Imidacloprid is a systemic insecticide that acts as an insect neurotoxin and belongs to a class of chemicals called neonicotinoids acting on the central nervous system of insects. Chemicals work by disrupting the transmission of excitability in the insect nervous system. In particular, it causes the blockage of nicotinergic neuronal pathways. By blocking nicotinic acetylcholine receptors, imidacloprid prevents acetylcholine from transmitting impulses between nerves, resulting in insect paralysis and eventual death. It is effective on contact and through stomach acts. Because imidacloprid binds more strongly to insect neuron receptors than mammalian neuron receptors, these insecticides are more toxic to insects than to mammals.
In 1999, imidacloprid was the most widely used insecticide in the world. Although there is now no patent, the main producer of this chemical is Bayer CropScience (part of Bayer AG). It is sold with many names for many uses; it can be applied by soil injection, tree injections, application for plant skin, leaf broadcasting, soil application as granular or liquid formulation, or as a treatment of pesticide-coated seeds. Imidacloprid is widely used for pest control in agriculture. Other uses include applications to the foundation to prevent termite damage, pest control for lawns and gardens, pet care for flea control, tree protection from dull insects, and in preservative care of several types of wood products.
Video Imidacloprid
Official use
Imidacloprid is the most widely used insecticide in the world. Its main uses include:
- Agriculture - Leaf aphid control, sugarcane beetle, thrips, rotting insects, grasshoppers, and various other plant-damaging insects
- Arboric - An emerald ash pest, a hairy hemlock adelgid, and other insects that attack trees (including hemlock, maple, oak, and birch)
- Home Protection - Termite controls, wood ants, cockroaches, and moisture-like insects
- Domestic animals - Flea control (applied to the neck)
- Grass - Japanese beetle larvae control
- Gardening - Controlling aphids and other pests
When used on plants, imidacloprid, which is systemic, is gradually taken up by plant roots and gradually transplanting plants through xylem tissue.
Maps Imidacloprid
Application to tree
When used on trees, it can take 30-60 days to reach the top (depending on size and height) and insert leaves in high enough quantities to be effective. Imidacloprid can be found in stems, branches, twigs, leaves, leaflets, and seeds. Many trees are pollinated by the wind. But others like fruit trees, lindens, catalpas, and black grasshoppers are bees and pollinated winds and imidacloprids are likely to be found in small flowers. Higher doses should be used to control insects that are boring than other types.
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On January 21, 1986, a patent was filed, and granted on May 3, 1988, to imidacloprid in the United States (US Pat. No. 4,742,060) by Nihon Tokushu Noyaku Seizo K.K. from Tokyo, Japan.
On March 25, 1992, Miles, Inc. (later Bayer CropScience) applied for the registration of imidacloprid for turfgrass and ornamentals in the United States. On March 10, 1994, the US Environmental Protection Agency approved the enrollment of imidacloprid.
On January 26, 2005, the Federal Register notes the establishment of '(Pesticide Tolerance for) Emergency Relief' for Imidacloprid. The use is given to Hawaii for the use of these pesticides in bananas (,) and the State of Minnesota, Nebraska, and North Dakota to use (from) these pesticides on sunflower (s) .
Biochemistry
Imidacloprid is a systemic chloronikolin pesticide, including a class of neonicotinoid insecticides. This works by disrupting the transmission of nerve impulses in insects by binding irreversibly to certain nicotinic acetylcholine receptors.
As a systemic pesticide, imidacloprid translocates or moves easily in plant xylem from soil to leaves, fruit, pollen, and plant nectar. Imidacloprid also exhibits excellent translaminar movements in plants and can penetrate the leaf cuticle and move easily to the leaf tissue.
Because imidacloprid is efficacious at very low levels (nanograms and picograms), imidacloprid may be used at lower concentrations (eg 0.05-0.12 lb/acre or 55-140 g/ha) than other insecticides. The availability of imidacloprid and its beneficial toxicity packages compared with other insecticides on the market in the 1990s enabled EPA to replace more toxic insecticides including acetylcholinesterase inhibitors, organophosphorus compounds, and methylcarbamate.
