The Impact of Pesticides - Academy Publish

In a randomised controlled trial, Pawar et al. (2006) studied the effect of very-highdose pralidoxime iodide (2 g loading dose, then 1 g either every hour or every 4 hfor 48 h, then 1 g every 4 h until recovery) in 200 patients with moderate OPpoisoning (excluding severely ill patients). Among OP pesticides involved therewere chlorpyrifos (diethyl OP) and dimethoate (dimethyl OP). The high-doseregimen was associated with reduced case fatality, fewer cases of pneumonia, andreduced time on mechanical ventilation. This study suggests that large doses ofPAM-2 could have benefit if patients are treated early and have good supportivecare.CLINICAL ASPECTS AND MEDICAL MANAGEMENT OFPOISONING WITH CARBAMATESCases of accidental overexposure to or suicide attempts with various CB pesticideshave followed similar clinical courses characteristic of cholinergic poisoning likethat in poisoning with OP. Differences in severity, duration, and outcome havecorresponded to differences in effective doses and in promptness andappropriateness of treatment. Spontaneous recovery without medical treatment hasoccurred generally within 4 hr of exposures producing symptoms of headache,dizziness, weakness, excessive salivation, nausea, or vomiting. More severesymptoms have generally prompted medical treatment. Following treatment withsufficient atropine, individuals have recovered from poisoning that produced suchsymptoms as visual disturbances, profuse sweating, abdominal pain, incoordination,fasciculations, breathing difficulties, or changes in pulse rate. Recovery has beencomplete in some cases within 2 hr and in all cases within one day. CB poorly passthe blood-brain barrier and effects on central nervous system seen in OP poisoningare absent or minimal. Deaths have resulted in severe cases where treatment wasdelayed and/or insufficient atropine was administered. It is important to note,however, that treatment with atropine combined with general supportive treatment,such as artificial respiration and administration of fluids, has resulted in recoveryeven in cases where symptoms progressed to pulmonary edema or coma (Baron,1991; Rotenberg et al., 1995; Jokanović, 2009a).Carbamylation of AChE is apparently a short-lived phenomenon, as CB arereversible AChE inhibitors that spontaneously reactivate with a half-life in the orderof an hour or less. Although the immediate clinical picture of CB poisoning issimilar to that of OP, reversible inhibition with spontaneous hydrolysis of thecarbamylated AChE moiety results in less severe and less prolonged toxicity.Dimethyl compounds are a special case: they produce a carbamylated AChE, whichmay be reactivated with oximes. However, oximes are harmful when employed inanimals poisoned with monomethyl carbamate, and a man who ingested carbaryldied 6 hours after a PAM-2 treatment (Karchmar, 2007). The use of oximes in thecase of CB poisoning is controversial and considered contraindicated by someauthors. Lieske et al. (1992) have found that pyridinium oximes (obidoxime,trimedoxime, pralidoxime, HI-6) enhance inhibition of both eel AChE and humanserum ChE induced by carbaryl. The authors have proposed that oximes act asallosteric effectors of cholinesterases in carbaryl poisoning resulting in enhancedinhibition rates and potentiation of carbaryl toxicity. Inspite of this, some authorshave reported beneficial effects of pralidoxime in aldicarb poisoning in humans(Garber, 1987; Burges et al., 1994). In experimental studies, oximes have beenshown to be beneficial, alone and/or with atropine, in countering the toxicity of thecarbamates isolan, thimetilan, pyramat, dimetilan, aldicarb, neostigmine,physostigmine, pyridostigmine and others (Bošković et al., 1976; Sterri et al., 1979;AcademyPublish.org - The Impact of Pesticides53