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Pyrethroid
Pyrethroid
Pyrethroid
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Chemical structure of Allethrin isomers
Chemical structure of Permethrin isomers

A pyrethroid is an organic compound similar to the natural pyrethrins, which are produced by the flowers of pyrethrums (Chrysanthemum cinerariaefolium and C. coccineum). Pyrethroids are used as commercial and household insecticides.[1]

In household concentrations pyrethroids are generally harmless to humans.[1] However, pyrethroids are toxic to insects such as bees, dragonflies, mayflies, gadflies, and some other invertebrates, including those that constitute the base of aquatic and terrestrial food webs.[2] Pyrethroids are toxic to aquatic organisms, especially fish.[3] They have been shown to be an effective control measure for malaria outbreaks, through indoor applications.[4]

Mode of action

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Pyrethroids are excitotoxic to axons. They act by preventing the closure of the voltage-gated sodium channels in the axonal membranes. The sodium channel is a membrane protein with a hydrophilic interior. This interior is shaped precisely to allow sodium ions to pass through the membrane, enter the axon, and propagate an action potential. When the toxin keeps the channels in their open state, the nerves cannot repolarize, leaving the axonal membrane permanently depolarized, thereby paralyzing the organism.[5] Pyrethroids can be combined with the synergist piperonyl butoxide, a known inhibitor of microsomal P450 enzymes which are important in metabolizing the pyrethroid. By that means, the efficacy (lethality) of the pyrethroid is increased.[6] It is likely that there are other mechanisms of intoxication also.[7] Disruption of neuroendocrine activity is thought to contribute to their irreversible effects on insects, which indicates a pyrethroid action on voltage-gated calcium channels (and perhaps other voltage-gated channels more widely).[7]

Chemistry and classification

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(1R,3R)- or (+)-trans-chrysanthemic acid.

Pyrethroids are classified based on their mechanism of biological action, as they do not share a common chemical structure. Many are 2,2-dimethylcyclopropanecarboxylic acid derivatives, like chrysanthemic acid, esterified with an alcohol. However, the cyclopropyl ring does not occur in all pyrethroids. Fenvalerate, which was developed in 1972, is one such example and was the first commercialized pyrethroid without that group.

Pyrethroids which lack an α-cyano group are often classified as type I pyrethroids and those with it are called type II pyrethroids. Pyrethroids that have a common name starting with "cy" have a cyano group and are type II. Fenvalerate also contains an α-cyano group.

Some pyrethroids, like etofenprox, also lack the ester bond found in most other pyrethroids and have an ether bond in its place. Silafluofen is also classified as a pyrethroid and has a silicon atom in the place of the ester. Pyrethroids often have chiral centers and only certain stereoisomers work efficiently as insecticides.[8]

Examples

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Safety

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Environmental effects

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Pyrethroids are toxic to insects such as bees, dragonflies, mayflies, gadflies, and some other invertebrates, including those that constitute the base of aquatic and terrestrial food webs.[2] They are toxic to aquatic organisms including fish.[3]

Pyrethroids are usually broken apart by sunlight and the atmosphere in one or two days, however when associated with sediment they can persist for some time.[better source needed][9]

Pyrethroids are unaffected by conventional secondary treatment systems at municipal wastewater treatment facilities. They appear in the effluent, usually at levels lethal to invertebrates.[better source needed][10]

Humans

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Pyrethroid absorption can happen via skin, inhalation or ingestion.[11] Pyrethroids often do not bind efficiently to mammalian sodium channels.[12] They also absorb poorly via skin and human liver is often able to metabolize them relatively efficiently. Pyrethroids are thus much less toxic to humans without liver problems than to insects.[13]

It is not well established if chronic exposure to small amounts of pyrethroids is hazardous or not.[14] However, large doses can cause acute poisoning, which is rarely life threatening. Typical symptoms include facial paresthesia, itching, burning, dizziness, nausea, vomiting and more severe cases of muscle twitching. Severe poisoning is often caused by ingestion of pyrethroids and can result in a variety of symptoms like seizures, coma, bleeding or pulmonary edema.[11] There is an association of pyrethroids with poorer early social-emotional and language development.[4]

Other organisms

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Pyrethroids are very toxic to cats, but not to dogs. Poisoning in cats can result in seizures, fever, ataxia and even death. Poisoning can occur if pyrethroid containing flea treatment products, which are intended for dogs, are used on cats. The livers of cats detoxify pyrethroids via glucuronidation more poorly than dogs, which is the cause of this difference.[15] Aside from cats, pyrethroids are typically not toxic to mammals or birds.[16] They are often toxic to fish, reptiles and amphibians.[17]

Resistance

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Further information: Insecticide resistance

The use of pyrethroids as insecticides has led to the development of widespread resistance to them among some insect populations, especially mosquitoes.[18]

