted to the pollen which bees then collect and take back to the hive.
If the pollen is contaminated then the poison is transmitted to the young bees and the queen, both of whom eventually die. In the event of a hive already harbouring a disease, the effects of the contamination can be disastrous.
There is scientific evidence that if certain fungicides are inadvertently mixed with some neonicotinoids their toxicity is increased 1000% (3). Neonics are also very toxic to aquatic animals, so washing out the spray tank and allowing the water to flow to a water course is unacceptable.
The coating of seeds before planting, such as happens with a lot of canola crops and many other plants (4), allows the plant to repel insect pests. However the problem is the pesticide can’t distinguish between insect species so a bee landing on the flower to pollinate it will possibly take poisoned pollen back to the hive.
What does this mean for beekeepers who put their hives in an orchard for pollination? One scenario is that a strong hive may go to pollination and return as a weak hive even though no spraying was done while the bees were on site. Hives could deteriorate in the weeks after they are removed, and checking the spray log of the orchardist (which they are required to keep by law) may show that the orchardist has sprayed some three weeks before the bees got there with a neonicotinoid.
The testing regimes in Australia to prove contamination do not appear to be accurate enough to determine the small amount of contamination in dead bees. (Refer to studies at Harvard University 5.)Authorities seem not to care if they cannot find a cause for death during pollination, arguing if the contaminate cannot be measured that it must be all right (www.apvma.gov.au). We have to have more accurate testing (www.plosone.org).
The questions that must be answered are:
- What if these pesticides get into the food chain and in the food that we eat?
- These pesticides (Neonics) attack the brain function of insects; would they attack human brain cells over time?
- Why cannot we debate the use of these Neonics in our Agricultural industries?
Various articles recently in the press and in the scientific community (6,7,8) point to deaths in bees in France, England, Germany and Slovenia. Birds that feed on insects have been reduced in numbers because of the drop in insect population.
An e-mail campaign to protest at the recent AGM of a chemical company raised in excess of one million signatures worldwide (see website: avaaz.com).
In the face of this increasing global concern about neonics what is happening in Australia to protect our bees and our livelihoods? What if we suffer the same losses in as has happened in other countries? Where does that leave our industry and what happens in the long term to our Agricultural industry if bees are wiped out?
We should be asking our DPI to test bees which we suspect may have died from contact with Neonics and not taking the attitude of expecting losses when you pollinate.
Some beekeepers recall the time before Neonics when they put bees on canola and the hives grew extremely large. "Boiling with bees ..." was the expression they used. Now when they pollinate canola the hives do not produce and usually come out weaker. So much so that they now only produce honey from forest areas and do not pollinate (9).
In the September issue of ABJ, Leo Kuter summarised some of the prevailing fears that honeybee decline is due to the use of neonicotinoids, a new class of systemic pecticides. Recent and widely-reported research (Henry et. al. 2012a) even suggests neonicotinoids might provide a mechanism for Colony Collapse Disorder (CCD), although it is worth noting that honeybee decline is also happening where CCD has never been reported.
Everybody likes a simple cause and effect – something we can point to and say (ommitting a few choice words to the perpetrators), 'Fix this and the bees will be right again.' Reality is rarely so straightforward. As the bee decline has progressed I've lost count of the simple 'causes' that have been presented. Among the more memorable are:
- mobile 'phones (the absolute 'definite cause' of choice a couple of years ago)
- mobile base stations, power lines and other strong electromagnetic sources (a perennial favourite for any malaise)
- alien abduction (hopefully they have smaller probes for abducted bees...)
- God's punishment (pro gay-marriage states in the USA have more cases of CCD)
Leo’s article shows neonicotinoids are at least a plausible candidate and they are surely not good for bees, but the argument for these being the explicit 'cause' of global bee decline is still not particularly strong. The risk here is that the media and vocal lobbyists are going off on a righteous crusade to the detriment of more diligent, and maybe less newsworthy, efforts to get to the root of a complex problem.
