Imidacloprid

From Wikipedia, the free encyclopedia

This is an old revision of this page, as edited by 222.165.255.198 (talk) at 01:00, 29 February 2012 (plenty of citations now, but an ongoing months-long POV edit war). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

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 systemic insecticide which acts as an insect neurotoxin and belongs to a class of chemicals called the neonicotinoids. Neonicotinoids are a class of insecticides which act on the central nervous system of insects with lower toxicity to mammals. 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 Admire, Advantage (Advocate) (flea killer for pets), Gaucho, Mallet, Merit, Nuprid, Prothor, Turfthor, Confidor, Conguard, Dominion 2L, Hachikusan, Kohinor, Optrol, Premise, Prothor, Provado, Intercept, Winner, and Xytect. Imidacloprid is one of the most widely used insecticides and can be applied by soil injection, tree injection, application to the skin, broadcast foliar, ground application as a granular or liquid formulation, or as a pesticide-coated seed treatment.[2][3]

Authorized 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.

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.


Background

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 works by interfering with the transmission of nerve impulses in insects by binding irreversibly to specific insect nicotinic acetylcholine receptors. [7]

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. [8] 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 insecticides, The availability of imidacloprid and its favorable toxicity package as compared to other insecticides on the market in the 1990's, allowed the EPA to cancel and replace far more toxic insecticides including the acetylcholinesterase inhibitors, the organophosphorus compounds and methylcarbamates. Cite error: A <ref> tag is missing the closing </ref> (see the help page).

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. [9]

Imidacloprid is persistent and highly 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. Major soil metabolites include imidacloprid nitrosimine, imidacloprid desnitro, hydroxynicotinic acid, and imidacloprid urea, which ultimately degrade to chloronicotinic acid, CO2, and bound residues. [10] [11] [12]

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. [13] [14] 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." [15]

Toxicology

Based on laboratory rat studies, imidacloprid is rated as "moderately toxic" on an acute oral basis to mammals and low toxicity on a dermal basis by the World Health Organization and the United States Environmental Protection Agency‎ (class II or III, requiring a "Warning" or "Caution" label). 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). [16] [17] Tolerances for imidacloprid residues in food range from 0.02 mg/kg in eggs to 3.0 mg/kg in hops.[18]

Animal toxicity is moderate when ingested orally and low when applied dermally. The oral LD50 of imidacloprid is 450 mg a.i./kg body weight in rats and 131 mg a.i./kg bw in mice; the 24-hour dermal LD50 in rats is greater than >5000 mg a.i./kg bw. It is not irritating to eyes or skin in rabbits and guinea pigs (although some commercial preparations contain clay as an inert ingredient, which may be an irritant). The acute inhalation LD50 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 measurements. [19] [20]

Bees and other insect pollinators

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. [21] 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." [22] 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. [23] 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. [24] [25]

Imidacloprid is one of the most highly toxic insecticides 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. Other systemic pesticides with a similar high acute toxicity to honey bees include clothianidin, thiamethoxam, dinotefuran, fipronil, emamectin benzoate, and spinosad.[26] Pesticide Reregistration Status USEPA [27] Regulations.gov U.S.

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.[28][29][30][31] The olefine and hydroxy metabolites of imidacloprid, which are found in plants, are very toxic to honeybees.[31] 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.[32][33][34][35][36][37][38][39] 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.[40][41]

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.[42]

Birds

In bobwhite quail (Colinus virginianus), imidacloprid was determined to be moderately toxic with an acute oral LD50 of 152 mg a.i./kg. (this is a relatively large amount and exposure to this amount in real situations is highly unlikely) 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. [43] [44]

Imidacloprid is highly toxic to four bird species: Japanese quail, house sparrow, canary, and pigeon. The acute oral LD50 for Japanese quail (Coturnix coturnix) is 31 mg a.i./kg bw with a NOAEL = 3.1 mg a.i./kg. The acute oral LD50 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 LD50s 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 LC50 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. [45] [46] 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. [47] [48]

Aquatic life

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. [49] [50] Although direct toxicity to fish appears low, there is the possibility of secondary risks to fish through altercations in food chains that involve aquatic invertebrates.

