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Fenvalerate is an exogenous solid with the formula C25H22ClNO3 and an average molecular weight of 419.90 g/mol. Fenvalerate belongs to the fatty acid esters, a subclass of fatty acyls within the organic compounds. It is utilized industrially as an insecticide, as well as a pyrethroid ester insecticide and acaricide (PMC3282909 ). This compound is released from various sources, including building and construction materials such as floors and tents or canopies; household cleaning and consumer products including soap detergents, perfumes within detergents and soaps, and cigar cigarettes; food, food processing and cookware including the preparation of malt, molasses and treatment of molasses, and food preservation; and electrical and electronic equipment including discharge lamps, amplifiers, conductors or conductive bodies characterised by the conductive materials, electrically stimulated smoking devices, and hybrid capacitors.
Fenvalerate targets 22 recorded proteins. It acts as an axonic poison by prolonging the open phase of sodium channel gates when a nerve cell is excited, blocking the closing of the gates and prolonging the return of the membrane potential to its resting state; this leads to nervous system hyperactivity, which can result in death and/or paralysis. Affected sodium channel proteins include SCN1A, SCN10A, SCN11A, and SCN2A. Additionally, fenvalerate inhibits Ca2+ and Mg2+ ATPase and Na+/K+ ATPase, including ATP2A1, ATP2A2, and ATP2C1, which are essential for transporting calcium across membranes. This inhibition results in the accumulation of intracellular free calcium ions, promoting the release of neurotransmitters from storage vesicles, the depolarization of adjacent neurons, and the propagation of stimuli throughout the central nervous system. Other protein targets include VDR, CYP19A1, NR1I2, and PPARG.
Belongs to the class of organic compounds known as pyrethroids. These are organic compounds similar to the pyrethrins. Some pyrethroids containing a chrysanthemic acid esterified with a cyclopentenone (pyrethrins), or with a phenoxybenzyl group.
Both type I and type II pyrethroids exert their effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. They appear to bind to the membrane lipid phase in the immediate vicinity of the sodium channel, thus modifying the channel kinetics. This blocks the closing of the sodium gates in the nerves, and thus prolongs the return of the membrane potential to its resting state. The repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential produces effects quite similar to those produced by DDT, leading to hyperactivity of the nervous system which can result in paralysis and/or death. Other mechanisms of action of pyrethroids include antagonism of gamma-aminobutyric acid (GABA)-mediated inhibition, modulation of nicotinic cholinergic transmission, enhancement of noradrenaline release, and actions on calcium ions. They also inhibit calium channels and Ca2+, Mg2+-ATPase. (11, 13, 8)
3, not classifiable as to its carcinogenicity to humans. (4)
Minimum Risk Level
Not Available
Symptoms
Following oral exposure, severe fine tremor, marked reflex hyperexcitability, sympathetic activation can occur. Nausea, vomiting and abdominal pain commonly occur and develop following ingestion. Sudden bronchospasm, swelling of oral and laryngeal mucous membranes, and anaphylactoid reactions have been reported after inhalation. Hypersensitivity reactions characterized by pneumonitis, cough, dyspnea, wheezing, chest pain, irritability to sound and touch, and bronchospasm may occur too. Dermatitis is the main effect of a dermal exposure fenvalerate. (14)
Treatment
Following oral exposure, the treatment is symptomatic and supportive and includes monitoring for the development of hypersensitivity reactions with respiratory distress. Provide adequate airway management when needed. Gastric decontamination is usually not required unless the pyrethrin product is combined with a hydrocarbon. Following inhalation exposure, move patient to fresh air. monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with inhaled beta2 agonist and oral or parenteral corticosteroids. In case of eye exposure, irrigate exposed eyes with copious amounts of room temperature water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist, the patient should be seen in a health care facility. If the contamination occurs through dermal exposure, Remove contaminated clothing and wash exposed area thoroughly with soap and water. A physician may need to examine the area if irritation or pain persists. Vitamin E topical application is highly effective in relieving parenthesis. (5)
Soil?Soil serves as a critical medium for plant growth and sustains various ecological functions; however, it can become a reservoir for synthetic chemical contamination.
Stormwater runoff?Stormwater runoff refers to the flow of rainwater or melted snow that does not soak into the ground and instead collects pollutants as it travels over impervious surfaces such as roads and parking lots.
Ballast water?Ballast water, taken on by ships to maintain stability and balance, often contains a diverse array of microorganisms, including bacteria, viruses, and plankton.
Bilge water?Bilge water is a byproduct generated from the accumulation of water in the lowest part of a ship's hull, which may include a mixture of seawater, oil, fuel residues, and various contaminants.
