Carbon tetrachloride poisoning

In most situations, adequate, usuaHy forced, ventilation is necessary to prevent excessive exposure. Persons who drink alcohol excessively or have Hver, kidney, or heart diseases should be excluded from any exposure to carbon tetrachloride. AH individuals regularly exposed to carbon tetrachloride should receive periodic examinations by a physician acquainted with the occupational hazard involved. These examinations should include special attention to the kidneys and the Hver. There is no known specific antidote for carbon tetrachloride poisoning. Treatment is symptomatic and supportive. Alcohol, oHs, fats, and epinephrine should not be given to any person who has been exposed to carbon tetrachloride. FoHowing exposure, the individual should be kept under observation long enough to permit the physician to determine whether Hver or kidney injury has occurred. Artificial dialysis may be necessary in cases of severe renal faHure. 

Therefore, in spite of remarkably increased liver injury, the animals are able to overcome injury and survive the potentiated liver toxicity (Kodavanti et al. 1992 Mehendale 1990, 1991, 1992). DDT increased the sensitivity of rats to carbon tetrachloride poisoning (McLean and McLean 1966), and mice fed 100 ppm polybrominated biphenyls (PBBs) or 200 ppm polychlorinated biphenyls (RGBs) in their diet for 28 days experienced increased carbon tetrachloride hepatotoxicity (Kluwe et al. 1979). Potentiation of renal dysfunction was also found in the PBB-pretreated mice. All of these compounds are broad-spectrum MFO inducers. 

Barnes R, Jones RC. 1967. Carbon tetrachloride poisoning. Am Ind Hyg Assoc J 28 557-560. 

Burkhart KK, Hall AH, Gerace R, et al. 1991. Hyperbaric oxygen treatment for carbon tetrachloride poisoning. Drug Safety 6 332-338. 

Conaway HB, Hoven F. 1946. Electrocardiographic changes in carbon tetrachloride poisoning. U.S. Navy Med Bull 46 593-595. 

Dawkins MJR. 1963. Carbon tetrachloride poisoning in the liver of the new- born rat. J Pathol Bact 85 189-196. 

De Toranzo EG, Villarruel MC, Castro JA. 1978b. Early destruction of cytochrome P-450 in testis of carbon tetrachloride poisoned rats. Toxicology 10 39-44. 

Deng JF, Wang JD, Shih TS, et al. 1987. Outbreak of carbon tetrachloride poisoning in a color printing factory related to the use of isopropyl alcohol and air conditioning systems in Taiwan. Am J Ind Med 12 11-19. 

Durden WD Jr., Chipman DW. 1967. Gasoline sniffing complicated by acute carbon tetrachloride poisoning. Arch Intern Med 119 371-374. 

Foxell AWH. 1951. Three cases of carbon tetrachloride poisoning with one fatality. Br Med J 1 397. 

Gardner GH, Gove RC, Gustafson RK, et al. 1925. Studies on the pathological histology of experimental carbon tetrachloride poisoning. Bulletin of Johns Hopkins Hospital 36 107-133. 

Garner RC, McLean AEM. 1969. Increased susceptibility to carbon tetrachloride poisoning in the rat after pretreatment with oral phenobarbitone. Biochem Pharmacol 18 645-650. 

Gray I. 1947. Carbon tetrachloride poisoning - Report of seven cases with two deaths. NY State J Med 47 2311-2315. 

Hardin BL. 1954. Carbon tetrachloride poisoning. A review. Ind Med Surg 23 93-105. 

Jennings RB. 1955. Fatal fulminant acute carbon tetrachloride poisoning. Arch Pathol 59 269-284. 

Kittleson KD, Borden CW. 1956. Acute renal failure due to carbon tetrachloride poisoning. Northwestern University Medical School Magazine 30 117-123. 

Lundh HAB. 1964. Sequence comparison between kidney and liver lesions in the rat following carbon tetrachloride poisoning. J Occup Med 6 123-128. 

MacMahon HE, Weiss S. 1929. Carbon tetrachloride poisoning with microscopic fat in the pulmonary artery. Am J Pathol 5 623-630. 