Pyrethroids have been used against bedbugs, but resistant populations have developed to them.[19][20][21][22] Populations of diamondback moths have also commonly developed resistance to pyrethroids[23][better source needed] – including in U.S. states North Dakota[24] and Wisconsin[25] while pyrethroids are still recommended in California.[26] Various mosquito populations have been discovered to have a high level of resistance, including Anopheles gambiae s.l. in West Africa by Chandre et al 1999 through Pwalia et al 2019, A. arabiensis in Sudan by Ismail et al 2018 and The Gambia by Opondo et al 2019, and Aedes aegypti in South East Asia by Amelia-Yap et al 2018, Papua New Guinea by Demok et al 2019, and various other locations by Smith et al 2016.[18]

Knockdown resistance (kdr) is one of the stronger kinds of resistance.[27] kdr mutations confer target-site resistance to DDT and pyrethroids and cross-resistance to DDT.[27] Most kdr mutations are within or proximate to the two arthropod sodium channel genes.[27]

History

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Pyrethroids were introduced by a team of Rothamsted Research scientists in the 1960s and 1970s following the elucidation of the structures of pyrethrin I and II by Hermann Staudinger and Leopold Ružička in the 1920s.[28] The pyrethroids represented a major advancement in the chemistry that would synthesize the analog of the natural version found in pyrethrum. Its insecticidal activity has relatively low mammalian toxicity and an unusually fast biodegradation. Their development coincided with the identification of problems with DDT use. Their work consisted firstly of identifying the most active components of pyrethrum, extracted from East African chrysanthemum flowers and long known to have insecticidal properties. Pyrethrum rapidly knocks down flying insects but has negligible persistence — which is good for the environment but gives poor efficacy when applied in the field. Pyrethroids are essentially chemically stabilized forms of natural pyrethrum and belong to IRAC MoA group 3 (they interfere with sodium transport in insect nerve cells).[29]

The first-generation pyrethroids, developed in the 1960s, include bioallethrin, tetramethrin, resmethrin, and bioresmethrin. They are more active than the natural pyrethrum but are unstable in sunlight. With the 91/414/EEC review,[30] many 1st-generation compounds have not been included on Annex 1, probably because the market is not big enough to warrant the costs of re-registration (rather than any special concerns about safety).

By 1974, the Rothamsted team had discovered a second generation of more persistent compounds notably: permethrin, cypermethrin and deltamethrin. They are substantially more resistant to degradation by light and air, thus making them suitable for use in agriculture, but they have significantly higher mammalian toxicities. Over the subsequent decades these derivatives were followed with other proprietary compounds such as fenvalerate, lambda-cyhalothrin and beta-cyfluthrin. Most patents have now expired, making these compounds cheap and therefore popular (although permethrin and fenvalerate have not been re-registered under the 91/414/EEC process).

References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Pyrethroid

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Pyrethroids are a class of synthetic insecticides chemically derived from the natural pyrethrins, which are neurotoxic esters extracted from the flowers of Chrysanthemum cinerariaefolium (also known as ). These compounds mimic the structure of pyrethrins but are modified for enhanced stability, potency against , and resistance to environmental degradation, such as in sunlight. Pyrethroids target the nervous systems of by binding to voltage-gated sodium channels, prolonging their opening and causing repetitive nerve firing, , and death, while exhibiting lower toxicity to mammals due to differences in body temperature and detoxification mechanisms. Developed in the mid-20th century to overcome the limitations of natural pyrethrins—such as rapid breakdown in light and air—pyrethroids emerged commercially in the , with key innovations like the synthesis of allethrin in 1949 and in 1973. By the 1980s, they accounted for approximately 25% of the global market, covering over 33 million hectares of annually. They are classified into two main types based on chemical structure: Type I pyrethroids (e.g., , allethrin), which lack an α-cyano group and typically induce repetitive tremors in exposed organisms; and Type II pyrethroids (e.g., , ), which include the α-cyano group and cause more severe symptoms like choreoathetosis with salivation. This influences their potency and toxicological profiles, with Type II variants often being more effective against a broader range of pests. Pyrethroids are extensively used in agriculture for crop protection against insects, in public health programs for vector control (such as malaria and Zika prevention via insecticide-treated mosquito nets recommended by the World Health Organization), and in household products for pest management, including lice shampoos and pet treatments. Over 1,000 pyrethroid compounds have been synthesized, though fewer than a dozen are commonly registered for use in the United States, often formulated as emulsifiable concentrates, aerosols, or dusts. Their lipophilic nature allows them to penetrate insect cuticles effectively, and they are frequently combined with synergists like to enhance efficacy by inhibiting detoxification enzymes. Despite their benefits, concerns include environmental persistence in sediments, in aquatic organisms, and emerging insect resistance, prompting ongoing research into sustainable alternatives.

Chemical Properties

Structure and Stereochemistry

Pyrethroids are synthetic esters structurally analogous to natural pyrethrins, consisting of a cyclopropanecarboxylic moiety esterified to an alcohol moiety. The component typically features a 2,2-dimethylcyclopropane ring substituted at the 3-position with groups such as a 2,2-dichlorovinyl (as in ) or isobutenyl chain. The alcohol moiety varies by type: Type I pyrethroids often use primary or secondary alcohols like 3-phenoxybenzyl alcohol or allethrolone (a cyclopentenolone), while Type II incorporate an α-cyano group on the alcohol, such as in 3-(2,2-dibromovinyl)-2,2-dimethylcyclopropanecarboxylic esterified with α-cyano-3-phenoxybenzyl alcohol (as in ). These structural modifications enhance stability and potency compared to pyrethrins. Pyrethroids exhibit complex due to multiple chiral centers. The ring introduces at the 3-substituent, with trans isomers generally more bioactive. Most pyrethroids have at least two chiral centers: the 1- and 3-positions of the (configuring as 1R,3R or 1S,3S for active forms). Type I compounds like have two centers (four stereoisomers), while Type II like have three (including the α-carbon, yielding eight stereoisomers). Insecticidal activity is highly stereospecific, with the (1R,trans)-acid and specific alcohol configurations (e.g., (S)-α-cyano for Type II) being most potent; commercial products are often mixtures enriched for active isomers.

