In 2019, the International Agency for Research on Cancer re-evaluated the carcinogenicity of night-shift work and reported that there is limited evidence that night-shift work is carcinogenic for the development of prostate cancer. Therefore, in 2020 and 2021, the Korean Epidemiologic Investigation Evaluation Committee concluded that 2 cases of prostate cancer were occupational diseases related to the night-shift work. Here, we report the 2 cases of prostate cancer in night-shift workers which were first concluded as occupational diseases by the Korean Epidemiologic Investigation Evaluation Committee.

Patient A: A 61-year-old man worked as a city bus driver for approximately 17 years, from 2002 to 2019, and was exposed to night-shift work during this period. In March 2017, the patient was diagnosed with high-grade prostate cancer through core-needle biopsy after experiencing stinging pain lasting for 2 months. Patient B: A 56-year-old man worked as an electrician and an automated equipment operator in a cement manufacturing plant for 35 years from 1976 to 2013 and was exposed to night-shift work during this period. In 2013, the patient was diagnosed with high-grade prostate cancer through core needle biopsy at a university hospital because of dysuria that lasted for 6 months.

The 2 workers were diagnosed with high-grade prostate cancer after working night shifts for 17 and 35 years respectively. Additionally, previous studies have reported that high-grade prostate cancer has a stronger relationship with night-shift work than low or medium-grade prostate cancer. Therefore, the Korean Epidemiologic Investigation Evaluation Committee concluded that night-shift work in these 2 patients contributed to the development of their prostate cancer.

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.

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.

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.