HCFC-123-induced toxic hepatitis and death at a Korean fire extinguisher manufacturing facility: a case series
10.1186/s40557-018-0231-2
- Author:
Mu Young SHIN
1
;
Jong Soo PARK
;
Hae Dong PARK
;
Jihye LEE
Author Information
1. Occupational Safety and Health Research Institute, Korea Occupational Safety and Health Agency, Ulsan, Republic of Korea.
- Publication Type:Case Report
- Keywords:
2,2-dichloro-1,1,1-trifluoroethane;
HCFC-123;
Toxic hepatitis;
Drug-induced liver injury;
Fire extinguisher manufacturing facility
- MeSH:
Alanine Transaminase;
Alkaline Phosphatase;
Appetite;
Aspartate Aminotransferases;
Bilirubin;
Biopsy;
Drug-Induced Liver Injury;
Emergencies;
Employment;
Fever;
Fires;
Hepatitis;
Hospitals, General;
Humans;
Korea;
Liver;
Liver Failure, Acute;
Male;
Occupational Exposure;
Transferases
- From:Annals of Occupational and Environmental Medicine
2018;30(1):20-
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Exposure to sustained high concentrations of HCFC-123 is known to be hepatotoxic. We report two simultaneous cases of toxic hepatitis related to exposure to 2,2-dichloro-1,1,1-trifluoroethane (HCFC-123), a common refrigerant, at a Korean fire extinguisher manufacturing facility. CASE PRESENTATION: Patients A and B were men aged 21 and 22 years, respectively, with no notable medical histories. They had recently started working for a manufacturer of fire extinguishers. During the third week of their employment, they visited the emergency center of a general hospital due to fever, lack of appetite, and general weakness. At the time of their visit, they were suspected as having hepatitis due to elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), and total bilirubin levels and were hospitalized. However, as their condition did not improve, they were moved to a tertiary general hospital. After conservative treatment, one patient improved but the other died from acute hepatic failure. Assessments of the work environment showed that the short-term exposure levels of HCFC-123 for valve assembly processes were as high as 193.4 ppm. A transjugular liver biopsy was performed in patient A; the results indicated drug/toxin-induced liver injury (DILI). Given the lack of a medical history and the occupational exposure to high levels of HCFC-123, a hepatotoxic agent, the toxic hepatitis of the workers was likely related to HCFC-123 exposure. CONCLUSIONS: Work environment assessments have not included this agent. To the best of our knowledge, we are the first to report a case of death related to HCFC-123-induced liver damage. Our findings suggest that exposure standards and limits for HCFC-123 must be developed in Korea; work environments will have to be improved based on such standards.
