Names | |
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IUPAC name 2-methyl-4-oxo-3-prop-2-yn-1-ylcyclopent-2-en-1-yl-2,2-dimethyl-3-(2-methylprop-1-en-1-yl)cyclopropanecarboxylate | |
Identifiers | |
3D model (JSmol) | |
ChEBI | |
ChemSpider | |
ECHA InfoCard | 100.041.246 |
KEGG | |
PubChem CID | |
UNII | |
CompTox Dashboard (EPA) | |
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Properties | |
C19H24O3 | |
Molar mass | 300.40 g/mol |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa). |
Prallethrin is a pyrethroid insecticide. Prallethrin 1.6% w/w liquid vaporizer is a repellent insecticide which is generally used for the control of mosquitoes in the household.
It is marketed as a mosquito repellent by Godrej as "GoodKnight Silver Power", SC Johnson as "All Out" and Southern Labs as "Quit Mozz" in India. It is also the primary insecticide in certain products for killing wasps and hornets, including their nests. It is the main ingredient in the consumer product "Hot Shot Ant & Roach Plus Germ Killer" spray. [1]
The vaporizer contains Prallethrin in isoparaffin solvents. The liquid is drawn up through a porous clay carbon wick by capillary action then vaporized with a heater.
The World Health Organization published in 2004 that "Prallethrin is of low mammalian toxicity, with no evidence of carcinogenicity" and "is very toxic to bees and fish but of low toxicity to birds." [2]
Prallethrin is a member of the pyrethroid class of insecticides. Pyrethroids have historically been classified into two groups, Type I and Type II, based upon chemical structure and neurotoxicological effect. Type I pyrethroids lack an alpha-cyano moiety and induce a syndrome in rats consisting of aggressive sparring, altered sensitivity to external stimuli, and fine tremor progressing to whole-body tremor and prostration. These Type I pyrethroid-specific behaviors are collectively described as the T-syndrome. Type II pyrethroids contain an alpha-cyano moiety and produce a syndrome in rats that includes pawing, burrowing, salivation, and coarse tremors leading to choreoathetosis. These Type II pyrethroid-specific behaviors are collectively described as the CS-syndrome (Verschoyle and Aldridge 1980; Lawrence and Casida 1982). Prallethrin is structurally similar to Type I pyrethroids. The adverse outcome pathway (AOP) shared by pyrethroids involves the ability to interact with voltage-gated sodium channels (VGSCs) in the central and peripheral nervous system, leading to changes in neuron firing, and ultimately neurotoxicity. [3]
Prallethrin has been evaluated for a variety of toxic effects in experimental toxicity studies. Neurotoxicity was observed throughout the database and is the most sensitive endpoint. Effects were seen across species, sexes, and routes of administration. In the acute rat neurotoxicity study, decreased exploratory behavior was seen at the time of peak effect. Reduced motor activity and transient tremors were also observed in the study. In the subchronic rat neurotoxicity study, a higher arousal rate was observed in animals at the highest dose tested. Clinical signs of neurotoxicity were also observed in other toxicity studies (subchronic and chronic oral studies in dogs, developmental toxicity studies in the rat and rabbit, 21-day dermal and 28-day inhalation studies in rats). No neurotoxic effects were observed in rats in the chronic toxicity study. [3]
Effects were also observed in the liver (rats, mice, and dogs), heart (dogs), and thyroid gland (rats). Some effects were also seen in the kidney (mice and rats). However, neurotoxicity was the most sensitive endpoint in the toxicology database, and other effects were generally seen in the presence of neurotoxicity and/or at higher doses. Liver effects observed included increased weight, elevated serum cholesterol and alkaline phosphatase activity, centrilobular hepatocyte vacuolation, histiocytic infiltration, enlarged liver, and perilobular hepatocellular hypertrophy. In dogs, myocardial fiber degeneration was seen in females in the subchronic study at the highest dose tested. Heart effects were also seen in one mid-dose female in the chronic study (hemorrhage and red discoloration). However, there was no dose response for the observed heart lesions in the study. Thyroid effects were observed in rats and consisted of increases in the number of small follicles and follicular cell hypertrophy and hyperplasia. The thyroid effects were seen in short-term studies in the presence of liver effects. Kidney effects observed were increased weights and histopathology. [3]