Rather than reviewing the evidence here, I recommend a visit to Randy Oliver's website where his two recent articles from the American Bee Journalon this topic can be found, along with some further commentary on his home page. Interested readers can also directly access the study by Henry et. al. (2012a), the commentry on this study by Creswell and Thompson (2012), the response to the comment (Henry et. al. 2012b) and to the meta-analysis of toxicological studies on imidacloprid by Creswell (2010). An example of one such study is Cutler and Scott-Dupree (2007). Links to all are included below. These are original material rather than reportage and demonstrate the complexity of the issue.
As food for thought, I'll leave you with the following:
- Neonicotinoids are widely used in Australia and our bees are not (yet) in decline.
- The 1999 and 2005 neonicotinoid bans in France did not lead to improved colony survival. Anecdotal reports of short-term improvements post-2005 are now attributed to a mild winter and losses have risen again.
- Canadian bee losses remain fairly steady despite the bulk of the honey crop coming from neonicotinoid treated canola.
Chris Strudwick, VAA member
Some further notesOn submitting this article I was asked to expand on the situation in France and Canada, so here is some more information for those who want to dig deeper.
Situation in France: Most of the material is in French but I have included a range of interesting reports. Data collection in France was patchy until 2008, however the pan-European COLOSS (prevention of COlony LOSSes) research program has lead to much better monitoring. Post the 1999/2005 bans, French winter colony losses remain higher than the long-term expected historical rate, ranging between 20-30%. The latest statistics are in www.coloss.org/publications/feb-2012-workshop-proceedings-wg1-york (France is on page 19).
The statistics come from an AFFSA/ANSES report. The French bee research institute, ITSAP, publishes reports on Winter losses for professional beekeepers. The OPERA research centre has a nice summary report in English, but is slightly out-of-date now www.pollinator.org/PDFs/OPERAReport.pdf.
Situation in Canada: CAPA www.capabees.com collects statistics and issues annual reports on their website. Winter losses are generally steady around 30-35% against a long-term historical value of about 15%, with lower losses in the milder winter of 2009-10. This is similar to the USA and some other Varroa affected countries, however Canadian bees have high exposure to neonicotinoid treated canola, with over 300,000 colonies, or half Canada's commercial bees, primarily working canola according to the Canadian Honey Council www.honeycouncil.ca. CCD however has not been reported in Canada.
Creswell, JE & Thompson, HM 2010, 'A meta-analysis of experiments testing the effects of a neonicotinoid insecticide (imidacloprid) on honey bees', Ecotoxicology, vol. 20, no. 1, pp. 149-157, accessed from http://link.springer.com/article/10.1007%2Fs10646-010-0566-0
Synopsis: Field-realistic doses of neonicotinoids are well below lethal levels but could affect forager performance by 6-20%. Existing studies are not statistically powerful enough to detect this small effect which may have been missed in evaluating impacts on honey bees, including those that find no observable impact.
Creswell, JE 2012, 'Comment on "A common pesticide decreases foraging success and survival in honey bees", Science, vol. 337, pp. 1453, accessed from http://www.sciencemag.org/content/337/6101/1453.2.full.html
Synopsis: Henry's model is sensitive to colony growth parameters. 'Colony collapse' disappears when more realistic parameters are applied, even with the predicted increase in forager mortality.
Cutler, GC & Scott-Dupree, 2007, 'Exposure to clothianidin seed-treated canola has no long-term impact on honey bees', Journal of Ecomonic Entomology, vol. 100, no. 3, pp. 765-772, accessed from http://dspace.lib.uoguelph.ca/xmlui/bitstream/handle/10214/2621/32546.pdf?sequence=1
Synopsis: No observable differences between colonies foraging on treated or non-treated canola. No difference in colony winter survival. Raises a couple of issues: Creswell shows the experiment can't detect the small effect that might be present, however if the effect is there the colonies appear to cope anyway.
