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Case Study 8: Carbon Tetrachloride Toxicity
Pages 249-266

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From page 249...
... This monograph is one in a series of self-instructional publications designed to increase the primary care provider's knowledge of hazardous substances in the environment and to aid in the evaluation of potentially exposed patients. See page 18 for more information about continuing medical education credits and continuing education units.
From page 250...
... You learn that the workers were handling several dozen barrels of a sweet-smelling hazardous waste liquid in a hot, unventilated room. Their work required taking samples from barrels, which were obtained from a defunct chlorofluorocarbon manufacturing plant.
From page 251...
... Sources producing concentrations that are above background levels include industrial locations where CCI4 is still used and chemical waste sites where emissions into air, water, Orson are not controlled properly. In 1983, the average atmospheric background level in rural areas was 0.13 parts per billion (ppb)
From page 252...
... Other populations at risk of exposure to CCI4 include people living near chemical waste sites where CCI4 is improperly stored. The toxic metabolites of CCI4 are produced from reactions mediated by mixed function oxidase (M FO)
From page 253...
... Persons with preexisting hepatic necrosis or cirrhosis or underlying renal disease appear to have increased susceptibility to CCI4-induced toxicity and are at increased risk of subsequent liver cancer. Although CCI4 is not toxic to the fetus in most animal models, results of studies indicate that the human fetal MFO enzyme system may be operational in the later stages of development and can be induced by certain maternal exposures (e.g., cigarette smoke)
From page 254...
... Bioactivation of CCI4 has become the model for chemical toxicity induced by free radicals a mechanism of toxic inju ry similar to that associated with radiation and the aging process. The results of studies with experimental animals indicate that the first step in CCI4 metabolism may involve the formation of a trichloromethyl free radical ( CCI3)
From page 255...
... Adverse effects to other organs are likely to be secondary to CNS, liver, or kidney damage. CC14 iS classified as a potential human carcinogen based on results of studies that indicate ingested CCI4 increases the frequency of liver tumors in experimental animals.
From page 256...
... In addition, a dramatic increase in calcium concentration occurs in hepatic mitochondria, accompanied by alterations in electrolyte distributionwith swelling of hepatic ceils and depletion of liver glycogen. Hepatic injury, which usually manifests after CNS effects have subsided, typically occurs 1 to 4 days after acute exposure.
From page 257...
... One to six days after an acute exposure, a patient may develop severe hepatic necrosis and renal failure, which can affect the cardiovascular and pulmonary systems. Toxic hepatitis, necrosis, and cirrhosis have been reported after chronic exposure to high levels of CCI4.
From page 258...
... should be performed, and urine output and fluid balance should be O Regardless of CCI4 exposure route, CNS effects predominate initially; symptoms of hepatic and renal damage may manifest later. O Any detectable amount of CCI4 in the blood Indicates exposure, although not necessarily adverse effects.
From page 259...
... , chest X ray, and electrocardiogram are warranted forbaseline and monitoring purposes. If liveror renal injury is severe, patients should be evaluated for spontaneous bleeding with serial hematocrits and tests for stool occult blood.
From page 260...
... Future hepatocellular carcinoma in persons with residual liver damage is a possibility. Exposed patients should be instructed to avoid stimulants and other hepatotoxicants including ethanol.
From page 261...
... For his potentially exposed coworkers? Standards and Regulations NIOSH considers CCI4 a probable human carcinogen and ACGIH considers CCI4 a suspected human carcinogen.
From page 262...
... Water The EPA maximum contaminant level for CCI4 in drinking water is 5 parts per billion (ppb)
From page 263...
... Government Documents Agency for Toxic Substances and Disease Registry. Toxicological profile for carbon tetrachloride.
From page 264...
... Other secondary health effects reported include coagulation disorders, cardiac dysrhythmias, and pulmonary edema; these effects are not likely to resolve without improvement in the intercurrent kidney and liver disorders. Because of the patient's multiple exposures to hepatotoxic agents (i.e., recent heavy consumption of ethanol and potential occupational exposure)
From page 265...
... Some solvents may cause dysrhythmias and pulmonary edema (probably secondary to renal toxicity) ; thus, a baseline electrocardiogram and chest X ray should be obtained.
From page 266...
... The patient's cardiac and pulmonary systems and clotting ability should also be evaluated periodically since abnormalities can occur secondary to hepatic and renal damage. If the patient shows no improvement, liver biopsy may be considered since liver enzyme levels are not always reliable predictors of liver damage.


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