Document ID: chunk:federal_register_of_legislation:F2013C00288:reg:1:p5
Version: federal_register_of_legislation:F2013C00288
Segment Type: reg
Provision Reference: reg 1 (pt 5/13)
Character Range: 2377229–2380249

tissue (or peel) and remain there bound to lipids in cell walls; transfer into the inner root or xylem is very slow or non-existent. CCME (2008) notes that the general consensus in the literature is that the root uptake pathway of organic contaminants such as hydrocarbons and PAH constituents from the soil by plants is extremely limited, particularly for the heavier PAHs such as BaP.

On the basis of the above, plant uptake has not been considered in the derivation of HIL A. However it is noted that if plant uptake were considered (using the equations presented in Appendix B), intakes derived from this source are low and do not significantly contribute to the HIL (<1%).

    1.3.5         Intakes from Other Sources – Background
Intakes of BaP from sources other than soil have been considered by Fitzgerald (1991) to range from 0.1661.6 µg/day (US EPA 1980) with intakes derived from food identified as the most significant. While more detailed reviews are available on potential intakes of BaP (CCME 2008), background intakes are not considered in the derivation of an HIL for BaP, as a non-threshold approach has been adopted.

1.4              Identification of Toxicity Reference Values

    1.4.1         Classification
The International Agency for Research on Cancer (IARC 2010) has classified BaP as
1—human carcinogen.
The US EPA has classified BaP as B2—probable human carcinogen.

    1.4.2         Review of Available Values/Information
BaP has been shown to be carcinogenic via all routes of exposure. BaP is an indirect carcinogen, that is, its carcinogenicity results from its metabolites, primarily various epoxides, as opposed to BaP itself. Several different types of tumours have been observed as a result of exposure to BaP, although tumour development is closely related to route of administration, i.e. dermal application induces skin tumours and oral administration induces gastric tumours. Exposure to BaP causes disruption to cellular genetic material, in particular DNA adducts are formed as a result of exposure and BaP is considered to be a genotoxic carcinogen (WHO 1998).

In addition BaP has been demonstrated to be a skin irritant and dermal sensitiser (WHO 1998).

US EPA (2005) has concluded that BaP (and carcinogenic PAHs assessed on the basis of a TEF) acts via a mutagenic mode of action and recommends that susceptibility associated with early lifetime exposures be addressed. No non-threshold values available for BaP have been derived to specifically address early lifetime susceptibility and hence these issues may need to be addressed when characterising exposure to BaP.
On this basis, a peer-reviewed non-threshold reference value is recommended for BaP. The following non-threshold values are available from Level 1 Australian and International sources:
Source              Value                                     Basis/Comments
Australian
ADWG (NHMRC 2011)   Not available                             Current guideline of 0.00001 mg/L established in ADWG (NHMRC