Brushes?Brushes used in personal care and cosmetics can be a source of synthetic chemical contamination due to the materials and coatings used in their manufacturing.
Floors?Floors in built environments can be a significant source of synthetic chemical contamination due to the materials and finishes used in their construction.
Tents Or Canopies?Tents and canopies used in various applications can be a source of synthetic chemical contamination primarily due to the materials from which they are made.
Amplifiers?Amplifiers, commonly used in various electronic devices to enhance signal strength, can be a source of synthetic chemical contamination due to the materials and processes involved in their production and disposal.
Conductors Or Conductive Bodies Characterised By The Conductive Materials?Conductors, or conductive bodies, are materials that allow the flow of electrical current, typically made from metals such as copper, aluminum, or silver.
Discharge Lamps?Discharge lamps, including fluorescent and high-intensity discharge (HID) lamps, are commonly used for lighting applications due to their energy efficiency and brightness.
Electrically Stimulated Smoking Devices?Electrically stimulated smoking devices, commonly known as e-cigarettes or vape pens, utilize electrical components to heat a liquid solution, often containing nicotine, flavorings, and other additives, to produce an aerosol for inhalation.
Hybrid Capacitors?Hybrid capacitors are energy storage devices that combine the properties of electrolytic and supercapacitors, utilizing a combination of electrochemical principles to achieve higher energy density and power density.
Line Transmission Systems?Line Transmission Systems, commonly used for the distribution of electrical energy, can be a source of synthetic chemical contamination through the insulation materials and coatings utilized in their construction.
Food Preservation?Food preservation often involves the use of synthetic chemicals, such as preservatives, flavor enhancers, and color additives, to extend shelf life and enhance the sensory qualities of food products.
Molasses And Treatment Of Molasses?Molasses is a thick, viscous byproduct of sugar production, derived from the extraction of sugar cane or sugar beet juice.
Preparation Of Malt?Malt preparation involves the germination and drying of cereal grains, primarily barley, to produce malt for brewing and food products.
Perfumes Within Detergents And Soaps?Perfumes within detergents and soaps are synthetic fragrance compounds added to enhance the sensory experience of cleaning products.
Soap Detergents?Soap detergents are synthetic surfactants designed to enhance the cleaning efficacy of water by reducing surface tension, allowing for better interaction with dirt and grease.
Manufacture Preparation Of Tobacco Products?The manufacture and preparation of tobacco products involve various processes that can result in the introduction of synthetic chemicals into the environment.
Anchoring Equipment?Anchoring equipment, commonly used in marine applications, can be a source of synthetic chemical contamination due to the materials and coatings utilized in their manufacturing.
Chemosterilants?Chemosterilants are synthetic chemicals designed to induce sterility in target pest populations, thereby controlling their reproduction and mitigating damage to crops.
Fertiliser Distributors?Fertiliser distributors play a critical role in the supply of synthetic fertilizers, which are widely used to enhance soil fertility and crop yield.
Molluscicides?Molluscicides are synthetic chemicals specifically designed to control and eliminate mollusks, such as snails and slugs, which can be detrimental to crops and agricultural productivity.
Nematocides?Nematocides are synthetic chemicals specifically designed to control nematodes, which are microscopic roundworms that can cause significant damage to crops and plants.
Rodenticides(1)?Rodenticides are synthetic chemicals specifically formulated to control rodent populations, serving as a crucial tool in managing pests that can damage crops and spread diseases.
Rodenticides?Rodenticides are chemical substances specifically designed to control rodent populations by causing death through various mechanisms, including anticoagulation or neurotoxicity.
Aftersun Products?Aftersun products are designed to soothe and hydrate the skin after sun exposure, often containing various synthetic chemicals such as emollients, preservatives, and fragrances.
Anti Perspirants Or Body Deoderants?Antiperspirants and body deodorants commonly contain synthetic chemicals such as aluminum compounds, parabens, and synthetic fragrances.
Depilatories?Depilatories are products designed to remove unwanted hair through the application of synthetic chemicals that break down the protein structure of hair, facilitating its removal.
Essential Oils Or Perfumes?Essential oils and perfumes are complex mixtures of volatile compounds derived from natural or synthetic sources, commonly used for their aromatic properties.
Eye Makeup Products?Eye makeup products, including mascaras, eyeliners, and eyeshadows, often contain a variety of synthetic chemicals such as pigments, preservatives, and film-forming agents.
Lip Care Products?Lip care products, including lipsticks, balms, and glosses, often contain a variety of synthetic chemicals such as parabens, phthalates, and synthetic fragrances.
Lip Makeup Products?Lip makeup products, such as lipsticks, lip glosses, and lip liners, often contain a variety of synthetic chemicals, including pigments, preservatives, and emollients.
