Imidacloprid

Imidacloprid[1]
Names
IUPAC name
N-{1-[(6-Chloro-3-pyridyl)methyl]-4,5-dihydroimidazol-2-yl}nitramide
Identifiers
138261-41-3 YesY
3D model (Jmol) Interactive image
ChEBI CHEBI:39169 YesY
ChEMBL ChEMBL406819 YesY
ChemSpider 77934 YesY
DrugBank DB07980 YesY
ECHA InfoCard 100.102.643
KEGG C11110 YesY
PubChem 86418
UNII 3BN7M937V8 YesY
Properties
C9H10ClN5O2
Molar mass 255.661
Appearance Colorless crystals
Melting point 136.4 to 143.8 °C (277.5 to 290.8 °F; 409.5 to 416.9 K)
0.51 g/L (20 °C)
Pharmacology
QP53AX17 (WHO)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
YesY verify (what is YesYN ?)
Infobox references

Imidacloprid is a systemic insecticide which acts as an insect neurotoxin and belongs to a class of chemicals called the neonicotinoids which act on the central nervous system of insects, with much lower toxicity to mammals. The chemical works by interfering with the transmission of stimuli in the insect nervous system. Specifically, it causes a blockage of the nicotinergic neuronal pathway. By blocking nicotinic acetylcholine receptors, imidacloprid prevents acetylcholine from transmitting impulses between nerves, resulting in the insect's paralysis and eventual death. It is effective on contact and via stomach action.[1] Because imidacloprid binds much more strongly to insect neuron receptors than to mammal neuron receptors, this insecticide is more toxic to insects than to mammals.[2]

As of 1999, Imidacloprid was the most widely used insecticide in the world.[3] Although it is now off patent, the primary manufacturer of this chemical is Bayer CropScience (part of Bayer AG). It is sold under many names for many uses; it can be applied by soil injection, tree injection, application to the skin of the plant, broadcast foliar, ground application as a granular or liquid formulation, or as a pesticide-coated seed treatment.[4][5] Imidacloprid is widely used for pest control in agriculture. Other uses include application to foundations to prevent termite damage, pest control for gardens and turf, treatment of domestic pets to control fleas,[2] protection of trees from boring insects,[6] and in preservative treatment of some types of lumber products (e.g., Ecolife brand).[7]

Recent research suggests that widespread agricultural use of imidacloprid and other pesticides may be contributing to honey bee colony collapse disorder, the decline of honey bee colonies in Europe and North America observed since 2006.[8][9][10] As a result, several countries have restricted use of imidacloprid and other neonicotinoids.[8] 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, or even deceptive.[11][12]

Authorized uses

Imidacloprid is the most widely used insecticide in the world. Its major uses include:

When used on plants, imidacloprid, which is systemic, is slowly taken up by plant roots and slowly translocated up the plant via xylem tissue.

Application to trees

When used on trees, it can take 30–60 days to reach the top (depending on the size and height) and enter the leaves in high enough quantities to be effective. Imidacloprid can be found in the trunk, the branches, the twigs, the leaves, the leaflets, and the seeds. Many trees are wind pollinated. But others such as fruit trees, linden, catalpa, and black locust trees are bee and wind pollinated and imidacloprid would likely be found in the flowers in small quantities. Higher doses must be used to control boring insects than other types.[6]

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.[15]

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.[16]

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).[17]

Brand names

Imidacloprid has many brands and formulations for a wide range of uses, from delousing or defleaing animals to protecting trees. Selected brand names include Admire, Advantage (Advocate) (flea killer for pets), Centerfire 75, Confidor, Conguard, Gaucho, Hachikusan, Intercept, InVict, Kohinor, Mallet, Maxforce Quantum, Merit, Nuprid, Optrol, Premise, Prothor, Provado, Turfthor, Temprid (Bayer), Winner, and Xytect.