Environmental fate
The main routes of imidacloprid dissipation in the environment are water photolysis (half-life = 1-4 hours) and plant uptake. The major photonabolites include imidacloprid desnitro, imidacloprid olefine, urea imidacloprid, and five minor metabolites. The end product of photodegradation is chloronicotinic acid (CNA) and finally carbon dioxide. Because imidacloprid has a low vapor pressure, it is usually not volatile.
Although the imidacloprid decomposes rapidly in the water in the presence of light, it remains persistent in water in the absence of light. It has a water solubility of 0.61 g/L, which is relatively high. In the dark, at a pH between 5 and 7, it is very slow, and at pH 9, the half-life is about 1 year. In soil under aerobic conditions, imidloprid is persistent with a half-life of 1-3 years. At the soil surface, the half-life is 39 days. Main soil metabolism includes imidacloprid nitrosimine, imidacloprid desnitro and urea imidacloprid, which eventually decreases to 6-chloronicotinic acid, CO 2 , and the residue is bound. 6-Chloronicotinic acid has recently been shown to mineralized through the nicotinic acid pathway (vitamin B3) in soil bacteria.
On the ground, imidacloprid greatly binds organic matter. When not exposed to light, imidacloprid breaks slowly in water, and thus has the potential to survive in groundwater for a long time. However, in a groundwater survey in the United States region that has been treated with imidacloprid for emerald ash borer, imidacloprid is usually undetectable. When detected, it is present at very low levels, mostly at concentrations less than 1 part per billion (ppb) with a maximum of 7 ppb, which is below the level of concern for human health. Detection generally occurs in areas with rocky or porous soils that are porous with little organic matter, where the risk of washing is high - and/or where the water level is close to the surface.
Based on its high water solubility (0,5-0,6 g/L) and perseverance, both the US Environmental Protection Agency and the Pest Control Management Agency in Canada consider imidacloprid to have a high potential to run into surface waters and to seep into groundwater and warning not to apply it in areas where soil can be penetrated, especially if the surface is shallow.
According to the standards set by the Canadian environmental ministry, if used correctly (at the recommended level, without irrigation, and when heavy rain is not predicted), imidacloprid does not typically enter deeper soil coatings despite 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), where imidloprid is applied to sugar beet bundles, it consistently shows that no washing of the detected imidacloprid to the 10-20 cm soil layer occurs. Imidacloprid was applied to cornfields in Minnesota, and no imidacloprid residues were found in the sample column segments below 0-15.2 cm depth segments (Rice et al., 1991, as reviewed in Mulye 1995).
However, the 2012 water monitoring study by the state of California, conducted by collecting agricultural runoff during the planting season of 2010 and 2011, found imidacloprid in 89% of the sample, with rates ranging from 0.1-3.2 Âμg/L. 19% of the sample exceeds the EPA threshold for chronic toxicity for aquatic invertebrates of 1.05 Âμg/L. The authors also point out that the Canada and European guidelines are much lower (0.23 Ã,Âμg/L and 0.067 Ã,Âμg/L, respectively) and exceeded in 73% and 88% of the samples, respectively. The authors concluded that "imidacloprid generally moves off site and contaminates surface water at concentrations that can harm aquatic invertebrates".
Toxicology
Based on laboratory mouse studies, imidacloprid is rated as "toxic" on an acute oral basis for mammals and low dermal toxicities by the World Health Organization and the United States Environmental Protection Agency (class II or III, requiring "Warning" or "Attention" label). It is rated as a "impossible" carcinogen and as a weak mutagenic by US EPA (group E). It is not listed for reproductive or developmental toxicity, but is listed on the EPA Tier 1 Screening Order for chemicals to be tested under the Endocrine Disruptor Screening Program (EDSP). Tolerance for imidacloprid residues in the food range of 0.02 mg/kg in eggs to 3.0 mg/kg in leaps.
