Environmental Medicine Integrating a Missing Element into Medical Education (1995) / Chapter Skim
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Case Study 47: Vinyl Chloride Toxicity
Case Study 47: Vinyl Chloride Toxicity
Pages 793-811
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From page 793... ...
Hepatic angiosarcoma has not been reported in workers who were exposed to vinyl chloride after 1974, when permissible workplace air levels were drastically reduced. This f nding, however, may reflect an incomplete latency period.
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From page 794... ...
Questioning reveals that he has been a car salesman for 25 years. He is married, has 3 children, and has lived near an industrial park for the last 18 years.
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From page 795... ...
Other sources of airborne exposure include volatilization from new plastic parts and upholstery in car interiors. Release of residual vinyl chloride monomer from most othersolid PVC materials is generally of little consequence, although significant amounts of vinyl chloride may be released during burning of PVC products.
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From page 796... ...
Who's at Risk Those at greatest risk of vinyl chloride exposure are the 2.2 million workers concerned with the production, use, transport, storage, and disposal of this material. The highest health risk has been to workers exposed as a result of the polymerization process, especially to those who were lowered directly into the reactor vessels to remove solid polymer adhering to the inside.
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From page 797... ...
The formation of scar tissue, which results from vinyl chlorideinduced chronic liver disease, has been reported to cause hepatomas that can become malignant when ethanol is consumed. The fetus may also be at increased risk.
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From page 798... ...
Chronic Exposure Several epidemiologic studies have convincingly associated chronic vinyl chloride exposure with liver tumors, both malignant and nonmalignant, and have suggested, but not proved, an increased incidence of cancers in other parts of the body. Subtle necrologic effects have been noted in some workers chronically exposed to vinyl chloride.
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From page 799... ...
Nonmalignant hepatic manifestations of vinyl chloride exposure include noncirrhotic portal hypertension and cirrhosis, depending on the nature of exposure. In cases of acute exposure, the resulting chemical hepatitis rarely progresses into fulminant hepatic necrosis.
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From page 800... ...
There have been no cases of hepatic angiosarcoma recorded in workers due to vinyl chloride exposure after 1974, when allowable workplace air levels were drastically reduced. However, a sufficient latency period has not yet elapsed for carcinogenic effects to have appeared.
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From page 801... ...
The latency period for nonmalignant complications may be several months, while the latency period for angiosarcoma of the liver may be as brig as 40 years. Workers exposed before 1974, when permissible workplace levels were still high, are at increased risk forthe development of hepatic angiosarcoma into the next century.
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From page 802... ...
Chronic Exposure Chronic occupational exposures to vinyl chloride at levels of several hundred ppm have led, in the past, to vinyl chloride disease, a condition involving a number of organ systems and tissues and resulting in a variety of clinical symptoms. The reported period of exposure before the onset of this disease ranged from 1 month to 3 years.
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From page 803... ...
10 803 Laboratory Tests Short of liver biopsy, there are no definitive clinical clues to distinguish hepatic injury due to vinyl chloride from that of other etiologies such as viral hepatitis infection and ethanol toxicity. (Vitamin A overload, hemochromotosis, andcarbontetrachloride exposure have been reported to cause liver disease only rarely.)
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From page 804... ...
These bile acids, cholylglycine and conjugates of cholic acid, have been shown to be significantly elevated in asymptomatic workers with chemical exposure and histologically proven chemical liver injury. A screening panel of fasting serum bile acids and liver enzyme assays or ICG clearance rates is both sensitive (few false negatives)
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When serum bile acids, alkaline phosphatase, and SGPT (ALT) are all normal, there is a high probability of excluding latent liver disease due to any cause; only a liver biopsy is more definitive.
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From page 806... ...
Recovery from acute effects is usually rapid and complete with supportive therapy; there is no specify treatment or antidote for vinyl chloride exposure. Chronic Exposure In the past, symptoms associated with vinyl chloride disease tended to disappear within 1 or 2 years after the patient was removed from exposure.
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From page 807... ...
requires that a worker's exposure to airborne vinyl chloride monomer not exceed 1 ppm averaged over any 8-hourperiod and that a worker not be exposed to greater than 5 ppm for any period of time exceeding 15 minutes. Direct contact with the liquid is prohibited.
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From page 808... ...
Environment Air The 1982 EPA emission standards for chemicals released to the atmosphere set a limit for vinyl chloride of 10 ppm, measured at the source. Water Pursuant to the Safe Drinking Water Act, EPA has issued a maximum contaminant level for vinyl chloride of 2 micrograms per liter (I L)
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From page 809... ...
Fox AJ, Collier PF. Mortality experience of workers exposed to vinyl chloride monomer in the manufacture of polyvinyl chloride in Great Britain.
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From page 810... ...
As a car salesman, he may daily spend time inside new cars where the ambient air can contain significant amounts of vinyl chloride (1 to 10 ppm) released from plastic and upholstery, including the dashboard and seats.
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From page 811... ...
(11 ) Since the rest of the family and the nearby community may have had similar exposure to vinyl chloride, all should undergo periodic testing of transaminases, alkaline phosphatase, and serum bile acids to detect latent chemical injury.
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