A cross-sectional study of 1,039 tungsten carbide (TC) production workers was carried out. The purposes were (1) to evaluate the prevalence of interstitial lung disease (ILD) and work-related wheezing, (2) to assess correlations between cobalt exposure and pulmonary disease, (3) to compare lung disease in grinders of hard carbide versus nongrinders, and (4) to evaluate the effects of new and previous threshold limit values for cobalt of 50 and 100 micrograms/m3. We obtained medical and occupational histories, flow-volume loops, single breath carbon monoxide diffusing capacity (DLCO), and chest radiographs. Time-weighted average cobalt levels were determined at every step in the production process. Work-related wheeze occurred in 113 participants (10.9%). Profusion greater than or equal to 1/0 occurred in 26 (2.6%) and interstitial lung disease (defined as profusion greater than or equal to 1M, FVC or DLCO less than or equal to 70%, and FEV1/FVC% greater than or equal to 75) in 7 (0.7%). The relative odds of work-related wheeze was 2.1 times for present cobalt exposures exceeding 50 micrograms/m3 compared with exposures less than or equal to 50 micrograms/m3. The relative odds of profusion greater than or equal to 1/0 was 5.1 times for average lifetime cobalt exposures exceeding 100 micrograms/m3 compared with exposures less than or equal to 100 micrograms/m3 in those with latency exceeding 10 yr. ILD was found in three workers with very low average lifetime exposures (less than 8 micrograms/m3) and shorter latencies. Grinders of hard carbide had lower mean DLCO than nongrinders, even though their cobalt exposures were lower.(ABSTRACT TRUNCATED AT 250 WORDS)

In sarcoidosis and idiopathic pulmonary fibrosis, it has been reported that lymphocyte proportions in lung lavage predict the subsequent clinical course. Recent evidence has suggested that lymphocytes are important in the alveolitis of asbestosis. We hypothesized that a greater relative proportion of T-lymphocytes in lung lavage of asbestos-exposed subjects is associated with immune activation and may predict the subsequent clinical course. We assessed lymphocyte subsets in lung lavage and peripheral blood (PB) of 97 asbestos-exposed subjects and 10 unexposed normal, using flow cytometry analysis of monoclonal antibody-treated cells. T-cell alveolitis was defined as follows: [%lymphocytes in lavage x %CD3 in lavage] greater than 2 SD above that product in normals. Eighteen subjects had T-cell alveolitis (group 1) and 79 did not (group 2). There were no significant differences between the groups in age, smoking status, duration of exposure, lung function results, or frequency of plaques or profusion greater than or equal to 1/0. Percent CD2 was higher in lavage of group 1 compared with group 2. There was a trend for higher %Ia in lavage of group 1 compared with group 2. These results identify a subgroup of asbestos-exposed subjects with T-cell alveolitis but no present excess of asbestos-related disease who may be at risk for future asbestos-related disease.