Exposure to 2,2-dichloro-1,1,1-trifluoroethane (HCFC-123) and acute liver dysfunction: A causal inference

Acute liver dysfunction has been reported among workers repeatedly exposed to 2,2-dichloro-1,1,1-trifluoroethane (HCFC-123), a substitute for trichlorofluoromethane. Causality between occupational exposure to HCFC-123 and liver dysfunction was examined. Levels of exposure to HCFC-123 were estimated retrospectively by reproducing working conditions and by a job record survey. Health surveillance, including liver function and subjective symptoms, was done when two workers first complained of ill health. The mean HCFC-123 concentration in air was more than 200 ppm with a peak concentration of about 1,000 ppm in a processing area where HCFC-123 was used. HCFC-123 of 18-24 ppm was detected in the adjunct areas where HCFC-123 vapor was not generated. Workers (n=14) were then classified into high (n=5) and low (n=9) exposure groups according to the estimated exposure level, which was confirmed by determination of urinary trifluoroacetic acid. Mean serum AST and ALT levels were 236 IU// and 476 IU// among the high-exposed workers, and exceeded 500 IU// in three workers. Various types of symptoms involving the central nervous system and digestive organs, and irritation of the mucous membrane, were also experienced. The degree and prevalence of these health effects were higher in the high exposure group, which indicates the exposure- effect and exposure-response relationships. The consistency and temporality of the relationship between HCFC-123 exposure and the observed health effects were also confirmed. We conclude that repeated exposure to high concentrations of HCFC-123 for no more than five weeks causes acute severe liver dysfunction with various symptoms in humans. Biological plausibility must be clarified to confirm the causality.