A study of pulmonary reactions to inhaled metallic dusts in hard metal workers was conducted. The study group consisted of 26 workers (25 males), mean age 32.9 years, engaged in manufacturing hard metal tools (group-A) and five males, 21 to 26 years old, engaged in grinding hard metal tools using high speed diamond/cobalt wheels with oily coolants (group-B). The subjects were given physical examinations that included chest X-rays, lung function tests, patch testing with cobalt (7440484) and tungsten (7440337), and bronchoalveolar lavage (BAL). BAL fluid cytology was determined. Samples of BAL fluid, blood, urine, toenails, and pubic hair were analyzed for cobalt, tungsten, and tantalum (7440257). Information on personal and occupational histories was obtained. The mean years of exposure of group-A and group-B were 10.4 and 5 years, respectively. Eighteen group-A and four group-B subjects were smokers. Two group-A subjects had a history of work related asthma. Two group-B subjects complained of severe exertional dyspnea and weight loss. All group-A subjects had normal chest X- rays. A slight impairment in pulmonary gas diffusion was the only functional impairment seen. Nine group-A subjects had moderate to large increases in BAL fluid lymphocyte counts. The increase was mainly due to an increase in OKT8+ suppressor cells. The group-B subjects with dyspnea showed diffuse irregular opacities on their chest X-rays and had a significant restrictive ventilatory impairment. Their BAL fluid contained a significant increase in bizarre giant cells, eosinophils, and lymphocytes with inverted OKT4/OKT8 ratios. One subject had a positive patch test for cobalt. The other three group-B subjects had only a slight increase in BAL fluid lymphocyte counts. The concentrations of cobalt, tungsten, and tantalum in the biological samples from all subjects were highest in those with the longest exposures and not related to symptomatology. The authors conclude that immunological mechanisms may be involved in the pathogenesis of respiratory diseases in hard metal workers. The more severe pathological changes seen in group-B subjects reflect the higher risk associated with exposure to coolant fluids as well as hard metals.