Pesticide poisoning treatment

NPTN is based at Oregon State University and is cooperatively sponsored by the University and EPA. NPTN serves as a source of objective, science-based pesticide information on a wide range of pesticide-related topics, such as recognition and management of pesticide poisonings, safety information, health and environmental effects, referrals for investigation of pesticide incidents and emergency treatment for both humans and animals, and cleanup and disposal procedures. 

It has been proposed that parathion hydrolase, also known as organophosphorous phosphotriesterase, be used for pesticide detoxification as an alternative to more common treatment methods. Parathion hydrolase is produced by a number of bacteria including Pseudomonas sp., Flavobacte-rium sp. and a recombinant Streptomyces [17,54]. It has been shown to hydrolyze some of the most widely used organophosphate pesticides such as methyl and ethyl parathion, diazinon, fensulfothion, dursban, and couma-phos [18,19]. It should be noted that organophosphate pesticides constitute the major proportion of agricultural pesticides used at present and are implicated in an estimated 800,000 pesticide poisoning cases every year [18]. Hydrolysis accomplishes the detoxification of the pesticide and makes the products amenable to biological treatment. 

Thiermann, H., Szinicz, L., Eyer, P., Felgenhauer, N., Zilker, T., Worek, F. (2007). Lessons to be learnt from OP pesticide poisoning for the treatment of nerve agent poisoning. Toxicology 233 145-54. 

Kusic et al. (1991) have tested the oxime HI-6 in OP pesticide poisoning in 60 patients. HI-6 was administered four times a day as a single i.m. injection of 500 mg with atropine and diazepam treatment. Oxime therapy was started on admission and continued for 2 to 7 days. Most patients were treated with HI-6 and nine patients severely poisoned with quinalphos were treated 2-PAM Cl (1,000 mg four times per day). HI-6 rapidly reactivated human red blood cell AChE inhibited by diethoxy OPs (phorate, pyr-idaphenthion, quinalphos) as well as that inhibited by dichlorvos (a dimethoxy OP). AChE inhibited with other dimethoxy OPs (dimethoate and phosphamidon) was reported to be resistant to HI-6 treatment, whereas reactivation with malathion was slow (reactivation half-time 10 h). Both HI-6 and 2-PAM successfully reactivated AChE in quinalphos-poisoned patients, with HI-6 acting as a faster AChE reactivator than 2-PAM. 

Balali-Mood, M., Shariat, M. (1998). Treatment of organophos-phate poisoning. Experience of nerve agents and acute pesticide poisoning on the effects of oximes. J. Physiol. (Paris) 92 375-8. 

In two volumes, this comprehensive and timely compendium of scientific knowledge covers the toxic effects or pesticides in humans and animals. The 1st edition, edited by Hayes WJ and Laws ER, consists of three volumes that were updated and expanded versions of Toxicology of Pesticides (1975) and Pesticides Studied in Man (1982), both of which are out of print. Includes information on the diagnosis and treatment of pesticide poisonings. A true classic. 

Eddleston M, Dawson A, Karalliedde L et al. (2004b). Early management after self-poisoning with an organophosphorus or carbamate pesticide - a treatment protocol for junior doctors. Crit Care, 8, R391-R397. 

Marrs TC (2003). Diazepam in the treatment of organophosphorus ester pesticide poisoning. Toxicol Rev, 22, 75-81. 

Another area that would be of direct benefit to the medical personnel responsible for treating pesticide exposure in humans is the development of antidotal and symptomatic treatment for the various classes of pesticides. Although we have more specific antidotes available to treat pesticide poisoning than for any other single class of acute poisons, the number of antidotes is small for non-insecticidal pesticides and these cases must be treated symptomatically. The current acute toxicity protocols do not currently provide the kind of clinical information that is needed in such cases. 

In Sri Lanka, 700,(XX) kg a of pesticides ate imported to be used in food production. In 1986, pesticide poisoning was the 6th leading cause of mortality in major hospitals and accounted for 57% of hospital admissions [3]. Approximately 13,(XX) people a" present to government hospitals for treatment of pesticide poisoning (the number of deaths is around 1(X)0 a ). Among these, nearly 25% are occupational (V unintentional exposures. 

A number of novel approaches to the antidotal treatment of OPs have been studied, often using prophylactic protocols and mostly in relation to nerve agent poisoning, but some may be applicable, at least in principle, to OP pesticide poisoning. 

Clay minerals can also protect the digestive mueosa against pestieide damage. Diquat, a widely used non-seleetive desieeant herbicide, induees erosion of intestinal mucosa and fluid hypersecretion. Similarly, montmorillonite and bentonite are good adsorbents, and may be reeommended for the treatment of pesticide poisoning. 

In the study reported by Tsai et al. (2007), 2-PAM was administered to 56 patients within 48 h of OP pesticides poisoning. The average duration of 2-PAM treatment was 5.5 4.9 days and the mean total dose was 16.4 12.4 g. The mortality and length of stay did not improve with 2-PAM treatment. Days spent on ventilator support were decreased in patients treated with 2-PAM (6.7 1.9 days) compared with those who were not (23.0 4.8 days). However, there are many limitations in this study. For example, a relatively small number of treated patients, lack of data regarding the OP pesticides involved, dose taken, and AChE inhibition. 

Pralidoxime (2-PAM) Pralidoxime is a commonly used oxime and is rccom-mended for all cases of moderate-to-severe nerve agent poisoning. The optimal dosage is dependent on the nerve agent, time since exposure and the cholinesterase activity of the victim, i here has been considerable experience with pralidoxime and other oximes over many years in the treatment of OP pesticide poisoning. 

The presentation and initial treatment of the characteristic acute cholinergic syndrome following severe OP exposure was considered in earlier chapters. Experience with OP pesticide poisoning has shown that in most cases, the signs and symptoms resolve after about 18 h with continuing anticholinergic and oxime treatment. Ventilation, if it had been required, can be discontinued at this stage. 

EllenhomMJ. 1997. Pesticides Insecticides. In Ellenhom s medical toxicology Diagnosis and treatment of human poisoning. Baltimore, MD Williams Wilkins, 1614-1631. 

Pharmacologically, carbofuran inhibits cholinesterase, resulting in stimulation of the central, parasympathetic, and somatic motor systems. Sensitive biochemical tests have been developed to measure cholinesterase inhibition in avian and mammalian brain and plasma samples and are useful in the forensic assessment of carbamate exposure in human and wildlife pesticide incidents (Bal-lantyne and Marrs Hunt and Hooper 1993). Acute toxic clinical effects resulting from carbofuran exposure in animals and humans appear to be completely reversible and have been successfully treated with atropine sulfate. However, treatment should occur as soon as possible after exposure because acute carbofuran toxicosis can be fatal younger age groups of various species are more susceptible than adults (Finlayson et al. 1979). Carbofuran labels indicate that application is forbidden to streams, lakes, or ponds. In addition, manufacturers have stated that carbofuran is poisonous if swallowed, inhaled, or absorbed through the skin. Users are cautioned not to breathe carbofuran dust, fumes, or spray mist and treated areas should be avoided for at least 2 days (Anonymous 1971). Three points are emphasized at this juncture. First, some carbofuran degradation... 

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