Water Quality Standards

Summary information extracted from:  Guidelines for drinking-water quality, 2nd ed. - Vol. 1. Recommendations. - Geneva, World Health Organization, 1993. pp. 60-61.

Vinyl chloride is used primarily for the production of polyvinyl chloride. The background level of vinyl chloride in ambient air in western Europe is estimated to range from 0.1 to 0.5 µg/m3. Residual vinyl chloride levels in food and drinks are now below 10 µg/kg. Vinyl chloride has been found in drinking-water at levels of up to a few micrograms per litre, and, on occasion, much higher concentrations have been found in ground water. It can be formed in water from trichloroethene and tetrachloroethene.

Vinyl chloride is metabolized to highly reactive and mutagenic metabolites by a dose-dependent and saturable pathway.

The acute toxicity of vinyl chloride is low, but vinyl chloride is toxic to the liver after short- and long-term exposure to low concentrations. Vinyl chloride has been shown to be mutagenic in various test systems in vitro and in vivo.

There is sufficient evidence of the carcinogenicity of vinyl chloride in humans from industrial populations exposed to high concentrations, and IARC has classified vinyl chloride in Group 1. A causal association between vinyl chloride exposure and angiosarcoma of the liver is sufficiently proved. Some studies suggest that vinyl chloride is also associated with hepatocellular carcinoma, brain tumours, lung tumours, and malignancies of the lymphatic and haematopoietic tissues.

Animal data show vinyl chloride to be a multisite carcinogen. Vinyl chloride administered orally or by inhalation to mice, rats, and hamsters produced tumours in the mammary gland, lungs, Zymbal gland, and skin, as well as angiosarcomas of the liver and other sites.

Because there are no data on carcinogenic risk following oral exposure of humans to vinyl chloride, estimation of risk of cancer in humans was based on animal carcinogenicity bioassays involving oral exposure. Using results from the rat bioassay, which yields the most protective value, and applying the linearized multistage model, the human lifetime exposure for a 10-5 excess risk of hepatic angiosarcoma was calculated to be 20 µg per person per day. It was also assumed that, in humans, the number of cancers at other sites may equal that of angiosarcoma of the liver, so that a correction (factor of 2) for cancers other than angiosarcoma is justified. Using the lifetime exposure of 20 µg per person per day for a 10-5 excess risk of hepatic angiosarcoma, a guideline value for drinking-water of 5 µg/litre was calculated.