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Reverted back to Freestyle's version. If there is a problem with the information or sources, I suggest we discuss this in the Talk Page.
WIlling to discuss on talk page - but stop telling stories that have nothing to do with the science. If you look at the spread of the bee collapse - it is obviously an organism that spread. This product is too valuable to be blamed.
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'''Imidacloprid''' is a [[nicotine]]-based, systemic [[insecticide]], which acts as a [[neurotoxin]] and belongs to a class of chemicals called the [[neonicotinoids]]. Although it is now off patent, the primary manufacturer of this chemical is Bayer CropScience, (part of [[Bayer|Bayer AG]]). It is sold under the [[trade name]]s Kohinor, Admire, Advantage (Advocate) (flea killer for pets), Gaucho, Mallet, Merit, Nuprid, Prothor, Turfthor, Confidor, Conguard, Dominion 2L, Hachikusan, Premise, Prothor, Provado, Intercept, and Winner. Imidacloprid is one of the most widely used insecticides and can be applied by soil injection, tree injection, application to the skin, or broadcast foliar or ground application as a [[granular]] or liquid formulation or as a pesticide-coated [[seed treatment]].<ref>[http://www.riversedgeofellijay.com/Documents/Adelgid/122805_Imidacloprid.pdf] USDA Forest Service. Imidacloprid: Human Health and Ecological Risk Assessment. Final Report. Dec 28, 2005.</ref><ref>[http://npic.orst.edu/factsheets/imidagen.pdf] National Pesticide Information Center. Imidacloprid: General Fact Sheet. May 2010.</ref>
'''Imidacloprid''' is a [[nicotine]]-based, systemic [[insecticide]], which acts as an insect [[neurotoxin]] in certain insect species and belongs to a class of chemicals called the [[neonicotinoids]]. Although it is now off patent, the primary manufacturer of this chemical is Bayer CropScience, (part of [[Bayer|Bayer AG]]). It is sold under the [[trade name]]s Kohinor, Admire, Advantage (Advocate) (flea killer for pets), Gaucho, Mallet, Merit, Nuprid, Optrol, Prothor, Turfthor, Confidor, Conguard, Dominion 2L, Hachikusan, Premise, Prothor, Provado, Intercept, Winner and Xytect. Imidacloprid is one of the most widely used insecticides. Approximately 95% of this compound is used on crops as a foliage spray. It also has many other valuable uses in the landscape and around the home. It has become a very important tool in the fight against the Emerald ash borer and the Asian long horned beetle. It's low cost and ease of application, along with its high efficacy make it invaluable. In trees it can be applied by soil injection or tree injection. It is also used as a topical application to the skin for lice in humans and for fleas and ticks on pets. Other application methods include: broadcast foliar or ground application as a [[granular]] or liquid formulation or as a pesticide-coated [[seed treatment]].<ref>[http://www.riversedgeofellijay.com/Documents/Adelgid/122805_Imidacloprid.pdf] USDA Forest Service. Imidacloprid: Human Health and Ecological Risk Assessment. Final Report. Dec 28, 2005.</ref><ref>[http://npic.orst.edu/factsheets/imidagen.pdf] National Pesticide Information Center. Imidacloprid: General Fact Sheet. May 2010.</ref>


Imidacloprid has been suspected of being associated with honeybee colony collapse disorder in man made hives. It has not however been directly linked to this disorder and research in recent years now points at other causes such as miticide sprays used by bee keepers to control mite parasites that are directly sprayed on the hive, a virus, and a fly known to parasitize American bumble bees and wasps has recently been discovered parasitizing California honey bees, causing bees to abandon their colonies in the night. Bees parasitized by the phorid fly became disoriented, "turning into zombies", flying out into the night to die the next day. Parasitism was widespread in the study area near the San Francisco Bay. Parasitism was found at 77% of the sites they investigated. The highest rate of parasitism was 91% of the nocturnally active bees at one site.
In [[France]], [[beekeepers]] reported a significant loss of [[honeybees]] in the 1990s, which they [[Imidacloprid effects on bees|attributed to the use of imidacloprid]] (Gaucho). In response, the French Minister of Agriculture convened a panel of expert scientists (Comite Scientifique et Technique) to examine the impact of imidacloprid on bees. After reviewing dozens of laboratory and field studies conducted by Bayer CropScience and by independent scientists, the Panel concluded that there was a significant risk to bees from exposure to imidacloprid on sunflowers and maize (corn), the only crops for which they had exposure data. Following the release of this report, the French Agricultural Ministry suspended the use of imidacloprid on maize and sunflowers. After this suspension, beekeepers used fipronil, another systemic pesticide which is also highly toxic to bees. Thus, a noticeable increase in the bee population was not observed until fipronil was no longer used. In 2008, Italy, Germany, and Slovenia suspended seed treatment uses of neonicotinoids and fipronil based on concerns for bees.<ref>[http://www.guardian.co.uk/environment/2008/may/23/wildlife.endangeredspecies Pesticides: Germany bans chemicals linked to honeybee devastation] - UK Guardian</ref> <!-- Access on 08-12-2008 --> <ref>[http://agriculture.gouv.fr/IMG/pdf/rapportfin.pdf] French Scientific and Technical Report on the Impact of Imidacloprid to Bees. </ref>