Henry, M, Beguine, M, Requier, F, Rollin, O, Odoux, JF, Aupinel, P, Aptel, J, Tchamitchian, S & Decourtye, A 2012, 'A common pesticide decreases foraging success and survival in honey bees', Science, vol. 336, pp. 348-350, accessed from http://www.sciencemag.org/content/336/6079/348.full.html
Synopsis: presents a model of forager loss from sub-lethal neonicotinoid (thiamethoxan) exposure against colony growth and proposes the losses are sufficient to cause colony collapse. The data on forager loss (table S1 in the supplementary materials) in familiar and unfamiliar environments, with and without neonicotinoid exposure, is particularly interesting. Around 15% forager loss is apparently normal!
Henry, M, Beguine, M, Requier, F, Rollin, O, Odoux, JF, Aupinel, P, Aptel, J, Tchamitchian, S & Decourtye, A 2012, Response to Comment on "A common pesticide decreases foraging success and survival in honey bees" Science, vol. 337, p, 1453, accessed from http://www.sciencemag.org/content/337/6101/1453.3.full.html
Synopsis: The model is recalculated using the method of Cresswell (2012) to calculate a critical population parameter. Data from the ECOBEE program, which collects data from real colonies, is used to provide better estimates. The results still indicate a colony decline, if not collapse.
Oliver, R, scientificbeekeeping.com - see especially scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-scienceand scientificbeekeeping.com/neonicotinoids-trying-to-make-sense-of-the-science-part-2
Synopsis: if you haven't already visited Randy's website you have missed a treat. A very thoughtful approach to beekeeping and a willingness to experiment. His articles on the neonicotinoid debate in the American Bee Journal are brave, especially when he attributes some colony losses to 'PPB' or 'piss-poor beekeeping'! Randy also gives details of a new and better scientific trial of neonicotinoids happening in the near future.
In an earlier article I suggested the controversy over neonicotinoids might be the latest example of trying to attribute the honeybee's decline over most of its current range to a single, simple and understandable cause. This is a natural human tendency but not helpful should causes turn out to be neither single nor simple. I also pointed out that the situation in Australia provides some pause for thought, as our bee populations are still apparently healthy although many of the perceived pressures are the same as those in affected countries. What I did not attempt to do was either to propose an alternative cause or reject any candidates, or at least not those existing in the realms of sanity. I am not going to identify a 'cause' here either. Instead, I would like to look at a mechanism that seems to be implicated in the decline and which may have some practical lessons for beekeepers.
We all know our bees are tremendously industrious. Just how industrious can still come as a surprise. We have our attention on the honey crop, which represents the colonies winter food supplies plus – in a well managed hive – a surplus we can remove. Beekeeping brought down to its basics is largely about managing the strength of the colony while the bees are actively foraging so the bees store more honey than their smaller winter population can consume. What we do not see is the turnover of stores and bees. Estimates vary, but an average hive will get through around 200,000 bees over the course of the season and, in doing so, will consume upwards of 25kg of pollen and 100kg of honey just in going about its daily business, without even considering laying in winter stores. This huge requirement for energy is the penalty that ancestrally tropical honeybees pay for their success in colonising temperate regions. A bee colony collectively acts more like a warm-blooded mammal than a mass of cold-blooded insects. Unlike colonial wasps that die off at the end of the season leaving the young queens to hibernate over winter, thereby using very little energy, bees cannot survive the cold. A bee colony keeps the boilers stoked and maintains an overwintering population which is ready to go as soon as the weather is warm enough for them to fly. Throughout the year, honey provides concentrated energy for bees to burn for heating the brood nest and for fuelling foragers. Clearly, if bees are unable to supply their energy needs the colony will fail, and starvation is of course the single biggest killer of bees, both wild (or feral) or managed. In the latter case the problem is almost entirely avoidable as beekeepers' colonies should not starve unless other factors are at play. Unfortunately they still do.
