Acute and recurrent hepatitis induced by 2,2-dichloro-1,1,1-trifluoroethane (HCFC-123)

K. Omae, T. Takebayashi, S. Tanaka, K. Sasaki, H. Miyauchi, I. Kabe, K. Taneichi, H. Shibaki

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


A 49-yr-old female cleaning worker first visited a hospital because of acute hepatitis. On admission, laboratory examination revealed severe hepatic damage (AST 2125 IU/L, ALT 2391 IU/L, LDH 1279 IU/L, t-Bil 8.5 mg/d/), but failed to disclose any evidence of viral infection or morphological lesions. She recovered day by day without any specific treatment for hepatitis and was discharged one month later. On the 11th day after restarting her job, she was readmitted due to similar symptoms and signs. Serum biochemistry data again showed severe liver damage (AST 1354, ALT 1604, LDH 1119 t-Bil 2.6). Histopathological diagnosis based on hepatic needle biopsy was chronic active hepatitis with diffuse infiltration of lymphocyte-dominant inflammatory cells, bridging necrosis, intercellular fibrosis in a limited region, and with ballooning, degeneration, and/or necrosis of the hepatic cells. A job-related cause was suspected and 2,2-dichloro-1,1,1-trifluoroethane (HCFC-123), which has been proven to cause acute hepatitis in humans, was detected in a dry-cleaning solvent by gas chromatography-mass spectrometry analysis. A job simulation experiment suggested that the concentration of the patient's exposure to HCFC-123 exceeded 1,000 ppm during the busiest work period, which was sufficiently high to induce severe liver damage.

Original languageEnglish
Pages (from-to)235-238
Number of pages4
JournalJournal of occupational health
Issue number5
Publication statusPublished - 2000


  • 1,1-Dichrolo-1-fluoroethane (HCFC-141b)
  • 2,2-Dichloro-1,1,1-trifluoroethane (HCFC-123)
  • Acute hepatitis
  • Chlorofluorocarbon substitute

ASJC Scopus subject areas

  • Medicine(all)


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