Over the past 20 years there has been much conjecture and guessing at the cause of bee die off in man made hives. And while imidacloprid has been pointed at by some, it must be recognized that research now points at other causes and that this epidemic was not happening everywhere imidacloprid was being used, but spread much like a disease spreads. Even in France, despite the widespread use of Imidacloprid, not all hives in all areas experienced die off at the same time. While a serious issue in some places in the 1990's, it did not become recognized to be a serious issue in the United States until the mid 2000's.
In 2006, U.S. commercial migratory beekeepers reported sharp declines in their honey bee colonies. Unlike previous losses, adult bees were abandoning their hives. Scientists named this phenomenon [[colony collapse disorder]] (CCD). Reports show that beekeepers in most states have been affected by CCD. <ref>[http://www.fas.org/sgp/crs/misc/RL33938.pdf] Congressional Research Service Honey Bee Colony Collapse Disorder </ref> Although no single factor has been identified as causing CCD, the United States Department of Agriculture (USDA) in their progress report on CCD stated that CCD may be "a syndrome caused by many different factors, working in combination or synergistically." <ref>[http://www.ars.usda.gov/is/br/ccd/ccdprogressreport2010.pdf USDA Colony Collapse Disorder Progress Report. June 2010 </ref> Recently, USDA researcher Jeff Pettis published the results of his study, which showed that bees treated with sub-lethal or low levels of imidacloprid had higher rates of infection with the pathogen ''Nosema'' than untreated bees. <ref>[http://www.springerlink.com/content/p1027164r403288u/ Pesticide exposure in honey bees Pettis et al 2012 </ref> His research was confirmed by Alaux (2010) and Vidau (2011) who found that interactions between ''Nosema'' and neonicotinoids weakened bees and led to increased mortality. <ref>[http://onlinelibrary.wiley.com/doi/10.1111/j.1462-2920.2009.02123.x/abstract] Interactions between ''Nosema'' and a neonicotinoid Alaux et al 2010 </ref> <ref>[http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0021550] Exposure to sublethal doses of fipronil and thiacloprid. Vidau et al 2011 </ref>


As a systemic pesticide, imidacloprid translocates or moves readily from the soil into the leaves, flowers, fruiting bodies, pollen, nectar, and guttation fluid of plants. Imidacloprid has limited mobility in the soil and does not bioaccumulate. For imidacloprid to be ingested in bees, it has to be translocated into plants and then the flowers where the bees can ingest it as they forage for pollen. Imidacloprid and other pesticides have been shown to weaken bees, making them more susceptible to parasites and other health issues. However, scientists no longer point directly at imidacloprid as the cause of this disorder. In fact despite banning imidacloprid and other neonicotonoids in France in 1999, Bee colony collapse disorder continues to be a serious issue. In Australia, where imidacloprid is widely used, there are no reports of colony collapse disorder, and there are also none of the viruses and mites that have also been linked as possible causes.


==History==
==History==
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==Biochemistry==
==Biochemistry==


Imidacloprid is a [[systemic effect|systemic]] [[chloronicotinyl]] [[pesticide]], belonging to the class of [[neonicotinoid]] insecticides. It acts as a [[neurotoxin]] and interferes with the transmission of nerve impulses in insects by binding irreversibly to specific insect [[nicotinic acetylcholine receptors]]. <ref>[http://www.ccme.ca/assets/pdf/imidacloprid_ssd_1388.pdf] Canadian Water Quality Guidelines: Imidacloprid </ref> Several studies have shown that selected metabolites and analogues of imidacloprid bind tightly to mammalian acetylcholine receptors <ref>[http://www.sciencedirect.com/science/article/pii/S0048357597922847]Interaction of Imidacloprid Metabolites and Analogues with the Nicotinic Acetylcholine Receptors of Mouse Brain in Relation to Toxicity. Chao and Casida 1997</ref> <ref>[http://www.ncbi.nlm.nih.gov/pubmed/11312774]Neonicotinoid Insecticides. Tomizawa et al 2000</ref> <ref>[http://www.journalarchive.jst.go.jp/jnlpdf.php?cdjournal=jpestics1975&cdvol=27&noissue=2&startpage=145&lang=en&from=jnltoc] Evaluation of Affinity of Neonicotinoid Insecticides for Rat Brain Nicotinic Acetylcholine Receptors. Okumoto and Ozoe 2002 </ref>
Imidacloprid is a [[systemic effect|systemic]] [[chloronicotinyl]] [[pesticide]], belonging to the class of [[neonicotinoid]] insecticides. It acts as a [[neurotoxin]] and interferes with the transmission of nerve impulses in insects by binding irreversibly to specific insect [[nicotinic acetylcholine receptors]]. <ref>[http://www.ccme.ca/assets/pdf/imidacloprid_ssd_1388.pdf] Canadian Water Quality Guidelines: Imidacloprid </ref> [http://www.sciencedirect.com/science/article/pii/S0048357597922847]Interaction of Imidacloprid Metabolites and Analogues with the Nicotinic Acetylcholine Receptors of Mouse Brain in Relation to Toxicity. Chao and Casida 1997</ref> <ref>[http://www.ncbi.nlm.nih.gov/pubmed/11312774]Neonicotinoid Insecticides. Tomizawa et al 2000</ref> <ref>[http://www.journalarchive.jst.go.jp/jnlpdf.php?cdjournal=jpestics1975&cdvol=27&noissue=2&startpage=145&lang=en&from=jnltoc] Evaluation of Affinity of Neonicotinoid Insecticides for Rat Brain Nicotinic Acetylcholine Receptors. Okumoto and Ozoe 2002 </ref>


