Acetamiprid

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Acetamiprid
Acetamiprid Structural Formulae V.1.svg
Acetamiprid 3D ball.png
Names
IUPAC name
N-[(6-chloro-3-pyridyl)methyl]-N'-cyano-N-methyl-acetamidine
Other names
(1E)-N-[(6-Chlor-3-pyridinyl)methyl]-N'-cyan-N-methylethanimidamid;
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
ECHA InfoCard 100.111.622 OOjs UI icon edit-ltr-progressive.svg
KEGG
MeSH acetamiprid
PubChem CID
UNII
  • InChI=1S/C10H11ClN4/c1-8(14-7-12)15(2)6-9-3-4-10(11)13-5-9/h3-5H,6H2,1-2H3/b14-8+ Yes check.svgY
    Key: WCXDHFDTOYPNIE-RIYZIHGNSA-N Yes check.svgY
  • InChI=1/C10H11ClN4/c1-8(14-7-12)15(2)6-9-3-4-10(11)13-5-9/h3-5H,6H2,1-2H3/b14-8+
    Key: WCXDHFDTOYPNIE-RIYZIHGNBY
  • Clc1ncc(cc1)CN(\C(=N\C#N)C)C
Properties
C10H11ClN4
Molar mass 222.678
Appearancewhite powder
Density 1.17 g/cm3
Melting point 98.9 °C (210.0 °F; 372.0 K)
Hazards
Flash point 166.9 °C (332.4 °F; 440.0 K)
Pharmacology
Legal status
  • AU: S6 (Poison)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
X mark.svgN  verify  (what is  Yes check.svgYX mark.svgN ?)

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 [1] ) 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.

Contents

Acetamiprid belongs to the family of chloropyridinyl neonicotinoid insecticides introduced in the early 1990s. [2] It is also used for controlling domestic pests (such as fleas on cats and dogs).

Structure and reactivity

Acetamiprid is an α-chloro-N-heteroaromatic compound. It is a neonicotinoid with a chloropyridinyl group and it is comparable to other neonicotinoids such as imidacloprid, nitenpyram and thiacloprid. These substances all have a 6-chloro-3-pyridine methyl group but differ in the nitroguanidine, nitromethylene, or cyanoamidine substituent on an acyclic or cyclic moiety. [3]

There are two isomeric forms in acetamiprid with E and Z-configurations of the cyanoimino group. There are also a variety of stable conformers due to the rotation of single bonds in the N-pyridylmethylamino group. The E-conformer is more stable than the Z-conformer and assumed to be the active form. In solution, two different E-conformers exist which slowly change into each other. [4]

Mechanism of action

Acetamiprid is a nicotine-like substance and reacts to the body in a similar way as nicotine. [5]

Metabolism

The metabolism of acetamiprid has been primarily studied in plants and soil. However, a recent study (2005) focussed on the metabolism of acetamiprid in honey bees. The honey bees in this study were fed a sucrose solution that contained acetamiprid. Seven different metabolites were discovered, of which two could not be identified. The five most abundant of these metabolites were found in the abdomen of the bee. Within the first hour of ingestion, acetamiprid concentrations were highest in tissues with a high nicotinic acetylcholine receptor density such as the abdomen, thorax and head. [2]

Acetamiprid was rapidly distributed throughout the bee's body, but also rapidly metabolised into the seven compounds. The substance is not just broken down in the gut, but in the entire body of the bee. This is mainly done by Type I enzymes such as mixed function oxidases. These enzymes use O2 to catalyze a reaction and convert acetamiprid into more polar metabolites. This makes it easier to excrete the compounds because the compounds become more hydrophilic. [2] Phase I enzymes form the first step in metabolizing the compound. Phase I metabolites can be bioactive. [6]

Three metabolic pathways exist, based on the kinetics of the metabolites that were found. The first pathway starts with the oxidative cleavage of the nitromethylene bond of acetamiprid. This is followed by another oxidation that forms 6-chloronicotinic acid. 6-Chloronicotinic acid is then transformed in one of the unidentified compounds, with an increased polarity. The second possible pathway is based on N-demethylation reactions, followed by oxidation of the nitromethylene bond of the intermediates. This will also result in 6-chloronicotinic acid. [2]

The last pathway consists of the oxidative cleavage of the cyanamine group. In this reaction a 1-3 ketone derivative is formed. This compound will undergo N-deacetylation which forms a 1-4 ketone derivative. This compound is transformed by oxidative cleavage into 6-chloropicolyl alcohol. From here, the compound can be metabolized in two different ways: either it is oxidized into 6-chloronicotinic acid or it is converted into a glycoconjugate derivative. The latter is probably in favour of the oxidization. [2]

Efficacy and side effects

Efficacy

Acetamiprid is used to protect a variety of crops, plants and flowers. It can be used combined with another pesticide with a different mode of action. This way the developing of resistance by pest species can be prevented. According to the US EPA acetamiprid could play a role in battling resistance in the species: Bemisia , greenhouse whiteflies and western flower thrips. [7]

Neonicotinoids act as agonists for nAChR and are selectively toxic to insects versus mammals, because of a higher potency on insect than mammalian nAChRs. [3] This increases their suitability as pesticides.

