Imidacloprid

Last updated
Imidacloprid [1]
Imidacloprid.svg
Imidacloprid.png
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 OOjs UI icon edit-ltr-progressive.svg
KEGG
PubChem CID
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) Yes check.svgY
    Key: YWTYJOPNNQFBPC-UHFFFAOYSA-N Yes check.svgY
  • 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
AppearanceColorless 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 )
Legal status
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
Yes check.svgY  verify  (what is  Yes check.svgYX mark.svgN ?)

Imidacloprid is a systemic insecticide belonging to a class of chemicals called the neonicotinoids which act on the central nervous system of insects. 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. [3]

Contents

From 1999 [4] through at least 2018, [5] [6] imidacloprid was 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, or ground application as a granular or liquid formulation, or as a pesticide-coated seed treatment. [7] [3] [8] 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, [3] protection of trees from boring insects, [9] and in preservative treatment of some types of lumber products. [10]

A 2018 review by the European Food Safety Authority (EFSA) concluded that most uses of neonicotinoid pesticides such as Imidacloprid represent a risk to wild bees and honeybees. [11] [12] In 2022 the United States Environmental Protection Agency (EPA) concluded that Imidacloprid is likely to adversely affect 79 percent of federally listed endangered or threatened species and 83 percent of critical habitats. [13] The pesticide has been banned for all outdoor use in the entire European Union since 2018, but has a partial approval in the U.S. and other parts of the world, where it is widely used. [14] [15]

Authorized uses

Imidacloprid is the most widely used insecticide in the world. [4] [5] [6] 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.

United States

Imidacloprid use in the US to 2019 Imidacloprid use USA.png
Imidacloprid use in the US to 2019

The estimated annual use of the compound in US agriculture is mapped by the US Geological Service and shows an increasing trend from its introduction in 1994 to 2014 when it reached 2,000,000 pounds (910,000 kg). [18] However, use from 2015 to 2019 dropped following concerns about the effect of neonicotinoid chemicals on pollinating insects. [19] In May 2019, the Environmental Protection Agency revoked approval for a number of products containing imidacloprid as part of a legal settlement, although some formulations continue to be available. [20] [21]

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. [9]

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. [22]

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. [23]

On January 26, 2005, the Federal Register noted the establishment of the '(Pesticide Tolerances for) Emergency Exemptions' for imidacloprid. Its 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). [24]

Biochemistry

Imidacloprid is a systemic insecticide, belonging to the class of chloronicotinyl neonicotinoid insecticides. It works by interfering with the transmission of nerve impulses in insects by binding irreversibly to specific insect nicotinic acetylcholine receptors. [25]

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. [26]

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. [27] [28]

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 6-chloronicotinic acid (6-CNA) and ultimately carbon dioxide. Since imidacloprid has a low vapor pressure, it normally does not volatilize readily. [25]

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. [29] 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. [30] Major soil metabolites include imidacloprid nitrosimine, imidacloprid desnitro and imidacloprid urea, which ultimately degrade to 6-chloronicotinic acid, CO2, and bound residues. [16] [25] 6-Chloronicotinic acid is recently shown to be mineralized via a nicotinic acid (vitamin B3) pathway in a soil bacterium. [31]

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. [32]

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. [16] [25]

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). [25] 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). [16] [25]

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 to 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". [33]

Health effects

The effects of imidacloprid on human health depend on the dose, duration, and frequency of exposure. The effects may also depend on the health of a person and environmental factors. People 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. [3]

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). [23] [34] Tolerances for imidacloprid residues in food range from 0.02 mg/kg in eggs to 3.0 mg/kg in hops. [1]

Mammals

Imidacloprid and its nitrosoimine metabolite (WAK 3839) have been well studied in rats, mice and dogs.

In dogs the LD50 is 450 mg/kg of body weight (i.e., in any sample of medium-sized dogs weighing 13 kilograms (29 lb), half of them would be killed after consuming 5,850 mg of imidacloprid, or about 15th of an ounce). 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 dust.

