Uncontrolled occupational exposure to 1,1-dichloro-1-Fluoroethane (HCFC-141b) is associated with acute pulmonary toxicity.

BACKGROUND: The toxicity of 1,1-dichloro-1-fluoroethane (HCFC-141b), a hydrochlorofluorocarbon (HCFC), is low according to animal studies. However, pulmonary manifestations associated with acute HCFC exposure by inhalation have not been reported as yet in man. We evaluated the pulmonary effects of HCFC-141b inhalation, caused by an accident, in previously healthy individuals. METHODS: The subjects in this study were 15 workers in whom unpleasant symptoms developed after inhaling HCFC-141b at work. Clinical manifestations, radiologic findings, and changes in pulmonary function and airway hyperresponsiveness (AHR) over time were assessed, and BAL fluid analyses findings for four subjects were compared with those of four healthy volunteers (control subjects). RESULTS: (1) Cough, shortness of breath, and malaise developed in most patients, but only two patients complained of a sore throat. (2) A high-resolution CT scan of the chest revealed bilateral diffuse ground-glass opacities that were predominant in upper lung zones. (3) The mean (+/- SD) FVC was 71.4 +/- 18.86% predicted, and the mean FEV(1)/FVC ratio was 92.9 +/- 4.25%. Eleven patients (73%) showed restrictive ventilatory impairments during the initial tests. FVC gradually improved, and the FEV(1)/FVC ratio gradually decreased with time. (4) AHR was observed in four subjects during the initial tests. (5) BAL fluid samples revealed significantly higher neutrophil counts than those in control subjects. CONCLUSIONS: Overexposure to HCFC-141b was associated with parenchymal lung injury that was characterized by ground-glass opacities, elevated BAL neutrophil counts, and restrictive ventilatory impairment. Restrictive impairments improved with time after exposure.

Dimethylacetamide-induced hepatic injuries among spandex fibre workers.

OBJECTIVES: To investigate clinical features of dimethylacetamide-induced hepatic injuries (DIHIs). METHODS: Workers exposed to dimethylacetamide (DMAc) in two spandex factories were monitored for DIHI. We identified 38 DIHI cases as study subjects between 2001 and 2004. DMAc exposure was estimated with urinary N-methylacetamide (NMAc) results from 2003 to 2004. RESULTS: All 38 cases showed hepatocellular-type liver injury. The interval between first exposure and identification of hepatic injury (latent period) was mostly less than two months and never exceeded six months. In addition, three repeat DIHI cases showed much shorter latent periods for recurrence than their initial latent periods of hepatic injury. A 50% decline of serum alanine aminotransferase (ALT) levels after the cessation of DMAc exposure took less than 14 days and a 90% decline less than 31 days. The median urinary NMAc level of DIHI group (samples from the department of DIHI cases) was 25.1 mg/g Cr; higher than that of all other urinary NMAc results (11.8 mg/g Cr). CONCLUSIONS: Our data suggest that DMAc can induce hepatocellular-type liver injury and the mechanism of DIHI may be idiosyncratic. Although our exposure estimation was incomplete, the workers with DIHIs might be exposed to higher levels of environmental DMAc than the workers who did not develop DIHIs. All workers exposed to DMAc need to be closely observed for occurrence of hepatic injury for at least six months.