Developmental and reproduction studies are available for prallethrin. There was no evidence of increased quantitative or qualitative susceptibility in any of the studies. In the developmental studies, no toxic effects were noted in fetuses up to the highest doses tested. Maternal effects in the studies included tremors, salivation, exaggerated reflexes, and chromorhinorrhea (the discharge of a pigmented secretion from the nose). [4] In the reproduction study, decreased pup body weights were seen during the lactation period. Effects seen in parental animals were decreased body weights and body weight gains, increased liver weights and microscopic findings in the liver, kidney, thyroid, and pituitary. [3]
Prallethrin is classified as “Not Likely to be Carcinogenic to Humans.” No tumors were observed in rat and mouse carcinogenicity studies up to the highest doses tested. In both the rat and mouse studies, the animals could have tolerated higher dose levels; however, EPA determined that dose levels were adequate to assess potential carcinogenicity. [3]
Prallethrin tested negative in the majority of the genotoxicity studies. It also tested negative in an in vitro chromosomal aberration study in Chinese Hamster Ovary (CHO K1) cells without metabolic activation, but tested positive at all doses with metabolic activation. However, clastogenicity was not clearly dose-related, was seen at nontoxic and slightly toxic doses, and was not expressed in in vivo studies and structure-activity comparisons with the other pyrethroids revealed no correlations with clastogenicity. Other gene mutation, chromosomal aberration, and unscheduled DNA synthesis (UDS) studies were negative; therefore, there is no concern for genotoxicity. [3]
Acute lethality studies conducted with prallethrin indicate moderate acute toxicity via the oral and inhalation routes of administration (Category II) and low acute toxicity via the dermal route (Categories IV). It is not irritating to the skin (Category IV) but is minimally irritating to the eye (Category IV). It is not a dermal sensitizer. The weight of evidence from the available guideline, non-guideline, mechanism of action, and pharmacokinetics studies supports characterizing the toxicological profile of pyrethroids, including prallethrin, as being rapid in onset and associated with acute, peak exposures. Also, there is no apparent increase in hazard from repeated/chronic exposures to prallethrin. [3]
Cypermethrin (CP) is a synthetic pyrethroid used as an insecticide in large-scale commercial agricultural applications as well as in consumer products for domestic purposes. It behaves as a fast-acting neurotoxin in insects. It is easily degraded on soil and plants but can be effective for weeks when applied to indoor inert surfaces. It is a non-systemic and non-volatile insecticide that acts by contact and ingestion, used in agriculture and in pest control products. Exposure to sunlight, water and oxygen will accelerate its decomposition. Cypermethrin is highly toxic to fish, bees and aquatic insects, according to the National Pesticides Telecommunications Network (NPTN). It is found in many household ant and cockroach killers, including Raid, Ortho, Combat, ant chalk, and some products of Baygon in Southeast Asia.
Piperonyl butoxide (PBO) is a pale yellow to light brown liquid organic compound used as an adjuvant component of pesticide formulations for synergy. That is, despite having no pesticidal activity of its own, it enhances the potency of certain pesticides such as carbamates, pyrethrins, pyrethroids, and rotenone. It is a semisynthetic derivative of safrole and is produced from the condensation of the sodium salt of 2-(2-butoxyethoxy) ethanol and the chloromethyl derivative of hydrogenated safrole (dihydrosafrole); or through 1,2-Methylenedioxybenzene.
Bifenthrin is a pyrethroid insecticide. It is widely used against ant infestations.
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.
Ethion (C9H22O4P2S4) is an organophosphate insecticide. It is known to affect the neural enzyme acetylcholinesterase and disrupt its function.
Fumonisin B1 is the most prevalent member of a family of toxins, known as fumonisins, produced by multiple species of Fusarium molds, such as Fusarium verticillioides, which occur mainly in maize (corn), wheat and other cereals. Fumonisin B1 contamination of maize has been reported worldwide at mg/kg levels. Human exposure occurs at levels of micrograms to milligrams per day and is greatest in regions where maize products are the dietary staple.