As a systemic pesticide, imidacloprid [[translocates]] or moves easily in the xylem of plants from the soil into the leaves, fruit, pollen, and nectar of a plant. Imidacloprid also exhibits excellent translaminar movement in plants and can penetrate the leaf cuticle and move readily into leaf tissue. <ref>[http://www.cdpr.ca.gov/docs/emon/pubs/fatememo/Imidclprdfate2.pdf] Environmental Fate of Imidacloprid California Department of Pesticide Regulation 2006 </ref> Since imidacloprid is efficacious at very low levels (nanogram and picogram), it can be applied at lower concentrations (e.g., 0.05–0.125&nbsp;lb/acre or 55–140 g/ha) than other neurotoxins, particularly organophosphates. <ref>[http://www.efsa.europa.eu/en/efsajournal/pub/148r.htm]European Food Safety Authority. Conclusion regarding the peer review of the pesticide risk assessment of the active substance imidacloprid. July 28, 2008. </ref>
As a systemic pesticide, imidacloprid [[translocates]] or moves easily in the xylem of plants from the soil into the leaves, fruit, pollen, and nectar of a plant. Imidacloprid also exhibits excellent translaminar movement in plants and can penetrate the leaf cuticle and move readily into leaf tissue. <ref>[http://www.cdpr.ca.gov/docs/emon/pubs/fatememo/Imidclprdfate2.pdf] Environmental Fate of Imidacloprid California Department of Pesticide Regulation 2006 </ref> Since imidacloprid is efficacious at very low levels (nanogram and picogram), it can be applied at lower concentrations (e.g., 0.05–0.125&nbsp;lb/acre or 55–140 g/ha) than other neurotoxins, particularly organophosphates. <ref>[http://www.efsa.europa.eu/en/efsajournal/pub/148r.htm]European Food Safety Authority. Conclusion regarding the peer review of the pesticide risk assessment of the active substance imidacloprid. July 28, 2008. </ref>
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The main routes of dissipation of imidacloprid in the environment are [[aqueous]] [[photolysis]] (half-life = 1–4 hours) and plant uptake. The major photo-metabolites include [[imidacloprid desnitro]], [[imidacloprid olefine]], imidacloprid urea, and five minor metabolites. The end product of photodegradation is [[chloronicotinic acid]] (CNA). Since imidacloprid has a low [[vapor pressure]], it normally does not volatilize readily. <ref>[http://www.ccme.ca/assets/pdf/imidacloprid_ssd_1388.pdf] Canadian Water Quality Guidelines: Imidacloprid </ref>
The main routes of dissipation of imidacloprid in the environment are [[aqueous]] [[photolysis]] (half-life = 1–4 hours) and plant uptake. The major photo-metabolites include [[imidacloprid desnitro]], [[imidacloprid olefine]], imidacloprid urea, and five minor metabolites. The end product of photodegradation is [[chloronicotinic acid]] (CNA). Since imidacloprid has a low [[vapor pressure]], it normally does not volatilize readily. <ref>[http://www.ccme.ca/assets/pdf/imidacloprid_ssd_1388.pdf] Canadian Water Quality Guidelines: Imidacloprid </ref>


Imidacloprid is persistent and moderately soluble in water. At pH's 5 and 7, it is stable in water, and at pH 9, the half-life is about 1 year. In soil under aerobic conditions, imidacloprid is persistent with half-lives on the order of 1-3 years.
Imidacloprid is moderately soluble in water. It is not stable in water and in the presence of light breaks down rapidly. In water not in the presence of light, it's half life is longer. It does not bioaccumulate. In soil under aerobic conditions, imidacloprid has been shown to have half lives of 6 - 18 months. Ultimately, imidacloprid breaks into carbon dioxide. As it breaks down it transitions through metabolites that include imidacloprid nitrosimine, imidacloprid desnitro, hydroxynicotinic acid, and imidacloprid urea.
Major soil metabolites include imidacloprid nitrosimine, imidacloprid desnitro, hydroxynicotinic acid, and imidacloprid urea, which ultimately degrade to chloronicotinic acid, CO<sub>2</sub>, and bound residues. Long-term soil dissipation studies in apple orchards and with seed-treated barley crops showed accumulation of imidacloprid residues in soil with repeated applications.
<ref>[http://www.ccme.ca/assets/pdf/imidacloprid_ssd_1388.pdf] Canadian Water Quality Guidelines: Imidacloprid </ref>
<ref>[http://www.ccme.ca/assets/pdf/imidacloprid_ssd_1388.pdf] Canadian Water Quality Guidelines: Imidacloprid </ref>
<ref>[European Draft Assessment Report: Imidacloprid. Annex B, B.7. February 2006]</ref>
<ref>[European Draft Assessment Report: Imidacloprid. Annex B, B.7. February 2006]</ref>
Based on its high water solubility (0.5-0.6 g/L) and persistence, both the U.S. Environmental Protection Agency and the Pest Management Regulatory Agency in Canada consider imidacloprid to have a high potential to run off into surface water and to leach into ground water. <ref>[http://www.regulations.gov/#!searchResults;rpp=10;po=0;s=EPA-HQ-OPP-2008-0844-0003] Environmental Fate and Effects Division Problem Formulation for Imidacloprid </ref>
Both the U.S. Environmental Protection Agency and the Pest Management Regulatory Agency in Canada consider imidacloprid to have characteristic that give it potential to run off into surface water if used in flood plains and highly porous soils with very shallow ground water. In normal use however, runoff potential is virtually nil. When tested for in runoff during rain events, minuscule amounts have been detected. Typically in the .5 - 1 part per billion range. The EPA considers chronic exposure of 1770 ppb to be an issue.
<ref>[http://www.ccme.ca/assets/pdf/imidacloprid_ssd_1388.pdf] Canadian Water Quality Guidelines: Imidacloprid </ref> Recently the state of California published the results of a water monitoring study where researchers found that imidacloprid was detected in 89% of collected water samples with 19% of the samples exceeding EPA's aquatic life benchmark. The results of this study indicate that imidacloprid does "move offsite and contaminates surface water at concentrations that could harm aquatic organisms."
<ref>[http://www.ccme.ca/assets/pdf/imidacloprid_ssd_1388.pdf] Canadian Water Quality Guidelines: Imidacloprid </ref>
<ref>[http://www.springerlink.com/content/566t681j31233742/] Detections of Imidacloprid in Surface Waters. Starner and Goh 2012 </ref>
<ref>[http://www.springerlink.com/content/566t681j31233742/] Detections of Imidacloprid in Surface Waters. Starner and Goh 2012 </ref>


