Cigarette smoke, asbestos, and small irregular opacities

Our plain-English summary of Cigarette smoke, asbestos, and small irregular opacities, by W. Weiss (The American Review of Respiratory Disease, 1984).

The study

• Author: W. Weiss
• Journal: The American Review of Respiratory Disease
• Published: 1984;130(2):293-301
• Type of article: Review
• Cited by: 87 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. 000585).

Abstract

The long-term inhalation of cigarette smoke is associated with the appearance of diffuse small irregular opacities of mild profusion on chest roentogenograms of some subjects in a limited number of reports. Human histologic and experimental animal studies have shown the presence of pulmonary interstitial fibrosis. The radiographic abnormalities may be explained by interstitial fibrosis, although bronchiolar wall thickening may also be involved. Because asbestos causes diffuse pulmonary fibrosis, the literature was reviewed for evidence concerning an interaction between cigarette smoke and asbestos in the frequency of pulmonary asbestosis. A majority of 14 prevalence studies and 7 cohort studies of asbestos workers with information on smoking habits have shown a positive interaction between the 2 agents. The interaction appears to be additive rather than synergistic. Smoking may exert an effect on the frequency of pulmonary asbestosis by increasing the effective fiber dose retained in the lungs through interference with clearance.

In plain English

This was a review article. It examined published evidence that long-term cigarette smoking can scar the lungs (fibrosis), and whether smoking affects how often asbestos workers develop asbestosis. The author reported that a limited number of reports linked long-term smoking to mild small irregular opacities (fine shadows) on chest X-rays. The review covered 14 prevalence studies and 7 cohort studies of asbestos workers that had smoking information. Most showed asbestosis more often in smokers than in nonsmokers. The author tested the prevalence studies that were set out in tables and found their results varied too much to be combined statistically. In the largest survey, of 23,340 British dockyard workers, suspected or definite pulmonary fibrosis was found in 0.2% of nonsmokers, 0.8% of ex-smokers and 1.1% of current smokers. Studies of Quebec chrysotile miners did not show this pattern. The author concluded that the interaction appeared additive rather than synergistic. Smoking might act by increasing the fiber dose retained in the lungs. The author noted that differences in cumulative asbestos exposure between smokers and nonsmokers could have confounded the results.

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: Literature review ("State of the Art" article)
• Who was studied: Published studies: 14 prevalence studies and 7 cohort studies of asbestos workers with smoking information (including shipyard and dockyard workers, insulators, textile and factory workers, and miners in Quebec and Italy), plus earlier autopsy, animal and X-ray studies of smoking and lung fibrosis
• Exposure: Cigarette smoking combined with asbestos exposure. The studies involved chrysotile, amosite, crocidolite and mixtures; the Quebec and Italian miners were exposed to chrysotile only and the Paterson factory workers to amosite only
• Main results:
  • From the studies reviewed, the author reported that long-term cigarette smoking was associated with mild small irregular opacities on chest X-rays of some subjects, in a limited number of reports
  • Most prevalence studies showed small irregular opacities more often in asbestos workers who smoked than in those who did not
  • Among the tabulated prevalence studies, the smoker-to-nonsmoker prevalence ratios were above 1.00 except in the Selikoff study of shipyard workers and the Liddell study of Quebec miners
  • In the total-population survey of British dockyard workers (Harries 1976), crude prevalence of suspected or definite pulmonary fibrosis was 0.2% of nonsmokers, 0.8% of ex-smokers and 1.1% of current smokers
  • In the same dockyard survey, current smokers had the highest rate and nonsmokers the lowest at every duration of asbestos exposure
  • In the cohort studies, smoker-to-nonsmoker rate ratios were above 1.00 except for the Quebec chrysotile miners and the Paterson amosite factory workers
  • The cohort studies with statistically significant elevations of rate ratios all involved exposure to mixtures of asbestos types
  • The author judged the interaction between smoking and asbestos to appear additive rather than synergistic
  • The author suggested that smoking may increase the effective fiber dose retained in the lungs
• The authors' conclusion: The author concluded that most human radiographic studies reviewed were consistent with the hypothesis that cigarette smoking causes radiographically visible lung fibrosis and influences how often asbestosis occurs, and that further studies are needed to explain the few discrepant results
• Limitations the authors state:
  • The results reviewed may be confounded by differences in cumulative asbestos exposure between smokers and nonsmokers, and such exposure data were generally unavailable
  • The studies varied considerably in method, especially in how asbestosis was defined
  • A heterogeneity test showed that the results of the tabulated prevalence studies varied too much to be pooled
  • It is uncertain whether small irregular opacities in smokers reflect bronchiolar wall changes or interstitial fibrosis
  • The separate contribution of smoking and asbestos during combined exposure cannot be assessed with current knowledge

Topics

Medical terms in this study, explained in our Lexicon: Interstitial Fibrosis, Pulmonary Fibrosis, Asbestosis, Habit.

Related studies

• Cigarette smoke increases the penetration of asbestos fibers into airway walls — D. McFadden, J. Wright, et al. (1986)
• Effects of cigarette smoke and asbestos on airway, vascular and mesothelial cell proliferation — H. Sekhon, J. Wright, et al. (1995)
• Cigarette smoke makes airway and early parenchymal asbestos-induced lung disease worse in the guinea pig — V. Tron, J.L. Wright, et al. (1987)
• Synergistic effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor by alveolar macrophages of rats — Y. Morimoto, M. Kido, et al. (1993)
• Retinoid signaling and activator protein-1 expression in ferrets given beta-carotene supplements and exposed to tobacco smoke — X.D. Wang, C. Liu, et al. (1999)
• Cigarette smoke potentiates asbestos-induced airflow abnormalities — J.L. Wright, V. Tron, et al. (1988)

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