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. [35]

It is not irritating to eyes or skin in rabbits and guinea pigs. [1]

Bees

Imidacloprid is acutely toxic to honeybees: its LD50 ranges from 5 to 70 nanograms per bee. [36] Honeybee colonies vary in their ability to metabolize toxins, which explains this wide range. Imidacloprid is more toxic to bees than the organophosphate dimethoate (oral LD50 152 ng/bee) or the pyrethroid cypermethrin (oral LD50 160 ng/bee). [36] 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. [37]

In laboratory studies, sublethal levels of imidacloprid have been shown to impair navigation, foraging behavior, feeding behavior, and olfactory learning performance in honeybees (Apis mellifera). [36] [38] [39] [40] [41] [42] [43] [44] In general, however, despite the fact that many laboratory studies have shown the potential for neonicotinoid toxicity, the majority of field studies have found only limited or no effects on honeybees. [45]

In bumblebees, exposure to 10 ppb imidacloprid reduces natural foraging behaviour, increases worker mortality and leads to reduced brood development. [46] [47] The probable mechanism is that the mevalonate pathway is substantially downregulated by the chronic imidacloprid exposure, which can help to explain the imidacloprid impairment of the cognitive functions. [48]

Birds

Imidacloprid is considered acutely toxic to birds, and to cause avian reproductive toxicity. [25]

In bobwhite quail (Colinus virginianus), imidacloprid was determined to be moderately toxic with an 14-day 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. [23] [25]

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. [23] [25]

According to the European Food Safety Authority, imidacloprid poses a potential high acute risk for both herbivorous and insectivorous birds. [28] Chronic risk has not been well established. [25]

A 2014 observational study conducted in the Netherlands correlated declines in some bird populations with environmental imidacloprid residues, although it stopped short of concluding that the association was causal. [49]

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; [1] however, the EPA has requested review of secondary effects on fish with food chains that include sensitive aquatic invertebrates. [16] Research published in 2018 demonstrated accumulation of imidacloprid in the blood of rainbow trout, contradicting claims from Bayer that persistence (bioaccumulation) does not occur with imidacloprid. [50] [51]

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. [52] Imidacloprid has been shown to increase the rate of photosynthesis in upland cotton temperatures above 36 degrees Celsius. [53]

Regulation

European Union

In the mid to late 1990s, French beekeepers reported a significant loss of bees, which they attributed to the use of imidacloprid.[ citation needed ] In 1999, the French Minister of Agriculture suspended the use of imidacloprid on sunflower seeds and appointed a team of expert scientists to examine the impact of imidacloprid on bees. In 2003, this panel issued a report which concluded that imidacloprid posed a significant risk to bees. [54] In 2004, the French Minister of Agriculture suspended the use of imidacloprid as a seed treatment for sunflowers and maize (corn). Certain imidacloprid seed treatments were also temporarily banned in Italy, following preliminary monitoring studies that identified correlations between bee losses and the use of neonicotinoid pesticides. [55]

In January 2013, a European Food Safety Authority (EFSA) report concluded that neonicotinoids posed an unacceptably high risk to bees: "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." [28] The EFSA also identified a number of gaps in the scientific evidence and were unable to finalize risk assessments for some uses authorized in the European Union (EU). Following the report, EU member states voted to restrict the use of the three main neonics, including imidacloprid, for seed treatment, soil application (granules) and foliar treatment in crops attractive to bees. [56]

In February 2018, the European Food Safety Authority published a further report concluding that neonicotinoids posed a serious danger to bees. [28] In April 2018, the member states of the EU decided to ban the neonicotinoids for all outdoor uses. [57]

United States

On July 1, 2022, the Commonwealth of Massachusetts in the United States banned commercial sales of imidacloprid and other neonicotinoids acetamiprid, clothianidin, dinotefuran, thiacloprid, and thiamethoxam to the general public for all outdoor uses. [58] Licensed dealers will be able to sell only to pesticide-licensed and certified individuals. The states of Maryland, Connecticut and Vermont also restrict use of neonicotinoid pesticides. [59]