Animal toxicity is moderate when ingested orally and low when used dermally. This does not irritate the eyes or skin of rabbits and guinea pigs (although some commercial preparations contain clays as an inert material, which may be irritating). Acute inhalation lD 50 in mice was not achieved at the highest attainable concentration, 69 milligrams per cubic meter of air as aerosol, and 5.323 mg ai/m 3 of air as dust. In mice fed for two years, no effect was observed at 100 parts per million (ppm). In mice, the thyroid is the organ most affected by imidacloprid. Thyroid lesions occur in male rats at LOAEL 16.9 mg/kg/day. In a one-year study of dogs, no effect was observed at 1,250 ppm, while rates of up to 2,500 ppm resulted in hypercholesterolaemia and increased cytochrome p-450 liver measurements.
Bees and other insects
For members of the Apis mellifera species, the western honey bee, imidacloprid is one of the most toxic chemicals ever made as an insecticide. Acute oral LD ​​ 50 of the imidacloprid range from 5 to 70 nanograms per bee. Honey bee colonies vary in their ability to metabolize toxins, which explain this wide range. Imidacloprid is more toxic to bees than dimethoate organophosphates (oral LD ​​ 50 152 ng/bee) or pyrethroid cypermethrin (oral LD ​​ 50 160 ng/bee). The toxicity of imidacloprid to bees differs from most insecticides because they are more toxic orally than through contact. Acute LD contact 50 is 0.024 Âμg active ingredient per bee.
Imidacloprid was first used extensively in the United States in 1996 because it replaced three broad classes of insecticides. In 2006, US commercial migrant bee breeders reported a sharp decline in their honey bee colony. Such a decline has occurred in the past; But unlike the case at the previous loss, the adult bees leave their nest. Scientists call this phenomenon a collapse of colony disorder (CCD). Reports indicate that beekeepers in most states have been affected by CCDs. Although no single factor was identified as a CCD cause, the United States Department of Agriculture (USDA) in their progress report on the CCD stated that CCDs may be "syndromes caused by many different factors, working in combination or in synergies." Several studies have found that sub-lethal levels of imidacloprid increase the susceptibility of honeybees to Nosema pathogens.
Dave Goulson (2012) from Stirling University suggests that the trivial effects of imidacloprid in the laboratory and greenhouse experiments can translate into great effects in the field. The study found that bees consuming pesticides suffered 85% loss on the number of queens that their hives produced, and doubling the number of unsuccessful bees returned from food-seeking trips.
Lu et al. (2012) reported they were able to replicate CCDs with sub-lethal doses of imidacloprid. Imidacloprid-treated sponge is almost 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 honeybees were treated with small doses of imidacloprid, comparable to what they would receive in the nectar and were previously considered safe amounts, to be "voter eaters", rejecting the nectar from lower sweet taste and prefer to feed only on sweet nectar. It was also found that the bees exposed to imidacloprid perform a "dance shake", a movement the bees use to tell the nest couple at the location of the feeding plants, at a lower rate.
Researchers from the Canadian Forest Service point out that imidacloprid used in trees at realistic field concentrations reduces leaf litter damage due to adverse sublethal effects on non-target invertebrate land. The study found no significant indication that invertebrates, which usually describe leaf litter, uncontaminated leaves are preferred, and conclude that invertebrates can not detect imidacloprid.
The 2012 research in situ provides strong evidence that exposure to subacial levels of imidacloprid to high fructose corn syrup (HFCS) used to feed honeybees when forages are not available causes bees to show consistent symptoms against a 23-week CCD. post dosage of imidacloprid. The researchers suggest that "delayed mortality observed in honeybees caused by imidacloprid in HFCS is a new and plausible mechanism for CCD, and should be validated in future studies".
