Hard metal particles and lung disease: coincidence or causality?

Accessible online at: www.karger.com/journals/res Hard metal is essentially produced by heating tungsten carbide together with cobalt powder at about 1,500°C. The resultant product consists of about 80% tungsten carbide, 10–20% cobalt, and may also contain minor amounts of other metals, frequently titanium. The combination of tungsten carbide with cobalt may – obviously in a synergistic way [1] – induce a particular lung disease, which has been described in workers exposed to hard metal dust [2] and in laboratory animals [3]. The development of hard metal lung disease (HMLD) is a rare event and is almost unrelated to the duration and extent of exposure, an observation which has been attributed to the presence of a particular individual sensitivity [4]. An autoimmune mechanism has been suspected. HMLD is clinically characterized largely by a restrictive lung disease with reduced diffusion capacity due to alveolitis with progression to fibrosis. The prognosis is rather poor [5], and progression after cessation of exposure is frequent. In most cases steroid therapy was attempted with minor effects only [6]. Histologically tungsten carbide particles can be demonstrated in the macrophages and fibrotic tissue, whereas cobalt cannot be found in most cases due to rapid clearance from lung tissue [6]. When HLMD is suspected because of occupational exposure, alveolitis and lung fibrosis, the diagnosis is further supported by demonstration of tungsten carbide particles in lung tissue or BAL, and it is ascertained by the histologic demonstration of pathognomonic multinuclear giant cells in the alveolar space [7–9]. In this issue of Respiration Hahtola et al. [10] describe a 45-year-old female hard metal worker with alveolitis and lung fibrosis and tungsten carbide particles in her lung tissue. Histologically, however, the lung biopsy showed a pattern suggestive of sarcoidosis with epitheloid cell granuloma. Multinucleated giant cells are not described. Consistent with sarcoidosis rather than HMLD are enlarged hilar lymph nodes, the development of arthralgia, and a rapid clinical improvement when therapy with steroids was initiated. In fact, sarcoidosis must always be considered as an alternative diagnosis to HMLD [11]. The authors discuss the resemblance of the clinical, radiological, and histological findings with sarcoidosis, but the title of their article suggests that HMLD is proven in this case. This diagnosis, however, is solely based on the demonstration of tungsten carbide particles in the patient’s lung, being a consequence of working at a grinding machine for 5 years. Therefore the hard metal dust particles in the patient’s lung do not mean that hard metal dust is causal to her disease, in particular when the latter is atypical for HMLD. A lot of foreign material is deposited in the lungs. It can be used as an indicator of exposure, but not as an indicator of disease. If this were not the case, then the sole presence of asbestos bodies in the patient’s lungs would prompt a diagnosis of ‘atypical