Registrations

Among others, imidacloprid is sold under the brand names: Confidor (Bayer CropScience India), [60] Marathon (OHP, US). [61] [62]

See also

Related Research Articles

<span class="mw-page-title-main">Pesticide</span> Substance used to destroy pests

Pesticides are substances that are used to control pests. They include herbicides, insecticides, nematicides, fungicides, and many others. The most common of these are herbicides, which account for approximately 50% of all pesticide use globally. Most pesticides are used as plant protection products, which in general protect plants from weeds, fungi, or insects. In general, a pesticide is a chemical or biological agent that deters, incapacitates, kills, or otherwise discourages pests. Target pests can include insects, plant pathogens, weeds, molluscs, birds, mammals, fish, nematodes (roundworms), and microbes that destroy property, cause nuisance, or spread disease, or are disease vectors. Along with these benefits, pesticides also have drawbacks, such as potential toxicity to humans and other species.

<span class="mw-page-title-main">Insecticide</span> Pesticide used against insects

Insecticides are pesticides used to kill insects. They include ovicides and larvicides used against insect eggs and larvae, respectively. Acaricides, which kill mites and ticks, are not strictly insecticides, but are usually classified together with insecticides. The major use of Insecticides is agriculture, but they are also used in home and garden, industrial buildings, vector control and control of insect parasites of animals and humans. Insecticides are claimed to be a major factor behind the increase in the 20th-century's agricultural productivity. Nearly all insecticides have the potential to significantly alter ecosystems; many are toxic to humans and/or animals; some become concentrated as they spread along the food chain.

<span class="mw-page-title-main">Bifenthrin</span> Chemical compound

Bifenthrin is a pyrethroid insecticide. It is widely used against ant infestations.

<span class="mw-page-title-main">Chlorpyrifos</span> Chemical compound

In organic chemistry, chlorpyrifos (CPS), also known as chlorpyrifos ethyl, is an organophosphate pesticide that has been used on crops, animals, and buildings, and in other settings, to kill several pests, including insects and worms. It acts on the nervous systems of insects by inhibiting the acetylcholinesterase enzyme. Chlorpyrifos was patented in 1966 by Dow Chemical Company.

Pesticides vary in their effects on bees. Contact pesticides are usually sprayed on plants and can kill bees when they crawl over sprayed surfaces of plants or other areas around it. Systemic pesticides, on the other hand, are usually incorporated into the soil or onto seeds and move up into the stem, leaves, nectar, and pollen of plants.

<span class="mw-page-title-main">Fipronil</span> Chemical compound

Fipronil is a broad-spectrum insecticide that belongs to the phenylpyrazole chemical family. Fipronil disrupts the insect central nervous system by blocking the ligand-gated ion channel of the GABAA receptor and glutamate-gated chloride (GluCl) channels. This causes hyperexcitation of contaminated insects' nerves and muscles. Fipronil's specificity towards insects is believed to be due to its greater binding affinity for the GABAA receptors of insects than to those of mammals, and for its action on GluCl channels, which do not exist in mammals. As of 2017, there does not appear to be significant resistance among fleas to fipronil.

Neonicotinoids are a class of neuro-active insecticides chemically similar to nicotine, developed by scientists at Shell and Bayer in the 1980s.

<span class="mw-page-title-main">Spinosad</span> Medication

Spinosad is an insecticide based on chemical compounds found in the bacterial species Saccharopolyspora spinosa. The genus Saccharopolyspora was discovered in 1985 in isolates from crushed sugarcane. The bacteria produce yellowish-pink aerial hyphae, with bead-like chains of spores enclosed in a characteristic hairy sheath. This genus is defined as aerobic, Gram-positive, nonacid-fast actinomycetes with fragmenting substrate mycelium. S. spinosa was isolated from soil collected inside a nonoperational sugar mill rum still in the Virgin Islands. Spinosad is a mixture of chemical compounds in the spinosyn family that has a generalized structure consisting of a unique tetracyclic ring system attached to an amino sugar (D-forosamine) and a neutral sugar (tri-Ο-methyl-L-rhamnose). Spinosad is relatively nonpolar and not easily dissolved in water.