==Toxicology==
==Toxicology==


Imidacloprid is one of the most highly toxic insecticides to honey bees with a contact acute LD<sub>50</sub> = 0.078&nbsp;ug a.i./bee and an acute oral LD<sub>50</sub> = 0.0039&nbsp;ug a.i./bee. <ref>[http://www.regulations.gov/#!searchResults;rpp=10;po=0;s=EPA-HQ-OPP-2008-0844-0003] Environmental Fate and Effects Division Problem Formulation for the Registration Review of Imidacloprid </ref> Other systemic pesticides with a similar high acute toxicity to honey bees include clothianidin, thiamethoxam, dinotefuran, fipronil, emmamectin benzoate, and spinosad. <ref>[http://www.epa.gov/pesticides/reregistration/status.htm]Pesticide Reregistration Status USEPA </ref> <ref>[regulations.gov]Regulations.gov U.S.</ref>
Imidacloprid is toxic to honey bees with a contact acute LD<sub>50</sub> = 0.078&nbsp;ug a.i./bee and an acute oral LD<sub>50</sub> = 0.0039&nbsp;ug a.i./bee. <ref>[http://www.regulations.gov/#!searchResults;rpp=10;po=0;s=EPA-HQ-OPP-2008-0844-0003] Environmental Fate and Effects Division Problem Formulation for the Registration Review of Imidacloprid </ref> Other systemic pesticides that have a higher acute toxicity to honey bees include clothianidin, thiamethoxam, dinotefuran, fipronil, emmamectin benzoate, and spinosad. <ref>[http://www.epa.gov/pesticides/reregistration/status.htm]Pesticide Reregistration Status USEPA </ref> <ref>[regulations.gov]Regulations.gov U.S.</ref>


Several 10-day chronic oral studies published in peer-reviewed literature have demonstrated [[NOAEC]] values for imidacloprid ranging from < 4 ppb to 10 ppb in honey bees and bumble bees.<ref>Moncharmont, F.D., A. Decourtye, C.H. Hantier, O. Pons, M. Pham-Delegue. 2003. Statistical analysis of honeybee survival after chronic exposure to insecticides. Environ Toxicol Chem 22(12): 3088-94</ref><ref>Decourtye, A, Lacassie, E, Pham-Delegue, MH (2003) Learning performances of honeybees (''Apis mellifera L'') are differentially affected by imidacloprid according to the season. Pest Manage Sci 59:269–278</ref><ref>Mommaerts, V., Reynders, S., Boulet, J., Besard, L., Sterk, G., Smagghe, G. Risk assessment for side-effects of neonicotinoids against bumblebees with and without impairing foraging behavior. Ecotoxicology 19:207-215</ref><ref name="Suchail">Suchail, S., Guez,D., and Belzunces, L.P. 2001. Discrepancy between acute and chronic toxicity induced by imidacloprid and its metabolites in Apis mellifera. Environ. Toxicol. Chem. 20: 2482–2486</ref> The olefine and hydroxy metabolites of imidacloprid, which are found in plants, are very toxic to honeybees.<ref name="Suchail" /> A large number of published studies have also shown that low levels of imidacloprid and its metabolites produce sublethal and behavioral effects in bees, including [[disorientation]] and effects on foraging, learning performance, motor coordination, and food consumption.<ref>Yang, E.C., Chuang, Y.C., Chen, Y.L., and Chang, L.H. 2008. Abnormal foraging behavior induced by sublethal dosage of imidacloprid in the honeybee (Hymenoptera: Apidae). J. Econ Entomology 101(6):1743-1748</ref><ref>Medrzycki P., Montanari, R., Bortolotti, L., Sabatini, A. G., Maini, S., and Porrini, C. 2003. Effects of imidacloprid administered in sub-lethal doses on honey bee behaviour. Laboratory tests. Bulletin of Insectology 56 (1): 59-62</ref><ref>Desneux, N., Decourtye, A., and Delpuech, J-M. 2007. The sublethal effects of pesticides on beneficial arthropods. Annual Review of Entomology 52: 81–106</ref><ref>Armengaud, C., Lambin, M., and Gauthier, M. 2002. Effects of imidacloprid on the neural processes of memory. In J. Devillers and M.H. Pham-Delegue(eds). Honey bees: estimating the environmental impact of chemicals (pp. 85-100). New York: Taylor & Francis</ref><ref>Bonmatin, J.M., Moineau, I., Charvet, R., Collin, M.E., Fleche, C., and Bengsch, E.R. 2005. Behavior of Imidacloprid in Fields. In E.Lcihtfourse, J. Schwarzbauer, and D. Robert (eds). Toxicity for Honey Bees in Environmental Chemistry: Green Chemistry and Pollutants in Ecosytems. New York: Springer</ref><ref>Aliouane, Y., Kacimi El Hassani, A., Gary, V., Armengaud, C., Lambin, M., Gauthier, M. (2009) Subchronic exposure of honeybees to sublethal doses of pesticides: effect on behavior. Environ
Toxicol Chem 28:113–122</ref><ref>Bortolotti, L., Montanari, R., Marcelino, J., Medrzycki, P., Maini, S., and Porrini, C. 2003. Effects of sub-lethal imidacloprid doses on the homing rate and foraging activity of honey bees. Bulletin of Insectology 56(1): 63-67</ref><ref>Decourtye, A., Lacassie, E., Pham-Delegue, MH. (2003) Learning performances of honeybees (''Apis mellifera L'') are differentially affected by imidacloprid according to the season. Pest Manage Sci 59:269–278</ref> Chronic or long-term toxicity to bees is still not well understood despite the large number of field studies that have been conducted. Effects of imidacloprid on brood and queen are also not known.<ref name="agriculture.gouv">[http://agriculture.gouv.fr/IMG/pdf/rapportfin.pdf] French Scientific and Technical Report on the Impact of Imidacloprid to Bees.</ref><ref>[http://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2008-0844-0003] Environmental Fate and Effects Problem Formulation for the Registration Review of Imidacloprid. Nov 13, 2008. USEPA</ref>