Sublethal doses (& lt; 10 ppb) for aphids have been found to cause changed behavior, such as wandering and eventually starvation. Very low concentrations also reduce nymph viability. In bee exposure to imidacloprid 10 ppb reduces natural foraging behavior, increases worker mortality and causes poor parent development. A 2013 study showed that bee colonies affected by 10 ppb imidacloprid began to fail after three weeks when mortality rates increased and birth rates decreased. The researchers connect this with open colonies to important tasks, such as feeding, thermoregulation and parental care, less well than unexposed colonies. This suggests that subletal imidacloprids lead to the failure of colonies through diminished colonic function.
In January 2013, the European Food Safety Authority declared that neonicotinoids pose a very high risk to bees, and that industry-sponsored science in which security claims from regulatory bodies could be wrong, concluding that, "The high acute risk to honeybees is identified from exposure through dust deviations to the use of seed treatment in maize, grains and wheat.Higher acute risks are also identified from exposure through residues in nectar and/or pollen. "A study author of a study which encourages the EFSA review suggests that industrial science related to neonicotinoids may have been deliberately deceptive, and the British Parliament has asked Bayer Crop Science manufacturers to explain the differences in evidence they have submitted to an investigation.
Bird
In quail bobwhite ( Colinus virginianus ), imidacloprid is determined to be quite toxic with acute oral LD ​​ 50 of 152 mg a.i./kg. It was slightly toxic in a 5-day dietary study with acute oral LC 50 of 1,420 mg diet a.i./kg, NOAEC from & lt; Dietary 69 mg/kg/kg, and diet LOAEC = 69Ã, mg a.i./kg. Exposed birds show ataxia, decreased wings, opisthotonos, immobility, hyperactivity, a plant full of fluid and intestines, and a heart that changes color. In a study of reproductive toxicity with incandescent bobwhite, NOAEC = 120Ã, mg diet a.i./kg and diet LOAEC = 240Ã, mg a.i./kg. Thin egg shells and adult weight loss were observed on a 240 mg/kg diet.
Imidacloprid is highly toxic to four species of birds: Japanese quail, sparrows, walnuts, and pigeons. Acute oral LD ​​ 50 for Japanese quail ( Coturnix coturnix ) is 31 mg/kg bw with NOAEL = 3.1 mg/kg. Acute oral LD ​​ 50 for house sparrow ( Passer domesticus ) is 41 mg ai/kg bb with NOAEL = 3 mg ai/kg and NOAEL = 6 mg ai/kg. LD 50 s for doves ( Columba livia ) and walnuts ( Serinus canaria ) are 25-50 mg a.i./kg. Mallard duck is more resistant to the effects of imidakloprid with LC diet 5 days 50 of & gt; 4,797 ppm. NOAEC for weight and feed consumption is diet 69Ã, mg a.i./kg. Studies of reproduction with mallard ducks showed the thinning of eggshells on a 240Ã, mg diet. A.i./kg. According to the European Food Safety Authority, imidacloprid has a potentially high acute risk for herbivorous birds and insectivores and granivorous mammals. Chronic risks are not well established. The hypothesis that imidacloprid has a negative impact on insectivorous bird populations is supported by a study of the propensity of bird populations in the Netherlands, where correlations have been identified between imidacloprid surface water concentrations and population decline. At an imidacloprid concentration of more than 20 nanograms per liter, the bird population tends to decrease 3.5 percent on average each year. Additional analysis in this study revealed that the spatial pattern of decline in bird populations only emerged after the introduction of imidacloprid to the Netherlands, in the mid-1990s, and that this correlation was not related to other land use factors.
Aquatic life
Imidacloprid is highly toxic on an acute basis for aquatic invertebrates, with EC 50 values ​​= 0.037 - 0.115 ppm. It is also highly toxic to water invertebrates on a chronic basis (effects on growth and movement): NOAEC/LOAEC = 1,8/3,6 ppm in daphnids; NOAEC = 0.001 at 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 a review of secondary effects on fish with food chains that include sensitive aquatic invertebrates.
