Document ID: chunk:federal_register_of_legislation:F2013C00288:reg:1:p3
Version: federal_register_of_legislation:F2013C00288
Segment Type: reg
Provision Reference: reg 1 (pt 3/10)
Character Range: 2742322–2745263

of the above, the use of the more commonly adopted equations for quantifying plant uptake (as presented in the text of Schedule B7) that do not address uptake of volatiles (from air) rather than the root, or transformations within the plant, are not considered appropriate and relevant for the assessment of TCE.

It is expected that the potential for plant uptake will be of less significance in the derivation of a soil HIL, when compared with the assessment of vapour inhalation, and given the limitations involved in providing a meaningful evaluation of plant uptake, it has not been considered in the derivation of HILs.

    1.4.4         Intakes from Other Sources – Background
As TCE is highly volatile, background intakes will be dominated by inhalation exposures. Concentrations of TCE in industrial, urban and regional areas are available in Australia. Data collected in NSW (DEC 2003) from urban and regional areas in NSW report average concentrations of TCE of approximately 0.1 ppbv (0.0005 mg/m3), close to the analytical limit of reporting with most samples noted to be not detected, with a maximum concentration in the Sydney CBD of 3.6 ppbv (0.019 mg/m3). Concentrations in an industrial area in Brisbane (Hawas et. al. 2001) have been reported with average and maximum concentrations of 0.0002 mg/m3 (also close to the limit of reporting) and 0.0005 mg/m3 respectively. Background air concentrations in Canada (CCME 2007) are considered to be approximately 0.0014 mg/m3, consistent with the range reported by DEC (2003). Background intakes (dominated by inhalation) were estimated by WHO (2011) to be approximately 0.04 µg/kg/day for children and 0.01 µg/kg/day for adults. Based on average concentrations reported in NSW and in Brisbane, intakes by young children are estimated to be approximately 0.3 µg/kg/day. These intakes comprise approximately 10% of the recommended inhalation TRVs for non-carcinogenic effects. It is noted that other sources found indoors (from a wide range of common products) are likely to be present and may contribute more significantly to background exposures. These sources may need to be addressed on a site-specific basis.

1.5              Identification of Toxicity Reference Values

    1.5.1         Classification
The International Agency for Research on Cancer (IARC 1995) has classified TCE as Group 2A—probably carcinogenic to humans.

Review by US EPA (2011) characterised TCE as carcinogenic in humans by all routes of exposure. This conclusion is based on convincing evidence of a causal association between TCE exposure in humans and kidney cancer. The human evidence of carcinogenicity from epidemiologic studies of TCE exposure is strong for non-Hodgkin Lymphoma but less convincing than for kidney cancer, and more limited for liver and biliary tract cancer. Less human evidence is found for an association between TCE exposure and other types of cancer, including bladder,