Document ID: chunk:federal_register_of_legislation:F2013C00288:reg:5:p3
Version: federal_register_of_legislation:F2013C00288
Segment Type: reg
Provision Reference: reg 5 (pt 3/7)
Character Range: 2822430–2825407

highly volatile and not persistent, background intakes will be dominated by inhalation exposures. Concentrations of vinyl chloride in industrial, urban and regional areas are available in Australia. Data collected in NSW (DEC 2003) from urban and regional areas in NSW note that vinyl chloride was rarely detected (<1% of samples) with the maximum reported from the Sydney CBD of 0.3 ppbv (0.0008 mg/m3). Vinyl chloride was not detected in ambient air sampling undertaken in Perth (WA DEP 2000). In addition, vinyl chloride has not been detected in drinking water and low levels are expected in food (NHMRC 2011). Low levels have been historically reported in some consumer products. Background intakes expected from vinyl chloride are expected to be low, with conservative intakes estimated by Health Canada (1992) of approximately 0.005 mg/kg/day and RIVM (2001) of approximately 0.00006 mg/kg/day (predominantly from inhalation). It is noted that, as the most sensitive end point is carcinogenicity, which is assessed on the basis of a non-threshold approach, background intakes are not used in the derivation of the HIL.

5.5              Identification of Toxicity Reference Values

    5.5.1         Classification
The International Agency for Research on Cancer (IARC 2008) has classified vinyl chloride as Group 1—carcinogenic to humans.

Vinyl chloride is also classified as a known human carcinogen (Category A) by US EPA for the inhalation route of exposure, and by analogy for the oral route of exposure. It is also considered highly likely to be carcinogenic by the dermal route.

    5.5.2         Review of Available Values/Information
Exposure to vinyl chloride via inhalation has been associated with increases in liver cancer, including a rare form of angiosarcoma and biliary tract cancer. Other studies have indicated increase incidence of CNS and brain cancer. While most data is associated with inhalation exposures, ingestion studies suggest evidence of carcinogenicity via oral exposure (WHO 1999 and ATSDR 2006).

Vinyl chloride has been identified as genotoxic and mutagenic (WHO 1999, ATSDR 2006 and US EPA 2000). The US EPA (2000) review notes that vinyl chloride toxicity occurs via a genotoxic pathway (identified from a number of lines of evidence) that is understood in some detail. On this basis, the assessment of carcinogenicity on the basis of a non-threshold (linear) approach is appropriate.

The US EPA (2000) review also noted that chemically induced human liver carcinogenicity is associated with mutational alteration of multiple genes, consistent with a mutagenic mode of action. In addition, several studies of partial lifetime exposure suggest that the lifetime cancer risk depends on age at exposure, with higher lifetime risks attributable to exposures at younger ages. This is also noted by WHO (2000; 2011). Consistent with US EPA guidance, the derivation of non-threshold values for vinyl chloride has incorporated factors that