Synthesis

The extraction of natural pyrethrins from the dried flowers of Chrysanthemum cinerariaefolium (also known as ) provided the basis for early insecticides, where flowers are harvested, dried, and subjected to solvent extraction using organic solvents like or to isolate the crude pyrethrin mixture, followed by purification steps such as or to obtain the active esters. This natural extraction method, while effective for small-scale production, was limited by seasonal availability and low yields (typically 1-2% pyrethrins content), prompting the development of synthetic pyrethroid analogs. Modern pyrethroid synthesis primarily involves the esterification of cyclopropanecarboxylic derivatives, such as halomethyl-substituted chrysanthemic , with specific alcohols to mimic the linkage in natural pyrethrins. A key route entails reacting the of the component with an alcohol under basic conditions; for instance, the reaction of (S)-allethrolone with chrysanthemoyl in the presence of a base like yields bioallethrin, a first-generation synthetic pyrethroid, with the of the alcohol ensuring high insecticidal activity. Similarly, 3-phenoxybenzyl alcohol is esterified with 3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropanecarboxylic to form , often using coupling agents like dicyclohexylcarbodiimide to facilitate the reaction. These esterifications typically occur in aprotic solvents at controlled temperatures to minimize side reactions and preserve stereoisomers. Industrial-scale production of pyrethroids like employs multi-step processes starting from readily available precursors, including the synthesis of the ring via addition to dienes and the introduction of double bonds using the on aldehydes to form the vinyl substituent. Stereoselective steps, such as asymmetric with chiral catalysts, are incorporated to favor the bioactive trans-isomers, followed by purification via or to achieve high enantiomeric purity. These processes are optimized for large-scale reactors, enabling continuous production with yields exceeding 80% for key intermediates. Synthetic pyrethroids offer significant advantages over natural pyrethrins, including greater through chemical that bypasses agricultural dependencies and reduced production costs, as well as enhanced stability via modifications like the addition of an alpha-cyano group to the alcohol moiety, which prolongs insecticidal efficacy in and heat. The cyclopropane ring motif in these synthetics is often derived from precursors but adapted for efficient laboratory assembly.

Classification and Examples

Types of Pyrethroids

Pyrethroids are primarily classified into two categories based on the presence or absence of an α-cyano group in their molecular structure: Type I pyrethroids, which lack this group and typically induce rapid knockdown through repetitive neuronal firing, and Type II pyrethroids, which contain the α-cyano group and cause prolonged via modification of sodium tail currents. This distinction arises from differences in their chemical makeup and resulting toxicological effects, with Type I compounds often producing shorter-lived symptoms compared to the more persistent actions of Type II. Pyrethroids can also be categorized by generations, reflecting advancements in their development for improved stability and efficacy. First-generation pyrethroids, such as simple esters like allethrin, were developed in the 1940s and 1950s but suffered from photolability, limiting their outdoor use. Second-generation pyrethroids, exemplified by photostable compounds like , emerged in the 1970s and addressed this issue through structural modifications that enhanced resistance to light degradation. Some sources refer to more advanced Type II compounds like , introduced in the 1980s, as third-generation pyrethroids due to their enhanced potency and environmental persistence. Functionally, pyrethroids are distinguished as knockdown agents, which immobilize pests quickly but may allow recovery without , versus lethal agents that ensure higher mortality rates through sustained effects. Formulation types further differentiate them, with oil-soluble variants suitable for solvent-based applications and water-dispersible forms, such as emulsions or granules, enabling easier mixing and application in aqueous systems despite their inherent low . At a group level, structure-activity relationships highlight the α-cyano group's pivotal role, as its addition to Type I scaffolds increases insecticidal potency by 10- to 100-fold, primarily by prolonging the duration of neuronal disruption. This enhancement underscores the evolution from earlier, less potent designs to more effective modern pyrethroids, guiding their selection for diverse pest control needs.