Adverse effects

Acetamiprid has a high potential for bioaccumulation and is highly toxic to birds and moderately toxic to aquatic organisms. [8] Excessive use of the pesticide could pose a threat to bird populations and other parts of the food chain. On the other hand, the metabolites that are produced after the absorption of acetamiprid in the honey bee are less toxic than those of other neonicotinoides. The half-life time of acetamiprid is also rather short, approximately 25–30 minutes, whereas other neonicotinoides can have a half-life of 4–5 hours. However, some metabolites are still present in the honey bee after 72 hours. This might be a toxicological risk for honey bees, as chronic exposure can increase the toxicity of certain compounds. [2] The EPA considers it "only moderately toxic" to bees; however, some media sources and the recent documentary Vanishing of the Bees have blamed neonicotinoids like acetamiprid for colony collapse disorder.

According to a report of the EPA from 2002, acetamiprid poses low risks to the environment compared to other insecticides. It degrades rapidly in soil and has therefore a low chance of leaching into groundwater. The degradation products will be able to reach the groundwater but are predicted to not be of toxicological significance. [9]

Toxicity

Insect studies

Extensive studies in the honeybee showed that acetamiprid LD50 is 7.1 μg with a 95% confidence interval of 4.57-11.2 μg/bee. In comparison, the LD50 of imidacloprid is 17,9 ng per bee. The difference in these comparable substances may be explained by a slightly weaker affinity of acetamiprid for nAChr when compared with imidacloprid. [10]

Neonicotinoids with a nitroguanidine group, such as imidacloprid, are most toxic to honey bees. Acetamiprid has an acyclic group instead of a second heterocyclic ring and is therefore much less toxic to honey bees than nitro-substituted compounds. [11]

Humans

As of now, two human case-studies have been described with acute poisoning by ingestion of an insecticide mixture containing acetamiprid whilst trying to commit suicide. Both patients were transported to an emergency room within two hours, and were instantly experiencing nausea, muscle weakness, convulsions and low body temperature (33.7 °C and 34.3 °C respectively). Symptoms such as muscle weakness seem to be similar to organophosphate insecticide exposure. Hypothermia and convulsions can be directly explained by the active acetamiprid compound which react with acetylcholine- and nicotinic receptors. Although mammalian toxicity is recorded as low, high doses of acetamiprid are recorded to be toxic to humans. [12]

Safety indications

Acetamiprid is classified as unlikely to be a human carcinogen. Acetamiprid has a low acute and chronic toxicity in mammals with no evidence of carcinogenicity, neurotoxicity or mutagenicity. It is classified as toxicity category rating II in acute oral studies with rats, toxicity category III in acute dermal and inhalation studies with rats, and toxicity category IV in primary eye and skin irritation studies with rabbits. It is mobile in soil, but degrades rapidly via aerobic soil metabolism, with studies showing its half-life between <1 and 8.2 days. The U.S. Environmental Protection Agency (EPA) does not consider it to be environmentally persistent.

A recent study has implicated acetamiprid as a cause of erectile dysfunction in human males and may be implicated in the problem of declining human fertility, and called into question its safety, particularly where its use may be subject to abuse. [13]

To ensure that application rates do not exceed limits which may be toxic to non-target vertebrates, the US proposes a maximum application rate of 0.1 to 0.6 pounds per acre (0.11 to 0.67 kg/ha) of active ingredient per season of agricultural land, differentiating between different crop types. [14] In China, the maximum dose is lower than in the US. The recommended dose that is used in agriculture ranges from 0.055 to 0.17 pounds of active ingredient per acre. [1]

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">Imidacloprid</span> Chemical compound

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. 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.

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

Chlorfenvinphos is an organophosphorus compound that was widely used as an insecticide and an acaricide. The molecule itself can be described as an enol ester derived from dichloroacetophenone and diethylphosphonic acid. Chlorfenvinphos has been included in many products since its first use in 1963. However, because of its toxic effect as a cholinesterase inhibitor it has been banned in several countries, including the United States and the European Union. Its use in the United States was discontinued in 1991.

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

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.

<span class="mw-page-title-main">Phosmet</span> Organophosphate non-systemic insecticide

Phosmet is a phthalimide-derived, non-systemic, organophosphate insecticide used on plants and animals. It is mainly used on apple trees for control of codling moth, though it is also used on a wide range of fruit crops, ornamentals, and vines for the control of aphids, suckers, mites, and fruit flies.

