Organophosphates intoxication symptoms

Developmental Effects. Adverse effects of methyl parathion on hirman fetal development have not been reported. Based on studies in animals, such effects appear to be possible if pregnant women were exposed during the first trimester to high concentrations of methyl parathion that resulted in significant depression of cholinesterase levels, particularly if concomitant signs and symptoms of organophosphate intoxication occur. Such an exposure scenario may occur with occupational exposure, exposure in homes or offices illegally sprayed with methyl parathion, or accidental exposure to methyl parathion, but is less likely as a result of low-level exposure. 

Since it is impossible to measure the inhibition inside the synapses, it is customary in cases of carbamate and organophosphate intoxication to measure the residual enzymatic activity in the blood of the victim and to calculate the percentage of inhibition. Normally, light symptoms appear not before 30% of inhibition, becoming an imminent life-threatening condition when this figure is above the 90-95% level. 

Due to the lack of gas masks and other protective clothes and gear, the total number of victims poisoned with sarin in Matsumoto who needed professional help (600) included not only residents, but also members of the rescue team and health care professionals. Seven out of 58 residents admitted to the hospitals died. A physician from the duty ambulance vehicle and seven rescuers out of the 95 engaged, had mild symptoms of organophosphate intoxication [13],... 

A classification of organophosphate poisoning has been proposed by Tafuri and Roberts (1987) modified from Namba et al. (1971). Clinical signs and symptoms of intoxication may occur when serum cholinesterase levels drop to below 50% of the normal value. Mild poisoning, with the patient still ambulatory, may occur when serum cholinesterase levels are 20-50% of normal moderate poisoning with inability to walk with levels 10-20% of normal and severe poisoning with respiratory distress and unconsciousness with serum cholinesterase levels <10% of normal. 

Cellular and molecular mechanisms of neurotoxicity are also influenced by the fact that neurons are postmitotic and do not divide. Thus, the capacity for replacement of damaged cells does not exist in the nervous system, whereas most other organ systems have a well-established capacity for regeneration. Many neurotoxins can cause encephalopathy and an important concept in neurotoxicology is the delayed manifestation of symptoms sometimes up to years after the exposure started. Several agents show a lag time between exposure and neurotoxicity. Examples are the organophosphate chemical warfare agents [245], bismuth intoxications [246] and methylmercury... 

The mode of action of the carbamate insecticides is similar to that of the organophosphates. As shown in Figure 7.15, the reaction yields a carbamylated AChE, followed by decarbamylation via hydrolysis. Carbamates also attack the CNS system, and the symptoms of intoxication are similar to those with the organophosphates. However, unlike the organophosphates, decarbamylation of acetylcholinesterase is rapid, typically in minutes, and therefore carbamate insecticides are regarded as reversible acetylcholinesterase inhibitors. 

A. Oximes are used to treat poisoning caused by cholinesterase inhibitor insecticides and nerve agents, ie, organophosphates, mixtures of organophospho-ms and carbamate insecticides, or pure carbamate insecticide intoxication with nicotinic-associated symptoms. Because of its low toxicity, possible ineffectiveness if treatment is delayed until after the cholinesterase enzyme has aged, ability to reverse nicotinic as well as muscarinic effects, and ability to reduce atropine requirements, pralidoxime should be used early and empirically for suspected cholinesterase inhibitor poisoning. 

Inhibition of AChE is irreversible, preventing the substrat (ACh) from reacting with the esterase site. Consequently, accumulation of ACh results in all symptoms of acetylcholine poisoning caused by organophosphates (Santos et al. 2007). Symptoms of intoxication appear after approximately 50 % of the AChE is inhibited and the typical effects are agitation, muscle weakness, muscle fasciculations, hypersalivation and sweat. Severe poisonings may cause respiratory failure, unconsciousness, confusion, convulsions and/or death (Sogorb and Vilanova 2002 Duysen et al. 2012). 

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