Specific Compounds

Permethrin is a broad-spectrum Type I pyrethroid insecticide, notable for its mixture of cis and trans isomers, with the cis form exhibiting greater potency and persistence. It has a molecular formula of C₂₁H₂₀Cl₂O₃ and a molecular weight of 391.3 g/mol, appearing as a viscous yellow-brown liquid with a melting point around 34 °C (ranging 34-39 °C for the mixture, higher for pure isomers). Its solubility in water is very low at 0.006 mg/L at 20 °C, and it possesses a logP of 6.5, indicating high lipophilicity; it remains stable under heat for over two years at 50 °C but undergoes some photochemical degradation upon exposure to light. Commercially available under trade names such as Ambush and Dragnet, permethrin was produced and used globally at approximately 600 tonnes per year in the 1980s. Cypermethrin, a Type II pyrethroid distinguished by its α-cyano group, offers high potency particularly against lepidopteran pests and exists as a of eight stereoisomers, with alpha-cypermethrin being one of the most active forms. Its molecular formula is C₂₂H₁₉Cl₂NO₃ with a molecular weight of 416.3 g/mol; it is a viscous to or crystalline with a of 60-80 °C for technical grade. solubility is minimal at 0.004 mg/L at 20 °C, and its logP is 6.60, reflecting strong partitioning into organic phases; it is stable in neutral to weakly acidic conditions (optimal at 4) and shows good photostability in field applications, though it hydrolyzes in alkaline media. Trade names include Cymbush and Ripcord, and it is widely formulated for agricultural and structural . Deltamethrin represents one of the most potent Type II pyrethroids, featuring an α-cyano group and resolved primarily to its active (1R)-cis for enhanced efficacy. With a molecular formula of C₂₂H₁₉Br₂NO₃ and molecular weight of 505.2 g/mol, it forms colorless to white odorless crystals with a of 98 °C and a density of 1.5 g/cm³. It exhibits negligible solubility (<0.0001 mg/L at 20 °C) and a high logP around 6.4, contributing to its low mobility; notably, deltamethrin demonstrates excellent UV stability, resisting photodegradation better than earlier pyrethroids. Commercial products bear names like Decis and K-Othrine, reflecting its broad adoption in pest management. Allethrin, the first synthetic pyrethroid developed in 1949, is a Type I compound primarily suited for indoor applications due to its rapid knockdown effect on flying insects. Its molecular formula is C₁₉H₂₆O₃ with a molecular weight of 302.4 g/mol, existing as a clear to pale yellow viscous liquid with a low melting point near 4 °C and boiling point of 140 °C at 0.1 mm Hg. Insoluble in water and with a logP of 4.78, it is more stable to UV light than natural pyrethrins but still decomposes under direct sunlight and in alkaline conditions. It is marketed under trade names such as Pynamin and is often used in aerosol formulations. Among minor variants, tetramethrin is a Type I pyrethroid with a phthalimide structure, appearing as white crystals (melting point 65-80 °C) that are insoluble in water and volatile, making it effective for space sprays against household pests; it is commercially available as Neo-Pynamin. Resmethrin, another early Type I compound, features a furan ring and was noted for its low mammalian toxicity but limited by instability to light and air (melting point ~62 °C, low water solubility); its registrations were voluntarily canceled in 2010, leading to discontinuation of sales by 2015 due to these stability issues.
CompoundTypeKey Physical PropertiesNotable StabilityTrade Names
PermethrinIMW: 391.3 g/mol; MP: 34 °C; Water sol.: 0.006 mg/L; logP: 6.5Heat-stable; moderate photodegradationAmbush, Dragnet
CypermethrinIIMW: 416.3 g/mol; MP: 60-80 °C; Water sol.: 0.004 mg/L; logP: 6.60pH-stable (acidic); good photostabilityCymbush, Ripcord
DeltamethrinIIMW: 505.2 g/mol; MP: 98 °C; Water sol.: <0.0001 mg/L; logP: ~6.4Excellent UV stabilityDecis, K-Othrine
AllethrinIMW: 302.4 g/mol; MP: ~4 °C; Water sol.: Insoluble; logP: 4.78Better than pyrethrins but UV-sensitivePynamin
TetramethrinIMW: 331.4 g/mol; MP: 65-80 °C; Water sol.: LowVolatile; light-unstableNeo-Pynamin
ResmethrinI (discontinued)MW: 338.4 g/mol; MP: ~62 °C; Water sol.: LowUnstable to light/air(Former: SBP-1382)

Biological Activity

Mode of Action

Pyrethroids exert their insecticidal effects primarily by binding to voltage-gated sodium channels (VGSCs) in neuronal membranes of insects, where they interact with specific receptor sites known as pyrethroid receptor sites 1 and 2 (PyR1 and PyR2), located in the transmembrane segments of the channel. These sites are situated in the inner pore region, involving domains I-III of the channel's alpha subunit, allowing pyrethroids to preferentially associate with the open state of the channel. Upon binding, pyrethroids inhibit the deactivation and inactivation processes of the VGSC, thereby prolonging the open state and extending the influx of sodium ions (Na⁺) during action potentials. This prolongation of Na⁺ conductance leads to repetitive nerve firing and sustained depolarization of the neuronal membrane, resulting in hyperexcitation followed by tremors and eventual paralysis in target insects. The effects differ between type I and type II pyrethroids: type I compounds, lacking an α-cyano group (e.g., ), induce short bursts of repetitive discharges by modestly slowing channel closure, while type II pyrethroids, possessing the α-cyano group (e.g., ), produce longer tail currents that more profoundly suppress excitability and promote depolarization-dependent block. Both types stabilize the open conformation but with varying kinetics, emphasizing the role of chemical structure in modulating channel gating. The binding of pyrethroids to VGSCs exhibits high stereospecificity, with only specific isomers demonstrating potent activity; for instance, the 1R-trans isomers of compounds like tetramethrin bind effectively with high affinity, achieving dissociation constants (K_d) in the range of 58-300 nM, whereas other stereoisomers show markedly reduced potency. This selectivity arises from the precise fit required at the receptor sites, where enantiomeric configuration influences interaction strength and subsequent channel modification. Synthetic pyrethroids share a similar mode of action with their natural precursors, the pyrethrins extracted from flowers, both targeting VGSCs to disrupt nerve function, but pyrethroids incorporate structural modifications such as halogen substitutions to enhance metabolic stability and prolong efficacy in the environment.