<span class="mw-page-title-main">Nitenpyram</span> Insecticide

Nitenpyram is a chemical frequently used as an insecticide in agriculture and veterinary medicine. The compound is an insect neurotoxin belonging to the class of neonicotinoids which works by blocking neural signaling of the central nervous system. It does so by binding irreversibly to the nicotinic acetylcholine receptor (nACHr) causing a stop of the flow of ions in the postsynaptic membrane of neurons leading to paralysis and death. Nitenpyram is highly selective towards the variation of the nACHr which insects possess, and has seen extensive use in targeted, insecticide applications.

<span class="mw-page-title-main">Clothianidin</span> Chemical compound

Clothianidin is an insecticide developed by Takeda Chemical Industries and Bayer AG. Similar to thiamethoxam and imidacloprid, it is a neonicotinoid. Neonicotinoids are a class of insecticides that are chemically similar to nicotine, which has been used as a pesticide since the late 1700s. Clothianidin and other neonicotinoids act on the central nervous system of insects as an agonist of nAChR, the same receptor as acetylcholine, the neurotransmitter that stimulates and activating post-synaptic acetylcholine receptors but not inhibiting AChE. Clothianidin and other neonicotinoids were developed to last longer than nicotine, which is more toxic and which breaks down too quickly in the environment.

<span class="mw-page-title-main">Colony collapse disorder</span> Aspect of apiculture

Colony collapse disorder (CCD) is an abnormal phenomenon that occurs when the majority of worker bees in a honey bee colony disappear, leaving behind a queen, plenty of food, and a few nurse bees to care for the remaining immature bees. While such disappearances have occurred sporadically throughout the history of apiculture, and have been known by various names, the syndrome was renamed colony collapse disorder in early 2007 in conjunction with a drastic rise in reports of disappearances of western honey bee colonies in North America. Beekeepers in most European countries had observed a similar phenomenon since 1998, especially in Southern and Western Europe; the Northern Ireland Assembly received reports of a decline greater than 50%. The phenomenon became more global when it affected some Asian and African countries as well. From 1990 to 2021, the United Nation’s FAO calculated that the worldwide number of honeybee colonies increased 47%, reaching 102 million.

<span class="mw-page-title-main">Acetamiprid</span> Chemical compound

Acetamiprid is an organic compound with the chemical formula C10H11ClN4. It is an odorless neonicotinoid insecticide produced under the trade names Assail, and Chipco by Aventis CropSciences. It is systemic and intended to control sucking insects (Thysanoptera, Hemiptera, mainly aphids) on crops such as leafy vegetables, citrus fruits, pome fruits, grapes, cotton, cole crops, and ornamental plants. It is also a key pesticide in commercial cherry farming due to its effectiveness against the larvae of the cherry fruit fly.

<span class="mw-page-title-main">Health effects of pesticides</span> How pesticides affect human health

Health effects of pesticides may be acute or delayed in those who are exposed. Acute effects can include pesticide poisoning, which may be a medical emergency. Strong evidence exists for other, long-term negative health outcomes from pesticide exposure including birth defects, fetal death, neurodevelopmental disorder, cancer, and neurologic illness including Parkinson's disease. Toxicity of pesticides depend on the type of chemical, route of exposure, dosage, and timing of exposure.

<span class="mw-page-title-main">Thiamethoxam</span> Chemical compound

Thiamethoxam is the ISO common name for a mixture of cis-trans isomers used as a systemic insecticide of the neonicotinoid class. It has a broad spectrum of activity against many types of insects and can be used as a seed dressing.

