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Occupational and Environmental Lung Disease |

Inhalational Nickel Carbonyl Poisoning in Waste Processing Workers*

Raymond CS. Seet, MRCP; Azman Johan, FRCP; Cuthbert ES Teo, FAMS(Path); Siok Lin Gan, MSc(OccMed); Kang Hoe Lee, MRCP
Author and Funding Information

*From the Department of Medicine (Drs. Seet and Lee), National University Hospital; Department of Medicine (Dr. Johan), Alexandra Hospital; Centre for Forensic Medicine (Dr. Teo), Health Sciences Authority; and Occupational Health Department (Dr. Gan), Ministry of Manpower, Singapore.

Correspondence to: Raymond CS. Seet, MRCP, Department of Medicine, National University Hospital, 5 Lower Kent Ridge Rd, Singapore 119074; e-mail: raymond_seet@nus.edu.sg



Chest. 2005;128(1):424-429. doi:10.1378/chest.128.1.424
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Background: Nickel carbonyl is formed when carbon monoxide comes into contact with active nickel. The inhaled nickel carbonyl is rapidly absorbed and distributed mainly to the lungs, brain, adrenal glands, and kidneys. In severe cases, acute nickel carbonyl exposure has been reported to cause death.

Design: Descriptive study.

Patients: Seven young men presented with fever, chills, substernal pleuritic chest pain, and exertional dyspnea. Extensive microbiological and toxicological investigations (including blood, urine, and bronchial specimens) for known pathogens and occupational toxins were performed. The clinical course and radiologic findings of each patient, including autopsy findings of three patients who died, were described.

Results: Four patients received treatment in the ICU. Elevated urinary nickel concentration was detected in all patients. Results of extensive microbiological investigations were unremarkable. No patients received chelating agents. Pulmonary consolidation, edema, hemorrhage, and fibrosis were observed at autopsy in patients who died. An out-of-date chemical used during neutralization of nickel waste was implicated as the source of nickel carbonyl poisoning.

Conclusions: High mortality was reported in patients who presented subacutely following nickel carbonyl exposure. Further studies should be performed to clarify the role of chelation therapy in the subacute phases following nickel carbonyl exposure.

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