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.
Aldrin is an organochlorine insecticide that was widely used until the 1990s, when it was banned in most countries. Aldrin is a member of the so-called "classic organochlorines" (COC) group of pesticides. COCs enjoyed a very sharp rise in popularity during and after World War II. Other noteworthy examples of COCs include dieldrin and DDT. After research showed that organochlorines can be highly toxic to the ecosystem through bioaccumulation, most were banned from use. Before the ban, it was heavily used as a pesticide to treat seed and soil. Aldrin and related "cyclodiene" pesticides became notorious as persistent organic pollutants.
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.
Benzotrichloride (BTC), also known as α,α,α-trichlorotoluene, phenyl chloroform or (trichloromethyl)benzene, is an organic compound with the formula C6H5CCl3. Benzotrichloride is an unstable, colorless or somewhat yellowish, viscous, chlorinated hydrocarbon with a penetrating odor. Benzotrichloride is used extensively as a chemical intermediate for products of various classes, i.e. dyes and antimicrobial agents.
1,1,2,2-tetrachloroethane (TeCA), also known by the brand names Bonoform, Cellon and Westron, is an organic compound. It is colorless liquid and has a sweet odor. It is used as an industrial solvent and as a separation agent. TeCA is toxic and it can be inhaled, consumed or absorbed through the skin. After exposure, nausea, dizziness or even liver damage may occur.
Organophosphate poisoning is poisoning due to organophosphates (OPs). Organophosphates are used as insecticides, medications, and nerve agents. Symptoms include increased saliva and tear production, diarrhea, vomiting, small pupils, sweating, muscle tremors, and confusion. While onset of symptoms is often within minutes to hours, some symptoms can take weeks to appear. Symptoms can last for days to weeks.
Methiocarb is a carbamate pesticide which is used as an insecticide, bird repellent, acaricide and molluscicide since the 1960s. Methiocarb has contact and stomach action on mites and neurotoxic effects on molluscs. Seeds treated with methiocarb also affect birds. Other names for methiocarb are mesurol and mercaptodimethur.
Hexachlorocyclopentadiene (HCCPD), also known as C-56, Graphlox, and HRS 1655, is an organochlorine compound with the formula C5Cl6. It is a precursor to pesticides, flame retardants, and dyes. It is a colourless liquid, although commercial samples appear lemon-yellow liquid sometimes with a bluish vapour. Many of its derivatives proved to be highly controversial, as studies showed them to be persistent organic pollutants. An estimated 270,000 tons were produced until 1976, and smaller amounts continue to be produced today.
Microcystin-LR (MC-LR) is a toxin produced by cyanobacteria. It is the most toxic of the microcystins.
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.
Triazofos is a chemical compound used in acaricides, insecticides, and nematicides.
EPN is an insecticide of the phosphonothioate class. It is used against pests such as European corn borer, rice stem borer, bollworm, tobacco budworm, and boll weevil.
Novaluron, or (±)-1-[3-chloro-4-(1,1,2-trifluoro-2-trifluoro- methoxyethoxy)phenyl]-3-(2,6-difluorobenzoyl)urea, is a chemical with pesticide properties, belonging to the class of insecticides called insect growth regulators. It is a benzoylphenyl urea developed by Makhteshim-Agan Industries Ltd.. In the United States, the compound has been used on food crops, including apples, potatoes, brassicas, ornamentals, and cotton. Patents and registrations have been approved or are ongoing in several other countries throughout Europe, Asia, Africa, South America, and Australia. The US Environmental Protection Agency and the Canadian Pest Management Regulatory Agency consider novaluron to pose low risk to the environment and non-target organisms and value it as an important option for integrated pest management that should decrease reliance on organophosphorus, carbamate and pyrethroid insecticides.
Nivalenol (NIV) is a mycotoxin of the trichothecene group. In nature it is mainly found in fungi of the Fusarium species. The Fusarium species belongs to the most prevalent mycotoxin producing fungi in the temperate regions of the northern hemisphere, therefore making them a considerable risk for the food crop production industry.