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Organophosphorus Poisoning: an Overview

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Organophosphorus Poisoning: an Overview International Journal of Health Sciences and Research www.ijhsr.org ISSN: 2249-9571 Review Article Organophosphorus Poisoning: An Overview Singh Yatendra1, Subhash Chandra joshi2, Makrand Singh2, Arun Joshi2, Jainendra Kumar3 1Assistant Professor, 2Associate Professor, 3Post Graduate Resident, Department of Medicine, Government Medical College, Haldwani, Uttarakhand (India). Corresponding Author: Singh Yatendra Received: 24/06//2014 Revised: 23/07/2014 Accepted: 24/07/2014 ABSTRACT Organophosphorus pesticides are used widely for agriculture, vector control, and domestic purposes. Despite the apparent benefits of these uses acute organophosphorus pesticide poisoning is an increasing worldwide problem, particularly in rural areas. Their toxicity has been recognised since the 1930s, when they were also developed for use as chemical warfare agents. Our aim is to provide an evidence based review of the pathophysiology, diagnosis and management of acute organophosphorus pesticide poisoning. We emphasize that in future, especially in developing countries, Government authorities should be encouraged to control organophosphate product licensing, manufacture, storage, import, methods of use and delivery, food contamination and disposal. Key words: Atropine, Organophosphorus poisoning, Pesticide, pralidoxime Key Messages: In developing countries, especially in India, organophosphorus pesticide use is widespread as most population is mainly rural with farming as a major occupation. Acute poisoning is a medical emergency. It is important to know the nature, severity and outcome of acute poisoning cases in order to take up appropriate planning, prevention and management techniques. INTRODUCTION octomethyl pyrophosphotetramide (OMPA). Organophosphorus (OP) compounds [2-4] Some OP esters are still used to treat have been widely used for a few decades in glaucoma (Ecothiopate). In addition to these agriculture for crop protection and pest beneficial agricultural, veterinary, and control, thousands of these compounds have medical uses, some highly potent OP been screened and over one hundred of them anticholinesterase compounds, including have been marketed for these purposes. [1] tabun, sarin, soman, and VX have been used Some have also been used in the medical as “nerve gases” in chemical warfare. They treatment of myasthenia gravis, e.g. are also been used as plasticizers, stabilizers diisopropyl phosphorofluoridate (DFP), in lubricating and hydraulic oils, flame tetraethyl pyrophosphate (TEPP) and retardants, and gasoline additives. [5] International Journal of Health Sciences & Research (www.ijhsr.org) 245 Vol.4; Issue: 8; August 2014 Acute poisoning is an important management of organophosphorous cause of morbidity and mortality in poisoning with emphasis on optimization developing countries like India. In medical and monitoring of usage of OP compounds. emergency 10% of admissions are due to Epidemiology: poisoning and organophosphorus poisoning The organophosphate compounds are contributes to nearly 50% of it. [6] most commonly associated with serious Acute poisoning with human toxicity, accounting for more than organophosphate compounds is common in 80% of pesticide-related hospitalizations. [11] northwest India and is generally as a result In contrast to the past, when chlorinated of suicidal ingestion. In India, hydrocarbon compounds such as DDT were Organophosphorus compounds (OPCs) are commonly used, organophosphate freely available in shops and widely used as insecticides have become increasingly insecticides in agriculture and at home. In popular for both agricultural and home use the past, a high mortality was reported but in because their unstable chemical structure recent years, with intensive care, mortality leads to rapid hydrolysis and little long-term has considerably declined. [7] accumulation in the environment. [12] A Organophosphates cause poisoning recent national survey in Bangladesh by inhibition of the enzyme cholinesterase showed that 14% of all deaths (3971 of with subsequent accumulation of 28,998) of women between 10 and 50 years acetylcholine and symptoms relating to of age were due to self-poisoning, the overactive cholinergic action. The majority with pesticides. [13] mechanism of inhibition is phosphorylation The importance of pesticides in India of the esteratic locus on the enzyme with the can be understood from the fact that formation of a stable chemical complex agriculture is a major component of the which is biologically inactive. Indian economy: It contributes 22% of the In parts of developing world nation’s GDP and is the livelihood of nearly pesticide poisoning causes more deaths than 70% the country’s workforce. Globally, due