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">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">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">Terbufos</span> Chemical compound

Terbufos is a chemical compound used in insecticides and nematicides. It is part of the chemical family of organophosphates. It is a clear, colourless to pale yellow or reddish-brown liquid and sold commercially as granulate.

<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">Profenofos</span> Chemical compound

Profenofos is an organophosphate insecticide. It is a liquid with a pale yellow to amber color and a garlic-like odor. It was first registered in the United States in 1982. As of 2015, it was not approved in the European Union.

<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 Yao, Xiao-hua; Min, Hang; Lü, Zhen-hua; Yuan, Hai-Ping (2006-04-01). "Influence of acetamiprid on soil enzymatic activities and respiration". European Journal of Soil Biology. 42 (2): 120–126. doi:10.1016/j.ejsobi.2005.12.001. ISSN   1164-5563.
  2. 1 2 3 4 5 6 Brunet, Jean-Luc; Badiou, Alexandra; Belzunces, Luc P (2005-08-01). "In vivo metabolic fate of [14C]-acetamiprid in six biological compartments of the honeybee, Apis mellifera L". Pest Management Science. 61 (8): 742–748. doi:10.1002/ps.1046. ISSN   1526-4998. PMID   15880574.
  3. 1 2 Ford, Kevin A.; Casida, John E. (2006-07-01). "Chloropyridinyl Neonicotinoid Insecticides: Diverse Molecular Substituents Contribute to Facile Metabolism in Mice". Chemical Research in Toxicology. 19 (7): 944–951. doi:10.1021/tx0600696. ISSN   0893-228X. PMID   16841963.
  4. ↑ Nakayama, Akira; Sukekawa, Masayuki; Eguchi, Yoshiyuki (1997-10-01). "Stereochemistry and active conformation of a novel insecticide, acetamiprid". Pesticide Science. 51 (2): 157. doi:10.1002/(sici)1096-9063(199710)51:2<157::aid-ps620>3.0.co;2-c. ISSN   1096-9063.
  5. ↑ Kimura-Kuroda, Junko; Komuta, Yukari; Kuroda, Yoichiro; Hayashi, Masaharu; Kawano, Hitoshi (2012-02-29). "Nicotine-Like Effects of the Neonicotinoid Insecticides Acetamiprid and Imidacloprid on Cerebellar Neurons from Neonatal Rats". PLOS ONE. 7 (2): e32432. Bibcode:2012PLoSO...732432K. doi: 10.1371/journal.pone.0032432 . ISSN   1932-6203. PMC   3290564 . PMID   22393406.
  6. ↑ Casida, John E. (2011-04-13). "Neonicotinoid Metabolism: Compounds, Substituents, Pathways, Enzymes, Organisms, and Relevance". Journal of Agricultural and Food Chemistry. 59 (7): 2923–2931. doi:10.1021/jf102438c. ISSN   0021-8561. PMID   20731358.
  7. ↑ US Environmental Protection Agency Office of Pesticide Programs. (2010). Response Letter for Extension of the Exclusive Use Data Protection Period for Acetamiprid and Acetamiprid Technical.
  8. ↑ University of Hertfordshire. (2018). Pesticide Properties DataBase. "acetamiprid". Retrieved from: Archived 2018-05-14 at the Wayback Machine
  9. ↑ US Environmental Protection Agency. (2002). Pesticide Fact Sheet: Acetamiprid.
  10. ↑ Tomizawa, Motohiro; Casida, and John E. (2003). "Selective Toxicity of Neonicotinoids Attributable to Specificity of Insect and Mammalian Nicotinic Receptors". Annual Review of Entomology. 48 (1): 339–364. doi:10.1146/annurev.ento.48.091801.112731. PMID   12208819.
  11. ↑ Iwasa, Takao; Motoyama, Naoki; Ambrose, John T; Roe, R.Michael (2004-05-01). "Mechanism for the differential toxicity of neonicotinoid insecticides in the honey bee, Apis mellifera". Crop Protection. 23 (5): 371–378. doi:10.1016/j.cropro.2003.08.018. ISSN   0261-2194.
  12. ↑ Tomonori Imamura, Youichi Yanagawa, Kahoko Nishikawa, Naoto Matsumoto & Toshihisa Sakamoto (2010)Two cases of acute poisoning with acetamiprid in humans, Clinical Toxicology, 48:8, 851-853.
  13. ↑ Kaur, R.P; Gupta, V; Christopher, A.F; Bansal, P (2015). "Potential pathways of pesticide action on erectile function – A contributory factor in male infertility". Asian Pacific Journal of Reproduction. 4 (4): 322–330. doi: 10.1016/j.apjr.2015.07.012 .
  14. ↑ US Environmental Protection Agency Office of Pesticide Programs, Health Effects Division, Science Information Management Branch: "Chemicals Evaluated for Carcinogenic Potential" (2006)
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