Effects on Target Pests

Pyrethroids exert their effects on target pests primarily through disruption of voltage-gated sodium channels in the nervous system, leading to a characteristic sequence of physiological responses. Upon exposure, insects initially exhibit hyperactivity and hyperexcitation, manifested as rapid, uncoordinated movements and convulsions, due to repetitive firing of action potentials. This phase quickly progresses to loss of coordination and knockdown, where pests display prostration, fine tremors (in Type I exposures), or more severe choreoathetosis and salivation (in Type II exposures), resulting in immobilization within minutes. Paralysis follows as nerve function collapses from sustained depolarization, typically occurring within hours, and culminates in death from systemic nervous system failure over 1 to 48 hours, depending on dose and species. The spectrum of activity encompasses a broad range of arthropods, including insects (such as those in orders Coleoptera, Diptera, Hemiptera, Hymenoptera, Lepidoptera, Orthoptera, and Thysanoptera), mites, and ticks, primarily via contact but also ingestion, with higher bioavailability through oral routes in some cases. Efficacy is demonstrated by low lethal doses; for example, the LD50 for permethrin against houseflies (Musca domestica) is approximately 0.023 μg per fly, equivalent to about 1-2 μg/g body weight. Factors influencing these effects include dose-dependent responses, where higher concentrations accelerate symptom onset; at application rates of 10-100 mg/m², pyrethroids achieve 90% knockdown in 10-30 minutes for many flying and crawling insects. Residual activity persists for weeks on treated surfaces, particularly for photostable formulations like , enabling prolonged control through contact exposure. Differences in effects arise between Type I and Type II pyrethroids: Type I compounds (lacking an α-cyano group, e.g., ) induce rapid knockdown ideal for flying insects, causing transient repetitive discharges and shorter-lived tremors, but with quicker recovery if not lethal. In contrast, Type II pyrethroids (with α-cyano group, e.g., ) prolong sodium channel opening, leading to more intense paralysis, higher lethality, and extended residual kill lasting weeks, suitable for sustained pest management.

Uses and Applications

Agricultural and Horticultural

Pyrethroids are widely used in agriculture to control insect pests on various crops, including grains (such as corn and wheat), vegetables (like tomatoes and leafy greens), fruits, nuts, cotton, and soybeans. They target a broad spectrum of pests, including aphids, beetles, caterpillars, and mites, often applied as foliar sprays, dusts, or granular formulations at concentrations typically ranging from 0.1% to 0.5% active ingredient. For example, is commonly used on vegetables to manage aphids and leafhoppers, while is applied to cotton for lepidopteran pests like bollworms. In field crops, pyrethroids such as lambda-cyhalothrin are standard for protecting against corn rootworms and soybean aphids in regions like the US Midwest. In horticulture, pyrethroids are employed for pest management on ornamental plants, turf, and greenhouse crops, controlling whiteflies, thrips, and spider mites. Bifenthrin, for instance, is used on lawns and landscape plants to suppress ants and sod webworms. These applications often incorporate synergists like piperonyl butoxide to improve efficacy against resistant populations. Global agricultural use accounts for the majority of pyrethroid consumption, though concerns over resistance and environmental impact have led to integrated pest management recommendations.

Public Health and Domestic

Pyrethroids play a crucial role in vector control programs aimed at preventing the transmission of diseases such as malaria, dengue, and Zika by targeting mosquito vectors. Long-lasting insecticidal nets (LLINs) impregnated with permethrin at concentrations of 2% w/w (20 g/kg net) provide a physical barrier and insecticidal effect, reducing the incidence of uncomplicated malaria episodes by approximately 50% in areas of stable transmission. Indoor residual spraying (IRS) using deltamethrin at 25 mg/m² on interior walls offers prolonged protection, killing mosquitoes that rest indoors after feeding and thereby interrupting disease cycles. In domestic settings, pyrethroids are widely incorporated into household products for managing common pests like cockroaches and fleas. Aerosol sprays and surface treatments typically contain or similar pyrethroids at 0.25-2% concentrations, applied to cracks, crevices, and infested areas to achieve rapid knockdown and control. Flea collars for pets often utilize -impregnated materials that release the insecticide gradually, providing extended protection against ectoparasites in home environments. The public health impact of pyrethroids is significant, as endorsed by the World Health Organization (WHO) for controlling vectors of dengue and Zika viruses, where they achieve 80-95% mortality of adult mosquitoes within 24 hours in susceptible populations. These insecticides contribute to broader disease prevention efforts, with pyrethroids accounting for about 20% of global insecticide use in vector control and household applications. Specialized formulations, such as ultra-low volume (ULV) fogging with pyrethroids like deltamethrin, are deployed during urban outbreaks to disperse fine aerosol droplets that target flying mosquitoes, enhancing rapid response in densely populated areas.