<span class="mw-page-title-main">Thiacloprid</span> Chemical compound

Thiacloprid is an insecticide of the neonicotinoid class. Its mechanism of action is similar to other neonicotinoids and involves disruption of the insect's nervous system by stimulating nicotinic acetylcholine receptors. Thiacloprid was developed by Bayer CropScience for use on agricultural crops to control of a variety of sucking and chewing insects, primarily aphids and whiteflies.

<span class="mw-page-title-main">Ethoprophos</span> Chemical compound

Ethoprophos (or ethoprop) is an organophosphate ester with the formula C8H19O2PS2. It is a clear yellow to colourless liquid that has a characteristic mercaptan-like odour. It is used as an insecticide and nematicide and it is an acetylcholinesterase inhibitor.

<span class="mw-page-title-main">Sulfoxaflor</span> Chemical compound

Sulfoxaflor, also marketed as Isoclast, is a systemic insecticide that acts as an insect neurotoxin. A pyridine and a trifluoromethyl compound, it is a member of a class of chemicals called sulfoximines, which act on the central nervous system of insects.

<span class="mw-page-title-main">Fenpropathrin</span> Chemical compound

Fenpropathrin, or fenopropathrin, is a widely used pyrethroid insecticide in agriculture and household. Fenpropathrin is an ingestion and contact synthetic pyrethroid. Its mode of action is similar to other natural (pyrethrum) and synthetic pyrethroids where in they interfere with the kinetics of voltage gated sodium channels causing paralysis and death of the pest. Fenpropathrin was the first of the light-stable synthetic pyrethroids to be synthesized in 1971, but it was not commercialized until 1980. Like other pyrethroids with an α-cyano group, fenpropathrin also belongs to the termed type II pyrethroids. Type II pyrethroids are a more potent toxicant than type I in depolarizing insect nerves. Application rates of fenpropathrin in agriculture according to US environmental protection agency (EPA) varies by crop but is not to exceed 0.4 lb ai/acre.

<span class="mw-page-title-main">Flupyradifurone</span> Chemical compound

Flupyradifurone is a systemic butenolide insecticide developed by Bayer CropScience under the name Sivanto. Flupyradifurone protects crops from sap-feeding pests such as aphids and is safer for non-target organisms compared to other insecticides. Sivanto was launched in 2014 since it obtained its first commercial registration in central America. Insecticide Resistance Action Committee (IRAC) classified Flupyradifurone as 4D subset (butenolide) and it is the first pesticide in the butenolide category. It was approved by European Union in 2015.

