Poisoning parathion

The hazards of human poisoning by the parathions have stimulated the development of safer analogues. Two chlorinated derivatives have gready reduced mammalian toxicides. Dicapthon [2463-84-5], 0,0-dimethyl 0-(2-chloro-4-nitrophenyl) phosphorothioate (63) (mp 53°C), has rat LD qS of 400, 330 (oral) and 790, 1250 (dermal) mg/kg. Chlorthion [500-20-8], 0,0-dimethyl 0-(3-chloro-4-nitrophenyl) phosphorothioate (64) (mp 21°C, <71.437), has rat LD qS of 890, 980 (oral) and 4500, 4100 (dermal) mg/kg. These compounds have been used as household insecticides. 

Northern New England Poison Center, 313, 318 Norwegian Occupational Hygiene Association, 276 Nova Chemicals Corporation, 149 NOVAFOS-M , parathion, 100... 

Several medical tests can determine whether you have been exposed to methyl parathion. The first medical test measures methyl parathion in your blood or measures 4-nitrophenol, which is a breakdown product of methyl parathion, in your urine. These tests are only reliable for about 24 hours after you are exposed because methyl parathion breaks down quickly and leaves your body. These tests cannot tell whether you will have harmful health effects or what those effects may be. The next medical test measures the levels of a substance called cholinesterase in your blood. If cholinesterase levels are less than half of what they should be and you have been exposed to methyl parathion, then you may get symptoms of poisoning. However, lower cholinesterase levels may also only indicate exposure and not necessarily harmful effects. The action of methyl parathion may cause lower cholinesterase levels in your red blood cells or your blood plasma. Such lowering, however, can also be caused by factors other than methyl parathion. For example, cholinesterase values may already be low in some people, because of heredity or disease. However, a lowering of cholinesterase levels can often show whether methyl parathion or similar compounds have acted on your nerves. Cholinesterase levels in red blood cells can stay low for more than a month after you have been exposed to methyl parathion or similar chemicals. For more information, see Chapters 3 and 7. 

The controls were patients who had undergone appendicitis or hernia surgery, and were matched for sex, age, and socioeconomic status with a larger set of 31 pesticide poisoning eases, of whieh the methyl parathion eases were a subset. Limitations of this study include the small number of methyl parathion eases, and the use of appendieitis and other surgery patients as eontrols. 

Diagnosis of organophosphate poisoning (including methyl parathion) can be confirmed by evaluation of serum (plasma) cholinesterase and erythrocyte cholinesterase. However, cholinesterase inhibition is not specific for organophosphates. For example, carbamate insecticides also result in cholinesterase inhibition, which is usually transitory. Erythrocyte cholinesterase measurement is a specific test for... 

This section will describe clinical practice and research concerning methods for reducing toxic effects of exposure to methyl parathion. However, because some of the treatments discussed may be experimental and unproven, this section should not be used as a guide for treatment of exposures to methyl parathion. When specific exposures have occurred, poison control centers and medical toxicologists should be... 

Following inhibition by methyl parathion, acetylcholinesterase activity recovers as a result of the synthesis of new enzyme, generally at a rate of approximately 1% per day. However, the symptoms of methyl parathion poisoning usually resolve much more rapidly. Therefore, even though they are symptom-free, persons poisoned by methyl parathion may be hypersusceptible to its effects and should avoid reexposure for several weeks (Aaron and Howland 1998 Proctor et al. 1988). 

De Bleecker J, Willems J, Van Den Neucker K, et al. 1992. Prolonged toxicity with intermediate syndrome after combined parathion and methyl parathion poisoning. Clin Toxicol 30 333-345. 

Fazekas GI. 1971. [Macroscopic and microscopic changes in Wofatox (methyl parathion) poisoning]. Zeitschift fur Rechtsmedizin 68 189-194. (German)... 

Fazekas IG, Rengei B. 1965. [Fatal methyl parathion (Wofatox) poisoning]. Arch Toxikol 30 323-326. (German)... 

Lukaszewicz-Hussain A, Moniuszko-Jakoniuk J, Pawlowska D. 1985. Blood glucose and insulin concentration in rats subjected to physical exercise in acute poisoning with parathion-methyl. Pol J Pharmacol Pharm 37 647-651. 

Tiess D, Wegener R, Tamme A. 1982. [A case of accidental parathion-methyl (Wofatox) poisoning with lethal result]. Deutsch Gesundheitswes 37 1540-1542. (German)... 

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. 

The deliberate poisoning of harmful birds leads to unexpected consequences. In three districts of the former GDR in 1964-65, com was sprayed with methyl parathion and grain with zinc phosphide to fight rooks. As was expected, a large number of birds died, but rooks made up only 3% of the total [32]. 

Which of the following is an agent useful in the treatment of severe poisoning by organophosphorus insecticides, such as parathion ... 

Such reductions may result in loss or diminution of the harmful effects as microorganisms convert the broad-spectrum poison 2,4-dinitrophenol to 2-amino-4-and 4-amino-2-nitrophenol, the fungicide pentachloronitrobenzene to penta-chloroaniline, and the insecticide Parathion to aminoparathion. 

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. ... 

Aging is of clinical interest in the treatment of poisoning because cholinesterase reactivators such as pralidoxime (2-PAM, Protopam) chloride are ineffective after aging has occurred. Measurement of metabolites of methyl parathion, p ra-nitrophenol, and dimethylphosphate in the urine has been used to monitor exposure to workers. ... 

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). 

---