|This article's factual accuracy is disputed. (August 2014)|
|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)|
Except where noted otherwise, data is given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
|what is: / ?)(|
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 in the nicotinergic neuronal pathway. By blocking nicotinic acetylcholine receptors, imidacloprid prevents acetylcholine from transmitting impulses between nerves resulting in the insect's paralysis, and eventually death. It is effective on contact and via stomach action. Because imidacloprid binds much more strongly to insect neuron receptors than to mammal neuron receptors, this insecticide is selectively more toxic to insects than mammals.
Imidacloprid is currently the most widely used insecticide in the world. 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. 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, protection of trees from boring insects, and in preservative treatment of some types of lumber products (e.g., Ecolife brand).
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. As a result, several countries have restricted use of imidacloprid and other neonicotinoids. 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 on may be flawed, or even deceptive.
Imidacloprid is the most widely used insecticide in the world. Its major uses include:
- Agriculture - Control of aphids, cane beetles, thrips, stink bugs, locusts, and a variety of other insects that damage crops
- Arboriculture - Control of the emerald ash borer and other insects that attack trees (including hemlock, maple, oak, and birch)
- Home Protection - Control of termites, carpenter ants, cockroaches, and moisture-loving insects
- Domestic animals - Control of fleas (applied to the neck)
- Turf - Control of Japanese beetle larvae
- Gardening - Control of aphids and other pests
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.
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.
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).
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), Confidor, Conguard, Gaucho, Hachikusan, Intercept, Kohinor, Mallet, Maxforce Quantum, Merit, Nuprid, Optrol, Premise, Prothor, Provado, Turfthor, Temprid (Bayer), Winner, and Xytect.
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.
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.
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.
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.
Imidacloprid breaks down rapidly in water in the presence of light (half-life = 1–4 hours) but is persistent in water in the absence of light. It has a water solubility of .61 g/L, which is relatively high. 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. Major soil metabolites include imidacloprid nitrosimine, imidacloprid desnitro and imidacloprid urea, which ultimately degrade to 6-chloronicotinic acid, CO2, and bound residues. 6-Chloronicotinic acid is recently shown to be mineralized via a nicotinic acid (vitamin B3) pathway in a soil bacterium.
In soil, imidacloprid strongly binds to organic matter. When not exposed to light, imidacloprid and dinotefuran break down slowly in water, and thus have the potential to persist in groundwater for extended periods. In surveys of groundwater, 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.
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.
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). 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).
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]".
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). Tolerances for imidacloprid residues in food range from 0.02 mg/kg in eggs to 3.0 mg/kg in hops.
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.
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). (For comparison, the weight of just the DNA of a human cell is about 7 picograms.) 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.
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. 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." Several studies have found that sub-lethal levels of imidacloprid increase honey bee susceptibility to the pathogen Nosema.
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.
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.
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.
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.
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".
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." 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.
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.
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. 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. 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. 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 other land usage factor.
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.
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.
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.
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.
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.
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.
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