References

  1. 1 2 3 4 5 "Pesticide Information Profiles: Imidacloprid Breaz". Extension Toxicology Network. Retrieved April 7, 2012.
  2. "Health product highlights 2021: Annexes of products approved in 2021". Health Canada . 3 August 2022. Retrieved 25 March 2024.
  3. 1 2 3 4 5 6 Gervais et al. 2010.
  4. 1 2 Yamamoto, Izuru (1999). "Nicotine to Nicotinoids: 1962 to 1997". In Yamamoto, Izuru; Casida, John (eds.). Nicotinoid Insecticides and the Nicotinic Acetylcholine Receptor. Tokyo: Springer-Verlag. pp. 3–27.
  5. 1 2 Casida, John E. (2018-01-07). "Neonicotinoids and Other Insect Nicotinic Receptor Competitive Modulators: Progress and Prospects". Annual Review of Entomology . 63 (1). Annual Reviews: 125–144. doi:10.1146/annurev-ento-020117-043042. ISSN   0066-4170. PMID   29324040.
  6. 1 2 Ihara, Makoto; Matsuda, Kazuhiko (2018). "Neonicotinoids: molecular mechanisms of action, insights into resistance and impact on pollinators". Current Opinion in Insect Science . 30. Elsevier: 86–92. doi:10.1016/j.cois.2018.09.009. ISSN   2214-5745. PMID   30553491. S2CID   58767188.
  7. "Imidacloprid: Human Health and Ecological Risk Assessment. Final Report" (PDF). USDA Forest Service. 2005. Archived from the original (PDF) on May 13, 2021. Retrieved July 23, 2021.
  8. 1 2 "Bayer seedgrowth". Bayer SeedGrowth. Archived from the original on January 17, 2021. Retrieved April 11, 2021.
  9. 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. Archived from the original (PDF) on January 26, 2016. Retrieved April 7, 2012.
  10. International Code Council Evaluation Service Report ESR-1851, dated August 2011. Archived 2018-12-12 at the Wayback Machine
  11. "Neonicotinoids: risks to bees confirmed | EFSA". www.efsa.europa.eu. 2018-02-28. Retrieved 2023-06-23.
  12. "Conclusion on the peer review of the pesticide risk assessment for bees for the active substance clothianidin". EFSA Journal. 11: 3066. 2013. doi:10.2903/j.efsa.2013.3066.
  13. US EPA, OCSPP (2022-06-16). "EPA Finalizes Biological Evaluations Assessing Potential Effects of Three Neonicotinoid Pesticides on Endangered Species". www.epa.gov. Retrieved 2023-06-23.
  14. Carrington, Damian (2018-04-27). "EU agrees total ban on bee-harming pesticides". The Guardian. ISSN   0261-3077 . Retrieved 2023-06-23.
  15. Milman, Oliver (2022-03-08). "Fears for bees as US set to extend use of toxic pesticides that paralyse insects". The Guardian. ISSN   0261-3077 . Retrieved 2023-06-23.
  16. 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.
  17. Preston, Richard (2007). "A Death in the Forest". The New Yorker.
  18. 1 2 US Geological Survey (2021-10-12). "Estimated Annual Agricultural Pesticide Use for imidacloprid, 2019" . Retrieved 2022-01-24.
  19. "EPA Actions to Protect Pollinators". US EPA. 3 September 2013. Retrieved 24 January 2022.
  20. Allington A (21 May 2019). "EPA Curbs Use of 12 Bee-Harming Pesticides". Bloomberg . Retrieved 24 January 2022.
  21. Bayer (April 2021). "Neonicotinoid insecticides" (PDF). Retrieved 2022-01-24.
  22. U.S. Pat. No. 4,742,060 Archived 2018-09-20 at the Wayback Machine - uspto.gov
  23. 1 2 3 4 "Index for Imidacloprid (Pc Code 129099) – Pesticides". US EPA. July 27, 2011. Retrieved July 24, 2021.
  24. Imidacloprid; Pesticide Tolerances for Emergency Exemptions Federal Register: January 26, 2005 (Volume 70, Number 16), Page 3634-3642- epa.gov
  25. 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. Archived from the original (PDF) on 2013-03-19. Retrieved February 13, 2012.
  26. Environmental Fate of Imidacloprid Archived March 16, 2012, at the Wayback Machine California Department of Pesticide Regulation 2006
  27. "Imidacloprid: Risk Characterization Document – Dietary and Drinking Water Exposure" (PDF). California Environmental Protection Agency. February 9, 2006. Retrieved April 7, 2012.