Buckles?Buckles, commonly used as fasteners in clothing, accessories, and furniture, can be a source of synthetic chemical contamination due to the materials and coatings employed in their production.
Footwear?Footwear production often involves the use of various synthetic chemicals, such as adhesives, dyes, and treatments, which can contribute to environmental contamination.
Yarns Or Threads?Yarns or threads used in textiles can be a source of synthetic chemical contamination due to the production processes and treatments they undergo.
Airplanes And Helicopters?Airplanes and helicopters are significant sources of synthetic chemical contamination primarily through the use of aviation fuels, lubricants, and de-icing agents.
Unmanned Aerial Vehicles?Unmanned Aerial Vehicles (UAVs), commonly known as drones, utilize various synthetic chemicals in their manufacturing, operation, and maintenance processes.
Nitrogenous Fertilisers?Nitrogenous fertilizers are synthetic chemical compounds primarily used to enhance plant growth by supplying essential nitrogen, a crucial nutrient for photosynthesis and protein synthesis.
Glass Coatings?Glass coatings are synthetic chemical formulations applied to glass surfaces to enhance properties such as durability, UV resistance, and aesthetic appeal.
Silica Glass?Silica glass, primarily composed of silicon dioxide (SiO2), is widely used in various applications, including windows, glass facades, and insulation materials.
Nanotechnology?Nanotechnology involves the manipulation of materials at the molecular or atomic level, typically within the range of 1 to 100 nanometers.
Water, Wastewater, & Sewage Treatment?Water, wastewater, and sewage treatment processes are critical for managing and mitigating pollutants in water systems.
This pyrethroid exerts its profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. This pyrethroid is a axonic poison that block the closing of the sodium gates in the nerves, and, thus, prolongs the return of the membrane potential to its resting state leading to hyperactivity of the nervous system which can result in paralysis and/or death. Type I Pyrethroid esters (lacking the alpha-cyano substituents) affect sodium channels in nerve membranes, causing repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential, the effects being quite similar to those produced by DDT (L857, A560).
This pyrethroid exerts its profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. This pyrethroid is a axonic poison that block the closing of the sodium gates in the nerves, and, thus, prolongs the return of the membrane potential to its resting state leading to hyperactivity of the nervous system which can result in paralysis and/or death. Type I Pyrethroid esters (lacking the alpha-cyano substituents) affect sodium channels in nerve membranes, causing repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential, the effects being quite similar to those produced by DDT (L857, A560).
This pyrethroid exerts its profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. This pyrethroid is a axonic poison that block the closing of the sodium gates in the nerves, and, thus, prolongs the return of the membrane potential to its resting state leading to hyperactivity of the nervous system which can result in paralysis and/or death. Type I Pyrethroid esters (lacking the alpha-cyano substituents) affect sodium channels in nerve membranes, causing repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential, the effects being quite similar to those produced by DDT (L857, A560).
This pyrethroid exerts its profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. This pyrethroid is a axonic poison that block the closing of the sodium gates in the nerves, and, thus, prolongs the return of the membrane potential to its resting state leading to hyperactivity of the nervous system which can result in paralysis and/or death. Type I Pyrethroid esters (lacking the alpha-cyano substituents) affect sodium channels in nerve membranes, causing repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential, the effects being quite similar to those produced by DDT (L857, A560).
This pyrethroid exerts its profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. This pyrethroid is a axonic poison that block the closing of the sodium gates in the nerves, and, thus, prolongs the return of the membrane potential to its resting state leading to hyperactivity of the nervous system which can result in paralysis and/or death. Type I Pyrethroid esters (lacking the alpha-cyano substituents) affect sodium channels in nerve membranes, causing repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential, the effects being quite similar to those produced by DDT (L857, A560).
This pyrethroid exerts its profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. This pyrethroid is a axonic poison that block the closing of the sodium gates in the nerves, and, thus, prolongs the return of the membrane potential to its resting state leading to hyperactivity of the nervous system which can result in paralysis and/or death. Type I Pyrethroid esters (lacking the alpha-cyano substituents) affect sodium channels in nerve membranes, causing repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential, the effects being quite similar to those produced by DDT (L857, A560).
This pyrethroid exerts its profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. This pyrethroid is a axonic poison that block the closing of the sodium gates in the nerves, and, thus, prolongs the return of the membrane potential to its resting state leading to hyperactivity of the nervous system which can result in paralysis and/or death. Type I Pyrethroid esters (lacking the alpha-cyano substituents) affect sodium channels in nerve membranes, causing repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential, the effects being quite similar to those produced by DDT (L857, A560).
