Accumulating evidence points to cancer potential. Exercise caution with this substance, explore your exposure routes and consider complete avoidance. See further details under Toxins.
Metabolic Interference or Disruption
Interferes with human metabolism. This can be a very serious thing. Some of these interference mechanics are well established. However, often long term effects and health consequences remain largely unknown. Additionally an emerging area of concern and one that is not currently studied, is the combined synergistic effects these metabolically disrupting chemicals have on human health.
Metabolic interference happens when the substance produces highly reactive and often damaging intermediates during detoxification or when the substance binds to specific enzymes, important structural groups on molecules, receptors and membranes or targets DNA or mimics key nutrients.
Exposure Produces Health Symptoms
Symptoms maybe short term or long term depending on the exposure duration and intensity and effects areas like Cardiovascular, Gastrointestinal, Cognition, Fatigue. A substance with this attribute may cause an allergic skin reaction, serious eye irritation, allergy or asthma symptoms or breathing difficulties if inhaled.
These attributes are ONLY based on peer-reviewed evidence. See link to Data Sources below. Everyone benefits from knowing this stuff. Please Share.
- CATEGORIES: Pesticide | Household Toxin | Food Toxin | Synthetic Toxin | PESTICIDE active ingredient | organic | insecticide | acaricide | ixodicide | Pesticide or Plant Growth Regulator Approved in Australia | Pesticide approved in USA (California) | Pesticide approved or pending approval in EU
- SUBSTANCE LINEAGE: Organic Compounds | Lipids and Lipid-Like Molecules | Fatty Acyls | Fatty Acid Esters | Pyrethroids
- SYNONYMS: a-Cyano-3-phenoxybenzyl 2-(4-chlorophenyl)-3-methylbutyrate | Agrofen | alpha-Cyano-3-phenoxybenzyl 2-(4-chlorophenyl)isovalerate | Aqmatrine | Asana | Belmark | Cyano(3-phenoxyphenyl)methyl 4-chloro-a-(1-methylethyl)benzeneacetate | 9CI | Ectrin | Esfenvalerate | Evercide 2362 | Fenaxin | Fenkem | Fenkill | Fenoxin | Fenval | Fenvaleric acid | Phenoxin | Phenvalerate | Pydrin | Sumicidin
- DESCRIPTION: Agricultural, public health and animal husbandry insecticide.Fenvalerate is an insecticide. It is a mixture of four optical isomers which have different insecticidal activities. The 2-S alpha (or SS) configuration is the most insecticidally active isomer. Fenvalerate consists of about 23% of this isomer. (Wikipedia) Fenvalerate has been shown to exhibit steroidogenic function (A7791). Fenvalerate belongs to the family of Pyrethroids. These are organic compounds similar to the pyrethrins. Some pyrethroids containing a chrysanthemic acid esterified with a cyclopentenone (pyrethrins), or with a phenoxybenzyl.
- COMMENTS: Residues of this pesticide are tested for on Australian Foods | Pesticide approved in Australia
- FORMULA: C25H22ClNO3
- DATA SOURCES: DATA SOURCES: T3DB | PubChem | IARC | Consolidated Pesticide Information Dataset (CPI) from the USA EPA | Compendium of Pesticide Common Names | APVMA | DPR | EU Pesticides
- LAST UPDATE: 28/04/2018
Mostly focused on Health Implications of Long Term Exposure to this substance
- 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. (T36)
- POSSIBLE HEALTH CONSEQUENCES: Pyrethroid effects typically include rapid onset of aggressive behavior and increased sensitivity to external stimuli, followed by fine tremor, prostration with coarse whole body tremor, elevated body temperature, coma, and death. Paresthesia, severe corneal damage, hypotension and tachycardia, associated with anaphylaxis, can also occur following pyrethriod poisoning. (L857) | Following ingestion, pyrethriods are hydrolysed by various digestive enzymes in the gastro-intestinal tract. However, a small portion of the insecticidally active compounds or its derivatives are absorbed, as shown by their toxicity and their effect on the liver. Pyrethriods may also be absorbed following inhalation or dermal contact. They are rapidly distributed to most tissues, particularly to those with a high lipid content, and are concentrated in central and peripheral nervous tissues. Pyrethriods or their metabolites are not known to be stored in the body or to be excreted in the milk, but no study of the matter has employed modern methods. The major metabolic pathways for pyrethriods are hydrolysis of the central ester bond, oxidative attacks at several sites, and conjugation reactions, to produce a complex array of primary and secondary water-soluble metabolites that undergo urinary excretion. Metabolism is believed to involve nonspecific microsomal carboxyesterases and microsomal mixed function oxidases, which are located in nearly all tissue types, with particularly high activities in the liver. Metabolites are excreted in the urine and faeces. (L857, L889)
- ACTION OF TOXIN: 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. (T10, T18, L857) | 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).
- TOXIN SITES OF ACTION IN CELL: "Extracellular", "Membrane"
- Additional Exposure Routes: Fenvalerate is used as an insecticide, mostly to control insects in food, feed, and cotton products, and for the control of flies and ticks in barns and stables. (L606)
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