  28. 1 2 3 4 "Conclusion on the peer review of the pesticide risk assessment for bees for the active substance clothianidin". EFSA Journal. 11: 3066. 2013. doi:10.2903/j.efsa.2013.3066.
  29. 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.
  30. Matthew Fossen (2006). "Environmental Fate of Imidacloprid" (PDF). Archived from the original (PDF) on March 16, 2012. Retrieved April 16, 2016.
  31. Shettigar M, Pearce S, Pandey R, Khan F, Dorrian SJ, Balotra S, Russell RJ, Oakeshott JG, Pandey G (2012). "Cloning of a novel 6-chloronicotinic acid chlorohydrolase from the newly isolated 6-chloronicotinic acid mineralizing Bradyrhizobiaceae strain SG-6C". PLOS ONE. 7 (11): e51162. Bibcode:2012PLoSO...751162S. doi: 10.1371/journal.pone.0051162 . PMC   3511419 . PMID   23226482.
  32. 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" Archived 2012-08-01 at the Wayback Machine . University of Michigan Extension, Michigan State University, The Ohio State University Extension.
  33. 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. S2CID   18454777.
  34. Endocrine Disruptor Screening Program: Tier 1 Screening Order Issuing Announcement. Federal Register Notice, Oct 21, 2009. Vol. 74, No. 202, pp. 54422-54428
  35. 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.[ dead link ]
  36. 1 2 3 Suchail, Séverine; Guez, David; Belzunces, Luc P. (November 2001). "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. S2CID   22209995.
  37. Suchail, Séverine; Guez, David; Belzunces, Luc P. (July 2000). "Characteristics of imidacloprid toxicity in two Apis mellifera subspecies" (PDF). Environmental Toxicology and Chemistry. 19 (7): 1901–1905. doi:10.1002/etc.5620190726. S2CID   84822758.
  38. Armengaud, C.; Lambin, M.; Gauthier, M. (2002), "Effects of imidacloprid on the neural processes of memory", in Devillers, J; Pham-Delegue, M.H. (eds.), Honey bees: estimating the environmental impact of chemicals, New York: Taylor & Francis, pp. 85–100, ISBN   9780415275187
  39. Decourtye, A; Lacassie, E; Pham-Delegue, M-H (2003). "Learning performances of honeybees (Apis mellifera L) are differentially affected by imidacloprid according to the season". Pest Manag. Sci. 59 (3): 269–278. doi:10.1002/ps.631. PMID   12639043.
  40. Decourtye, A.; Armengaud, C.; Devillers, R.M.; Cluzeau, S. (2004). "Imidacloprid impairs memory and brain metabolism in the honeybee (Apis mellifera L)". Pesticide Biochem Phys. 78 (2): 83–92. doi:10.1016/j.pestbp.2003.10.001.
  41. Guez, D.; Suchail, S.; Gauthier, M.; Maleszka, R.; Belzunces, L. (2001). "Contrasting effects of imidacloprid on habituation in 7- and 8-day-old honeybees (Apis mellifera)". Neurobiology of Learning and Memory. 76 (2): 183–191. doi:10.1006/nlme.2000.3995. PMID   11502148. S2CID   17822619.
  42. Pham-Delegue, M.H.; Cluzeau, S. (1999), "Effets des produits phytosanitaires sur l'abeille; incidence du traitement des semences de tournesol par Gaucho sur les disparitions de butineuses", Rapport final de synthese au Ministere de l'Agriculture et de la Peche
  43. Lambin, M.; Armengaud, C.; Ramond, S.; Gauthier, M. (2001). "Imidacloprid-induced facilitation of the proboscis extension reflex habituation in the honeybee". Archives of Insect Biochemistry and Physiology. 48 (3): 129–134. doi:10.1002/arch.1065. PMID   11673842.
  44. Williamson, S.M.; Wright, G.A (2013). "Exposure to multiple cholinergic pesticides impairs olfactory learning and memory in honeybees" (PDF). Journal of Experimental Biology. 216 (10): 1799–1807. doi:10.1242/jeb.083931. ISSN   0022-0949. PMC   3641805 . PMID   23393272.
  45. "Neonicotinoids". Pollinator Network @ Cornell. Retrieved May 10, 2019.