McLean AEM, McLean EK. 1966. The effect of diet and 1,1,1-trichloro-2,2-bis-(p-chlorophenyl)ethane (DDT) on microsomal hydroxylating enzymes and on sensitivity of rats to carbon tetrachloride poisoning. Biochem J 100 564- 571. 

Norwood WD, Fuqua PA, Scudder BC. 1950. Carbon tetrachloride poisoning. Arch Ind Hyg Occup Med 1 90-100. 

Phelps BM, Hu CH. 1924. Carbon tetrachloride poisoning. Report of two fatal cases and a series of animal experiments. J Am Med Assoc 82 1254-1256. 

Ruprah M, Mant TGK, Flanagan RJ. 1985. Acute carbon tetrachloride poisoning in 19 patients implications for diagnosis and treatment. Lancet, May 4, 1 1027-1029. 

Sirota JFI. 1949. Carbon tetrachloride poisoning in man. I. The mechanism of renal failure and recovery. J Clin Invest 28 1412-1422. 

Tracey, JP, Sherlock P. 1968. Flepatoma following carbon tetrachloride poisoning. New York Journal of Medicine 68 2202-2204. 

Umiker W, Pearce J. 1953. Nature and genesis of pulmonary alterations in carbon tetrachloride poisoning. Arch Pathol 55 203-217. 

Villarruel MC, Fernandez G, Aguilar EG, et al. 1987. Early biochemical alternations in liver mitochondria from carbon tetrachloride poisoned rats. J AppI Toxicol 7 173-177. 

Metabolites of carbon tetrachloride may also give a positive result with tiiis test, but carbon tetrachloride is only partially metabolised to trichloromethyl compounds and the test may fail to detect this agent. If carbon tetrachloride poisoning is suspected, evidence of hepato-toxicity should be sought by carrying out appropriate serum-enzyme assays. 

F2. Fleisher, C. A., and Wakim, K. G., Transaminase in canine serum and cerebrospinal fluid after carbon tetrachloride poisoning and injection of transaminase concentrates. Proc. Staff Meetings Mayo Clin. 31, 640 (1956). 

Zinc atoms in some of the enzyme molecules participate in catalysis and also appear to be essential for maintenance of structmre of apoen-zymes. Zinc also plays a role in stabilization of biomembrane structure and polynucleotide conformation. Inasmuch as zinc appears to have a protective influence in hepatic cellular damage induced by carbon tetrachloride poisoning, it is reasonable to suggest that zinc also may have a direct effect on free radicals. 

The kidney is also a major target of carbon tetrachloride toxicity. The characteristic injuries observed are nephritis, nephrosis, and proteinuria. Delayed pulmonary edema and renal failure may follow hepatic damage. Renal failure is the most frequent cause of death in carbon tetrachloride poisonings. 

AID. Alston, W. C., Hepatic and renal complications arising from accidental carbon tetrachloride poisoning in the human subject. /, Clin. Pathol. 23, 249-253 (1970). 

S12a. Slater, T. F., Strauli, V. D., and Sawyer, B. C., Changes in liver nucleotide concentrations in experimental liver injury. 1. Carbon tetrachloride poisoning. Biochem. J. 93, 260-266 (1964). 

Leach BE, Forbes JC (1941) Sulfonamide drugs as protective agents against carbon tetrachloride poisoning. Proc Soc Exp Biol Med 48 361-363... 

Canary-yellow crystals from carbon tetrachloride. Poisonous. Dimorphous. The stable form occurs as orthorhombic crystals d l. 65 mp 195 tap 410 (decompn). Sublimes readily. Vapor press, at 20 = 2 x ]0-u mm volatility 0.02 mg/cu m beat of volatilization S4.8 cal spec heat 0.268 cal. Practically insol in water. Slightly sol in benzene, xylene, carbon tetrachloride. Corrodes iron, bronze, brass. [The metastable form melts at 186 if monoclinic, and at 182 if triclinic.]... 

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