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.[18]

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.[19]

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 1990s allowed the EPA to replace more toxic insecticides including the acetylcholinesterase inhibitors, the organophosphorus compounds, and methylcarbamates.[20][21]

Environmental fate

The main routes of dissipation of imidacloprid in the environment are aqueous photolysis (half-life = 1–4 hours) and plant uptake. The major photometabolites include imidacloprid desnitro, imidacloprid olefine, imidacloprid urea, and five minor metabolites. The end product of photodegradation is chloronicotinic acid (CNA) and ultimately carbon dioxide. Since imidacloprid has a low vapor pressure, it normally does not volatilize readily.[18]

Although imidacloprid breaks down rapidly in water in the presence of light, it remains persistent in water in the absence of light. It has a water solubility of .61 g/L, which is relatively high.[22] In the dark, at pH between 5 and 7, it breaks down very slowly, and at pH 9, the half-life is about 1 year. In soil under aerobic conditions, imidacloprid is persistent with a half-life of the order of 1–3 years. On the soil surface the half-life is 39 days.[23] Major soil metabolites include imidacloprid nitrosimine, imidacloprid desnitro and imidacloprid urea, which ultimately degrade to 6-chloronicotinic acid, CO2, and bound residues.[13][18][24] 6-Chloronicotinic acid is recently shown to be mineralized via a nicotinic acid (vitamin B3) pathway in a soil bacterium.[25]

In soil, imidacloprid strongly binds to organic matter. When not exposed to light, imidacloprid breaks down slowly in water, and thus has the potential to persist in groundwater for extended periods. However, in a survey of groundwater in areas of the United States which had been treated with imidacloprid for the emerald ash borer, imidacloprid was usually not detected. When detected, it was present at very low levels, mostly at concentrations less than 1 part per billion (ppb) with a maximum of 7 ppb, which are below levels of concern for human health. The detections have generally occurred in areas with porous rocky or sandy soils with little organic matter, where the risk of leaching is high — and/or where the water table was close to the surface.[26]

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 and thus warn not to apply it in areas where soils are permeable, particularly where the water table is shallow.[13][18]

According to standards set by the environmental ministry of Canada, if used correctly (at recommended rates, without irrigation, and when heavy rainfall is not predicted), imidacloprid does not characteristically leach into the deeper soil layers despite its high water solubility (Rouchaud et al. 1994; Tomlin 2000; Krohn and Hellpointner 2002).[18] In a series of field trials conducted by Rouchaud et al. (1994, 1996), in which imidacloprid was applied to sugar beet plots, it was consistently demonstrated that no detectable leaching of imidacloprid to the 10–20 cm soil layer occurred. Imidacloprid was applied to a corn field in Minnesota, and no imidacloprid residues were found in sample column segments below the 0-15.2 cm depth segment (Rice et al. 1991, as reviewed in Mulye 1995).[13][18]

However, a 2012 water monitoring study by the state of California, performed by collecting agricultural runoff during the growing seasons of 2010 and 2011, found imidacloprid in 89% of samples, with levels ranging from 0.1-3.2 µg/L. 19% of the samples exceeded the EPA threshold for chronic toxicity for aquatic invertebrates of 1.05 µg/L. The authors also point out that Canadian and European guidelines are much lower (0.23 µg/L and 0.067 µg/L, respectively) and were exceeded in 73% and 88% of the samples, respectively. The authors concluded that "imidacloprid commonly moves offsite and contaminates surface waters at concentrations that could harm aquatic invertebrates".[27]

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][28] Tolerances for imidacloprid residues in food range from 0.02 mg/kg in eggs to 3.0 mg/kg in hops.[1]

Animal toxicity is moderate when ingested orally and low when applied dermally. 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.[1][18]

