Rhodium triiodide

Endpoint summary

Key value for chemical safety assessment

Genetic toxicity in vitro

Description of key information

In a guideline study, to GLP, rhodiumtriiodide was mutagenic in Salmonella typhimurium strains TA 98, TA 100 and TA 1537, when tested in the absence and presence of a rat liver metabolic activation system (S9), as well as in strain TA 1535 in the absence of S9. In Escherichia coli WP2uvrA, an ambiguous result was seen in the absence of S9 (Cincelli & Brightwell, 2006).

Endpoint conclusion

Endpoint conclusion:

adverse effect observed (positive)

Genetic toxicity in vivo

Description of key information

No data identified.

Endpoint conclusion

Endpoint conclusion:

no study available

Mode of Action Analysis / Human Relevance Framework

No data identified.

Additional information

In an OECD Test Guideline 471 study, conducted according to GLP, rhodiumtrijodide was examined for the ability to induce gene mutations in Salmonella typhimurium (strains TA 1535, TA 1537, TA 98, and TA 100) and Escherichia coli (WP2 uvrA) in the presence and absence of phenobarbital/betanaphthoflavone-induced rat liver metabolic activation system (S9). A preliminary solubility trial identified dimethylsulphoxide (DMSO) as a suitable solvent for the test material. An initial experiment (in triplicate) was conducted for each strain using the plate incorporation method, involving concentrations of up to 5000 µg/plate, based on observed precipitation (in DMSO) in the preliminary trial. Large increases in the number of revertant colonies were observed in strains TA 98 and TA 100, in both the presence and absence of S9 when the plate incorporation method was used. Further testing of the remaining strains using the pre-incubation method (also in triplicate) revealed small, but significant and dose-related increases in TA 1535 in the absence of S9 and in TA 1537 in both the presence and absence of S9. No evidence of cytotoxicity was apparent; precipitation occurred at the highest tested dose, though scoring was reportedly unaffected. Overall, rhodiumtrijodide was found to be mutagenic in S. typhimurium strains TA 1537, TA 98 and TA 100 in the absence and presence of S9, as well as in strain TA 1535 in the absence of S9 alone, under the conditions of the test. However, the authors do not comment on an ambiguous result seen in E. coli WP2 uvrA in the absence of metabolic activation, where treatment at the maximum tested dose level induced a near-doubling in the number of revertant colonies (Cincelli & Brightwell, 2006). The test results therefore indicate that rhodium triiodide is potentially mutagenic; however, the relevance of these findings is currently unclear due to the use of the DMSO solvent. It is possible that DMSO has influenced the outcome of this Ames test, e.g. via the formation of soluble (and potentially DNA-reactive) rhodium(III)-DMSO complexes [Complexation with DMSO has been observed for both rhodium (I) and rhodium (III) compounds (James and Morris, 1980), as well as with ruthenium (II) compounds (Jaswal et al., 1990).]. As such, the relevance of these findings for the assessment of the mutagenic potential of rhodium triiodide and its consequent classification is currently uncertain.

 

No in vivo genotoxicity data were identified for rhodium triiodide or any other poorly soluble rhodium (III) compounds.

 

In 2002, the Dutch Expert Committee on Occupational Standards (DECOS) reviewed the genotoxic and carcinogenic potential of rhodium and rhodium compounds. In its evaluation, the Committee found that several water-soluble rhodium (III) compounds were genotoxic and, as such, a human health concern. No data regarding poorly soluble rhodium (III) compounds were reported by DECOS, although the Expert Group did imply a distinction between the soluble and insoluble rhodium (III) species, regarding their potential mutagenicity (DECOS, 2002).

 

The results of a proprietary bacterial reverse mutation assay (conducted in accordance with OECD Test Guideline 471 and GLP) for rhodium trihydroxide, a poorly soluble rhodium (III) compound, indicate a lack of bacterial mutagenicity (when tested as a suspension). Similarly, the preliminary findings for another proprietary OECD Test Guideline 471 Ames test indicate a lack of mutagenicity for dirhodium trioxide, another poorly soluble rhodium (III) compound. A number of water-soluble rhodium (III) compounds have shown mutagenic potential in various studies, and these substances are considered separate from the insoluble/poorly water-soluble rhodium (III) compounds.

 

Based on the limited available data, the mutagenic potential of the poorly-soluble and insoluble rhodium (III) compounds currently remains uncertain. However, bio-elution information may prove to be a more accurate means of assessing and grouping these substances, notably as their mutagenic activity is likely associated with their ability to release rhodium(III)-ionic species in solution. Indeed, bio-elution assays have been commissionedto further elucidate the genotoxicity profileof this class of compounds.

 

 

References

DECOS (2002). Dutch Expert Committee on Occupational Standards, a committee of the Health Council of the Netherlands. Rhodium and compounds: Evaluation of the carcinogenicity and genotoxicity.  

 

James BR and Morris RH (1980). Sulfur-bonded sulfoxide complexes of rhodium(III) and rhodium(I). Canadian Journal of Chemistry 58(4), 399-408.

 

Jaswal JS, Rettig SJ and James BR (1990). Ruthenium(III) complexes containing dimethylsulfoxide or dimethylsulfide ligands, and a new route to trans-dichlorotetrakis(dimethylsulfoxide)ruthenium(II). Canadian Journal of Chemistry 68(10), 1808-1817.

Justification for classification or non-classification

Based on the existing data set, rhodium triiodide does not currently meet the criteria for classification as a germ cell mutagen (category 1A or 1B) under EU CLP criteria (EC 1272/2008). However, this conclusion should be revisited when the results of the commissioned bio-elution assays are available.