Description
General Information
- Metabolism: 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)
- Uses/Sources: Pyrethroids are used as insecticides. (L857)
- Health Effects: 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)
- Symptoms: Spilling on the head, face and eyes can result in pain, lacrimation, photophobia, congestion, and edema of the conjunctiva and eyelids. Ingestion cases epigastric pain, nausea, vomiting, headache, dizziness, anorexia, fatigue, tightness in chest, blurred vision, paresthesia, palpitations, coarse muscular fasciculations, and disturbances of conciousness. In servere poisonings, convulsive attacks with opisthotonos and loss of conciousness have occurred. (T10)
- 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. (L363)
Mechanism of Action
Target Name | Mechanism of Action | References |
---|---|---|
Calcium-transporting ATPase type 2C member 1 Calcium-transporting ATPase type 2C member 2 Sarcoplasmic/endoplasmic reticulum calcium ATPase 1 Sarcoplasmic/endoplasmic reticulum calcium ATPase 2 Sarcoplasmic/endoplasmic reticulum calcium ATPase 3 |
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) |
2003 |
Sodium channel subunit beta-1 Sodium channel subunit beta-2 Sodium channel subunit beta-3 Sodium channel subunit beta-4 Sodium channel protein type 1 subunit alpha Sodium channel protein type 10 subunit alpha Sodium channel protein type 11 subunit alpha Sodium channel protein type 2 subunit alpha Sodium channel protein type 3 subunit alpha Sodium channel protein type 4 subunit alpha Sodium channel protein type 7 subunit alpha Sodium channel protein type 8 subunit alpha Sodium channel protein type 5 subunit alpha Sodium channel protein type 9 subunit alpha |
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). |
2003 15950969 1995 |