JACC Report 47 – 1,1-Dichloro-2,2,2-trifluoroethane (HCFC-123) Third edition

JACC 047 : 1,1-Dichloro-2,2,2-trifluoroethane (HCFC-123)CAS No. 306-83-2 (Third Edition) | July 2005

This report has been produced as part of the ECETOC Joint Assessment of Commodity Chemicals (JACC) programme. It updates an earlier ECETOC review¹and presents a critical evaluation of the available toxicity and ecotoxicity data on 1,1-dichloro-2,2,2-trifluoroethane (HCFC-123), including results of new toxicological studies conducted by the Programme for Alternative Fluorocarbon Toxicity Testing (PAFT)². HCFC-123 is a volatile liquid that is used, for example, as a refrigerant in air-conditioning installations and as an intermediate in the production of various chemicals. HCFC-123 is a transitional replacement (to be phased out by 2020) for chloro- and bromo-fluorocarbons. It has a low potential for ozone depletion (2% of that of CFC-11, trichlorofluoromethane) and global warming (76 relative to carbon dioxide; this compares to 4,000 for CFC-11). Any HCFC-123 released to the environment will rapidly volatilise to the atmosphere, where it will be slowly degraded, mainly to trifluoroacetic acid, which will partition into water and possibly accumulate there, although predicted concentrations are below toxic thresholds.

HCFC-123 is not readily biodegradable, but is not likely to bio-concentrate in fish and other aquatic organisms. It is slightly to moderately toxic to fish, invertebrates, and algae. Thus, HCFC-123 is unlikely to pose a significant hazard to the aquatic environment; it is also not persistent in water. HCFC-123 has a low toxicity in laboratory animals upon single brief exposure to the liquid or vapour. The liquid is not irritant or sensitising to the skin, but produces eye irritation. For humans, the most relevant critical effects from single, brief single exposure to HCFC-123, such as from the discharge of a fire extinguisher, are depression of the central nervous system and increased likelihood of cardiac arrhythmia. Repeated exposure to HCFC-123 may yield liver lesions.

In reproductive toxicity studies in animals, the growth of neonates was retarded, probably because the milk of the dams contained trifluoroacetic acid, the main metabolite of HCFC-123. HCFC-123 is not genotoxic in vivo, although there was clastogenetic activity at high doses in vitro. HCFC-123 caused statistically significant increases in benign tumours in rat liver, testis and pancreas. The formation of liver tumours can be linked with the rodent-specific peroxisome proliferation potential of HCFC-123, while the testicular tumours may have resulted from enhanced hormonal disturbances in senescent rats. Thus, the hepatic and testicular tumours are not relevant for human health hazard assessment. The mechanism of pancreatic acinar cell tumour formation is not understood, and the significance of those tumours for humans remains uncertain. ¹ECETOC. 1996. Joint assessment of Commodity Chemicals report No. 33 ²A cooperative research effort (1987-2000) sponsored by 16 of the leading CFC producers [http://www.afeas.org/paft/]