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.[51]


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] Environmental Fate of Imidacloprid California Department of Pesticide Regulation 2006
  9. ^ [6] Canadian Water Quality Guidelines: Imidacloprid
  10. ^ [7] Canadian Water Quality Guidelines: Imidacloprid
  11. ^ [European Draft Assessment Report: Imidacloprid. Annex B, B.7. February 2006]
  12. ^ [8] Environmental Fate and Effects Division Problem Formulation for Imidacloprid
  13. ^ [9] Environmental Fate and Effects Division Problem Formulation for Imidacloprid
  14. ^ [10] Canadian Water Quality Guidelines: Imidacloprid
  15. ^ [11] Detections of Imidacloprid in Surface Waters. Starner and Goh 2012
  16. ^ [12]Imidacloprid Cleared Science Reviews. U.S. EPA.
  17. ^ [13]Endocrine Disruptor Screening Program: Tier 1 Screening Order Issuing Announcement. Federal Register Notice, Oct 21, 2009. Vol. 74, No. 202, pp. 54422-54428
  18. ^ [14]EXTOXNET. Imidacloprid
  19. ^ Cornell Extension Toxicology NetworkEXTOXNET. Imidacloprid
  20. ^ [15]Water Quality Guidelines: Imidacloprid, Scientific Support Document. 2007. Canadian Council of Ministers of the Environment.
  21. ^ [16] Congressional Research Service Honey Bee Colony Collapse Disorder
  22. ^ [http://www.ars.usda.gov/is/br/ccd/ccdprogressreport2010.pdf USDA Colony Collapse Disorder Progress Report. June 2010
  23. ^ [http://www.springerlink.com/content/p1027164r403288u/ Pesticide exposure in honey bees Pettis et al 2012
  24. ^ [17] Interactions between Nosema and a neonicotinoid Alaux et al 2010
  25. ^ [18] Exposure to sublethal doses of fipronil and thiacloprid. Vidau et al 2011
  26. ^ [19]
  27. ^ [www.regulations.gov]
  28. ^ 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
  29. ^ 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.
  30. ^ 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.
  31. ^ a b 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.
  32. ^ 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.
  33. ^ 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.
  34. ^ Desneux, N., Decourtye, A., and Delpuech, J-M. 2007. The sublethal effects of pesticides on beneficial arthropods. Annual Review of Entomology 52: 81–106
  35. ^ 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
  36. ^ 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.
  37. ^ 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.
  38. ^ 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.
  39. ^ 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
  40. ^ [20] French Scientific and Technical Report on the Impact of Imidacloprid to Bees.
  41. ^ [21] Environmental Fate and Effects Problem Formulation for the Registration Review of Imidacloprid. Nov 13, 2008. USEPA.
  42. ^ [22] Imidacloprid in leaves from systemically treated trees may inhibit litter breakdown by non-target invertebrates. Kreutzweiser and Thompson 2009.
  43. ^ [23]Canadian Water Quality Guidelines: Imidacloprid, Scientific Support Document. 2007. Canadian Council of Ministers of the Environment.
  44. ^ [24]Imidacloprid Cleared Science Reviews. U.S. EPA.
  45. ^ [25]
  46. ^ [26]Imidacloprid Cleared Science Reviews. U.S. EPA.
  47. ^ [27]European Food Safety Authority. Conclusion regarding the peer review of the pesticide risk assessment of the active substance imidacloprid. July 28, 2008.
  48. ^ [28]Water Quality Guidelines: Imidacloprid, Scientific Support Document. 2007. Canadian Council of Ministers of the Environment.
  49. ^ [29] Environmental Fate and Effects Division Problem Formulation for the Registration Review of Imidacloprid
  50. ^ [30]Imidacloprid Cleared Science Reviews. U.S. EPA.
  51. ^ R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 764-765.

Sources

External links

Retrieved from "https://en.wikipedia.org/w/index.php?title=Imidacloprid&oldid=479392718"