Bees and other insects

To members of the genus Apis, the honey bees, imidacloprid is one of the most toxic chemicals ever created as an insecticide. The acute oral LD50 ranges from 5 to 70 picograms of active ingredient per bee, making it more toxic to bees than the organophosphate dimethoate (oral LD50 0.152 µg/bee) or the pyrethroid cypermethrin (oral LD50 0.160 µg/bee).[29] (For comparison, the weight of just the DNA of a human cell is about 7 picograms.[30]) The toxicity of imidacloprid to bees differs from most insecticides in that it is more toxic orally than by contact. The contact acute LD50 is 0.024 µg active ingredient per bee.[31]

Imidacloprid was first widely used in the United States in 1996 as it replaced three broad classes of insecticides. In 2006, U.S. commercial migratory beekeepers reported sharp declines in their honey bee colonies. Such declines had happened in the past; however unlike the case in 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.[32] 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."[33] Several studies have found that sub-lethal levels of imidacloprid increase honey bee susceptibility to the pathogen Nosema.[34][35][36]

Dave Goulson (2012) of the University of Stirling showed that trivial effects of imidacloprid in lab and greenhouse experiments can translate into large effects in the field. The research found that bees consuming the pesticide suffered an 85% loss in the number of queens their hives produced, and a doubling of the number of bees who failed to return from food foraging trips.[8][9]

Lu et al. (2012) reported they were able to replicate CCD with sub-lethal doses of imidacloprid. The imidacloprid-treated hives were nearly empty, consistent with CCD, and the authors exclude Varroa or Nosema as contributing causes.[10]

In May 2012, researchers at the University of San Diego released a study showing that honey bees treated with a small dose of imidacloprid, comparable to what they would receive in nectar and formerly considered a safe amount, became "picky eaters," refusing nectars of lower sweetness and preferring to feed only on sweeter nectar. It was also found that bees exposed to imidacloprid performed the "waggle dance," the movements that bees use to inform hive mates of the location of foraging plants, at a lower rate.[37]

Researchers from the Canadian Forest Service showed that imidacloprid used on trees at realistic field concentrations decreases leaf litter breakdown owing to adverse sublethal effects on non-target terrestrial invertebrates. The study did not find significant indication that the invertebrates, which normally decompose leaf litter, preferred uncontaminated leaves, and concluded that the invertebrates could not detect the imidacloprid.[38]

A 2012 in situ study provided strong evidence that exposure to sublethal levels of imidacloprid in high fructose corn syrup (HFCS) used to feed honey bees when forage is not available causes bees to exhibit symptoms consistent to CCD 23 weeks post imidacloprid dosing. The researchers suggested that "the observed delayed mortality in honey bees caused by imidacloprid in HFCS is a novel and plausible mechanism for CCD, and should be validated in future studies".[39][40]

Sublethal doses (<10 ppb) to aphids have been found to lead to altered behavior, such as wandering and eventual starvation. Very low concentrations also reduced nymph viability.[41] In bumblebees exposure to 10 ppb imidacloprid reduces natural foraging behaviour, increases worker mortality and leads to reduced brood development.[42] A 2013 study showed that bumblebee colonies exposed to 10 ppb of imidacloprid started failing after three weeks when the death rate increased and the birth rate decreased. The researchers attributed this to exposed colonies performing essential tasks, such as foraging, thermoregulation and brood care, less well than unexposed colonies.[43] This suggests that sublethal imidacloprid causes colony failure through reduced colony function.

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 might be flawed, concluding that, "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."[11] An author of a Science study prompting the EFSA review suggested that industry science pertaining to neonicotinoids may have been deliberately deceptive, and the UK Parliament has asked the manufacturer Bayer Crop Science to explain discrepancies in evidence they have submitted to an investigation.[12]

Birds

In bobwhite quail (Colinus virginianus), imidacloprid was determined to be moderately toxic with an acute oral LD50 of 152 mg a.i./kg. 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.[16][18]

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 canaria) 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.[16][18] 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.[18][21] The hypothesis that imidacloprid has a negative impact on insectivorous bird populations is supported by a study of bird population trends in the Netherlands, where correlation has been identified between surface-water concentrations of imidacloprid and population decline. At imidacloprid concentrations of more than 20 nanograms per litre, bird populations tended to decline by 3.5 per cent on average annually.[44] Additional analyses in this study revealed that spatial pattern of bird population decline appeared only after the introduction of imidacloprid to the Netherlands, in the mid-1990s, and that this correlation is not linked to any other land usage factor.

