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In vitro

HCFC 123 was negative when tested in standard Ames assays (Central Toxicology Laboratory, 1989; Longstaff et al., 1984).

In an earlier study, HCFC 123 was tested for mutagenicity in a series of suspension and plate assays using Salmonella typhimurium tester strains (Ames), as well as Saccharomyces cerevisiae strain D4 (forward mutation assay), in the presence and absence of S9. HCFC 123 was found to be negative in both of these assays.

HCFC 123 was evaluated for clastogenic potential in 3 in vitro cytogenetic assays using human lymphocytes both in the presence and absence of rat liver-derived S9 mix.

In one study, human lymphocytes were exposed to HCFC-123 at dose levels of 50, 250 and 500 μg/ml in the absence of S9 mix and 100, 500 and 1,000 μg/ml in the presence of S9 mix (Central Toxicology Laboratory, 1992). In the presence of S9 mix, no increases in the frequency of chromosomal aberrations were observed. In the absence of S9 mix, dose-related increases in the chromosomal aberration frequency were observed which were statistically and biologically significant at 500 μg/ml.

A study in the liquid phase and in the vapour phase was carried out by Life Science Research (1991a and 1991b).

When tested in the liquid phase at 0.005% (v/v), positive response in the absence of S9, but no significant evidence for a positive response in the presence of S9 were observed (Life Science Research 1991a).

In the vapour phase study, cultured human lymphocytes were exposed to 25,000 ppm or 100,000 ppm HCFC-123 in the absence of S9, and to 300,000 ppm in the presence of S9. In both cases, biologically and statistically significant positive responses were produced (Life Science Research 1991b). In vivo HCFC-123 was tested for the ability to induce unscheduled DNA synthesis (UDS) in an rat hepatocyte assay incorporating an auto-radiographic technique. Male Alderley Park (Alpk:APfSD) rats were exposed by inhalation at 8,000, 12,500 or 20,000 ppm HCFC-123 for 6 hours. Hepatocytes from exposed rats were assessed for the induction of UDS at the two highest dose levels. At in vivo at exposure levels up to 20,000 ppm, HCFC-123 did not induce DNA repair in rat hepatocytes (Central Toxicology Laboratory, 1993). An in vivo micronucleus assay was conducted to evaluate the genotoxic potential of HCFC-123 (Hoechst, 1988). NMRI mice were exposed to levels of 2,000, 6,000 or 18,000 ppm in air for 6 hours. Under the conditions of this assay, exposure to HCFC-123 did not result in an increased number of micronuclei. HCFC-123 was further evaluated for genotoxic activity in an chromosome aberration study with peripheral blood lymphocytes from Sprague-Dawley rats (Hazelton, 1992). The blood samples were taken from male rats that had been exposed (6 h/d, 7 d/wk) over a period of 14 weeks to HCFC-123 concentrations of 300, 1,000 or 5,000 ppm HCFC-123. Chromosome aberrations were determined only in the high dose group. The authors concluded that HCFC-123 was not genotoxic in this assay. Conclusions HCFC 123 showed no mutagenic potential in bacterial mutation assays. In vitro chromosomal aberration studies showed unconclusive results. However, negative results were obtained in an in vivo chromosomal aberration study in rat blood lymphocytes and in an in vivo micronucleus study in mouse bone marrow erythrocytes. Negative results were observed also in an UDS study in rat hepatocytes. Overall HCFC 123 is to be considered as not genotoxic or mutagenic.

Endpoint Conclusion: No adverse effect observed (negative)

Justification for classification or non-classification

HCFC 123 does not meet the classification criteria for genotoxicity and mutagenicity in accordance withEU Directive 67/548/EEC and EU Classification, Labeling and Packaging of Substances and Mixtures (CLP) Regulation (EC) No. 1272/2008.