  46. Gill R.J.; Ramos-Rodriguez O.; Raine N.E. (2012). "Combined pesticide exposure severely affects individual-and colony-level traits in bees". Nature. 491 (7422): 105–108. Bibcode:2012Natur.491..105G. doi:10.1038/nature11585. PMC   3495159 . PMID   23086150.
  47. Bryden, John; Gill, Richard J.; Mitton, Robert A. A.; Raine, Nigel E.; Jansen, Vincent A. A. (2013). "Chronic sublethal stress causes bee colony failure". Ecology Letters. 16 (12): 1463–1469. doi:10.1111/ele.12188. PMC   4299506 . PMID   24112478.
  48. Erban T.; Sopko B.; Talacko P.; Harant K.; Kadlikova K.; Halesova T.; Riddellova K.; Pekas A. (2019). "Chronic exposure of bumblebees to neonicotinoid imidacloprid suppresses the entire mevalonate pathway and fatty acid synthesis". J Proteomics. 196: 69–80. doi:10.1016/j.jprot.2018.12.022. PMID   30583045. S2CID   58641344.
  49. Hallmann CA, Foppen RP, van Turnhout CA, de Kroon H, Jongejans E (July 2014). "Declines in insectivorous birds are associated with high neonicotinoid concentrations". Nature. 511 (7509): 341–3. Bibcode:2014Natur.511..341H. doi:10.1038/nature13531. hdl: 2066/130120 . PMID   25030173. S2CID   4464169.
  50. Frew JA, Brown JT, Fitzsimmons PN, Hoffman AD, Sadilek M, Grue CE, Nichols, JW (February 2018). "Toxicokinetics of the neonicotinoid insecticide imidacloprid in rainbow trout (Oncorhynchus mykiss)". Comp Biochem Physiol C. 205: 34–42. doi:10.1016/j.cbpc.2018.01.002. PMC   5847319 . PMID   29378254.
  51. "Risk-benefit analysis of Bayer's imidacloprid". greenstarsproject.org. March 21, 2021. Retrieved December 14, 2021.
  52. Cheng Y, Shi ZP, Jiang LB, Ge LQ, Wu JC, Jahn GC (March 2012). "Possible connection between imidacloprid-induced changes in rice gene transcription profiles and susceptibility to the brown plant hopper Nilaparvatalugens Stål (Hemiptera: Delphacidae)". Pestic Biochem Physiol. 102–531 (3): 213–219. doi:10.1016/j.pestbp.2012.01.003. PMC   3334832 . PMID   22544984.
  53. Gonias, Evangelos D.; Oosterhuis, Derrick M.; Bibi, Androniki C. (2007). "Physiologic Response of Cotton to the Insecticide Imidacloprid under High-Temperature Stress". Journal of Plant Growth Regulation. 27 (1): 77–82. doi:10.1007/s00344-007-9033-4. ISSN   0721-7595. S2CID   20930112.
  54. Comité Scientifique et Technique (18 September 2003). "Imidaclopride utilisé en enrobage de semences (Gaucho) et troubles des abeilles: Rapport final" [Imidacloprid used in coating seeds (Gaucho) and disorders of bees: Final report](PDF) (in French). Archived from the original (PDF) on 16 March 2012. Retrieved 18 April 2012.
  55. "Colony Collapse Disorder: European Bans on Neonicotinoid Pesticides – Pesticides – US EPA". epa.gov. June 23, 2010. Archived from the original on September 4, 2011. Retrieved July 24, 2021.
  56. McDonald-Gibson, Charlotte (29 April 2013). "'Victory for bees' as European Union bans neonicotinoid pesticides blamed for destroying bee population". The Independent. Archived from the original on 1 May 2013. Retrieved 1 May 2013.
  57. "EU to fully ban neonicotinoid insecticides to protect bees". Reuters. 27 April 2018. Retrieved 29 April 2018.
  58. "FREQUENTLY ASKED QUESTIONS, Pesticides Containing Neonicotinoids Registration Change".
  59. "Massachusetts regulators to restrict consumer use of bee-toxic neonicotinoid pesticides".
  60. "Insecticide-Confidor". Bayer CropScience India. Retrieved 2021-04-11.
  61. US EPA (United States Environmental Protection Agency) (2015-04-21). "Label Amendment – minor label revisions Product Name: Marathon 1% Granular Greenhouse and Nursery Insecticide EPA Registration Number: 59807-15 Application Date: March 17, 2015 Decision Number: 502678" (PDF). Archived from the original (PDF) on 2021-04-11.
  62. OHP. "MARATHON 1% Granular" (PDF). Archived from the original (PDF) on 2018-05-16.