Aquatic life

Imidacloprid is highly toxic on an acute basis to aquatic invertebrates, with EC50 values = 0.037 - 0.115 ppm. It is also highly toxic to aquatic invertebrates on a chronic basis (effects on growth and movement): NOAEC/LOAEC = 1.8/3.6 ppm in daphnids; NOAEC = 0.001 in Chironomus midge, and NOAEC/LOAEC = 0.00006/0.0013 ppm in mysid shrimp. Its toxicity to fish is relatively low; however, the EPA has requested review of secondary effects on fish with food chains that include sensitive aquatic invertebrates.[13]

Plant life

Imidacloprid has been shown to turn off some genes that some rice varieties use to produce defensive chemicals. While imidacloprid is used for control of the brown planthopper and other rice pests, there is evidence that imidacloprid actually increases the susceptibility of the rice plant to planthopper infestation and attacks.[45]

Health impact

Imidacloprid and its nitrosoimine metabolite (WAK 3839) have been well studied in rats, mice and dogs. In mammals, the primary effects following acute high-dose oral exposure to imidacloprid are mortality, transient cholinergic effects (dizziness, apathy, locomotor effects, labored breathing) and transient growth retardation. Exposure to high doses may be associated with degenerative changes in the testes, thymus, bone marrow and pancreas. Cardiovascular and hematological effects have also been observed at higher doses. The primary effects of longer term, lower-dose exposure to imidacloprid are on the liver, thyroid, and body weight (reduction). Low- to mid-dose oral exposures have been associated with reproductive toxicity, developmental retardation and neurobehavioral deficits in rats and rabbits. Imidacloprid is neither carcinogenic in laboratory animals nor mutagenic in standard laboratory assays.[46]

No studies have been published involving human subjects chronically exposed to imidacloprid. Effects of imidacloprid on human health and the environment depend on how much imidacloprid is present and the length and frequency of exposure. Effects also depend on the health of a person and/or certain environmental factors.[47]

A study conducted in tissue culture of neurons harvested from newborn rats showed that Imidacloprid and acetamiprid, another neonicotinoid, excited the neurons in a way similar to nicotine, so the effects of neonicotinoids on developing mammalian brains might be similar to the adverse effects of nicotine.[48]

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 (i.e., in any sample of medium sized dogs weighing, say, 13 kilograms (29 lb), half of them would be killed after consuming 5,850 mg of imidacloprid, or about  1⁄5th of an ounce) . Blood imidacloprid concentrations may be measured to confirm diagnosis in hospitalized patients or to establish the cause of death in postmortem investigations.[49]

