Robert Boileau

Airway function in lifetime-nonsmoking older asbestos workers

Previous studies of lung function in asbestos workers have documented airflow limitation in many of the workers, but the specific influence of asbestos exposure could not be clearly differentiated from the effects of the cigarette smoking habit. In this study, airway function was evaluated in lifetime-nonsmoking, long-term workers of the mines and mills of Québec. The 17 asbestos workers in this study had worked for an average of 28 years in the mines and mills of the local asbestos industry and did not have any other respiratory industrial dust exposure. They did not have a history of previous pulmonary disease and did not meet the usual diagnostic criteria for chronic bronchitis, emphysema, or asthma. Seven of the workers met the diagnostic criteria for asbestosis and 10 workers did not. The latter group of workers did not differ from a matched control group except in terms of a higher isoflow volume (p less than 0.05). The workers with asbestosis, however, had a restrictive pattern of lung function, increased isoflow volume, and increased upstream resistance at low lung volumes (p less than 0.01). Lung biopsy in three of the patients with the disease demonstrated peribronchiolar alveolitis and fibrosis with obliteration and narrowing of the small airways. These data on lifetime-nonsmoking, long-term asbestos workers provide further evidence of small airway obstruction associated with asbestos exposure and independent of the smoking habit. This airflow limitation was observed predominantly in workers with a restrictive pattern of lung function associated with peribronchiolar alveolitis. The lifetime-nonsmoking asbestos workers without restrictive patterns of lung function had minimal dysfunction of the peripheral airways.

Enzyme activities of lung lavage in asbestosis.

We analyzed lung lavage supernatant for amylase, lactate dehydrogenase (LD), alkaline phosphatase (ALP), beta-glucuronidase (beta G), and albumin, and a differential count was made of the cellular component of lung lavage in 18 normal controls and 36 long-term asbestos workers of the mines and mills of Québec. The men were concomitantly evaluated by the usual clinical, radiological, functional parameters and 67Ga lung scan. In 7 workers without asbestosis and normal 67Ga scan, lavage enzyme activities, albumin and cell counts were comparable to those of controls. Of 9 without sufficient criteria for asbestosis but increased 67Ga lung uptake, cell counts documented significant increases in the mean number of macrophages (X 2), lymphocytes (X 2) and neutrophils (X 3). Supernatant analyses showed significant increases in amylase (X 4-5), LD (X 2.5), ALP (X 1.5) and beta G (X 2-4). These changes were comparable to those in the lavage of workers with well established asbestosis except that in the latter, the lymphocyte count was slightly lower but the neutrophil count higher (p less than 0.05). These data document that enzyme activities of lung lavage can differentiate asbestos workers with early or late asbestosis from controls and asbestos workers without disease.

Elevated histamine content of lung lavage in human asbestosis

Increased histamine levels in lung lavage have been previously reported in humans with idiopathic fibrosing alveolitis and mast cell proliferation was documented on lung tissue. Similarly, mast cell proliferation has been documented in experimental asbestosis. To evaluate the relevance of these observations to human asbestosis, we performed bronchoalveolar lavage in 10 normal volunteers (group N) and 22 long-term asbestos workers from the mines and mills of Quebec. The 22 asbestos workers were evaluated by standard clinical, functional, radiographic, and gallium-67 lung uptake tests. Five did not have any abnormality suggestive of asbestosis and constituted group A. The 6 in group B were without sufficient criteria for well-established asbestosis, but their lung pressure-volume curve was rigid and67Ga lung uptake was increased; the 11 in group C had well-established asbestosis. In addition to standard parameters of BAL cellularity and biochemistry, we measured histamine levels by fluorometric method. In normals, histamine levels were 1.0 ± 0.3 ng/ml, in group A 1.25 ± 0.37 ng/ml (NS), in group B 2.26 ± 0.86 ng/ml (P < 0.05 B vs A or N), and in group C it was 2.65 ± 0.44 ng/ml (P < 0.05 C vs A or N). BAL eosinophils were absent in normals and group A, 272 ± 136/ml in group B, and 764 ± 350 in group C (P < 0.05 for groups B and C vs normals and group A), but did not correlate with histamine content of BAL. This study provides evidence of an elevated content of histamine in the bronchoalveolar milieu of patients with early and late asbestosis. This finding is of interest in relation to the potential role of the mast cell in the disease process.