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Sunflower and corn seed treatments of the active ingredient imidacloprid are suspended in France; other imidacloprid seed treatments, such as for sugar beets and cereals, are allowed, as are foliar uses.<ref name="epa_a" />
Sunflower and corn seed treatments of the active ingredient imidacloprid are suspended in France; other imidacloprid seed treatments, such as for sugar beets and cereals, are allowed, as are foliar uses.<ref name="epa_a" />

==Health effects on birds, aquatic invertebrates, and other wildlife==

In March 2013, the [[American Bird Conservancy]] published a review of 200 studies on neonicotinoids including industry research obtained through the US Freedom of Information Act, calling for a ban on neonicotinoid use as seed treatments because of their toxicity to birds, aquatic invertebrates, and other wildlife.<ref>{{cite web|title=The Impact of the Nation’s Most Widely Used Insecticides on Birds|url=http://www.abcbirds.org/abcprograms/policy/toxins/Neonic_FINAL.pdf|work=Neonicotinoid Insecticides and Birds|publisher=American Bird Conservancy|accessdate=19 March 2013|author=Pierre Mineau|coauthors=Cynthia Palmer|date=March 2013}}</ref>


==Health impact==
==Health impact==

Revision as of 17:58, 28 April 2013

Neonicotinoids are a class of neuro-active insecticides chemically related to nicotine. The development of this class of insecticides began with work in the 1980s by Shell and the 1990s by Bayer.[1] The neonicotinoids were developed in large part because they show reduced toxicity compared to previously used organophosphate and carbamate insecticides. Most neonicotinoids show much lower toxicity in mammals than insects, but some breakdown products are toxic.[2] Neonicotinoids are the first new class of insecticides introduced in the last 50 years, and the neonicotinoid imidacloprid is currently the most widely used insecticide in the world.[3]

Recently, the use of some members of this class has been restricted in some countries due to evidence of a connection to honey-bee colony collapse disorder.[4][5] In January 2013, the European Food Safety Authority stated that neonicotinoids pose an unacceptably high risk to bees, and that the industry-sponsored science upon which regulatory agencies' claims of safety have relied may be flawed.

In March 2013, the American Bird Conservancy published a review of 200 studies on neonicotinoids including industry research obtained through the US Freedom of Information Act, calling for a ban on neonicotinoid use as seed treatments because of their toxicity to birds, aquatic invertebrates, and other wildlife.[6] Also in March 2013, the US EPA was sued by a coalition of beekeepers, conservation and sustainable agriculture advocates who accused the agency of performing inadequate toxicity evaluations and allowing the pesticides' registration to stand on insufficient industry studies.[7]

Mode of action

Neonicotinoids, like nicotine, are nicotinic acetylcholine receptor agonists. This receptor is normally activated by the neurotransmitter acetylcholine. These receptors are located in both the central and peripheral nervous systems of mammals but are limited to the CNS in insects. While low to moderate activation of these receptors causes nervous stimulation, high levels overstimulate and block the receptors.[3][8] This receptor blockage causes paralysis and death. Normally, acetylcholine is broken down by acetylcholinesterase to terminate signals from these receptors. However, acetylcholinesterase cannot break down neonicotinoids, and the binding is irreversible.[8] Because most neonicotinoids bind much more strongly to insect neuron receptors than to mammal neuron receptors, these insecticides are selectively more toxic to insects than mammals.[9]

Basis of selectivity

R-nicotine
Desnitro-imidacloprid
R-nicotine (top) and desnitro-imidacloprid are both protonated in the body

