Parathion poisoning from

K. Kanagaratnam, W.H. Boon, and T.K. Hoh, Parathion poisoning from contaminated barley. Lancet 1 538, 1960... 

Stomach wash samples in nonfatal cases were found to contain large quantities of insecticide, thereby indicating that the major part of the insecticide was excreted by the body. Only trace amounts of pesticides would have remained in the body which did not prove fatal. The distribution pattern in different body organs is practically the same in all cases examined for parathion poisoning, as death generally occurred within an hour or two from administration of the poison. 

Clifford, N.J. and A.S. Nies (1989). Organophosphate Poisoning from Wearing a Laundered Uniform Previously Contaminated with Parathion, JAMA, 262, 3035-3036. 

Nisse K, Eorceville X, Cezard C, Ameri A, and Mathieu-Nolf M (1988) Intermediate syndrome with delayed distal polyneuropathy from ethyl parathion poisoning. Veterinary and Human Toxicology 40 349-352. 

Induction of emesis is contraindicated in the case of parathion poisoning due to the early onset of respiratory depression and seizures. Gastric lavage may be indicated if performed immediately after parathion ingestion. Activated charcoal/cathartic therapy may be adopted to retard the absorption from the gastrointestinal tract. Atropine should be administered intravenously until atropinization is achieved. In adults, 2-5 mg kg should be administered every 10-15 min and in children 0.05 mg kg must be... 

In a patient who had received obidoxime for 12 days and died 15 days after parathion poisoning, obidoxime concentrations in cartilage were 100-fold higher than in plasma (unpublished). These data indicate that the chondroitin sulfate-rich tissues may represent the deep compartment from which pyridinium aldoximes are slowly released. 

Nisse, P., Forceville, X., Cezard, C. C., Amcri, A., and Mathicu-Nolf, M. (1998). Intermediate syndrome with delayed di.stal polyneuropathy from ethyl parathion poisoning. Vet. Hum. Toxicol. 40, 166-168. 

Following absorption, OP compounds accumulate rapidly in fat, liver, kidneys, and salivary glands. The phos-phorothioates (P—S), such as diazinon, parathion, and bromophos, are more lipophilic than phosphates (P=0), such as dichlorvos, and are therefore stored extensively in fat, which may account for the prolonged intoxication and clinical relapse after apparent recovery that has been observed in poisoning from these OP in.sectieidcs. OP compounds vary in the case with which they cross the blood-brain barrier,... 

Because the phosphates are readily absorbed through the skin and are hazardous from exposure by any route, prevention of poisoning includes avoiding contact with the bare skin and avoidance of inhalation of the chemicals. It is recommended also that workers change their clothes completely and bathe with soap and water after every use of this material. Particular caution is indicated on the part of pilots engaged in airplane spraying because of the effects of the organic phosphates on the eyes. Parathion presents special problems because of its translocation into the plant. 

A few deaths have been reported after poisoning by EPN, most resulting from suicidal ingestion, but at least one death has been associated with EPN spraying. It is moderately to highly toxic in animals, but less potent than parathion. ... 

Deaths from occupational exposure have been reported, usually after massive accidental exposures. Data from human poisonings by methyl parathion are not sufficiently detailed to identify the range between the doses producing first symptoms and those producing severe or fatal intoxication.The probable oral lethal dose is 5-50mg/kg. Most animal data and limited human data indicate that methyl parathion is somewhat less acutely toxic than parathion. ... 

Hundreds of deaths associated with parathion exposure have been reported. These deaths have resulted from accidental, suicidal, and homicidal poisonings. It has been the cause of most crop worker poisonings in the United States. Fatal human poisonings have resulted from ingestion, skin exposure, and inhalation (with varying degrees of skin exposure). 

In the field, parathion is converted to varying degrees to paraoxon, which may persist on foliage and in soil. Exposure to paraoxon from weathered parathion residues by the dermal route on reentry by field-workers has resulted in anticholinesterase poisonings. ... 

C. Bronchoconstriction and secretion and muscular weaknesses occur from acetylcholine accumulation after inhibition of acetylcholinesterase. Parathion is an organophosphate insecticide that inhibits acetylcholinesterase, and it is readily available. Poisoning with compound 1080 (fluorocitrate) inhibits mitochondrial respiration and causes seizures and car-... 

Highly toxic groups will be found. They may be used to step up old nematocides or bring new ones to the fore. However, soil nematocides are contact killers and as such will be supplanted by chemotherapy. Plants will be fed materials toxic to the nematode. Such chemicals (stomach poisons) are already here, as indicated by sodium selenate. Plant parasitic nematodes can bathe in it, but unless it is absorbed by the plant and thus fed to the nematode, no injury is done. The mode of action of parathion is still uncertain. Plant parasitic nematodes placed in a saturated aqueous solution certainly survive for long periods, yet it has been found effective in the control of certain nematodes in living plants 16y 0), The next step is the introduction into the plant of nutriments to replace those taken from the plant by the nematode. The final step is the introduction into the plant of neutralizers of nemic enzymes. This may have already been done in the case of parathion, for it is said to inhibit cholinesterase formation in other animals. Chemotherapy will then have its day, but when that day is done physics may be expected to take over liie burdens of the control of plant diseases. We can expect the use of ultrasonics and radioactive fertilizers. 

In order to reach a conclusion when and how and, and to some extent, how much of a particular insecticide was administered, the form and quantity in which the insecticide exists in different tissues and in blood and urine may give valuable clues. Indeed, an intelligent deduction is also based on the knowledge of metabolic pathways and formation of other derivatives. Thus, as parathion is excreted in the urine ultimately as p-nitro-phenol, urinary p-nitrophenol levels may indicate the extent of exposure to parathion ). In cases of mild and moderate exposure, the excreted p-nitrophenol in urine was found to be of the order of 0.057 to 0.322 mg. percent. In severe and fatal cases of poisoning by parathion, the level of p-nitrophenol in urine was from 0.16 to 1.16 mg. percent. para-Nitrophenol thus is rapidly excreted in urine and no longer detected 48 hours after the exposure to the pesticide. 

Environmental Impacts Methyl parathion is highly toxic for aquatic invertebrates , and moderately toxic to mammals such as rats, dogs and rabbits . The chemical has been implicated in the deaths of waterfowl and the acute poisoning of fish, birds, cattle and wild animals. In 1995 a mixture of methyl parathion and endosulfan led to the death of over 240,000 fish in Alabama, when heavy rain washed the pesticides washed from the cotton fields and into rivers . 

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