The other part of the equation is population dynamics. Three important elements are productivity of the queen, longevity of foragers, and the contribution of various externally derived mortality factors. Most queens are prolific layers. Healthy bee colonies at full strength are normally around the 40,000 mark, implying a laying rate of about 1000 eggs per day just to maintain the population at that level. During the explosive early season growth phase the colony can increase by 40% per month, requiring a significant excess of eggs laid over deaths of mature bees. The laying capacity of a good queen provides a buffer to cope with losses, and of course bees know how to fix the problem of a poorly-performing queen. We still see a huge check in the progress of a colony if it ever becomes queenless, even briefly. Forager longevity is another matter and is in itelf a fascinating topic. In brief it is affected by the quality of feeding a young bee receives, workload and health. Overworked and poorly-fed bees die young. Come to think of it, that applies to beekeepers too! Sickness is more subtle. It can shorten life or make a forager become less efficient and consume more fuel. Either way, it affects the hives 'profit and loss' account. Likewise, if factors such as pesticides hit the foraging population and increase losses or decrease useful lifespan, the impacts will echo through the colony. Because of the fecundity of bees, that may show as a failure to thrive rather than as a collapse.
Australian beekeepers are aware that an abundance of foragers and a good source of nectar is not always a recipe for success. Poor quality pollen gathered by colonies working trees such as ironbarks can mean the loss of the growing generation. The colony goes from plenty of bees to none as brood starves and house bees fail to emerge to maintain the survivors, leading to a sudden decline. Likewise brood diseases can alter the balance by reducing worker brood survival rates. Sick brood that does survive gives rise to sick workers that will never become long-lived efficient foragers.
What seems to be a robust and thriving colony is easily disturbed by interrelated factors affecting population dynamics or energy balance. Bees can get hit at both ends, as well as in the middle. Disturbance can lead to a decline or dwindling in colony numbers, fast or slow depending on exactly which part of the system has been disrupted. Healthy bees have resilience and spare capacity, even so most wild colonies develop terminal problems after a while, hopefully after producing a few successful swarms. Unmanaged hives often go the same way after swarming themselves down to vulnerable remnant populations. What does this mean in practice? Well, if bee colonies are merely coping rather than thriving, they are on a knife edge. Chemical residues might impact a bee's immune system causing it to burn more energy and knocking a day or two off its lifespan. Diseases like Nosema might be doing the same, while both factors in combination appear to be worse. Normal forager loss rates may go up a few percent due to neonicotinoid or other pesticide action. Varroa mites in particular stress adult bees by causing large open wounds and spreading disease, while brood are decimated by transmitted viruses. None of these things in themselves might be sufficient to overcome a colony, but they do not have to be. All they need to do is put a big enough spanner in the works of those population dynamics and energy balance models and the system will eventually grind to a halt.
Research has failed to to find 'the cause' of bee decline or the more dramatic 'colony collapse disorder'. It has however turned up a worrying array of suspects, with the triumvirate of Varroa, Nosema ceranae and assorted viruses always in the background. Absence of Varroa is likely the saving factor in Australia because we seem to have all the others. Brood combs in the USA are laden with residues of varroicides, pesticides, herbicides and fungicides, some at barely sub-lethal doses. Fungicides in particular seem to be a much bigger threat than was formerly thought (and that is another story) while varroicides are universal and only slightly less toxic to bees than to Varroa. Without Varroa treatments the colonies would likely fail anyway, going fromn thriving to collapsing over the course of about four years. What are apparently 'normal' bees are often found to be carrying unusually high virus or Nosema loads. Meanwhile, monocultures of crops and the destruction of agricultural 'weeds' mean that bees may not be getting the variety of pollen they need to ensure healthy brood growth and fat, long-lived bees. Pervasive sub-lethal exposure to 'safer' pesticides chips away at the margins.