Most neonicotinoids, such as imidacloprid, show low affinity for mammalian nicotinic acetylcholine receptors (nAChRs) while exhibiting high affinity for insect nAChRs.[3][10] Mammals and insects have structural differences in nAChRs that affect how strongly particular molecules bind, both in the composition of the receptor subunits and the structures of the receptors themselves.[9][10] Nicotine, like the natural ligand acetylcholine, has a positively charged nitrogen (N) atom at physiological pH.[3][9] A basic nitrogen will become positively charged in neutral aqueous solution because it is protonated by water. This positive charge gives these compounds a strong affinity to mammalian nAChRs. At the same time, the charge on nicotine lowers its effectiveness as an insecticide, because the blood–brain barrier prevents free access of ions to the central nervous system, and insect nAChRs are only present in the central nervous system.[3][9] The blood–brain barrier does not prevent nicotine poisoning in mammals, because mammalian nAChRs are located in the peripheral nervous system and are necessary for vital functions such as breathing. The low mammalian toxicity of imidacloprid can be explained in large part by its lack of a charged nitrogen atom at physiological pH. The molecule shows weak affinity to mammalian nAChRs but strong affinity for insect nAChRs. Furthermore, the uncharged molecule can penetrate the insect blood–brain barrier, while the human blood–brain barrier filters it.[3] However, desnitro-imidacloprid, which is formed in a mammal's body during metabolism[9] as well as in environmental breakdown,[11] has a charged nitrogen and shows high affinity to mammalian nAChRs.[9] Desnitro-imidacloprid is quite toxic to mice.[2]

Independent studies show that while the photodegradation half-life time of most neonicotinoids is around 34 days when exposed to sunlight, it might take up to 1386 days (3.8 years) for these compounds to degrade in the absence of sunlight and micro-organism activity. Some activists are concerned that neonicotinoids applied agriculturally might accumulate in aquifers.[12]

History

Nicotine acts as an insecticide but is also toxic to mammals.[13] In fact, nicotine has a lower lethal dose for rats than flies.[3] This spurred a scientific search for compounds that retain the insecticidal properties of nicotine but have selectively less effect on mammals, but initial investigation of nicotine related compounds (nicotinoids) as insecticides was not successful.[13] The precursor to nithiazine was first synthesized by a chemist at Purdue University. Shell researchers found in screening that this precursor showed insecticide potential and refined it to develop nithiazine.[1] Nithiazine was later found to be a postsynaptic acetylcholine receptor agonist,[14] meaning it has the same mode of action as nicotine. Nithiazine does not act as an acetylcholinesterase inhibitor,[14] in contrast to the organophosphate and carbamate insecticides. While nithiazine has the desired specificity (i.e. low mammalian toxicity), it is not photostable (it breaks down in sunlight), so it was not commercially viable. Neonicotinoids were developed after the lack of commercial success of nithiazine. The first commercial neonicotinoid, imidacloprid, was developed by Bayer.[1]

Most neonicotinoids are water-soluble and break down slowly in the environment, so they can be taken up by the plant and provide protection from insects as the plant grows. During the late 1990s this class of pesticides, primarily imidacloprid, became widely used. Beginning in the early 2000s, two other neonicotinoids, clothianidin and thiamethoxam were in use as well. Currently, virtually all corn that is planted in the Midwest is treated with one of these two insecticides and various fungicides. In addition, most soybean seeds are also treated with a neonicotinoid insecticide, usually thiamethoxam. Clothianidin is one of the most toxic substances known for honey bees.[15]

US EPA reregistration

The US EPA has established a 15-year registration review cycle for all pesticides. As all neonicotinoids were registered after 1984, they were not subject to reregistration. The EPA granted a conditional, or temporary, registration to clothianidin in 2003. The same approval was given to thiamethoxam. Imidacloprid was registered in 1994. It was not conditional. The EPA is now re-evaluating the safety of neonicotinoids. According to Scott Black, the EPA has stated that the registration review process will take several years. At the earliest , the new verdict for imidacloprid will be in 2016 and 2017 for clothianidin and thiamethoxam. The registration review docket for imidacloprid opened in December 2008 and the docket for nithiazine opened in March 2009. Stated topics for review include uncertainty in the effects of neonicotinoids on pollinators, including reports of beekill incidents. The EPA states, "To better ensure a 'level playing field' for the neonicotinoid class as a whole, and to best take advantage of new research as it becomes available," the other neonicotinoids (acetamiprid, clothianidin, dinotefuran, thiacloprid and thiamethoxam) will begin registration review in 2012.[16]

