Asbestos exposure, cigarette smoking, and airflow limitation in long-term Canadian chrysotile miners and millers

Our plain-English summary of Asbestos exposure, cigarette smoking, and airflow limitation in long-term Canadian chrysotile miners and millers, by R. Bégin, R. Boileau, S. Péloquin (American Journal of Industrial Medicine, 1987).

The study

• Authors: R. Bégin, R. Boileau, S. Péloquin
• Journal: American Journal of Industrial Medicine
• Published: 1987;11(1):55-66
• Cited by: 31 articles, as counted by NIH iCite
• Read it: PubMed · Publisher
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 000945).

Abstract

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.

In plain English

This study measured detailed lung function in 331 long-term workers from the chrysotile asbestos mines and mills of Quebec's Eastern Townships. All had been referred for workers' compensation evaluation and were seen at the authors' institution between 1982 and 1984. Thirty-four had never smoked. The comparison group was 21 never-smoking manual workers with no asbestos exposure. The authors sorted the workers into three groups: no signs of asbestos lung damage (A), asbestos-related alveolitis without asbestosis (B), and asbestosis (C).

Among never-smokers, airflow conductance at the lowest lung volume, as a share of the controls' average, was 70% in group A, 50% in group B and 38% in group C. Group C never-smokers also had smaller lung volumes. Among smokers, conductance was reduced at all lung volumes: to about 25% of normal in group A, and to 19% at low lung volume in group B. Group C smokers were similar to group B smokers.

The authors concluded that these asbestos conditions limit airflow at low lung volumes, increasingly with disease severity, without lowering standard spirometry flow rates, and that this effect adds to that of smoking. They noted they lacked suitable smoking controls and could not fully rule out other mine and mill dusts.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Cross-sectional comparison of pulmonary function tests between groups of asbestos workers (by disease category and smoking status) and unexposed nonsmoking controls
• Who was studied: 331 long-term Canadian chrysotile miners and millers aged 43 to 74, of whom 34 were lifetime nonsmokers and 297 smokers. They were selected from workers referred to the local Workmen's Compensation Committee and tested in 1982 to 1984. Ex-smokers, workers with known past lung disease and workers with incomplete evaluations were excluded. Controls were 21 lifetime nonsmoking manual workers without asbestos exposure.
• Exposure: Canadian chrysotile asbestos only, in the mines and mills of the Eastern Townships of Quebec, for an average of 36 years (range 20 to 45). The authors note that the mine and mill dust also contains other minerals, including tremolite and actinolite.
• Main results:
  • Category A nonsmokers (8 workers without signs of asbestos lung damage) differed from controls only at the lowest lung volume, where airflow conductance was reduced to 70% of normal (p less than 0.05).
  • Category A smokers (85 workers) had airflow conductance reduced at all lung volumes, to about 25% of normal (p less than 0.001 at all points).
  • Category B nonsmokers (6 workers with asbestos alveolitis but not asbestosis) had normal conductance at high lung volumes, but conductance was reduced by 50% at 50% of total lung capacity.
  • Category B smokers (59 workers) had airflow conductance of 62% of normal at 70% of total lung capacity and 19% of normal at 50% of total lung capacity.
  • Category B smokers had lower total lung capacity and functional residual capacity than category A smokers, but higher expiratory flow rates.
  • Category C nonsmokers (20 workers with asbestosis) had smaller lung volumes and lower diffusion capacity than controls. Their airflow conductance was 38% of normal at 50% of total lung capacity.
  • Category C smokers (153 workers with asbestosis) had reductions in airflow conductance comparable to those of category B smokers.
• The authors' conclusion: The authors concluded that asbestos airway disease, asbestos alveolitis and asbestosis cause airflow limitation at low lung volumes, which increases with the severity of the disease, but do not reduce spirometric expiratory flow rates. They concluded that this effect is cumulative with that of smoking.
• Limitations the authors state:
  • The study had no appropriate smoking controls, so it could not directly say whether the effect of smoking in asbestos workers is additive or multiplying.
  • The authors could not completely rule out that other dusts and pollutants in the mines and mills contributed to the airway lesion.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Chrysotile.

Medical terms in this study, explained in our Lexicon: Asbestos Exposure, Chrysotile, Pulmonary Function Test (PFT), Obstructive Lung Disease.

Related studies

• The combination of effects on lung cancer of cigarette smoking and exposure in quebec chrysotile miners and millers — F.D. Liddell, B.G. Armstrong (2002)
• Long-term mortality experience of chrysotile miners and millers in Thetford Mines, Quebec — W.J. Nicholson, I.J. Selikoff, et al. (1979)
• Severe diffuse small airways abnormalities in long term chrysotile asbestos miners — J.L. Wright, A. Churg (1985)
• Mortality in Canadian miners and millers exposed to chrysotile — J.C. McDonald, F.D. Liddell (1979)
• Radiographic changes in a group of chrysotile miners and millers exposed to low asbestos dust concentrations — S. Cordier, G. Theriault, et al. (1984)
• Combined effect of asbestos exposure and tobacco smoking on Finnish anthophyllite miners and millers — L.O. Meurman, R. Kiviluoto, et al. (1979)

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