Insecticides and CCD, Part I
Bee Culture (July) Vol. 136 (7): 17-18
By
Dr. Malcolm T. Sanford
With the recent flap about CCD, insecticides have inevitably been identified as one of the possible causes of larger-than-normal bee loss. The history of the relationship between beekeeping and insecticide application goes back a long way. In the 1950s it took some sleuthing to finally figure out that arsenic dust was being collected by bees in the field as pollen to both their and their colony’s detriment. Given the advantages of hindsight, who now could possibly argue that dusting with this extremely toxic substance does not affect honey bees. This even includes the active material in treated wood.1 Another situation arose with the use of microencapsulated pesticides in the 1970s, especially a product called PennCap-M®.2 The capsules acted like pollen grains and were a time bomb in colonies, because they could be brought back without harm to the forager, only became a problem when consumed by young bees in an effort to feed larvae.
Insecticides were such a problem to beekeepers in the late1970s that congress authorized the beekeeper indemnity program, which provided payments to beekeepers from colonies lost to chemical application in both agricultural and urban (mosquito control) situations.3 However, this program became unwieldy because it was difficult to tell the difference between legitimate and falsely reported claims, and was finally discontinued. This era brought into use the current information on the effects of pesticides on honey bees, pioneered by Dr. Larry Atkins at the University of California, Riverside for which most extension publications continue to draw their information.4 This was based on topical exposure to workers in small cages (LD50), however, there is evidence that bees may be exposed through other routes, including contaminated nectar, and that measurement of toxicity (LC50) might be significantly different.5 In Florida, this became a hot issue with a material called Temk® used in citrus groves.6 The active ingredient in this material, aldicarb, is a systemic insecticide and was thought to translocate into the blooms contaminating nectar. And although the active ingredient is certainly harmful to honey bees, there is evidence that the metabolites (break down products) of this material may even be more toxic than the parent substance.
The use of pesticides inside colonies to control Varroa mites inevitably brought more direct exposure to chemical pesticides. The candidates used to control Varroa mites on any scale also became more toxic as time went on. Treatments began with the rather benign fluvalinate, a synthetic pyrethroid, (Mavrik®) first soaked into wooden strips with an “emergency” Section 18 label,10 quickly replaced by a formulation on a plastic strip (Apistan®) with a broader use (Section 3) label. Beekeepers got 10 years use out of this material until mites became generally resistant due to lack of resistance management in many cases.11
The next material to receive a label was called Bayer Bee Strips®, later formulated as CheckMite +®. The active ingredient is coumaphos in the class of pesticides known as organophosphates. When this material first became available, I wrote the following, “Coumaphos is in a class of highly toxic materials known as organophosphates (OPs). It is a cholinesterase inhibitor, which attacks the nervous system. Developments of this insecticide type were associated with German studies on related compounds, the so-called "nerve gases" (sarin, soman and tabun). Suffice it to say OPs are among the most toxic of insecticides. The LD50 of coumaphos for absorption through the skin (dermal), for example, is 860 milligrams per kilogram of body weight in rats. It is, therefore, much less benign than fluvalinate, the active ingredient in Apistan®, a synthetic pyrethroid, with a dermal LD50 in rats of 20,000 milligrams per kilogram of body weight.12 Organophosphates are the basis of many commonly used insecticides (malathion, Diazinon®, parathion, Dibrom®).”13
In localized areas coumaphos resistance has already shown up in Varroa. This leaves beekeepers with no other hard pesticides at present that are as effective controls, the so-called “magic bullets” of Varroa mite control. Thus, so-called “soft” pesticides like formic and oxalic acids and essential oils (thymol based Apiguard® and Api-Life Var®) are being scrutinized. These, in combination with other techniques such as open bottom boards, drone trapping, the sugar shake and breeding (Russian bees and Varroa-sensitive hygienic stock), are leading the beekeeping community into a more integrated control technology for Varroa mites. However, even the soft chemicals can be hard on bees, and cannot be discounted when it comes to additive effects of chemicals on colonies already under stress by increased manipulation and management
The above discussion was to provide
In a way, the beekeeping experience has mirrored other production agriculture, which also continues to search for effective insecticides as more and more resistance by pests (insects) emerges. Fortunately a new tool has emerged that appears to have incredible promise. Predictably it is another class of pesticides, the neonicotinoids.
In a review of this subject, Motohiro Tomizawa and John E. Casida state, “The neonicotinoids are the most important new class of synthetic insecticides of the past three decades. Although related to nicotine in action, and partially in structure, the neonicotinoids originated instead from screening novel synthetic chemicals to discover a lead compound. Once optimized to imidacloprid (IMI) and analogs, the neonicotinoids joined the earlier chlorinated hydrocarbons, organophosphorus compounds, methylcarbamates, and pyrethroids to constitute the five principal types of active ingredients, all of which are neuroactive insecticides.