See also

References

  1. 1 2 3 4 "Pesticide Information Profiles: Imidacloprid Breaz". Extension Toxicology Network. Retrieved April 7, 2012.
  2. 1 2 3 4 Gervais, J.A.; Luukinen, B.; Buhl, K.; Stone, D. (April 2010). "Imidacloprid Technical Fact Sheet" (PDF). National Pesticide Information Center. Retrieved 12 April 2012.
  3. ↑ Yamamoto, Izuru (1999). "Nicotine to Nicotinoids: 1962 to 1997". In Yamamoto, Izuru; Casida, John. Nicotinoid Insecticides and the Nicotinic Acetylcholine Receptor. Tokyo: Springer-Verlag. pp. 3–27.
  4. ↑ USDA Forest Service. Imidacloprid: Human Health and Ecological Risk Assessment. Final Report. Dec 28, 2005.
  5. ↑ National Pesticide Information Center. Imidacloprid: General Fact Sheet. May 2010.
  6. 1 2 3 Herms DA, McCullough DG, Smitley DR, Sadof C, Williamson RC, Nixon PL (2009). "Insecticide options for protecting ash trees from emerald ash borer" (PDF). North Central IPM Center Bulletin. Retrieved April 7, 2012.
  7. ↑ International Code Council Evaluation Service Report ESR-1851, dated August 2011.
  8. 1 2 3 Carrington, Damian (March 29, 2012). "Pesticides linked to honeybee decline". The Guardian. Retrieved April 7, 2012.
  9. 1 2 Whitehorn, P. R.; O'Connor, S.; Wackers, F. L.; Goulson, D. (2012). "Neonicotinoid Pesticide Reduces Bumble Bee Colony Growth and Queen Production". Science. 336 (6079): 351–2. doi:10.1126/science.1215025. ISSN 0036-8075. PMID 22461500.
  10. 1 2 Lu, Chensheng; Warchol, K. M.; Callahan, R. A. (2012). "In situ replication of honey bee colony collapse disorder (13 March 2012 corrected proof)" (PDF). Bulletin of Insectology. 65 (1). ISSN 1721-8861. Retrieved 7 April 2012.
  11. 1 2 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.
  12. 1 2 Damian Carrington (16 January 2013) "Insecticide 'unacceptable' danger to bees, report finds" The Guardian
  13. 1 2 3 4 5 6 Federoff, N.E.; Vaughan, Allen; Barrett, M.R. (13 November 2008). "Environmental Fate and Effects Division Problem Formulation for the Registration Review of Imidacloprid". US EPA. Retrieved 18 April 2012.
  14. ↑ Preston, Richard (2007). "A Death in the Forest". The New Yorker.
  15. ↑ U.S. Pat. No. 4,742,060 - uspto.gov
  16. 1 2 3 4 Index of Cleared Science Reviews for Imidacloprid (Pc Code 129099) U.S. EPA.
  17. ↑ Imidacloprid; Pesticide Tolerances for Emergency Exemptions Federal Register: January 26, 2005 (Volume 70, Number 16), Page 3634-3642- epa.gov
  18. 1 2 3 4 5 6 7 8 9 10 Canadian Council of Ministers of the Environment (2007). Canadian water quality guidelines: imidacloprid: scientific supporting document (PDF). Winnipeg, Man.: Canadian Council of Ministers of the Environment. ISBN 978-1-896997-71-1.
  19. ↑ Environmental Fate of Imidacloprid California Department of Pesticide Regulation 2006
  20. ↑ "Imidacloprid: Risk Characterization Document - Dietary and Drinking Water Exposure" (PDF). California Environmental Protection Agency. February 9, 2006. Retrieved April 7, 2012.
  21. 1 2 Conclusion regarding the peer review of the pesticide risk assessment of the active substance imidacloprid. European Food Safety Authority. July 28, 2008.