Active substances

Available neonicotinoid insecticides include:

Use

Imidacloprid, a representative neonicotinoid, is effective against sucking insects, some chewing insects, soil insects, and is also used to control fleas on domestic animals.[8]

Imidacloprid is possibly the most widely used insecticide, both within the mode of action group and in the worldwide market. It is now applied against soil, seed, timber and animal pests as well as foliar treatments for crops including: cereals, cotton, grain, legumes, potatoes,[17] pome fruits, rice, turf and vegetables. It is systemic with particular efficacy against sucking insects and has a long residual activity. Imidacloprid can be added to the water used to irrigate plants. Controlled release formulations of imidacloprid take 2–10 days to release 50% of imidacloprid in water.[18]

The application rates for neonicotinoid insecticides are much lower than older, traditionally used insecticides.

Main article: Imidacloprid effects on bees

Initially neonicotinoids were considered to have low-toxicity to many beneficial insects, including bees; however recently this claim has come into question. More recent research suggests a potential toxicity to bees and other beneficial insects through low level contamination of nectar and pollen with neonicotinoid insecticides used in agriculture. Although these low level exposures do not normally kill bees directly, they may impact some bees’ ability to forage for nectar, learn and remember where flowers are located, and possibly impair their ability to find their way home to the nest or hive.[19] Several recent studies suggest a relationship to what has become generally known as colony collapse disorder (CCD) which has devastated honey bee populations world-wide since about 2006.[20][21] A 2012 study suggested that neonicotinoids may be responsible for detrimental effects of pesticides on the bumble bee colony growth and queen production which may be related to a world-wide reduction in the number of wild bees.[22]

In 2012, several peer reviewed independent studies were published showing that neonicotinoids had previously undetected routes of exposure affecting bees including through dust, pollen, and nectar[23] and that sub-nanogram toxicity resulted in failure to return to the hive without immediate lethality,[24] the primary symptom of CCD.[25] Research also showed environmental persistence in agricultural irrigation channels and soil.[26] These reports prompted a formal peer review by the European Food Safety Authority which stated in January 2013 that neonicotinoids pose an unacceptably high risk to bees, and that the industry-sponsored science upon which regulatory agencies' claims of safety have relied may be flawed and contain several data gaps not previously considered. Their review concluded, "A high acute risk to honey bees was identified from exposure via dust drift for the seed treatment uses in maize, oilseed rape and cereals. A high acute risk was also identified from exposure via residues in nectar and/or pollen."[27][28] David Goulson, an author of one of the Science studies which prompted the EESA peer review, has suggested that industry science pertaining to neonicotinoids may have been deliberately deceptive, and the UK Parliament has asked manufacturer Bayer Cropscience to explain discrepancies in evidence they have submitted to an investigation.[29]

A two-year peer reviewed study published in 2012 showed the presence of two neonicotinoid insecticides, clothianidin and thiamethoxam, in bees found dead in and around hives situated near agricultural fields. Other bees at the hives exhibited tremors, uncoordinated movement and convulsions, all signs of insecticide poisoning. The insecticides were also consistently found at low levels in soil—up to two years after treated seed was planted—on nearby dandelion flowers and in corn pollen gathered by the bees. Insecticide-treated seeds are covered with a sticky substance to control its release into the environment, however they are then coated with talc to facilitate machine planting, which is released into the environment in large amounts. The study found that the exhausted talc showed extremely high levels of the insecticides—up to about 700,000 times the lethal contact dose for a bee. According to the research, "Whatever was on the seed was being exhausted into the environment. This material is so concentrated that even small amounts landing on flowering plants around a field can kill foragers or be transported to the hive in contaminated pollen. This might be why we found these insecticides in pollen that the bees had collected and brought back to their hives." Tests also showed that the corn pollen that bees were bringing back to hives tested positive for neonicotinoids at levels roughly below 100 parts per billion, an amount not acutely toxic, but enough to kill bees if sufficient amounts are consumed.[30]