My crystal ball is no better than anyone else's, but this is not a pretty story and has many routes to a sad ending. The nub of it is, whether or not something actually emerges as a 'cause', there are plenty of other and subtler ways to achieve disaster. Fortunately there are at least a few ways to help avoid it. Experience in the rest of the world shows that well-managed bees continue to cope. That appears to mean controlling serious conditions like Varroa and Nosema ceranae, managing brood diseases and making sure bees are well-fed, particularly when the colony is growing and when winter bees are developing, with protein being the critical factor. Sugar fuels bees, it does not grow them. We do not have Varroa yet and should make every effort to keep things that way. Unfortunately we do have Nosema ceranae. To my knowledge, nobody here actively assesses Nosema loads or treats for it (methods used overseas would not currently be legal), and it could be insidiously spreading and eroding away at colony health in preparation for the arrival of Varroa as the main event. As a final comment, there has also been a great decline in beekeepers over Europe and North America.
Amateur and small-scale beekeepers report the highest colony losses and commonly throw in the towel. Professional beekeepers – those that do not go bust - learn how to cope. Time for us all to brush up our skills.
Chris Strudwick, VAA Member, Email: firstname.lastname@example.org
Neonicotinoid pesticides have been in the news again, as usual not in a good way. I have seen some confusion in how this news has been interpreted and there is still some confusion over what the issues actually are. Before I get into the details, I should say that I am not yet taking sides on the pro/anti neonicotinoid argument. As a beekeeper I am no fan of agricultural pesticides as I have never come across one that does bees any good. We have to accept there is a place for pesticides in modern agriculture, like it or not, but we must keep a close eye on how and why they are used, as well as their impacts on the environment and on consumers of agricultural products. No question that pesticides are potentially harmful to bees and that the latest generation of neonicotinoids in particular are exceptionally toxic in miniscule quantities. The current debate as to whether neonicotinoid pesticides are actually responsible for the global decline of honeybees and Colony Collapse Disorder is quite another matter. Opinions are running thick and fast but hard evidence is still thin on the ground.
The debate is confusing because it conflates a number of issues. In particular, the acute effects of neonicotinoid toxicity are lumped together with the more subtle effects of sub-acute exposure. Mass die-offs of bees in Canada, France and Italy are the result of acute toxicity - bees directly poisoned from exposure to lethal doses of insecticide. Some of these instances are clearly down to neonicotinoids. This however is not what is concerning some researchers, after all we know that insecticides are designed to kill insects and neonicotinoids are very good at it. The researchers are more concerned that tiny doses of neonicotinoids that do not immediately kill the bees may cause behavioural disturbances, or reduce the viability of the colony through some mechanism, that will eventually lead to the colony failing. This does not involve a dramatic die-off of bees, just a terminal dwindling of bee colonies. There is good evidence now that these subtle effects can occur (and not just in honeybees), but there is argument as to whether the laboratory experiments really translate to what happens in the outside world. For instance, the experiments artificially feed the affected insects with different mixtures of sugar syrup and insecticide. Are the insects really taking in similar amounts of insecticide to those they would consume in reality? Is direct consumption the same as exposure to dust or pollen? The calculation of so-called ‘field-realistic’ dosages is a hot topic, and is just one of the parameters under question (1).
It is probably worth taking a step back and looking at how neonicotinoids are actually used. There are a number of related products and these have become increasingly effective as each new generation is developed. If you use ant baits you are exploiting the power of a substance such as fipronil, a close relative of the neonicotinoids, to be carried back to the colony and spread through it by the ants’ social behaviour, such as sharing of food. This kills the whole colony and not just the individual ant that takes the bait. It is a powerful attack on social insects such as wasps and termites and also semi-social insects such as cockroaches. By a twist of fate, it may yet prove our best weapon to stem the spread of Apis ceranae, the Asian Honeybee.
