d-cis-Phenothrin

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)

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)

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)

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, and bronchospasm may occur too . Dermatitis is the main effect of a dermal exposure to phenothrin. (T36)

d-Phenothrin is a fast acting insecticide, effective by contact and stomach action. It is rapidly metabolized and excreted by humans and has low human toxicity. For both cis- and trans- isomers, the product was metabolized by hydrolysis, oxidation and conjugation and a large part of d-Phenothrin is excreted unchanged in the urine and the faeces. Following oral administration of the (1R)- trans - isomer, the urine is the major excretory route. The isomer is extensively metabolized to oxidative and conjugated derivatives of the hydrolysed ester. Oxidative and conjugated derivatives of the (1R)- cis -isomer are also observed but hydrolysis of the ester linkage is a minor metabolic pathway. With this isomer the faeces is the major excretory route. The metabolic profiles aree similar following dermal application, although the rates of excretion for each isomer showed some differences between the two routes of administration. The major metabolite is 3-phenoxybenzyl alcohol (PBalc). Smaller amounts of PBacid and trace amounts of 4'-OH-PBacid are also found. It is stable to storage in the dark; d-Phenothrin is relatively unstable to sunlight or ultra violet irradiation, or in alkaline media. (L866, A561)