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Pulmonary Fibrosis Associated with Occupational Exposure to Hard Metal at a Metal-Coating Plant -- Connecticut, 1989
On July 21, 1989, a 35-year-old worker in an industrial plant was examined at a university-based occupational health clinic (OHC) in Connecticut because of a 21-month history of shortness of breath and interstitial abnormalities visible on chest radiograph. In addition, examination of an open-lung biopsy performed in June 1989 had shown interstitial fibrosis and the presence of numerous macrophages and multinucleated giant cells in the alveolar spaces. The clinical and pathologic findings were compatible with a diagnosis of hard-metal pulmonary disease, a condition associated with occupational exposure to metallic alloys of cobalt and tungsten carbide. An energy-dispersive radiographic analysis of the biopsy material identified particulate iron, potassium, calcium, zinc, and lesser amounts of other metals in the lung tissues, but cobalt and tungsten were not specifically identified. Based on these findings, the OHC initiated an investigation to determine the source of exposure.
The patient was employed as a helper in a detonation-gun coating process that used heated, aerosolized metal powder to coat premanufactured metal parts within an enclosed chamber; except for 12 months during 1982-1983, he had worked continuously on the process from 1981 through 1989. His duties included setting up the metal parts to be coated in an enclosed, well-ventilated chamber and then reentering the chamber after the coating process was completed to remove the finished parts. A review of information provided by his employers confirmed that powdered hard metal (tungsten carbide mixed with cobalt) was used routinely in the coating process.
During the period the process helper was employed at the plant, exposure levels for cobalt were measured routinely as part of the plant's industrial hygiene program. Although the patient had never been monitored directly, personal breathing-zone exposures measured for other workers in his department had not exceeded 100 ug/m3 (as an 8-hour, time-weighted average), the then-applicable Occupational Safety and Health Administration (OSHA) permissible exposure limit (PEL) for cobalt. However, cobalt concentrations within the coating chamber were not measured during process operation and probably exceeded this level. At the conclusion of the coating process, the chamber was thoroughly ventilated before the helper reentered it to remove the completed parts.
In 1988, a supervisor for the same coating-process department at the plant had died of a progressive, diffuse pulmonary fibrosis that was clinically and histopathologically diagnosed as hard-metal pulmonary disease. During 1984, a transbronchial lung biopsy had shown findings consistent with, but not specific for, hard-metal pulmonary fibrosis, including interstitial fibrosis with honeycombing, mononuclear cells, intraalveolar giant cells, and an increased number of alveolar macrophages. His exposure to hard metal may have occurred during earlier employment as a grinder of completed metal parts and/or while he supervised the detonation-gun coating process. As part of the OHC investigation, reexamination of biopsy materials confirmed the presence of large quantities of tungsten and lesser amounts of cobalt in his lung tissue.
An OSHA plant inspection conducted after the diagnosis of pulmonary fibrosis in the process helper documented one airborne cobalt level at 90% of the OSHA PEL. As a result of these two cases and the investigation findings reported here, the plant reviewed its industrial hygiene program for the metal-coating process and instituted a chest radiograph surveillance program for the approximately 40 coating-process employees. Reported by: WS Beckett, MD, S Figueroa, MD, B Gerstenhaber, MD, L Welch, MD, D Klimstra, MD, GJ Walker Smith, MD, Dept of Internal Medicine, Pathology, and Epidemiology, Dept of Public Health, Yale Univ School of Medicine, New Haven, Connecticut. Div of Respiratory Disease Studies, National Institute for Occupational Safety and Health, CDC.
Editorial Note: Exposure to respirable cobalt dust (particle size less than 10 um) has been recognized as a cause of respiratory disease since 1940, when illness occurred in industrial workers exposed to dust generated by metallurgic processes (1). Exposure to cobalt most commonly occurs during the production or use of hard metal, an extremely durable alloy of cobalt and tungsten carbide. A recent case series in the United States emphasized the spectrum of respiratory diseases associated with exposure to hard metal, including reversible airway obstruction, reversible hypersensitivity pneumonitis or alveolitis, and pulmonary fibrosis (2). Giant-cell interstitial pneumonia is a particular form of pulmonary fibrosis that, in an occupational setting, is believed to be highly specific for cobalt-induced disease (3).
Detonation welding -- the metal-coating process by which the two employees in this report were exposed -- has not previously been associated with hard-metal disease. This process and the allied process of plasma coating are widely used in industry to produce smooth, durable surface coatings by the generation and deposition of high volumes of finely divided metal aerosols; these processes can, at the same time, constitute potential respiratory hazards.
Exposure-response relations in hard-metal respiratory disease are complex. For example, in one survey of hard-metal production facilities, although the overall prevalence of interstitial lung disease among exposed active workers was low (0.7%), 10% had work-related manifestations of obstructive airway disease (4). Furthermore, the presence of interstitial disease was not strongly correlated with measured exposure levels, suggesting that susceptibility factors other than total dose are important in the causation of disease. It is not known whether the recently adopted OSHA PEL of 50 ug/m3 (5) prevents sensitization or protects persons who have become hypersensitive.
The failure to identify tungsten in the lung biopsy of the process helper is noteworthy. Because cobalt has a relatively high biological solubility, it often may not be detected in lung biopsy specimens obtained from workers with documented hard-metal disease; however, tungsten generally is present. The absence of tungsten in this case may be related to the character of the exposures associated with the specific process reported here; this process generates an unusually fine and highly heated aerosol characterized by particles that may be cleared more rapidly from the lung interstitium.
The diagnosis of hard-metal disease in these two workers is an example of an occupational sentinel health event (i.e., a condition that indicates both the failure to protect the affected worker from a preventable occupational illness and the existence of risk for similar illnesses for co-workers) (6,7) and indicates the occurrence of potentially fatal toxic exposures in a process previously considered to have adequate engineering controls. The episode also emphasizes the need for medical surveillance and a review of workplace practices in facilities that use cobalt in similar processes. Surveillance for the respiratory effects of cobalt may require a review of symptoms, spirometry, measurement of diffusing capacity, and chest radiographs.
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