A case of chlamydial septicemia--Quebec.
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Biomedical subjects
Publications and source records attributed to S Péloquin.
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To investigate further the relationships of asbestos exposure, cigarette smoking, and airflow limitation, we have obtained detailed pulmonary function tests (PFT) in 331 long-term Canadian chrysotile workers, 34 of whom were lifetime nonsmokers. Three disease categories were defined on the bases of standard diagnostic criteria, gallium-67 lung uptake, and the lung pressure-volume curve. Category A was composed of workers without changes suggestive of alveolitis or asbestosis. There were eight nonsmokers (ns), among whom we found a statistically significant 30% reduction in airflow conductance (Gus) at low lung volume, which is consistent with the concept of an asbestos airway lesion. The 85 smokers (sm) of category A had reduction of Gus at both high and low lung volumes. Category B was composed of workers without asbestosis but with evidence of asbestos alveolitis. In the six ns, Gus was significantly reduced to 50% normal at low lung volume. The 59 sm had reduction of Gus at both high and low lung volumes but less severely than sm in category A. Category C was composed of workers with asbestosis. The 20 ns had restrictive pattern of lung function, and Gus was decreased to 39% normal at 50% TLC. The 153 sm in C had airflow reduction comparable to sm in B. We concluded that asbestos exposure, which leads to asbestos airway disease, asbestos peribronchiolar alveolitis, and asbestosis, causes airflow limitation at low lung volume but does not reduce the expiratory flow rates on the flow-volume curve in lifetime nonsmokers. In the smoking asbestos workers with alveolitis or asbestosis, the major component of airflow limitation is a smoking effect. In these smoking workers, rigidity of the lung lessens airflow obstruction associated with smoking at the expense of increased work of breathing.
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To study the clinical usefulness of computed tomography (CT) scanning of the thorax in asbestos related pleuropulmonary disease, 127 long term asbestos workers of the mines and mills in the Eastern Townships of Québec were examined. The CT scan was compared with the standard posteroanterior (PA) chest film and the four view films using the ILO grading system for profusion of disease. Six lung areas and six pleural sites were studied. On the basis of the usual diagnostic criteria, 41% of the workers had asbestosis. For profusion of parenchymal disease, there was an excellent correlation (r = 0.96, p less than 0.001) between PA and four view films and the latter did not significantly increase the total profusion score; the CT scan correlated less well with the PA film (r = 0.79, p less than 0.01) and the scatter of the data was larger. In 10 of the 53 (19%) workers with asbestosis the pulmonary lesions were not recognised by CT scan. For profusion of pleural plaques, there was an excellent correlation (p = 0.91, p less than 0.001) between PA and four view films; scores were identical in 73%, higher for PA in 7%, and higher for four view films in 19%. CT scan scores, however, were identical with PA films in 31%, higher for CT scan in 13% (owing to higher scores on lateral pleural sites), and lower for CT scan in 56% (owing to lower scores at diaphragm and costophrenic angle sites). Pleural calcifications were identified in 24 workers for a total of 40 sites; 13 as possible, 31% identified by two modes, and 27 as definite. Of the latter, 14 were seen only on CT scan. In the workers with rigid pressure volume curve of the lung and increased Gallium-67 lung uptake only, CT scan total scores were not significantly higher than in those without these markers of early interstitial lung disease (5 +/- 1 v 4 +/- 1, p less than 0.05). Thus the four view films and CT scan appear to be useful mainly in the assessment of pleural disease. The four view film identifies more sites of pleural plaques and the CT scan more pleural calcified plaques.
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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.