  22. ↑ Flores-Céspedes, Francisco; Figueredo-Flores, Cristina Isabel; Daza-Fernández, Isabel; Vidal-Peña, Fernando; Villafranca-Sánchez, Matilde; Fernández-Pérez, Manuel (January 18, 2012). "Preparation and Characterization of Imidacloprid Lignin–Polyethylene Glycol Matrices Coated with Ethylcellulose". Journal of Agricultural and Food Chemistry. 60 (4): 1042–1051. doi:10.1021/jf2037483. PMID 22224401.
  23. ↑ Matthew Fossen (2006). "Environmental Fate of Imidacloprid" (PDF). Retrieved April 16, 2016.
  24. ↑ [European Draft Assessment Report: Imidacloprid. Annex B, B.7. February 2006]
  25. ↑ Madhura Shettigar, Stephen Pearce, Rinku Pandey, Fazlurrahman Khan, Susan J. Dorrian, Sahil Balotra, Robyn J. Russell, John G. Oakeshott, Gunjan Pandey. Cloning of a Novel 6-Chloronicotinic Acid Chlorohydrolase from the Newly Isolated 6-Chloronicotinic Acid Mineralizing Bradyrhizobiaceae Strain SG-6C. DOI: 10.1371/journal.pone.0051162 http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0051162
  26. ↑ Hahn, Jeffrey; Herms, Daniel A.; McCullough, Deborah G. (February 2011). "Frequently Asked Questions Regarding Potential Side Effects of Systemic Insecticides Used To Control Emerald Ash Borer". University of Michigan Extension, Michigan State University, The Ohio State University Extension.
  27. ↑ Starner, Keith; Goh, Kean S. (2012). "Detections of Imidacloprid in Surface Waters of Three Agricultural Regions of California, USA, 2010-2011". Bulletin of Environmental Contamination and Toxicology. 88 (3): 316–321. doi:10.1007/s00128-011-0515-5. PMID 22228315.
  28. ↑ Endocrine Disruptor Screening Program: Tier 1 Screening Order Issuing Announcement. Federal Register Notice, Oct 21, 2009. Vol. 74, No. 202, pp. 54422-54428
  29. ↑ Suchail, Séverine; Guez, David; Belzunces, Luc P. (November 2011). "Discrepancy between acute and chronic toxicity induced by imidacloprid and its metabolites in Apis mellifera". Environmental Toxicology and Chemistry. 20 (11): 2482–2486. doi:10.1002/etc.5620201113. PMID 11699773. Check date values in: |year= / |date= mismatch (help)
  30. ↑ R. L. Wysong (1 January 1976). The Creation-Evolution Controversy. Wysong Institute. p. 395. ISBN 978-0-918112-02-6.
  31. ↑ Suchail, Séverine; Guez, David; Belzunces, Luc P. (July 2000). "Characteristics of imidacloprid toxicity in two Apis mellifera subspecies". Environmental Toxicology and Chemistry. 19 (7): 1901–1905. doi:10.1002/etc.5620190726.
  32. ↑ Honey Bee Colony Collapse Disorder Congressional Research Service.
  33. ↑ "USDA Colony Collapse Disorder Progress Report" (PDF). USDA Agriculture Research Service. June 2010. Retrieved April 7, 2012.
  34. ↑ Alaux, Cédric; Brunet, Jean-Luc; Dussaubat, Claudia; Mondet, Fanny; Tchamitchan, Sylvie; Cousin, Marianne; Brillard, Julien; Baldy, Aurelie; Belzunces, Luc P.; Le Conte, Yves (2010). "Interactions between Nosema microspores and a neonicotinoid weaken honeybees (Apis mellifera)". Environmental Microbiology. 12 (3): 774–782. doi:10.1111/j.1462-2920.2009.02123.x. ISSN 1462-2912. PMC 2847190Freely accessible. PMID 20050872.
  35. ↑ Didier, Elizabeth; Diogon, Cyril; Aufauvre, Marie; Fontbonne, Julie; Viguès, Régis; Brunet, Bernard; Texier, Jean-Luc; Biron, Catherine; Blot, David G.; El Alaoui, Nicolas; Belzunces, Hicham; Delbac, Luc P.; Delbac, Frédéric (2011). Didier, Elizabeth, ed. "Exposure to Sublethal Doses of Fipronil and Thiacloprid Highly Increases Mortality of Honeybees Previously Infected by Nosema ceranae". PLoS ONE. 6 (6): e21550. doi:10.1371/journal.pone.0021550. ISSN 1932-6203. PMC 3125288Freely accessible. PMID 21738706.