Veterinary and Medical

Pyrethroids play a significant role in veterinary medicine for managing ectoparasites in livestock and companion animals. Permethrin pour-on formulations, typically at concentrations of 7.5-10%, are applied topically along the backline of cattle at dosages of 1.5-3 mL per 100 lbs body weight to control ticks, lice, and flies, providing residual protection for up to several weeks. Deltamethrin-impregnated collars for dogs and cats offer sustained release of the active ingredient, killing and repelling fleas and ticks for 4-6 months while remaining water-resistant. These products target contact toxicity to arthropods, disrupting nerve function upon exposure. In human medical applications, pyrethroids are employed as topical ectoparasiticides, particularly for infestations treatable without systemic drugs. Permethrin 1% lotion or cream is recommended as first-line therapy for head lice (pediculosis capitis), applied to dry hair and scalp for 10 minutes before rinsing, with a second application 9-10 days later to address newly hatched lice; historical efficacy reached 96% in susceptible strains, though rates have declined to 45-55% in areas with resistance. For scabies, 5% permethrin cream is applied from neck to toes and left on for 8-14 hours, achieving cure rates of 91-98% after one or two applications in clinical trials. Pyrethrin shampoos, often combined with piperonyl butoxide to enhance efficacy, are used similarly for head lice, killing live insects but requiring a follow-up treatment to eliminate nits. Ectoparasiticide dips for livestock, such as those containing synthetic pyrethroids like cypermethrin or deltamethrin, are diluted to concentrations of approximately 0.025-0.05% in water for plunge or spray applications, immersing animals weekly during peak infestation periods to control and mites. These formulations demonstrate variable efficacy against resistant strains, with some pyrethroids maintaining >90% mortality in moderately resistant populations over 24 hours, though high-level resistance reduces control in heavily affected areas. Administration involves thorough wetting of the animal's coat, with withholding periods of 1-7 days for or to ensure safety. The animal health segment represents about 10% of the global pyrethroid market, driven by demand for ectoparasiticide products in and pets. Many pyrethroid-based veterinary and medical treatments, including creams and collars, have received regulatory approval for over-the-counter use by agencies like the FDA and EPA, facilitating accessible application without prescription in non-severe cases.

Safety and Toxicology

Human Health Effects

Pyrethroids demonstrate low in humans and other mammals, with oral LD50 values generally exceeding 2000 mg/kg in rats for many compounds, such as (LD50 1000–2000 mg/kg) and (LD50 30–5000 mg/kg). This reduced toxicity compared to insects stems from rapid hydrolysis by mammalian carboxylesterases and enzymes, which quickly detoxify the compounds. Human exposure to pyrethroids occurs mainly via dermal contact, , and , with dermal being the predominant route in occupational and domestic settings. Dermal exposure often causes localized , such as or (tingling or burning sensations), particularly at concentrations above 5%, though systemic absorption is low (0.3–1.8% for ). of aerosols can lead to respiratory , including coughing, sneezing, , and mild dyspnea at high concentrations, while —typically accidental or suicidal—results in gastrointestinal symptoms like , , and , with rare progression to more severe effects such as tremors or seizures in large doses. Symptoms from acute exposure generally resolve within hours to days with supportive care, as the compounds do not accumulate significantly. Chronic low-level exposure to pyrethroids may involve potential neurotoxic effects, including persistent or the "Type I" characterized by tremors and , though human data remain limited and primarily derived from occupational cohorts. Epidemiological studies suggest associations with neurobehavioral alterations, such as cognitive deficits in children, but causality is not firmly established. Concerns over endocrine disruption, including reduced testosterone levels observed in animal models, persist but lack conclusive evidence in humans, with no definitive links to reproductive or developmental disorders. In occupational settings, pyrethroid exposure is managed through established air limits, such as the OSHA of 5 mg/m³ (8-hour time-weighted average) for pyrethrins, with similar guidelines applying to synthetic pyrethroids; actual measured levels during application often range from 0.005 to 0.055 mg/m³, below which significant effects are rare. Case studies document reactions, including allergic or respiratory , in a subset of workers, underscoring the need for .