“Neonicotinoids are increasingly used for systemic control of plant-sucking insects, replacing the organophosphorus compounds and methylcarbamates, which have decreased effectiveness because of resistance or increased restrictions due to toxicological considerations. Neonicotinoids are also important in animal health care (i.e. flea control). These developments were possible because of the selective toxicity of the neonicotinoids, which is attributable to the specificity of insect and mammalian nicotinic receptors as reviewed here. Neonicotinoids are more toxic to aphids, leafhoppers, and other sensitive insects than to mammals. The physicochemical properties of the neonicotinoids played an important role in their development. The principal target pests are aphids, leafhoppers, whiteflies, and other sucking insects due to the excellent plant-mobile (systemic) property conferred by the moderate water solubility.”
“About 90% of the synthetic organic insecticides and acaricides, by market share, are nerve poisons acting on only four targets: acetylcholinesterase (AChE) for organophosphorus compounds and methylcarbamates, the voltage-dependent sodium ion channel for DDT and pyrethroids, nAChR for the botanical nicotine and most recently synthetic neonicotinoids, and the γ-aminobutyric acid (GABA)-gated chloride channel for polychlorocycloalkanes and fipronil. From 1987 to 1997, the use of compounds acting at the cholinergic nAChR shifted from sixth to third in overall ranking, in the most part replacing AChE inhibitors, and this trend is expected to continue.
“The long-term future of neonicotinoids will depend on continued evidence for the human and environmental safety of current compounds, including low toxicity to predators, parasites, and pollinators, no adverse environmental distribution, and fate. It will be enhanced by the discovery of new compounds with a broader spectrum of useful properties including control of lepidopterous larvae and pest strains resistant to earlier analogs. These biological features must be combined with suitable hydrophilicity for transport in plants, hydrophobicity for contact activity, and photostability for residual efficacy. Much has been learned about neonicotinoids in the first decade of their use and about the nicotinic receptor as a target for selective toxicity between insects and mammals. The benefits of neonicotinoids in crop protection and animal health can be enjoyed for many decades ahead with attention to their proper use in pest management systems that delay or circumvent the development of resistance in pest insects.”
I have purposefully left intact the quotes above so readers can begin to understand some of the complexity of insecticides in general and neonicotinoids in specifics. Nevertheless, it is worth summarizing some of points made:
1. The reference material for neonicotinoids is imidacloprid (many products will have this as the active ingredient).
2. The benefits of the neonicotinoids include:
A. High toxicity to insects (especially sucking
insects like aphids, leafhoppers, fleas) and low toxicity to mammals (humans,
dogs, cats)
B. Water solubility so that
plants can use the materials in their vascular systems (systemic insecticides)
C. Different than other classes meaning insects
will have to start over in developing resistance so they should be effective
for a long period.
3. A 15% world market share and third ranking for the neonicotinoids by 2005 appears to be continuing”
Just how ubiquitous these products are becomes clear from one post to the Bee-L discussion list: “Imidacloprid is found in granules for controlling lawn grubs, liquid for tree and shrub pest control, and even in some potting soil mixes and fertilizers. Available at every Walmart in the country, I bet!”
In the southeast, we look to imidacloprid as truly a “miracle” substance for relief from one the region’s most irritating insects for humans and their pets. A pest control conference participant in a seminar confirmed for me that “flea jobs” had disappeared in the 1990s.
References:
1.<http://pubs.acs.org/cgi-bin/abstract.cgi/jafcau/1984/32/i05/f-pdf/f_jf00125a060.pdf?sessid=6006l3>
2. <http://www.canr.uconn.edu/ces/ctpep/ct_bee.html>
4. <http://en.wikipedia.org/wiki/Pesticide_toxicity_to_bees>
5. <http://apis.ifas.ufl.edu/apis86/apjun86.htm#2>
6. <http://apis.ifas.ufl.edu/apis88/apjan88.htm#2>
7. <http://apis.ifas.ufl.edu/apis87/apdec87.htm#1>
8. <http://apis.ifas.ufl.edu/apis88/apmay88.htm#2>
9. <http://apis.ifas.ufl.edu/apis96/apaug96.htm#1>
10. <http://apis.ifas.ufl.edu/apis92/apapr92.htm#4>
11. <http://apis.ifas.ufl.edu/apis99/apfeb99.htm#1>
12. <http://ace.orst.edu/info/extoxnet/pips/fluvalin.htm>
13. <http://apis.ifas.ufl.edu/apis99/apjan99.htm#1>
14. Motohiro Tomizawa and John E. Casida. 2003 Selectivity Toxicity or Neonicotinoids Attributable to Specificity of Insect and Mammalian Nicotinic Receptors, Annual Review of Entomology, Vol. 48: 339-364