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Organophosphates intoxication

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. [Pg.36]

At the 2 lowest doses, significant depression from day 2 through day 14 blood cholinesterase normal at day 21. At 60.75 mg/kg, blood cholinesterase decreased for entire 49-day posttreatment. No outward signs of organophosphate intoxication and normal food intake and demeanor At 24 h, whole milk had 0.24 mg famphur/L of which 76% was in the butterfat fraction after 72 h, residues in milk were <0.008 mg/L... [Pg.1082]

Over 25 years ago Carman and coworkers recognized the adverse potential of fieldworker exposure to pesticide residues ( ). Subsequent fieldworker acute organophosphate intoxications and resulting political pressure led to regulations by the Occupational Health and Safety Administration and the Environmental Protection Agency. These regulations and the worker reentry situation have been the subject of reviews (, 3). [Pg.59]

However, an examination of published worker reentry cases presents a frustrating problem. A compilation of incidents from 1949 to 1955 described cases of organophosphate intoxication from workers in pears, apples, grapes, citrus, and hops (18). Workers were picking, thinning, cultivating, and irrigating. [Pg.64]

Carbamates as Pre-Exposure Treatment against Organophosphate Intoxication... [Pg.284]

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. [Pg.285]

It can be seen that one of the quaternary carbamates has been chosen for this use, mainly because they are safer and also have fewer untoward effects, and since in the early years organophosphate intoxication was considered to be mainly a peripheral breathing problem (paralysis of the diaphragm muscles and edema of the lungs). The realization during the 1980s and 1990s that inhibition of the brain... [Pg.285]

Rubinshtein, R., Bar-Meir, E., Grubstein, A., Bitterman, H. (2002). Early onset of ventricular tachyarrhythmias in organophosphate intoxication. Israel Med. Assoc. J. 4 63-4. [Pg.506]

Organophosphate Intoxication Molecular Consequences Mechanisms and Solutions... [Pg.691]

Levy-Khademi, F., Tenenhaum, A.N., Wexler, I.D., Amitai, Y. (2007). Unintentional organophosphate intoxication in children. Pediatr. Emerg. Care 23 716-18. [Pg.948]

Bajgar, J., Fusek, J., Kuca, K., Bartosova, L., Jun, D. (2007). Treatment of organophosphate intoxication using cholinesterase reactivators facts and fiction. Mini Rev. Med. Chem. 7 461-6. [Pg.1017]

Cowan, J., Sinton, C.M., Varley, A.W., Wians, F.H., Haley, R.W., Munford, R.S. (2001). Gene therapy to prevent organophosphate intoxication. Toxicol. Appl. Pharmacol. 173 1-6. [Pg.1029]

Guven, M., Sungur, M., Eser, B., Sari, I., Altuntas, F. (2004). The effects of fresh frozen plasma on cholinesterase levels and outcomes in patients with organophosphate intoxication. Clin. Toxicol. 42 617-23. [Pg.1062]

Robenshtok E, Luria S, Tashma Z, and Hourvitz A (2002) Adverse reaction to atropine and the treatment of organophosphate intoxication. The Israel Medical Association Journal 4(7) 535-539. [Pg.192]

Methomyl exerts toxicity by inhibiting acetylcholinesterase. As with other carbamate insecticides, acetylcholinesterase inhibition is much less persistent than with organophosphate intoxication. [Pg.1642]

The examples provided above give only a brief overview of the variety of enzymatic functions that alter, biotransform, and biodegrade xenobiotics. In many instances numerous enzymes are known, as in the case of the mixed function oxidases. In order to provide a concrete example of a system of detoxification enzymes that is widely distributed, we have chosen the organophosphate acid anhydrolases — enzymes that may aid in the understanding of organophosphate intoxication and may also provide a means for the detoxification and bioremediation of these materials. [Pg.256]

Oehmichen M, Besserer K. Forensic significance of acetylcholine esterase histochemistry in organophosphate intoxication. Original investigations and review of the literature. Z Rechtsmed 1982 89 149-65. [Pg.165]


See other pages where Organophosphates intoxication is mentioned: [Pg.33]    [Pg.34]    [Pg.48]    [Pg.1080]    [Pg.384]    [Pg.496]    [Pg.611]    [Pg.284]    [Pg.1080]    [Pg.84]    [Pg.64]    [Pg.292]    [Pg.285]    [Pg.76]    [Pg.934]    [Pg.2353]    [Pg.2460]    [Pg.2520]   
See also in sourсe #XX -- [ Pg.64 ]




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