Neonicotinoids are also used in the same way as other common insecticides, for instance directly sprayed to protect blooming sunflower crops in France (2). This led to a number of incidents where honeybees were poisoned and caused an outcry against neonicotinoids in France, where some beekeepers also associated these chemicals with increased Winter mortality. While neonicotinoids will kill bees at tiny dosages, in essence this is no different to the countless poisonings of bees with other misapplied insecticides that have happened since insecticides were invented. The most valuable use of these new insecticides is as a ‘systemic’. When applied to seed as a dressing, sufficient insecticide is taken up by the growing plant to make it toxic to pests that consume it or suck its sap. These routes provide little direct threat to bees but the story does not end here. The first problem comes when the seed is sown. Seed is coated with neonicotinoid insecticide and talc, and insecticide is present in the dust that is created during sowing. Each gram of dust has the potential to kill hundreds of thousands of bees (3). Any bees flying through it while foraging, or that come into contact with dust settling downwind on forage plants, may receive high and lethal dosages. In 2011 1nd 2012 there were hundreds of reported cases of acute poisonings in a 200km radius of Ontario in Canada, believed due to this cause (4). A high percentage of dead bees sampled showed the presence of neonicotinoids, although this was not definitively the lethal agent. Such poisonings are accidental and obvious, but again the story continues.
Plants protected by systemic insecticides may transfer these substances into their nectar and pollen and also into ‘guttation droplets’, basically water droplets exuded onto the leaves at night. Bees may tap into any of these plant products and pick up traces of insecticides that are too small to be directly lethal. Such exposure may still affect the health and behaviour of individual bee. The toxin might also be brought back to the hive, perhaps in nectar or pollen, and spread through the colony’s food supply and via food-sharing behaviour. This is one of the primary areas of concern. Nobody yet knows whether the amounts involved are reliably small enough not to be causing problems – bees, like us, are constantly dealing with low levels of toxins from their environment – or whether something quietly sinister is happening.
This is not just a ‘bee problem’. Recent reports show a common fungicide to be highly lethal to frogs at ‘normal application levels’ (5). The manufacturer admits the toxicity of the product to frogs but claims the tests are not representative of field conditions and that frogs would never naturally be exposed in this way. Both views could be correct, but the example highlights that interpretation depends on just how well we can identify, quantify and verify the chain of risks.
This is exactly the problem at the heart of the recent announcement by the European Food Safety Authority (EFSA) that advises policy makers on issues of food safety, including regarding the regulation of pesticide use in food crops. Their announcement on Jan 16 th, entitled: EFSA identifies risks to bees from neonicotinoids (6) caused a stir. A good example is the current Avaaz campaign which is no doubt well-meant but seemingly based on misinterpretation (7). Unfortunately the title of the EFSA press release is very misleading as the statement in no way vindicates the argument for neonicotinoids being the cause of all our troubles. EFSA is responsible for doing risk assessments to help support decisions. What they are saying is, they did an absolutely terrible job of identifying and assessing the risks around this class of pesticides 8. No surprise to me. My experience is that even clever people are pathologically bad at assessing environmental risks.
Further, the evidence on which the assessments were based was incomplete in some fundamental respects, to the point where there was no way the risks could properly be quantified. My reading of the background studies shows holes in the process and available information rather than something critically dangerous being ignored or omitted. A prime example is not having enough data to say authoritatively how much build-up there is in the soil after repeated applications. The whole assessment process leaves me uncomfortable about how these analyses are conducted. I have no doubt it would all have passed under the radar if public interest in neonicotinoids as a possible cause of bee decline had not emerged and caused a fuss. Senior bureaucrats have been deeply embarrassed and no doubt more junior heads will roll. Will we learn some lessons? Well, perhaps but I am not betting on it.
Whatever the causes – pesticides, climate change, habitat destruction, human population growth, industrialisation of agriculture – it is not just honeybees that are in trouble. Many insects are disappearing (and the birds that depend on them), some of which are important pollinators of food crops and other plants and others that are just our fellow-travellers in life, and no less valuable for that. They are very hard to bring back once they are gone. I wonder just how much notice we would have taken had our bees not been affected.
