Abstract
Four treatment groups (80 male Sprague-Dawley rats/group) were used in a 2 X 2 factorial design: inhalation of 600 ppm vinyl chloride (VC) 4 hr/day, 5 days/week for 1 year; VC and ingestion of 5% ethanol in water (v/v); filtered air and ethanol; filtered air. Ingestion of ethanol was begun 4 weeks prior to inhalation of VC and continued for life or termination of the study at two and one-half years from the first VC exposure. In this model system, ethanol potentiated the carcinogenic response to VC in the liver and produced an excess of neoplasms in animals receiving ethanol alone. Inhalation of VC induced angiosarcoma of the liver in 23% of the exposed animals; ethanol in addition to VC inhalation increased the incidence to 50%. Concomitant administration of VC and ethanol also produced an excess of hepatocellular carcinoma and lymphosarcoma. Ethanol with or without VC had a strong tumorigenic effect on the endocrine system. These results indicate that ethanol is a cocarcinogen in relation to the carcinogen VC.
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Selected References
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