Plant life
Imidacloprid has proven to kill some genes that use some rice varieties to produce defensive chemicals. While Imidacloprid is used to control brown planthopper and other rice pests, there is evidence that imidacloprid actually increases the susceptibility of rice plants to aphid attack and aphis attack. Imidacloprid has been shown to increase the rate of photosynthesis in upland cotton at temperatures above 36 degrees Celsius.
Health impact
Imidacloprid and nitrosoimine metabolites (WAK 3839) have been studied well in mice, rats and dogs. In mammals, the main effects after oral exposure of high doses of acute to imidacloprid are mortality, transient cholinergic effects (dizziness, apathy, locomotor effects, depressed breathing) and temporary growth retardation. Exposure to high doses may be associated with degenerative changes in the testes, thymus, bone marrow and pancreas. Cardiovascular and hematologic effects have also been observed at higher doses. The main long-term effects, low-dose exposure to imidacloprid is in the liver, thyroid, and body weight (reduction). Low or moderate dose oral exposure has been associated with reproductive toxicity, developmental retardation and neurobehavioral deficits in rats and rabbits. Imidacloprids are not carcinogenic in laboratory or mutagenic animals in standard laboratory tests.
Midacloprid is quite toxic and is associated with neurotoxic, reproductive and mutagenic effects. It has been found highly toxic to bees and other beneficial insects. This substance is also toxic to the birds in the highlands, generally survive in the soil and can seep into the ground water. Health Canada has stated that chemical toxicity to bees and other insects is not present in a scientific dispute.
The effect of imidacloprid on human health and the environment depends on how much imidacloprid is present and the length and frequency of exposure. The effects also depend on one's health and/or certain environmental factors.
A study conducted in tissue culture of neurons taken from newborn mice suggests that Imidacloprid and acetamiprid, another neonicotinoid, move neurons in a way similar to nicotine, so the effects of neonicotinoids on mammalian brain development may be similar to the adverse effects of nicotine.
Overdose
People who may orally ingest acute amounts will experience emesis, diaphoresis, drowsiness and disorientation. This needs to be intentional because large amounts will need to be digested to experience a toxic reaction. In dogs, LD 50 is 450Ã, mg/kg body weight (ie, in a sample of medium-sized dog weighing 13 kilograms (29 pounds), half of them will be killed after consuming 5,850 mg of imidacloprid, or approximately 1 / 5 of an ounce). Blood imidacloprid concentration can be measured to confirm the diagnosis in the inpatient or to establish the cause of death on postmortem examination.
Rule
Neonicotinoids banned by the European Union
In February 2018, the European Food Safety Authority published a new report showing that neonicotinoids pose a serious danger to honeybees and wild bees. In April 2018, EU Member States decided to ban three major neonicotinoids (clothianidin, imidacloprid and thiamethoxam) for all outdoor use.
See also
- Fipronil
- Imidakloprid effect on bees
- Insecticides
- Neonicotinoid
- Pesticide poisoning in bees
References
Source
- PAN Pesticide Database
External links
- Van Dijk T. C., Van Staalduinen M. A., Van der Sluijs J. P. (2013). "Macro-Invertebrate Decrease in Surface Water Contaminated with Imidacloprid". PLoS ONE . 8 (5): e62374. doi: 10.1371/journal.pone.0062374. PMC 3641074 . PMID 23650513. CS1 maint: Many names: list of authors (links)
- [4] Decrease in insectivorous birds is associated with high concentrations of neonicotinoids
- Pesticide Information Profile from Extension Toxicology Network
- Imidacloprid Details Chart that forms a 2-chloro pyridine toxin
- Imidacloprid Fact Sheet, with 18 References, from Sierra Club of Canada
- "Expert Overview" Bayer "
- Imidacloprid in Pesticide Properties DataBase (PPDB)
Source of the article : Wikipedia
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