The references below are not necessarily the original sources but have been chosen because they are freely available on-line, written in English, offer some interpretation, and include the primary sources in their own reference lists.1. European Food Safety Authority 2012, Statement on the findings in recent studies investigating sub-lethal effects in bees of some neonicotinoids in consideration of the uses currently authorised in Europe, EFSA Journal 2012;10(6):2752, accessed at http://www.efsa.europa.eu/en/efsajournal/doc/2752.pdf
2. L Maxim and J P van der Sluijs 2010, Expert explanations of honeybee losses in areas of extensive agriculture in France: Gaucho ® compared with other supposed causal factors, Environ. Res. Lett. 5 014006, accessed at http://iopscience.iop.org/1748-9326/5/1/014006/
a. Fabio Sgolastra, Teresa Renzi, Stefano Draghetti, Piotr Medrzycki, Marco Lodesani, Stefano Maini, Claudio Porrini 2012, Effects of neonicotinoid dust from maize seed-dressing on honey bees, Bulletin of Insectology 65 (2): pp. 273-280, accessed at http://www.bulletinofinsectology.org/pdfarticles/vol65-2012-273-280sgolastra.pdfb. 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 accessed atc. Purdue University News Service, Jan 11 th 2012, Researchers: Honeybee deaths linked to seed insecticide exposure, accessed at
4. Toronto Sun, June 8 th 2012, Beekeepers blame pesticides for bee deaths, accessed at5. The Guardian Jan 24 th 2013, Common pesticides 'can kill frogs within an hour' accessed at6. European Food Safety Authority Press Release, Jan 16 th 2013, EFSA identifies risks to bees from neonicotinoids, accessed from8. European Food Safety Authority 2012, Scientific Opinion on the science behind the development of a risk assessment of Plant Protection Products on bees (Apis mellifera, Bombus spp. and solitary bees), EFSA Journal 2012;10(5):2668, accessed fromChris Strudwick, VAA Member, Email: email@example.com
It was a busy month for those following the neonicotinoid pesticide story. The media, and various other groups keen for attention, have got excited over the story of a 'ban' imposed by the EU while deeper and more important stories, as usual, have been overlooked. Level heads were in short supply, with Trevor Weatherhead from AHBIC, interviewed on Radio National, being a refreshing exception.
Brushing aside the commentary cluttering the media, here is a summary of the story so far. After coming under pressure following public concern over bee deaths, the European Food Safety Authority (EFSA) has revised its earlier findings on three neonicotinoid pesticides which they previously judged to meet safety standards. Some critical assessment information was found to be incomplete and a moratorium – not a 'ban' – has been approved by the EU regarding use on crops that are attractive to bees, in practice sunflowers and oilseed rape (canola) 1. The moratorium will last until the necessary information is supplied, which must be within the next two years. Meanwhile, the moratorium is not binding and not all EU members may choose to adopt it. I am not convinced this is the same as the story that is being presented to us in the press and elsewhere. Certainly it is a bit less of an environmental triumph and a bit more of a bureaucratic adjustment.
EFSA's job is to provide risk assessments which can be used by other bodies to inform policy decisions. EFSA makes no decisions itself nor provides definitive advice. It does not conduct research, nor does it set or enforce standards. If you are starting to wonder what it does do, its purpose is to evaluate the evidence – mostly supplied by the manufacturer – submitted in this case in support of an application to register a pesticide, that a product meets the required standards while taking the broader scientific picture into account. Despite the importance to all of us of in doing these assessments well, it transpires that EFSA is under-resourced to deal with complex submissions, has little direct power, and its advice is treated as guidance only. Is that a story?
