page_title: Colony collapse disorder
section_title: Pesticides
hierarchical_section_title: Colony collapse disorder / Possible causes / Pesticides
caption_attribution_description: English: Imidacloprid map of use, USA, 2012 (estimated) Deutsch: Geschätzte ausgebrachte Imidaclopridmenge in den USA 2012
context_page_description: Colony collapse disorder is an abnormal phenomenon that occurs when the majority of worker bees in a honey bee colony disappear, leaving behind a queen, plenty of food, and a few nurse bees to care for the remaining immature bees. While such disappearances have occurred sporadically throughout the history of apiculture, and have been known by various names, the syndrome was renamed colony collapse disorder in late 2006 in conjunction with a drastic rise in reports of disappearances of western honey bee colonies in North America. Beekeepers in most European countries have observed a similar phenomenon since 1998, especially in Southern and Western Europe; the Northern Ireland Assembly received reports of a decline greater than 50%. The phenomenon became more global when it affected some Asian and African countries as well.
  Colony collapse disorder causes significant economic losses because many agricultural crops worldwide depend on pollination by western honey bees.
context_section_description: According to the USDA, pesticides may be contributing to CCD. A 2013 peer-reviewed literature review concluded neonicotinoids in the amounts typically used harm bees and safer alternatives are urgently needed. At the same time, other sources suggest the evidence is not conclusive, and that clarity regarding the facts is hampered by the role played by various issue advocates and lobby groups.
  Scientists have long been concerned that pesticides, including possibly some fungicides, may have sublethal effects on bees, not killing them outright, but instead impairing their development and behavior. Of special interest is the class of insecticides called neonicotinoids, which contain the active ingredient imidacloprid, and other similar chemicals, such as clothianidin and thiamethoxam. Honey bees may be affected by such chemicals when they are used as a seed treatment because they are known to work their way through the plant up into the flowers and leave residues in the nectar. The containment of neonicotinoids to crops and fields designated for treatment is difficult, and many times inefficient. Run-off from treated fields and farm machinery that is not properly cleaned after field treatments can lead to exposure and uptake of pesticides by untreated plants. Therefore, honey bees are not only exposed to neonicotinoids by foraging on treated plants, but also by foraging on plants unintentionally exposed to these chemicals. The doses taken up by bees are not lethal, but possible chronic problems could be caused by long-term exposure. In a laboratory setting, both lethal and sub-lethal effects on foraging behavior, memory, and learning ability have been observed in honey bees exposed to neonicotinoids. However, these effects were not seen in field studies with field-realistic dosages. Most corn grown in the US is treated with neonicotinoids, and a 2012 study found high levels of clothianidin in pneumatic planter exhaust. In the study, the insecticide was present in the soil of unplanted fields near those planted with corn and on dandelions growing near those fields. Another 2012 study also found clothianidin and imidacloprid in the exhaust of pneumatic seeding equipment.
  A 2010 survey reported 98 pesticides and metabolites detected in aggregate concentrations up to 214 ppm in bee pollen; this figure represents over half of the individual pesticide incidences ever reported for apiaries. It was suggested that "while exposure to many of these neurotoxicants elicits acute and sublethal reductions in honey bee fitness, the effects of these materials in combinations and their direct association with CCD or declining bee health remains to be determined."
  Evaluating pesticide contributions to CCD is particularly difficult for several reasons. First, the variety of pesticides in use in the different areas reporting CCD makes it difficult to test for all possible pesticides simultaneously. Second, many commercial beekeeping operations are mobile, transporting hives over large geographic distances over the course of a season, potentially exposing the colonies to different pesticides at each location. Third, the bees themselves place pollen and honey into long-term storage, effectively meaning a delay may occur from days to months before contaminated provisions are fed to the colony, negating any attempts to associate the appearance of symptoms with the actual time when exposure to pesticides occurred.
  To date, most of the evaluation of possible roles of pesticides in CCD have relied on the use of surveys submitted by beekeepers, but direct testing of samples from affected colonies seems likely to be needed, especially given the possible role of systemic insecticides such as the neonicotinoid imidacloprid (which are applied to the soil and taken up into the plant's tissues, including pollen and nectar), which may be applied to a crop when the beekeeper is not present. The known effects of imidacloprid on insects, including honey bees, are consistent with the symptoms of CCD; for example, the effects of imidacloprid on termites include appa
caption: Imidacloprid map of use, US, 2012 (estimated)
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