This pyrethroid exerts its profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. This pyrethroid is a axonic poison that block the closing of the sodium gates in the nerves, and, thus, prolongs the return of the membrane potential to its resting state leading to hyperactivity of the nervous system which can result in paralysis and/or death. Type I Pyrethroid esters (lacking the alpha-cyano substituents) affect sodium channels in nerve membranes, causing repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential, the effects being quite similar to those produced by DDT (L857, A560).
This pyrethroid exerts its profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. This pyrethroid is a axonic poison that block the closing of the sodium gates in the nerves, and, thus, prolongs the return of the membrane potential to its resting state leading to hyperactivity of the nervous system which can result in paralysis and/or death. Type I Pyrethroid esters (lacking the alpha-cyano substituents) affect sodium channels in nerve membranes, causing repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential, the effects being quite similar to those produced by DDT (L857, A560).
This pyrethroid exerts its profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. This pyrethroid is a axonic poison that block the closing of the sodium gates in the nerves, and, thus, prolongs the return of the membrane potential to its resting state leading to hyperactivity of the nervous system which can result in paralysis and/or death. Type I Pyrethroid esters (lacking the alpha-cyano substituents) affect sodium channels in nerve membranes, causing repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential, the effects being quite similar to those produced by DDT (L857, A560).
This pyrethroid exerts its profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. This pyrethroid is a axonic poison that block the closing of the sodium gates in the nerves, and, thus, prolongs the return of the membrane potential to its resting state leading to hyperactivity of the nervous system which can result in paralysis and/or death. Type I Pyrethroid esters (lacking the alpha-cyano substituents) affect sodium channels in nerve membranes, causing repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential, the effects being quite similar to those produced by DDT (L857, A560).
This pyrethroid exerts its profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. This pyrethroid is a axonic poison that block the closing of the sodium gates in the nerves, and, thus, prolongs the return of the membrane potential to its resting state leading to hyperactivity of the nervous system which can result in paralysis and/or death. Type I Pyrethroid esters (lacking the alpha-cyano substituents) affect sodium channels in nerve membranes, causing repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential, the effects being quite similar to those produced by DDT (L857, A560).
This pyrethroid exerts its profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. This pyrethroid is a axonic poison that block the closing of the sodium gates in the nerves, and, thus, prolongs the return of the membrane potential to its resting state leading to hyperactivity of the nervous system which can result in paralysis and/or death. Type I Pyrethroid esters (lacking the alpha-cyano substituents) affect sodium channels in nerve membranes, causing repetitive (sensory, motor) neuronal discharge and a prolonged negative afterpotential, the effects being quite similar to those produced by DDT (L857, A560).
This pyrethroid inhibits Na+/K+ ATPase and Ca2+ and Mg2+ ATPase, which are essential for the transport of calcium across membranes. This results in the accumulation of intracellular free calcium ions, which promotes release of neurotransmitters from storage vesicles, the subsequent depolarization of adjacent neurons, and the propagation of stimuli throughout the central nervous system. (T10)
This pyrethroid inhibits Na+/K+ ATPase and Ca2+ and Mg2+ ATPase, which are essential for the transport of calcium across membranes. This results in the accumulation of intracellular free calcium ions, which promotes release of neurotransmitters from storage vesicles, the subsequent depolarization of adjacent neurons, and the propagation of stimuli throughout the central nervous system. (T10)
This pyrethroid inhibits Na+/K+ ATPase and Ca2+ and Mg2+ ATPase, which are essential for the transport of calcium across membranes. This results in the accumulation of intracellular free calcium ions, which promotes release of neurotransmitters from storage vesicles, the subsequent depolarization of adjacent neurons, and the propagation of stimuli throughout the central nervous system. (T10)
Leng G, Lewalter J, Rohrig B, Idel H: The influence of individual susceptibility in pyrethroid exposure. Toxicol Lett. 1999 Jun 30;107(1-3):123-30. [PubMed: 10414789]
Qu JH, Hong X, Chen JF, Wang YB, Sun H, Xu XL, Song L, Wang SL, Wang XR: Fenvalerate inhibits progesterone production through cAMP-dependent signal pathway. Toxicol Lett. 2008 Jan 4;176(1):31-9. Epub 2007 Sep 21. [PubMed: 18053657]
ATSDR - Agency for Toxic Substances and Disease Registry (2006). Toxicological profile for cyanide. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). - http://www.atsdr.cdc.gov/toxprofiles/tp8.html
International Agency for Research on Cancer (2014). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. - http://monographs.iarc.fr/index.php
ATSDR - Agency for Toxic Substances and Disease Registry (2003). Toxicological profile for pyrethrins and pyrethroids. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). - http://www.atsdr.cdc.gov/toxprofiles/tp155.html
