フルメトリン

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. (T36)

At high doses, signs of poisoning attributable to flumethrin include profuse salivation and pulmonary edema, clonic seizures, opisthotonos (i.e., the spine is bent forward such that a supine body rests on its head and heels), coma, and death. At lower doses, commonly observed effects include paresthesia and erythema. (L863)

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. (T18, L857)

The highest concentration is found in the liver, but high concentrations were also found in the spleen, kidney, lung, adrenal cortex, cartilage, bone marrow, pineal gland, pituitary, and subcutaneous adipose tissue; the lowest concentrations are found in the central nervous system. Flumethrin is excreted in the urine or the feces as unchanged compound or the metabolite, 3-[2-chloro-2-(4-chlorophenyl)ethenyl]-2,2-dimethylcyclopropanecarboxylic acid, flumethrin acid. 3-(4'-hydroxy-phenoxy)-4-fluorobenzoic acid and 3-phenoxy-4-fluorobenzoic acid can further be found in the urine as well as their glycine conjugates. The phenyl ring may be hydroxylated and, following ester bond hydrolysis, the cyano group is converted to SCN- and carbon dioxide and 3-phenoxybenzaldehyde is oxidized to the carboxylic acid. The resultant acids and phenols can then conjugate with glucuronic acid, sulfate, and/or amino acids. (L885)