Central nervous system poisoning

Potential Uses of These Polymers. We have studied the phenyl isocyanate modification of poly(vinyl alcohol) as a model system. Many uses exist for carbamates as medicines, pesticides and herbicides (67,68). For example, ethyl carbamate has been used to treat leukemia and multiple myeloma. Ethyl carbamate has also been used as an antidote for central nervous system poisoning by strychnine. The tranquilizer Meprobamate is a carbamate derivitive. Numerous pesticides and herbicides, such as Sevin and Propham, are also carbamate derivatives. Propham is isopropyl N-phenylcarbamate which bears a strong resemblence to the polymers of Equation 21, and this compound is used as a preemergence herbicide. Numerous other close analogs could be cited also. We might note also that the N-phenyl carbamoyl unit bears... 

All of the organophosphates except echothiophate are distributed to all parts of the body, including the central nervous system. Poisoning with these agents therefore includes an important component of central nervous system toxicity. 

SAFETY PROFILE Confirmed carcinogen. Poison by ingestion, intraperitoneal, subcutaneous, intravenous, and intramuscular routes. Moderately toxic by inhalation and skin contact. Human mutation data reported. A skin and eye irritant. Mutation data reported. The liquid is dangerous to the eyes. The vapor is irritating to mucous membranes and is a central nervous system poison. However, its low volatility reduces its toxicity effect. Ingestion of furfural has produced cirrhosis of the liver in rats. In industry there is a tendency to minimize the danger of acute effects resulting from exposure to it. This is particularly tme because of its low volatility. 

ACUTE HEALTH RISKS irritation of eyes, skin, and upper respiratory system destructive to tissues of mucous membranes central nervous system poison headache dangerous for acute effects resulting from exposure to furfural are minimized because of its low volatility. 

C. Central nervous system poisoning may cause agitation, seizures, and coma. 

Propylene oxide is a primary irritant, a mild protoplasmic poison, and a mild depressant of the central nervous system. Skin contact, even in dilute solution (1%), may cause irritation to the eyes, respiratory tract, and lungs. Propylene oxide is a suspected carcinogen in animals. The LC q (lowest lethal concentration by inhalation in tats) is 4000 mg/kg body weight. The LD q (oral) is 930 mg/kg. The LD q (dermal) is 1500 mg/kg. The TWA (8-h exposure) is 100 ppm and the STEP (15-min exposure) is 150 ppm. 

Health and Safety Factors. Carbonyl sulfide is dangerously poisonous, more so because it is practically odorless when pure. It is lethal to rats at 2900 ppm. Studies show an LD q (rat, ip) of 22.5 mg/kg. The mechanism of toxic action appears to iavolve breakdowa to hydrogea sulfide (36). It acts principally on the central nervous system with death resulting mainly from respiratory paralysis. Little is known regarding the health effects of subacute or chronic exposure to carbonyl sulfide a 400-p.g/m max level has been suggested until more data are available (37). Carbon oxysulfide has a reported inhalation toxicity in mice LD q (mouse) = 2900 ppm (37). 

Metals and metalloids that form alkyl compounds, eg, methylmercury and methylarsenic acid, tributjltin, deserve special concern because these compounds are volatile and accumulate in cells they are poisonous to the central nervous system of higher organisms. Because methylmercury or other metal alkyls may be produced at a rate faster than it is degraded by other organisms, it may accumulate in higher organisms such as fish. Hg species are also reduced to elementary Hg which is soluble in water but lost by volatilization to the atmosphere (40). 

Toxicity of 2-Ghloroethanol. Ethylene chlorohydrin is an irritant and is toxic to the Hver, kidneys, and central nervous system. In addition, it is rapidly absorbed through the skin (73). The vapor is not sufficiently irritating to the eyes and respiratory mucous membranes to prevent serious systemic poisoning. Contact of the Hquid in the eyes of rabbits causes moderately severe injury, but in humans corneal bums have been known to heal within 48 hours. Several human fataUties have resulted from inhalation, dermal contact, or ingestion. One fatahty was caused by exposure to an estimated 300 ppm in air for 2.25 hours. In another fatal case, autopsy revealed pulmonary edema and damage to the Hver, kidneys, and brain (73). 

Inhalation is the most common means by which ethers enter the body. The effects of various ethers may include narcosis, irritation of the nose, throat, and mucous membranes, and chronic or acute poisoning. In general, ethers are central nervous system depressants, eg, ethyl ether and vinyl ether are used as general anesthetics. 

Lotti M, Becker CE. 1982. Treatment of acute organophosphate poisoning Evidence of a direct effect on central nervous system by 2-PAM (pyridine-2-aldoxime methyl chloride). J Toxicol Clin Toxicol 19 121-127. 

Oral poisoning after accidental phenol ingestion has caused fulminant central nervous system depression, hepatorenal and cardiopulmonary failure [20]. No hepatorenal or central nervous system toxicities with properly performed chemical peels have been reported in the literature [21]. 

The mechanism whereby the bacteria produce the disease with its attendant symptoms is often due to the cells ability to produce specific poisons, toxins or aggressins (Chapter 14). Many of these are tissue-destroying enzymes which can damage the cellular structure ofthe body or destroy red blood cells. Others (neurotoxins) are highly specific poisons ofthe central nervous system, for example the toxin produced by Clostridium botulinum is, weight for weight, one ofthe most poisonous substances known. 

Attempts to diminish the overall metabolism of trichloroethylene might be useful (e.g., hypothermia, mixed-function oxidase inhibitors, competitive inhibitors of trichloroethylene metabolism [i.e., P-450 substrates]), if instituted soon enough after trichloroethylene exposure. Catecholamines (especially beta agonists) act in concert with trichloroethylene, increasing the risk of cardiac arrhythmias. Hence, catecholamines should be administered to patients only in the lowest efficacious doses and for certain limited presentations of trichloroethylene poisoning. Ethanol should also be avoided because concurrent exposure to trichloroethylene and ethanol can cause vasodilation and malaise and may potentiate central nervous system depression at high dosage levels of either compound. 

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