In the case of the three neonicotinoids in question there were several problems. Firstly, some of the required evidence was incomplete and the relevant assessment 'boxes' could not be 'ticked', including those for safety of bees collecting nectar and pollen from treated crops. This does not mean those crops are definitely unsafe for bees to forage, just that the evidence is not good enough to make an informed safety assessment. Consequently, permitting the use of these pesticides against an incomplete risk analysis was a significant failure in an important process and an abuse of public trust. That is one major missed story. The second issue is that the standards applied were inappropriate for the class of pesticides under assessment. Regulation struggles to keep up with advances in science. The systemic mode of action and the extremely small dosages needed to produce a toxic effect were a poor fit to a framework designed for previous generations of pesticides 2. In other words, even meeting the required measures would not provide the intended guarantee of safety. For me, that is another really important story.
There is yet another story, perhaps more of a back-story, that is of particular concern. This time it is not to do with EFSA but with changing agricultural practices and perceptions. Because systemic insecticides are often applied with seed on sowing and continue to work during the life of the crop, and possibly longer via soil residues that can be taken up by subsequent crops, farmers are now using them less as treatments and more as insurance. The cost of the pesticide is offset against the likely financial loss should the crop be attacked. Although neonicotinoids are rather expensive, their effectiveness means that only small quantities are needed. Farmers can treat their seed and then avoid doing much in the way of subsequent treatments, all without having to closely monitor their crops. The result is that crops are often treated whether they are threatened or not. Studies in Italy 3 often showed little difference in crop yields in treated and untreated maize, presumably because some of the measurements were made in years and localities where pests were not prevalent. It demonstrates how farmers are willing to take the treatment costs regardless in order to provide some extra security. This is also a much simpler proposition than applying integrated pest management.
Farmers are not out to massacre bees and other pollinators, it would be counter-productive for them to do so. The use of conventional pesticides presents hazards to non-target species including many beneficial insects, and these are disappearing at an alarming rate. Pesticides are nasty things and conventional spraying requires vastly larger quantities of chemicals to be applied, where they drift in the air, pollute water and accumulate in soil. Wax comb from beehives often captures a toxic record of historic pesticide applications. On the face of it, neonicotinoids seem to be an improvement. Small quantities can be used, they are specifically applied to the target crop and only pests attacking that crop were thought to be at risk. Reality turns out to be more complex but environmentally there is merit in the approach. However, the routine use of these highly toxic chemicals as insurance is disturbing. If misused or overused they are likely to be exceptionally harmful 4. They need to be applied much more thoughtfully, for instance when there is a high likelihood of pest attack in the growing season. Pest management strategies are necessary to farmers and beekeepers and environmentalists must engage with farmers to develop better ones.
As a final word, neonicotinoids are present in a number of garden pesticides at quite high concentrations. These tend to be used far less carefully and are under much less scrutiny than their agricultural equivalents. If this class of pesticides should be considered for banning, these garden products are a really good place to start as they are much less valuable 'protecting' our lawns and golf-courses than protecting our crops. Is that another neglected story?
European Commission press release, Brussels, 29 th April 2013 http://europa.eu/rapid/press-release_IP-13-379_en.pdf
Maxim, L., & Van der sluis, J. (2013). Late lessons from early warnings: science, precaution, innovation. Chapter 16: Some emerging issues | Seed-dressing systemic insecticides and honeybees.EEA Report No.1/2013: http://www.eea.europa.eu/publications/late-lessons-2/late-lessons-chapters/late-lessons-ii-chapter-16ApeNet. (2011). Effects of coated maize seed on honey bees - Report based on results obtained from the second year (2010) activity of the APENET project. Evaluation (pp. 1–100).
Dijk, T. C. Van, Staalduinen, M. A. Van, & Sluijs, J. P. Van Der. (2013). Macro-Invertebrate Decline in Surface Water Polluted with Imidacloprid. PLoS ONE, 8 (5), 1–10. doi:10.1371/journal.pone.0062374
Chris Strudwick, VAA Member, Email: firstname.lastname@example.org