Researchers Kreutzweiser and Thompson (2009) from the Canadian Forest Service showed that imidacloprid at realistic field concentrations inhibits non-target terrestrial invertebrates that decompose leaf litter. In their study, there was no significant indication that invertebrates detected or avoided imidacloprid-treated leaves. <ref>[http://www.ncbi.nlm.nih.gov/pubmed/18973940] Imidacloprid in leaves from systemically treated trees may inhibit litter breakdown by non-target invertebrates. Kreutzweiser and Thompson 2009 </ref>
Researchers Kreutzweiser and Thompson (2009) from the Canadian Forest Service showed that imidacloprid at realistic field concentrations inhibits non-target terrestrial invertebrates that decompose leaf litter. In their study, there was no significant indication that invertebrates detected or avoided imidacloprid-treated leaves. <ref>[http://www.ncbi.nlm.nih.gov/pubmed/18973940] Imidacloprid in leaves from systemically treated trees may inhibit litter breakdown by non-target invertebrates. Kreutzweiser and Thompson 2009 </ref>


In bobwhite quail (<i>Colinus virginianus</i>), imidacloprid was determined to be moderately toxic with an acute oral LD<sub>50</sub> of 152 mg a.i./kg. It was slightly toxic in a 5-day dietary study with an acute oral LC<sub>50</sub> of 1,420 mg a.i./kg diet, a NOAEC of < 69 mg a.i./kg diet, and a LOAEC = 69 mg a.i./kg diet. Exposed birds exhibited ataxia, wing drop, opisthotonos, immobility, hyperactivity, fluid-filled crops and intestines, and discolored livers. In a reproductive toxicity study with bobwhite quail, the NOAEC = 120 mg a.i./kg diet and the LOAEC = 240 mg a.i./kg diet. Eggshell thinning and decreased adult weight were observed at 240 mg a.i./kg diet. <ref>[http://www.ccme/ca/assets/pdf/imidacloprid_ssd_1388.pdf]Canadian Water Quality Guidelines: Imidacloprid, Scientific Support Document. 2007. Canadian Council of Ministers of the Environment. </ref> <ref>[http://www.epa.gov/pesticides/chemical/foia/cleared-reviews/reviews/129099/129099.htm]Imidacloprid Cleared Science Reviews. U.S. EPA.</ref>
In bobwhite quail (<i>Colinus virginianus</i>), imidacloprid was determined to be moderately toxic with an acute oral LD<sub>50</sub> of 152 mg a.i./kg. These levels are much higher than would realistically be encountered. It was slightly toxic in a 5-day dietary study with an acute oral LC<sub>50</sub> of 1,420 mg a.i./kg diet, a NOAEC of < 69 mg a.i./kg diet, and a LOAEC = 69 mg a.i./kg diet. Exposed birds exhibited ataxia, wing drop, opisthotonos, immobility, hyperactivity, fluid-filled crops and intestines, and discolored livers. In a reproductive toxicity study with bobwhite quail, the NOAEC = 120 mg a.i./kg diet and the LOAEC = 240 mg a.i./kg diet. Eggshell thinning and decreased adult weight were observed at 240 mg a.i./kg diet. <ref>[http://www.ccme/ca/assets/pdf/imidacloprid_ssd_1388.pdf]Canadian Water Quality Guidelines: Imidacloprid, Scientific Support Document. 2007. Canadian Council of Ministers of the Environment. </ref> <ref>[http://www.epa.gov/pesticides/chemical/foia/cleared-reviews/reviews/129099/129099.htm]Imidacloprid Cleared Science Reviews. U.S. EPA.</ref>


Imidacloprid is highly toxic to four bird species: Japanese quail, house sparrow, canary, and pigeon. The acute oral LD<sub>50</sub> for Japanese quail (<i>Coturnix coturnix</i>) is 31 mg a.i./kg bw with a NOAEL = 3.1 mg a.i./kg. The acute oral LD<sub>50</sub> for house sparrow (''Passer domesticus'') is 41 mg a.i./kg bw with a NOAEL = 3 mg a.i./kg and a NOAEL = 6 mg a.i./kg. The LD<sub>50</sub>s for pigeon (''Columba livia'') and canary (''Serinus canaries'') are 25-50 mg a.i./kg. Mallard ducks are more resistant to the effects of imidacloprid with a 5-day dietary LC<sub>50</sub> of > 4,797 ppm. The NOAEC for body weight and feed consumption is 69 mg a.i./kg diet. Reproductive studies with mallard ducks showed eggshell thinning at 240 mg a.i./kg diet. <ref>[http://www.ccme/ca/assets/pdf/imidacloprid_ssd_1388.pdf]</ref> <ref>[http://www.epa.gov/pesticides/chemical/foia/cleared-reviews/reviews/129099/129099.htm]Imidacloprid Cleared Science Reviews. U.S. EPA.</ref> According to the European Food Safety Authority, imidacloprid poses a potential high acute risk for herbivorous and insectivorous birds and granivorous mammals. Chronic risk has not been well established. <ref>[http://www.efsa.europa.eu/en/efsajournal/pub/148r.htm]European Food Safety Authority. Conclusion regarding the peer review of the pesticide risk assessment of the active substance imidacloprid. July 28, 2008.</ref> <ref>[http://www.ccme/ca/assets/pdf/imidacloprid_ssd_1388.pdf]Water Quality Guidelines: Imidacloprid, Scientific Support Document. 2007. Canadian Council of Ministers of the Environment.</ref>