infectious diseases. [7] Organophosphate to consolidation in the agrochemical insecticides account for more than 50% of industry, the top five multinational all acute poisoning in hospital practice, the companies control almost 60% of the majority of patients are younger than 30 yrs. market. [8] In teenagers and adults the poisoning is Overexposure to pesticides can occur generally due to suicidal intention although before spraying– because of easy access for accidental poisoning during spraying can children, lack of adequate labeling and also occur. [9] during mixing – during spraying and after Mortality ranges from 4% to 38% in spraying operations. Spray operators and Indian studies. The most common cause of bystanders can be affected. Having cheap death is respiratory failure. Early recognition and easily available highly hazardous and prompt ventilator support may improve pesticides at hand increases the incidence of the survival rate. The common use of intentional pesticide poisonings. [14] insecticides in public health and agricultural The effective number of cases of schedules has caused severe environmental pesticide poisoning occurring in India pollution and potential health hazards annually has been estimated by G. Ravi et al including severe acute and chronic cases of 2007 to be up to 76 000, much higher than human and animal poisonings. [10] So our the figure of NCRB. Furthermore, Gunell et aim is to discuss the clinical features and al, 2007 calculate that the number of International Journal of Health Sciences & Research (www.ijhsr.org) 246 Vol.4; Issue: 8; August 2014 intentional cases alone reaches some serum cholinesterase 126,000 cases annually. [15] The reasons for (pseudocholinesterase). [19] the suicide in males may include lack of Normally the cholinesterases rapidly employment, poverty, urbanization and hydrolyze the neurotransmitter acetylcholine various other stress related factors. In into inactive fragments of choline and acetic females, it may be due to marital acid after the completion of neurochemical disharmony. [16] transmission. The neurotransmitter CLASSIFICATION AND BIOLOGICAL acetylcholine is present in the terminal ASPECTS OF ORGANOPHOSPHORUS endings of all postganglionic COMPOUNDS: parasympathetic nerves, at myoneural Classification [9,17] junctions, and at both parasympathetic and Organophosphorus compounds are classified sympathetic ganglia. The major toxicity of as organophosphate compounds is the covalent I. By chemical structure: binding of phosphate radicals to the active A. Alkyl phosphates: HETP (Hexaethyl tetra sites of the cholinesterases, transforming phosphate), TEPP (tetraethyl them into enzymatically inert proteins. [19,20] pyrophosphate) tetron, fosvex etc Organophosphates thus act as irreversible B. Aryl phosphates : Paroxon (0,0, diethyl- cholinesterase inhibitors because the o-p-nitrophenyl phosphate) –E 600- organophosphate-cholinesterase bond is not mintacol, Parathion (0,0, diethyl-o-p- spontaneously reversible without nitrophenyl thiosulphate or diethyl pharmacological intervention. The inhibition thiophosphoric ester of p-nitrophenol-folidol of cholinesterase activity leads to the (bayer), Eketox (sandoz), kilphos, niran, accumulation of acetylcholine at synapses, rhyntox, oriental Bug’s bait etc. causing overstimulation and subsequent II. By toxicity [18] disruption of transmission in both the central Highly toxic (< D50 < 50mg/kg): and peripheral nervous systems. Exposure to Azinophos-methyl (Cruthion), Bomyl organophosphate compounds will, therefore, (Swat) interfere with synaptic transmission Carbophenthion (Trithion) etc. peripherally at muscarinic neuroeffector Moderate Toxicity (αD50 = 50-1000mg/kg): junctions and nicotinic receptors within Acephate (Orthene), Bensulide (Betasan), sympathetic ganglia and at skeletal Chloropyrofos (Durshan, Lorsban) etc. myoneural junctions. This is accomplished Low toxicity (αD50 = > 1000mg/kg) : by an overstimulation of acetylcholine Bromophos (Nexagan), Etrimfos (Ekanet), receptor sites that leads to a variety of Iodofenphos (Nuvanol N) etc. physiologic and metabolic derangements. (αD50 = lethal dose in experimental Disruption of transmission also will occur at animals) the acetylcholine receptor sites within the central nervous system. [20] MECHANISM OF ACTION: Organophosphate compounds avidly MODE OF INTOXICATION: [18,20,21] bind to cholinesterase molecules and Most OP compounds are extremely share a similar lipophilic. They are therefore readily chemical structure. In human beings, the two absorbed by passive diffusion across lung principal cholinesterases are RBC, or true and gastrointestinal system or skin. cholinesterase (acetylcholinesterase), and Deliberate ingestion is common with suicidal intensions in developing countries, International Journal of Health
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