causality, colony collapse disorder, complexity, controversy, neonicotinoids, pathology, pesticides, precautionary principle, standards of proof
The phrase ‘colony collapse disorder’ was first used in 2006 to refer to the phenomenon of dramatic, large scale and unexplained disappearances of commercial bee colonies, initially in Florida and California. Superseding the earlier term ‘Fall Dwindle Disease’, it was said to be distinguished from the periodic winter losses that are a normal hazard of beekeeping by a number of characteristics: firstly the sheer suddenness of the collapse – with large and apparently thriving colonies sometimes disappearing almost overnight; also by the presence of significant stores of honey remaining in the hive – ruling out lack of food supplies as a cause of the sudden evacuation; and by the absence of obvious invaders such as other bees, wax moths or beetles taking advantage of the empty hive to consume the honey. It was also associated with an almost complete absence of the bee carcasses that would normally be found within the hive and littered around the entrance to collapsed colonies. These features combined to create the sense that this was something new, never before encountered; hence ‘colony collapse disorder’ was born.
After some initial scepticism about early reports, the scale of colony losses across 22 states by the spring of 2007 had given credence to the idea that ‘CCD’ was real, and it began making headlines worldwide. In the context of a dawning awareness and rising alarm at the potential impact on food production and the agricultural economy if the rapid rate of colony losses continued, the first scientific research attempting to identify the cause of CCD began in 2007, initially at Penn State University in collaboration with the US Department of Agriculture research service. The most promising candidates for a cause included the widespread use of relatively new ‘neonicotinoid’ pesticides, which were believed by many to detrimentally affect the apian nervous system; the apparently unstoppable progress of parasites such as the parasitic Varroa mite and associated viruses such as nosema infection and Israeli Acute Paralysis Virus, introduced into vulnerable honeybee populations by the under-regulated transcontinental trade in honeybees; loss of genetic diversity due to poor breeding practices favoured by some commercial breeders; the unintended consequences of GM crops in weakening bee immune systems; over-intensive exploitation of honeybees in monocultural commercial pollination, leading to intolerable migratory stresses on that species and the crowding out of native pollinators; the increasing frequency of unseasonal weather associated with climate change, which is known to affect the reproductive and foraging cycles of bee colonies; and changing landscapes involving the loss of areas of diverse flora such as wildflower meadows that play such a vital role in sustaining native bee populations.
Despite ongoing investigations at numerous institutions, none of these has yet emerged as an entirely convincing candidate for a sole causal explanation, with multiple factors present in all cases examined and no single factor present in every case. It therefore seems increasingly likely that the phenomenon known as CCD is a hybrid or multiple rather than singular phenomenon, with several factors potentially interacting in complex ways. The absence of a single authoritative explanation has frustrated the search for the sort of relatively simple ‘single bullet’ solution sought by policymakers. To use other environmental crises for comparison, CCD is proving to be rather like climate change – a complex multi-causal problem requiring fundamental changes in social and material organisation.
Reports of dramatic honeybee losses across the world were soon being linked to ‘CCD’, in Canada, Taiwan, Spain, Portugal, Italy, France, Poland, Austria, Belgium, Holland, Croatia, and the UK. This was despite the insistence of some national governments that the bee losses in their country were not further manifestations of CCD, with its implication of a systemic and worldwide honeybee collapse, but were in fact unconnected contingent events. From a strictly analytical point of view this is not entirely unreasonable, given the difficulty of strictly distinguishing between ‘normal’ winter losses and CCD, not to mention the doubt as to whether ‘CCD’ is a singular phenomenon at all. But in practice this stance has often legitimised a political reluctance to significantly increase funding for research that might improve understanding of the factors contributing to the wider and longer-term pollinator decline, the occurrence of which is undisputed. Ironically the cautious scepticism of many pathologists and other experts – the very people in need of greater funding in order to more adequately address the problem – as to the existence of ‘CCD’ as a unitary phenomenon distinct from previous cycles of colony losses, has sometimes tended to shore up this political position.
In contrast, other parties to the debate, including many beekeepers whose livelihoods are under threat from colony collapse, have been convinced for some time on the basis of their lived experience and a wealth of anecdotal evidence not only that CCD is real, but that neonicotinoid pesticides are centrally to blame, and (particularly in France) many have campaigned vigorously for years alongside a range of environmental groups to have these chemicals banned. Meanwhile the big pesticide manufacturers whose profits rely upon routine agricultural use of their products have lobbied intensively against this, and have funded research designed to exonerate neonicotinoids under the guise of researching the causes of CCD. In this way the debate about CCD has become an intensely political and economic battleground rather than simply an arena of disinterested scientific investigation.
The beekeepers and anti-pesticide campaigners secured a significant victory in April 2013 when the EU banned the use of neonicotinoids for two years in member states. The rationale for the temporary ban was that it would provide breathing space for further investigations into CCD, including studies of the effect of neonicotinoids upon bee brains and nervous systems, as well as making it possible to observe the impact upon the bee population of eliminating these pesticides from the environment for the stipulated period. There are many doubts about the adequacy of the ban, especially given that it proscribes just 3 major neonicotinoid products – clothianidin, imidacloprid and thaimetoxam – when recent pollen studies suggest that bees are exposed to a whole ‘toxic soup’ of as many as 35 different chemicals, the synergistic and long term effects of which are not well understood. Nonetheless, by imposing the ban the EU significantly deployed the ‘precautionary principle’, according to which, if there is reason to suspect that a substance is causing significant harm to to health and/or the environment, then use of that substance is halted until its safety can be established beyond doubt.
This is in direct contrast to the ‘innocent until proven guilty’ approach that has been urged on governments by the pesticide companies, and which notably has been adopted by the UK government, which opposes the ban, with a DEFRA report published in March 2013 disputing the methodologies used in a number of studies that have shown detrimental effects upon bees of even sub-lethal doses of neonicotinoids. According to DEFRA’s approach, a substance should not be withdrawn from use – with the accompanying financial consequences for the manufacturer – merely on the basis of reasonable suspicion, but only when its harmfulness has been established beyond all doubt, something which the companies concerned will use all of their lobbying power to prevent or delay.
In either case, the question of what the appropriate standard of proof should be in the context of complex interactions between multiple causes becomes a political issue, with critics on all sides always able to use the absence of a single direct cause-and-effect relation or ‘smoking gun’ to create sufficient doubt to allow them to press their case. And with the evidence pointing to neonicotinoids as a sole or primary cause continuing to be less than decisive, unless there is a serious breakthrough in the next two years it seems inevitable that this debate will be revisited and that it will continue to be contested ferociously.
© Richie Nimmo 2013.