Based on laboratory rat studies, imidacloprid is rated as "moderately toxic" on an acute oral basis to mammals by the [[World Health Organization]] and the [[United States Environmental Protection Agency‎]] (class II or III, requiring a "Warning" or "Caution" label), and a "potential" [[ground water]] contaminant. It is rated as an "unlikely" [[carcinogen]] and as weakly mutagenic by the U.S.EPA (group E). It is not listed for [[reproductive]], or [[developmental]] toxicity, but is listed on EPA's Tier 1 Screening Order for chemicals to be tested under the Endocrine Disruptor Screening Program (EDSP). <ref>[http://www.epa.gov/pesticides/chemical/foia/cleared-reviews/reviews/129099/129099.htm]Imidacloprid Cleared Science Reviews. U.S. EPA.</ref> <ref>[http://www.epa.gov/endo/pubs/stakeholder/notices.htm]Endocrine Disruptor Screening Program: Tier 1 Screening Order Issuing Announcement. Federal Register Notice, Oct 21, 2009. Vol. 74, No. 202, pp. 54422-54428</ref> Tolerances for imidacloprid residues in food range from 0.02 mg/kg in eggs to 3.0 mg/kg in [[hops]].<ref>[http://pmep.cce.cornell.edu/profiles/extoxnet/haloxyfop-methylparathion/imidacloprid-ext.html]EXTOXNET. Imidacloprid </ref>

Animal toxicity is similar to that of the parent compound, nicotine, where animals exhibit [[fatigue (physical)|fatigue]], [[muscle contraction|twitch]]ing, [[cramp]]s, and [[fatigue (medical)|weakness]] leading to [[asphyxia]]. The oral [[median lethal dose|LD<sub>50</sub>]] of imidacloprid is 450 mg a.i./kg body weight in [[rat]]s and 131 mg a.i./kg bw in [[mouse|mice]]; the 24-hour [[dermal]] LD<sub>50</sub> in rats is greater than >5000 mg a.i./kg bw. It is not irritating to eyes or skin in [[rabbit]]s and [[guinea pig]]s (although some commercial preparations contain [[clay]] as an inert ingredient, which may be an [[Irritation|irritant]]). The acute [[inhalation]] LD<sub>50</sub> in rats was not reached at the greatest attainable concentrations, 69 milligrams per cubic meter of air as an aerosol, and 5,323 mg a.i./m³ of air as a dust. In rats subjected to a two-year feeding study, no observable effect was seen at 100 parts per million (ppm). In rats, the thyroid is the organ most affected by imidacloprid. Thyroid lesions occurred in male rats at a LOAEL of 16.9 mg a.i./kg/day. In a one-year feeding study in dogs, no observable effect was seen at 1,250 ppm, while levels up to 2,500 ppm led to [[hypercholesterolemia]] and elevated [[liver]] [[Cytochrome P-450#Drug metabolism|cytochrome p-450 measurements]]. <ref> [http://pmep.cce.cornell.edu/profiles/extoxnet/haloxyfop-methylparathion/imidacloprid-ext.html Cornell Extension Toxicology Network]EXTOXNET. Imidacloprid </ref> <ref>[http://www.ccme/ca/assets/pdf/imidacloprid_ssd_1388.pdf]Water Quality Guidelines: Imidacloprid, Scientific Support Document. 2007. Canadian Council of Ministers of the Environment.</ref>

Imidacloprid is very highly toxic on an acute basis to aquatic invertebrates (freshwater and estuarine/marine) with EC50 values = 0.037 - 0.115 ppm. It is also very highly toxic to aquatic invertebrates on a chronic basis: NOAEC/LOAEC = 1.8/3.6 ppm in dapnids; NOAEC = 0.001 in midge, and NOAEC/LOAEC = 0.00006/0.0013 ppm in mysid shrimp. <ref>[http://www.regulations.gov/#!searchResults;rpp=10;po=0;s=EPA-HQ-OPP-2008-0844-0003] Environmental Fate and Effects Division Problem Formulation for the Registration Review of Imidacloprid </ref> <ref>[http://www.epa.gov/pesticides/chemical/foia/cleared-reviews/reviews/129099/129099.htm]Imidacloprid Cleared Science Reviews. U.S. EPA.</ref>


==Overdosage==
==Overdosage==

Revision as of 21:12, 19 February 2012

Imidacloprid[1]
Names
IUPAC name
N-[1-[(6-Chloro-3-pyridyl)methyl]-4,5-dihydroimidazol-2-yl]nitramide
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
DrugBank
ECHA InfoCard 100.102.643 Edit this at Wikidata
KEGG
UNII
  • InChI=1S/C9H10ClN5O2/c10-8-2-1-7(5-12-8)6-14-4-3-11-9(14)13-15(16)17/h1-2,5H,3-4,6H2,(H,11,13) checkY
    Key: YWTYJOPNNQFBPC-UHFFFAOYSA-N checkY
  • InChI=1/C9H10ClN5O2/c10-8-2-1-7(5-12-8)6-14-4-3-11-9(14)13-15(16)17/h1-2,5H,3-4,6H2,(H,11,13)
    Key: YWTYJOPNNQFBPC-UHFFFAOYAZ
  • [O-][N+](=O)NC/1=N/CCN\1Cc2cnc(Cl)cc2
Properties
C9H10ClN5O2
Molar mass 255.661
Appearance Colorless crystals
Melting point 136.4–143.8 °C
0.51 g/L (20 °C)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
checkY verify (what is checkY☒N ?)