In July 2010 Dutch toxicologist Dr. Henk Tennekes published a scientific paper examining the toxicity of neonicotinoid pesticides in relation to exposure time.[31] He then authored and published a book in regards to his research called "A Disaster in the Making". The book explores the impact of neonicotinoids on the immune system of bees. The 2009 documentary Vanishing of the Bees suggests that a link between neonicotinoid pesticides and colony collapse disorder exists.[32]

Environmental impact

In 2008 Germany revoked the registration of clothianidin for use on seed corn after an incident that resulted in the death of millions of nearby honey bees.[33] Investigation of the incident revealed that it was caused by a combination of factors, among which were the failure to use a polymer seed coating known as a "sticker"; weather conditions that resulted in late planting when nearby canola crops were in bloom; a particular type of air-driven equipment used to sow the seeds which apparently blew clothianidin-laden dust off the seeds and into the air as the seeds were ejected from the machine into the ground; dry and windy conditions at the time of planting that blew the dust into the nearby canola fields where honey bees were foraging;[34] and a higher application rate which had been authorized for a severe root worm infestation. Clothianidin was also restricted for a short period for use on rapeseed; however, after evidence had shown that the problems resulting from maize seed were not transferable to rapeseed, its use was reinstated under the condition that the pesticide be fixed to the rapeseed grains by means of an additional sticker, so that abrasion dusts would not be released into the air.[35][36]

In 2009 the German Federal Office of Consumer Protection and Food Safety decided to continue to suspend authorization for the use of clothianidin on corn because it has not yet been fully clarified to what extent and in what manner had bees come into contact with the active substances in the pesticides belonging to the neonicotinoid group (clothianidin, thiamethoxam and imidacloprid) when used on corn. In addition, on the basis of new findings, the question arose as to whether drops of liquid from plants which are taken in by bees pose an additional risk.[37]

Neonicotinoid seed treatment uses are banned in Italy, but foliar uses are allowed. This action was taken based on preliminary monitoring studies showing that bee losses were correlated with the application of seeds treated with these compounds; Italy also based its decision on the known acute toxicity of these compounds to pollinators.[38][39]

Sunflower and corn seed treatments of the active ingredient imidacloprid are suspended in France; other imidacloprid seed treatments, such as for sugar beets and cereals, are allowed, as are foliar uses.[38]

Health impact

A study conducted on rats suggests that the neonicotinoids may adversely affect human health, especially the developing brain.[40]