Environmental Impact

Pyrethroids undergo degradation in environmental compartments primarily through photolysis and , exhibiting half-lives of 1 to 30 days in and under typical conditions. further contributes to their breakdown, though rates vary by compound and environmental factors such as exposure and microbial activity. Despite these degradation pathways, pyrethroids strongly adsorb to sediments and soils due to their high organic carbon-water partition coefficients (Koc values often exceeding 10,000, and reaching up to 3.14 × 10^6 for compounds like ), reducing their and mobility in but allowing accumulation in sedimentary layers. This adsorption is facilitated by their inherent structural . Bioaccumulation of pyrethroids is moderate in aquatic organisms, with bioconcentration factors (BCF) generally ranging from 100 to 1,000 in and , reflecting their lipophilic nature balanced by metabolic clearance. In contrast, is low in birds and mammals, as these taxa rapidly metabolize pyrethroids via enzymes, limiting tissue residue buildup. Agricultural runoff represents a primary vector for pyrethroid entry into aquatic ecosystems, transporting residues bound to and contributing substantially to pollution incidents, where pyrethroids are frequently detected in contaminated surface waters and implicated in up to 75% of samples showing presence in affected regions. This contamination disrupts broader ecological balance by altering and dynamics in receiving water bodies. Recent post-2020 research highlights emerging concerns regarding pyrethroid interactions with , which can adsorb these insecticides and potentially increase their environmental persistence by shielding them from degradation processes. Furthermore, effects, including rising temperatures and shifting hydrologic patterns, may alter pyrethroid degradation rates by influencing microbial activity and photolysis efficiency, thereby extending their in warming environments.

Effects on Non-Target Organisms

Pyrethroids are highly toxic to non-target aquatic organisms, particularly such as crustaceans (e.g., , LC50 0.01–0.2 μg/L) and insects, due to their on sodium channels, leading to and mortality at environmentally relevant concentrations. species, including (LC50 0.2–3.5 μg/L), also exhibit high sensitivity, with sublethal effects like impaired swimming and observed in chronic exposures. Terrestrial non-target organisms, including beneficial insects like honeybees, face risks from direct contact or drift, with topical LD50 values around 0.1–1 μg/bee, contributing to pollinator stress and colony losses. Birds and mammals are less affected, showing no acute toxicity at field rates, though bioaccumulation in food chains may pose indirect risks. Amphibians display variable sensitivity, with larvae often more vulnerable than adults. Overall, these effects underscore the need for targeted application to minimize impacts on biodiversity.

Resistance

Mechanisms of Resistance

Insect resistance to pyrethroids primarily arises through modifications that counteract the insecticides' disruption of voltage-gated sodium channels (VGSCs) in neuronal membranes, where pyrethroids normally bind to prolong sodium ion influx and cause hyperexcitation followed by paralysis. These adaptations include target-site alterations that reduce binding affinity, enhanced metabolic detoxification, and behavioral changes that limit exposure, often occurring in combination to confer high-level resistance. Target-site resistance, the most studied mechanism, involves mutations in the VGSC gene that decrease pyrethroid binding and efficacy. The canonical knockdown resistance (kdr) mutation, a leucine-to-phenylalanine substitution at position 1014 (L1014F), reduces channel sensitivity to pyrethroids by 100- to 1,000-fold, allowing insects to withstand doses that would otherwise cause rapid knockdown. This is widespread across pest species, including mosquitoes; for instance, in populations, L1014F frequencies reached up to 83% in resistant strains from a study in Côte d’Ivoire, and recent surveys as of 2025 indicate persistently high frequencies, such as 78.1% in forest zones of certain regions. Similar kdr variants, such as L1014S, have also been documented in vectors like , contributing to regional pyrethroid failure in control. Metabolic resistance enables insects to enzymatically degrade or sequester pyrethroids before they reach their target, often through overexpression of detoxification enzymes. Cytochrome P450 monooxygenases, particularly from the CYP6 family (e.g., CYP6P9a and CYP6P3), hydroxylate pyrethroids like deltamethrin, rendering them inactive and conferring resistance ratios exceeding 1,000-fold in malaria vectors such as Anopheles funestus. Glutathione S-transferases (GSTs) further contribute by conjugating pyrethroid metabolites for excretion, with elevated GST activity observed in resistant strains of agricultural pests like the cotton bollworm. These enzymes are upregulated via gene amplification or regulatory changes, imposing fitness costs but providing broad-spectrum protection against multiple insecticides. Behavioral resistance, though less prevalent than physiological mechanisms, involves evolved avoidance behaviors that reduce contact with treated surfaces. In pyrethroid-resistant strains of , mosquitoes exhibit heightened irritability or repellency, leading to quicker evasion of insecticide-impregnated nets or sprays, which can diminish control efficacy by up to 50% in field settings. This form of resistance is often secondary to metabolic or target-site changes but has been noted in urban pests like , where resistant individuals preferentially navigate untreated areas. Recent advances highlight intensified resistance through compounded genetic changes. Super-kdr , such as M918T or M918I in the VGSC linker domain, synergize with L1014F to substantially amplify resistance in species like the tropical bed bug Cimex hemipterus, as reported in Iranian populations post-2020, with knockdown ratios of 5- to 7-fold and overall high tolerance from multiple mechanisms. In bed bugs (), polygenic resistance dominates, involving a 6 Mb genomic superlocus with multiple P450 and genes, resulting in high tolerance (resistance ratios up to 199-fold in studied field strains) to common pyrethroids like . These developments underscore the polyvalent nature of resistance in urban and vector pests.