Imidacloprid is a nicotine-based, systemic insecticide, which acts as an insect neurotoxin in certain insect species and belongs to a class of chemicals called the neonicotinoids. Although it is now off patent, the primary manufacturer of this chemical is Bayer CropScience, (part of Bayer AG). It is sold under the trade names Kohinor, Admire, Advantage (Advocate) (flea killer for pets), Gaucho, Mallet, Merit, Nuprid, Optrol, Prothor, Turfthor, Confidor, Conguard, Dominion 2L, Hachikusan, Premise, Prothor, Provado, Intercept, Winner and Xytect. Imidacloprid is one of the most widely used insecticides. Approximately 95% of this compound is used on crops as a foliage spray. It also has many other valuable uses in the landscape and around the home. It has become a very important tool in the fight against the Emerald ash borer and the Asian long horned beetle. It's low cost and ease of application, along with its high efficacy make it invaluable. In trees it can be applied by soil injection or tree injection. It is also used as a topical application to the skin for lice in humans and for fleas and ticks on pets. Other application methods include: broadcast foliar or ground application as a granular or liquid formulation or as a pesticide-coated seed treatment.[2][3]

Imidacloprid has been suspected of being associated with honeybee colony collapse disorder in man made hives. It has not however been directly linked to this disorder and research in recent years now points at other causes such as miticide sprays used by bee keepers to control mite parasites that are directly sprayed on the hive, a virus, and a fly known to parasitize American bumble bees and wasps has recently been discovered parasitizing California honey bees, causing bees to abandon their colonies in the night. Bees parasitized by the phorid fly became disoriented, "turning into zombies", flying out into the night to die the next day. Parasitism was widespread in the study area near the San Francisco Bay. Parasitism was found at 77% of the sites they investigated. The highest rate of parasitism was 91% of the nocturnally active bees at one site.

Over the past 20 years there has been much conjecture and guessing at the cause of bee die off in man made hives. And while imidacloprid has been pointed at by some, it must be recognized that research now points at other causes and that this epidemic was not happening everywhere imidacloprid was being used, but spread much like a disease spreads. Even in France, despite the widespread use of Imidacloprid, not all hives in all areas experienced die off at the same time. While a serious issue in some places in the 1990's, it did not become recognized to be a serious issue in the United States until the mid 2000's.

As a systemic pesticide, imidacloprid translocates or moves readily from the soil into the leaves, flowers, fruiting bodies, pollen, nectar, and guttation fluid of plants. Imidacloprid has limited mobility in the soil and does not bioaccumulate. For imidacloprid to be ingested in bees, it has to be translocated into plants and then the flowers where the bees can ingest it as they forage for pollen. Imidacloprid and other pesticides have been shown to weaken bees, making them more susceptible to parasites and other health issues. However, scientists no longer point directly at imidacloprid as the cause of this disorder. In fact despite banning imidacloprid and other neonicotonoids in France in 1999, Bee colony collapse disorder continues to be a serious issue. In Australia, where imidacloprid is widely used, there are no reports of colony collapse disorder, and there are also none of the viruses and mites that have also been linked as possible causes.

History

On January 21, 1986 a patent was filed, and granted on May 3, 1988, for imidacloprid in the United States (U.S. Pat. No. 4,742,060) by Nihon Tokushu Noyaku Seizo K.K. of Tokyo, Japan.[4]

On March 25, 1992, Miles, Inc. (later Bayer CropScience) applied for registration of imidacloprid for turfgrass and ornamentals in the United States. On March 10, 1994, the U.S. Environmental Protection Agency approved the registration of imidacloprid.[5]

On January 26, 2005, the Federal Register notes the establishment of the '(Pesticide Tolerances for) Emergency Exemptions' for imidacloprid. It use was granted to Hawaii (for the) use (of) this pesticide on bananas(,) and the States of Minnesota, Nebraska, and North Dakota to use (of) this pesticide on sunflower(s).[6]

Biochemistry

Imidacloprid is a systemic chloronicotinyl pesticide, belonging to the class of neonicotinoid insecticides. It acts as a neurotoxin and interferes with the transmission of nerve impulses in insects by binding irreversibly to specific insect nicotinic acetylcholine receptors. [7] [18]Interaction of Imidacloprid Metabolites and Analogues with the Nicotinic Acetylcholine Receptors of Mouse Brain in Relation to Toxicity. Chao and Casida 1997</ref> [8] [9]

As a systemic pesticide, imidacloprid translocates or moves easily in the xylem of plants from the soil into the leaves, fruit, pollen, and nectar of a plant. Imidacloprid also exhibits excellent translaminar movement in plants and can penetrate the leaf cuticle and move readily into leaf tissue. [10] Since imidacloprid is efficacious at very low levels (nanogram and picogram), it can be applied at lower concentrations (e.g., 0.05–0.125 lb/acre or 55–140 g/ha) than other neurotoxins, particularly organophosphates. [11]

The main routes of dissipation of imidacloprid in the environment are aqueous photolysis (half-life = 1–4 hours) and plant uptake. The major photo-metabolites include imidacloprid desnitro, imidacloprid olefine, imidacloprid urea, and five minor metabolites. The end product of photodegradation is chloronicotinic acid (CNA). Since imidacloprid has a low vapor pressure, it normally does not volatilize readily. [12]

Imidacloprid is moderately soluble in water. It is not stable in water and in the presence of light breaks down rapidly. In water not in the presence of light, it's half life is longer. It does not bioaccumulate. In soil under aerobic conditions, imidacloprid has been shown to have half lives of 6 - 18 months. Ultimately, imidacloprid breaks into carbon dioxide. As it breaks down it transitions through metabolites that include imidacloprid nitrosimine, imidacloprid desnitro, hydroxynicotinic acid, and imidacloprid urea. [13] [14]

Both the U.S. Environmental Protection Agency and the Pest Management Regulatory Agency in Canada consider imidacloprid to have characteristic that give it potential to run off into surface water if used in flood plains and highly porous soils with very shallow ground water. In normal use however, runoff potential is virtually nil. When tested for in runoff during rain events, minuscule amounts have been detected. Typically in the .5 - 1 part per billion range. The EPA considers chronic exposure of 1770 ppb to be an issue. [15] [16]

