Document ID: chunk:federal_register_of_legislation:F2013C00288:reg:2:p4
Version: federal_register_of_legislation:F2013C00288
Segment Type: reg
Provision Reference: reg 2 (pt 4/6)
Character Range: 2102553–2105541

though it is noted that the evidence of carcinogenicity applies to the inhalation route only.

    2.4.2         Review of Available Values/Information
Available data with respect to carcinogenicity was reviewed by WHO (2001). The review provided is no different from that summarised by Di Marco & Buckett (1996). Beryllium and compounds are considered carcinogenic to humans with the most important  end point identified as lung cancer following inhalation exposures. WHO (2001) noted that the genotoxicity data for beryllium is mixed and it appears to be somewhat compound-dependent (NRC 2007). Although the bacterial assays have been largely negative, the mammalian test systems exposed to beryllium compounds have shown evidence of mutations, chromosomal aberrations, and cell transformations. ATSDR (2002) has considered beryllium compounds to be weakly genotoxic.

The mode of action for beryllium carcinogenicity is not well understood and the relevance of a non-threshold approach to the quantification of inhalation exposures is not clear. The following is noted by Di Marco & Buckett (1996) and is considered to remain relevant for the assessment of inhalation exposures:
'Whilst lung cancer is the most important  end point, it is unlikely to be a concern for beryllium in soil. Acute beryllium lung disease appears to occur prior to the development of lung cancer and may play a role in its induction. In addition, this disease has only been reported after exposure to high levels of specific beryllium compounds in the workplace; conditions which are unlikely to be achieved on exposures to dust generated from beryllium contaminated soil.'

This is supported by a more recent review by Hollins et al. (2009) where it was concluded that 'the increase in potential risk of lung cancer was observed among those exposed to very high levels of beryllium and that beryllium's carcinogenic potential in humans at exposure levels that exist in modern industrial settings should be considered either inadequate or marginally suggestive'.

Further review of carcinogenic risk associated with inhalation exposures in the current HIL by Di Marco & Buckett (1996) indicated that a soil concentration that is protective of carcinogenic risk via inhalation at a level of 1 in 100,000 (more than 1000 mg/kg) was well in excess of the derived HIL (20 mg/kg). This is consistent with calculations that would be conducted using current exposure assumptions.

On the basis of the above it is recommended that a threshold approach be adopted for the derivation of an HIL for beryllium in soil.  The following are available from Level 1 Australian and International sources:

Source              Value                       Basis/Comments
Australian
ADWG (NHMRC 2011)   TDI = 0.002 mg/kg/day       No quantitative evaluation is available in the previous ADWG (NHMRC 2004) due to lack of suitable oral data.
                                                TDI presented in ADWG (NHMRC 2011) and is