  36. ↑ Pettis, Jeffery S.; Vanengelsdorp, Dennis; Johnson, Josephine; Dively, Galen (2012). "Pesticide exposure in honey bees results in increased levels of the gut pathogen Nosema". Naturwissenschaften. 99 (2): 153–158. doi:10.1007/s00114-011-0881-1. ISSN 0028-1042. PMC 3264871Freely accessible. PMID 22246149.
  37. ↑ McDonald, Kim (23 May 2012). "Commonly Used Pesticide Turns Honey Bees Into 'Picky Eaters'". UCSD News Center. Retrieved 30 May 2012.
  38. ↑ Kreutzweiser, DP.; Thompson, DG.; Scarr, TA. (May 2009). "Imidacloprid in leaves from systemically treated trees may inhibit litter breakdown by non-target invertebrates". Ecotoxicol Environ Saf. 72 (4): 1053–7. doi:10.1016/j.ecoenv.2008.09.017. PMID 18973940.
  39. ↑ "Pesticide tied to bee colony collapse | Harvard Gazette". News.harvard.edu. Retrieved 2012-05-24.
  40. ↑ Chensheng Lu; Kenneth M. Warchol; Richard A. Callahan (2012). "In situ replication of honey bee colony collapse disorder" (PDF). Bulletin of Insectology. 65 (1): 1–8. Archived from the original (PDF) on May 26, 2012.
  41. ↑ Wollweber, Detlef; Tietjen, Klaus (1999). "Chloronicotinyl insecticides: a success of the new chemistry". In Yamamoto, Izuru; Casida, John. Nicotinoid Insecticides and the Nicotinic Acetylcholine Receptor. Tokyo: Springer-Verlag. pp. 109–125.
  42. ↑ Gill, R.J., Ramos-Rodriguez, O. and Raine, N.E., 2012. Combined pesticide exposure severely affects individual-and colony-level traits in bees. Nature, 491(7422), pp.105-108.
  43. ↑ Bryden, J., Gill, R.J., Mitton, R.A., Raine, N.E. and Jansen, V.A.A., 2013. Chronic sublethal stress causes bee colony failure. Ecology Letters, 16(12), pp.1463-1469.
  44. ↑ Hallmann, C.A.Hallman; Foppen, Ruud P. B.; Van Turnhout, Chris A. M.; De Kroon, Hans; Jongejans, Eelke (2014). "Declines in insectivorous birds are associated with high neonicotinoid concentrations". Nature. 511 (7509): 341–3. doi:10.1038/nature13531. PMID 25030173.
  45. ↑ Cheng, Yao; Shi, Zhao-Peng, Jiang, Li-Ben, Ge, Lin-Quan, Wu, Jin-Cai, Jahn, Gary C. (2012). "Possible connection between imidacloprid-induced changes in rice gene transcription profiles and susceptibility to the brown plant hopper Nilaparvata lugens Stål (Hemiptera: Delphacidae)". Pesticide Biochemistry and Physiology. 102 (3): 213–219. doi:10.1016/j.pestbp.2012.01.003. PMC 3334832Freely accessible. PMID 22544984.
  46. ↑ USDA, Forest Service ,Forest Health Protection (December 28, 2005). Imidacloprid - Human Health and Ecological Risk Assessment – Final Report "HUMAN HEALTH RISK ASSESSMENT / Overview. 3-1". United States Forest Service. Retrieved July 30, 2013.
  47. ↑ IMIDACLOPRID TECHNICAL FACT SHEET . National Pesticide Information Center Published April 2010, Retrieved July 30, 2013.
  48. ↑ Kimura-Kuroda J, Komuta Y, Kuroda Y, Hayashi M, Kawano H; Komuta; Kuroda; Hayashi; Kawano (2012). Okamoto, Shu-Ichi, ed. "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. PMC 3290564Freely accessible. PMID 22393406.
  49. ↑ R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 764-765.

Sources

External links

This article is issued from Wikipedia - version of the 11/11/2016. The text is available under the Creative Commons Attribution/Share Alike but additional terms may apply for the media files.