References

  1. ^ a b c Kollmeyer, Willy D.; Flattum, Roger F.; Foster, James P.; Powell, James E.; Schroeder, Mark E.; Soloway, S. Barney (1999). "Discovery of the Nitromethylene Heterocycle Insecticides". In Yamamoto, Izuru; Casida, John (eds.). Nicotinoid Insecticides and the Nicotinic Acetylcholine Receptor. Tokyo: Springer-Verlag. pp. 71–89Template:Inconsistent citations{{cite book}}: CS1 maint: postscript (link)
  2. ^ a b Chao, Shirley Lee; Casida, John E. (1997). "Interaction of Imidacloprid Metabolites and Analogs with the Nicotinic Acetylcholine Receptor of Mouse Brain in Relation to Toxicity". Pesticide Biochemistry and Physiology. 58: 77–88. doi:10.1006/pest.1997.2284.
  3. ^ a b c d e f g Yamamoto, Izuru (1999). "Nicotine to Nicotinoids: 1962 to 1997". In Yamamoto, Izuru; Casida, John (eds.). Nicotinoid Insecticides and the Nicotinic Acetylcholine Receptor. Tokyo: Springer-Verlag. pp. 3–27Template:Inconsistent citations{{cite book}}: CS1 maint: postscript (link)
  4. ^ "Nature Studies by Michael McCarthy: Have we learned nothing since 'Silent Spring'?" The Independent 7 January 2011
  5. ^ "Do people know perfectly well what’s killing bees?" IO9.com 6 January 2011
  6. ^ Pierre Mineau (March 2013). "The Impact of the Nation's Most Widely Used Insecticides on Birds" (PDF). Neonicotinoid Insecticides and Birds. American Bird Conservancy. Retrieved 19 March 2013. {{cite web}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  7. ^ Carrington, Damian (22 March 2013). "US government sued over use of pesticides linked to bee harm". The Guardian. Retrieved 25 March 2013.
  8. ^ a b c Gervais, J.A.; Luukinen, B.; Buhl, K.; Stone, D. (April 2010). "Imidacloprid Technical Fact Sheet" (PDF). National Pesticide Information Center. Retrieved 12 April 2012.{{cite web}}: CS1 maint: date and year (link)
  9. ^ a b c d e f Tomizawa, Motohiro (2004). "Neonicotinoids and Derivatives: Effects in Mammalian Cells and Mice". Journal of Pesticide Science. 29 (3): 177–183. doi:10.1584/jpestics.29.177Template:Inconsistent citations{{cite journal}}: CS1 maint: postscript (link) Cite error: The named reference "Tomizawa2004" was defined multiple times with different content (see the help page).
  10. ^ a b Tomizawa, Motohiro; Latli, Bachir; Casida, John E. (1999). "Structure and Function of Insect Nicotinic Acetylcholine Receptors Studied with Nicotinic Insecticide Affinity Probes". In Yamamoto, Izuru; Casida, John (eds.). Nicotinoid Insecticides and the Nicotinic Acetylcholine Receptor. Tokyo: Springer-Verlag. pp. 271–292Template:Inconsistent citations{{cite book}}: CS1 maint: postscript (link)
  11. ^ Svetlana, Koshlukova (9 February 2006). "Imidacloprid: Risk Characterization Document: Dietary and Drinking Water Exposure" (PDF). California Environmental Protection Agency, Department of Pesticide Regulation. Retrieved 11 April 2012.
  12. ^ "Interview with microbiologist: "This place is filled with multinational lobbyists"". Delo.si. 2011-05-14. Retrieved 2011-10-11.
  13. ^ a b Ujváry, István (1999). "Nicotine and Other Insecticidal Alkaloids". In Yamamoto, Izuru; Casida, John (eds.). Nicotinoid Insecticides and the Nicotinic Acetylcholine Receptor. Tokyo: Springer-Verlag. pp. 29–69Template:Inconsistent citations{{cite book}}: CS1 maint: postscript (link)
  14. ^ a b Schroeder, M. E.; Flattum, R. F. (October 1984). "The Mode of Action and Neurotoxic Properties of the Nitromethylene Heterocycle Insecticides". Pesticide Biochemistry and Physiology. 22 (2): 148–160. doi:10.1016/0048-3575(84)90084-1.{{cite journal}}: CS1 maint: date and year (link)
  15. ^ Neonicotinoid Seed Treatments and Honey Bee Health - eXtension
  16. ^ US EPA (April 2012). "Pesticides: Registration Review: Program Highlights". Retrieved 15 April 2012.{{cite web}}: CS1 maint: date and year (link)
  17. ^ Potato insecticides by group and mode of action (PDF)
  18. ^ Totan Adak, Jitendra Kumar, N. A. Shakil, S. Walia. 2012. Development of controlled release formulations of imidacloprid employing novel nano-ranged amphiphilic polymers. Journal of Environmental Science and Health, Part B, Vol. 47, Iss. 3, 2012.