Management Strategies

Management of pyrethroid resistance primarily involves integrating these insecticides into broader (IPM) frameworks to delay the evolution of resistance in pest populations. A key strategy is rotating pyrethroids with insecticides from different chemical classes, such as organophosphates or carbamates, to reduce selective pressure on pyrethroid target sites and metabolic pathways. For instance, alternating pyrethroids with neonicotinoids can help mitigate cross-resistance risks, though careful selection is needed to avoid shared resistance mechanisms. Additionally, incorporating synergists like (PBO) enhances pyrethroid efficacy by inhibiting enzymes responsible for metabolic detoxification, thereby restoring susceptibility in moderately resistant populations. Routine monitoring is essential for early detection and informed decision-making in resistance management. Bioassays, such as or tests, quantify resistance levels by calculating resistance ratios (RR), where an RR greater than 10-fold relative to susceptible strains indicates high resistance risk requiring intervention. Complementary genomic screening detects knockdown resistance (kdr) mutations in the voltage-gated , allowing proactive adjustments to control programs before phenotypic resistance becomes widespread. Emerging tactics focus on innovative combinations and molecular approaches to overcome resistance. Combination products pairing pyrethroids with chlorfenapyr, a pro-insecticide with a distinct targeting mitochondrial respiration, have demonstrated superior control of pyrethroid-resistant malaria vectors compared to pyrethroids alone. (RNAi) offers a targeted method by delivering double-stranded RNA to silence resistance-associated genes, such as those encoding detoxifying enzymes or kdr variants, thereby restoring pyrethroid susceptibility in treated insects. Global initiatives, particularly the World Health Organization's (WHO) guidelines for vector control, emphasize resistance management through diversified insecticide use and surveillance in malaria-endemic areas. These recommendations promote pyrethroid-PBO or pyrethroid-chlorfenapyr nets where resistance is confirmed, contributing to significant reductions in malaria incidence—up to 50% in some settings—while curbing resistance spread in monitored programs; as of April 2025, WHO expanded recommendations for dual-insecticide nets (pyrethroid-chlorfenapyr and pyrethroid-pyriproxyfen) to further address resistance. The WHO Global Plan for Insecticide Resistance Management further advocates for integrated vector management to sustain pyrethroid effectiveness long-term.

History and Regulation

Historical Development

Pyrethroids originated from efforts to synthesize analogs of natural pyrethrins, extracted from Chrysanthemum cinerariaefolium flowers, which had been used as insecticides since the early but suffered from rapid degradation in light and air. The first synthetic pyrethroid, allethrin, was developed in 1949 by Milton S. Schechter and others at the U.S. Department of Agriculture, marking the beginning of first-generation pyrethroids in the 1940s and 1950s. These early compounds, including bioallethrin, , and resmethrin introduced in the 1960s, improved potency but retained instability to environmental factors. To address , second-generation pyrethroids were developed in the late and early , featuring structural modifications for stability. Key innovations included , synthesized in 1973 by Michael Elliott and colleagues at Rothamsted Experimental Station, and fenvalerate, introduced commercially around the same time. These photostable variants enabled widespread agricultural and applications, with pyrethroids entering the market in the and comprising about 25% of the global market by the 1980s.

Current Regulations

In the United States, the Environmental Protection Agency (EPA) classifies many pyrethroids as reduced-risk pesticides due to their lower toxicity to mammals compared to older insecticides, facilitating expedited registration under the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA). Tolerances, or maximum residue limits (MRLs), for pyrethroids in crops vary by substance and commodity, typically ranging from 0.05 ppm to 20 ppm; for instance, tolerances reach 20 ppm in and 0.05 ppm in many . To mitigate environmental risks, EPA labels for pyrethroid products often mandate aquatic buffer zones, prohibiting applications within specified distances of water bodies to prevent runoff and protect sensitive aquatic organisms like and invertebrates. In the , pyrethroids are regulated under the Biocidal Products Regulation (BPR, EU No 528/2012) for non-agricultural uses and the Plant Protection Products Regulation (PPPR, EU No 1107/2009) for crop applications, with active substances like receiving renewed approvals through 2025 following risk assessments by the (ECHA). Due to their high to pollinators, phase-out considerations apply to high-risk uses, such as applications during bee-active periods, with restrictions on outdoor use near flowering crops to minimize exposure. EU MRLs for pyrethroids, set under Regulation (EC) No 396/2005, range from below 0.01 mg/kg (default for unlisted commodities) to 5 mg/kg in specific cases, such as 0.5 mg/kg for lambda-cyhalothrin in certain . The (WHO) and (FAO) recognize pyrethroids as essential for in malaria-endemic areas, recommending their use in long-lasting insecticidal nets (LLINs) and indoor residual spraying (IRS) where resistance is not prevalent. WHO guidelines emphasize integrated vector management, including pyrethroid-based interventions combined with surveillance, while FAO supports their agricultural applications under Codex standards; both organizations stress ongoing monitoring for insecticide resistance to sustain efficacy. Between 2021 and 2025, regulatory updates have focused on environmental protections, including California's State Water Resources Control Board amendments to basin plans, which impose stricter controls on pyrethroid discharges to waterways through measures like vegetated buffers and reduced application rates to address sediment toxicity in urban and agricultural runoff. Globally, the Commission has advanced harmonization of pyrethroid MRLs, recommending levels such as 0.05 mg/kg for in fruits to facilitate while aligning with WHO/FAO safety evaluations.

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