Toxicology

Imidacloprid is toxic to honey bees with a contact acute LD50 = 0.078 ug a.i./bee and an acute oral LD50 = 0.0039 ug a.i./bee. [17] Other systemic pesticides that have a higher acute toxicity to honey bees include clothianidin, thiamethoxam, dinotefuran, fipronil, emmamectin benzoate, and spinosad. [18] [19]


Researchers Kreutzweiser and Thompson (2009) from the Canadian Forest Service showed that imidacloprid at realistic field concentrations inhibits non-target terrestrial invertebrates that decompose leaf litter. In their study, there was no significant indication that invertebrates detected or avoided imidacloprid-treated leaves. [20]

In bobwhite quail (Colinus virginianus), imidacloprid was determined to be moderately toxic with an acute oral LD50 of 152 mg a.i./kg. These levels are much higher than would realistically be encountered. It was slightly toxic in a 5-day dietary study with an acute oral LC50 of 1,420 mg a.i./kg diet, a NOAEC of < 69 mg a.i./kg diet, and a LOAEC = 69 mg a.i./kg diet. Exposed birds exhibited ataxia, wing drop, opisthotonos, immobility, hyperactivity, fluid-filled crops and intestines, and discolored livers. In a reproductive toxicity study with bobwhite quail, the NOAEC = 120 mg a.i./kg diet and the LOAEC = 240 mg a.i./kg diet. Eggshell thinning and decreased adult weight were observed at 240 mg a.i./kg diet. [21] [22]


Overdosage

Persons who might orally ingest acute amounts would experience emesis, diaphoresis, drowsiness and disorientation. This would need to be intentional since a large amount would need to be ingested to experience a toxic reaction. In dogs the LD50 is 450 mg/Kg of body weight. Blood imidacloprid concentrations may be measured to confirm diagnosis in hospitalized patients or to establish the cause of death in postmortem investigations.[23]

Uses

The most widely used applications for imidacloprid in California are pest control in structures, turf pest control, grape growing, and head and leaf lettuce growing. Other widespread crop uses are rice, grains/cereals including corn (maize), potatoes, vegetables, sugar beets, fruit, cotton, and hops. Target insects include sucking insects (e.g., aphids, whiteflies, leafhoppers and planthoppers, thrips, scales, mealybugs, bugs, psyllids, and phylloxera), beetles (e.g., longhorn beetles, leaf beetles, Colorado potato beetles, rice water-weevils, wireworms, grubs, and flea beetles), and others (e.g., leafminers, some diptera, termites, locusts, and fleas).

As an insecticide spray, it is used on a wide variety of agricultural crops, ornamentals, and turf. It is also marketed for termite control, for flea control on pets, and for household cockroach control.

A systemic insecticide

Imidacloprid, which is a systemic pesticide, is readily taken up by plant roots and translocates up into the plant leaves, fruit, pollen, and nectar via the xylem. Insects that eat the leaves or plant fluids may be killed, and pollinators that feed on the pollen and nectar may be exposed to imidacloprid. The products Confidor and Admire are intended for application via irrigation, application to the soil, or on foliage, while Gaucho is intended for use as a seed dressing, applied to the seed before sowing.

Imidacloprid is the active ingredient in Bayer's Advantage brand flea drops.[24]

See also

References

  1. ^ Imidacloprid at Extoxnet
  2. ^ [1] USDA Forest Service. Imidacloprid: Human Health and Ecological Risk Assessment. Final Report. Dec 28, 2005.
  3. ^ [2] National Pesticide Information Center. Imidacloprid: General Fact Sheet. May 2010.
  4. ^ U.S. Pat. No. 4,742,060 - uspto.gov
  5. ^ [3] Imidacloprid Cleared Science Reviews. U.S. EPA.
  6. ^ Imidacloprid; Pesticide Tolerances for Emergency Exemptions Federal Register: January 26, 2005 (Volume 70, Number 16), Page 3634-3642- epa.gov
  7. ^ [4] Canadian Water Quality Guidelines: Imidacloprid
  8. ^ [5]Neonicotinoid Insecticides. Tomizawa et al 2000
  9. ^ [6] Evaluation of Affinity of Neonicotinoid Insecticides for Rat Brain Nicotinic Acetylcholine Receptors. Okumoto and Ozoe 2002
  10. ^ [7] Environmental Fate of Imidacloprid California Department of Pesticide Regulation 2006
  11. ^ [8]European Food Safety Authority. Conclusion regarding the peer review of the pesticide risk assessment of the active substance imidacloprid. July 28, 2008.
  12. ^ [9] Canadian Water Quality Guidelines: Imidacloprid
  13. ^ [10] Canadian Water Quality Guidelines: Imidacloprid
  14. ^ [European Draft Assessment Report: Imidacloprid. Annex B, B.7. February 2006]
  15. ^ [11] Canadian Water Quality Guidelines: Imidacloprid
  16. ^ [12] Detections of Imidacloprid in Surface Waters. Starner and Goh 2012
  17. ^ [13] Environmental Fate and Effects Division Problem Formulation for the Registration Review of Imidacloprid
  18. ^ [14]Pesticide Reregistration Status USEPA
  19. ^ [regulations.gov]Regulations.gov U.S.
  20. ^ [15] Imidacloprid in leaves from systemically treated trees may inhibit litter breakdown by non-target invertebrates. Kreutzweiser and Thompson 2009
  21. ^ [16]Canadian Water Quality Guidelines: Imidacloprid, Scientific Support Document. 2007. Canadian Council of Ministers of the Environment.
  22. ^ [17]Imidacloprid Cleared Science Reviews. U.S. EPA.
  23. ^ R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 764-765.
  24. ^ Advantage for Dogs, Bayer Animal Health Australia

Sources

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