  19. ^ http://citybugs.tamu.edu/factsheets/ipm/what-is-a-neonicotinoid/
  20. ^ Copping, Jasper (April 1, 2007). "Flowers and fruit crops facing disaster as disease kills off bees". The Telegraph.
  21. ^ Mysterious Bee Deaths Linked to Pesticides [dead link]
  22. ^ "Neonicotinoid Pesticide Reduces Bumble Bee Colony Growth and Queen Production". Science. Retrieved 2012-04-07.
  23. ^ Tapparo, Andrea (January 31, 2012). "Assessment of the Environmental Exposure of Honeybees to Particulate Matter Containing Neonicotinoid Insecticides Coming from Corn Coated Seeds" (PDF). Environmental Science and Technology. 46 (5): 2592–9. doi:10.1021/es2035152. PMID 22292570. Retrieved 27 March 2013. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  24. ^ Schneider, Christof W. (January 11, 2012). "RFID Tracking of Sublethal Effects of Two Neonicotinoid Insecticides on the Foraging Behavior of Apis mellifera" (PDF). PLOS One. 7 (1): e30023. doi:10.1371/journal.pone.0030023. PMC 3256199. PMID 22253863. Retrieved 27 March 2013. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: unflagged free DOI (link)
  25. ^ Pettis, Jeffery S. (February 2012). "Pesticide exposure in honey bees results in increased levels of the gut pathogen Nosema" (PDF). Naturwissenschaften. 99 (2): 153–8. doi:10.1007/s00114-011-0881-1. PMC 3264871. PMID 22246149. Retrieved 27 March 2013. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  26. ^ Krupke, Christian H. (January 3, 2012). "Multiple Routes of Pesticide Exposure for Honey Bees Living Near Agricultural Fields". PLOS One. 7 (1): e29268. doi:10.1371/journal.pone.0029268. PMC 3250423. PMID 22235278. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)CS1 maint: unflagged free DOI (link)
  27. ^ European Food Safety Authority (16 January 2013) "Conclusion on the peer review of the pesticide risk assessment for bees for the active substance clothianidin" EFSA Journal 11(1):3066.
  28. ^ European Food Safety Authority (2012) "Assessment of the scientific information from the Italian project 'APENET' investigating effects on honeybees of coated maize seeds with some neonicotinoids and fipronil" EFSA Journal 10(6):2792
  29. ^ Damian Carrington (16 January 2013) "Insecticide 'unacceptable' danger to bees, report finds" The Guardian
  30. ^ Purdue Newsroom - Researchers: Honeybee deaths linked to seed insecticide exposure
  31. ^ Tennekes, Henk A. (2010). "The significance of the Druckrey–Küpfmüller equation for risk assessment—The toxicity of neonicotinoid insecticides to arthropods is reinforced by exposure time" (PDF). Toxicology. 276 (1): 1–4. doi:10.1016/j.tox.2010.07.005. PMID 20803795.
  32. ^ "2009 documentary ''Vanishing of the Bees''". Vanishingbees.co.uk. 2011-02-03. Retrieved 2011-10-11.
  33. ^ Benjamin, Alison (23 May 2008). "Pesticides: Germany bans chemicals linked to honeybee devastation". The Guardian.
  34. ^ "EPA Acts to Protect Bees | Pesticides | US EPA". Epa.gov. Retrieved 2011-10-11.
  35. ^ "Press releases and background information - Background information: Bee losses caused by insecticidal seed treatment in Germany in 2008". BVL. Retrieved 2011-10-11.
  36. ^ "Background information: Bee losses caused by insecticidal seed treatment in Germany in 2008". German Federal Office of Consumer Protection and Food Safety (BVL). 2008-07-15.
  37. ^ "Maize seed may now be treated with "Mesurol flüssig" again". German Federal Office of Consumer Protection and Food Safety (BVL). 2002-02-09.
  38. ^ a b "Colony Collapse Disorder: European Bans on Neonicotinoid Pesticides | Pesticides | US EPA". Epa.gov. Retrieved 2011-10-11.
  39. ^ Brandon Keim (Dec 13, 2010). "Leaked Memo Shows EPA Doubts About Bee-Killing Pesticide". Wired.
  40. ^ Kimura-Kuroda J , Komuta Y , Kuroda Y , Hayashi M , Kawano H (2012) Nicotine-Like Effects of the Neonicotinoid Insecticides Acetamiprid and Imidacloprid on Cerebellar Neurons from Neonatal Rats. PLoS ONE 7(2): e32432. doi:10.1371/journal.pone.0032432
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