Pleuropulmonary disease among asbestos workers in relation to smoking and type of exposure

Our plain-English summary of Pleuropulmonary disease among asbestos workers in relation to smoking and type of exposure, by W. Weiss, P.A. Theodos (Journal of Occupational Medicine., 1978).

The study

• Authors: W. Weiss, P.A. Theodos
• Journal: Journal of Occupational Medicine.
• Published: 1978;20(5):341-5
• Cited by: 22 articles, as counted by NIH iCite
• Read it: PubMed
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 002158).

Abstract

The chest roentgenograms of employees aged 40 and over in two asbestos manufacturing plants were read by consensus without knowledge of the plant or smoking habits. Plant A used only chrysotile asbestos throughout its history and Plant B used amosite as well as chrysotile, the amosite being limited to the period 1950-64. The prevalence of pulmonary disease was 25% in Plant A and 33% in Plant B. The prevalence of pleural thickening was 18% in Plant A and 35% in Plant B. Neither age nor work duration were factors in these differences. In Plant A there was no obvious relationship between smoking and pleuropulmonary disease. In Plant B there was a definite relationship of smoking to pulmonary disease and perhaps to pleural thickening. Both type of asbestos and smoking habits appear to be determinants of pleuropulmonary disease in asbestos workers.

In plain English

This was a chest X-ray survey of men aged 40 or over at two asbestos products plants: 40 men in Plant A, which used only chrysotile, and 48 in Plant B, which also used amosite from 1950 to 1964. The authors read the 1975 films together by consensus, without knowing each man's plant or smoking habits. Pulmonary disease was seen in 25% in Plant A and 33% in Plant B, and pleural thickening in 18% and 35%. Because of small numbers, these differences were not statistically significant. In Plant A no relationship with smoking was found. In Plant B, pulmonary disease was absent in the ten nonsmokers but occurred in one-third of exsmokers and almost half of current smokers, a statistically significant relationship. Pleural thickening in Plant B was seen in one nonsmoker and in 42% of exsmokers and current smokers (P = 0.074, not quite significant). The authors called their conclusions tentative. They suggested amosite may be more potent than chrysotile, and that smoking must be seriously considered as a cause or a confounding factor in disease from amosite, but perhaps not chrysotile.

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 chest X-ray (roentgenogram) survey of employees. Both authors classified the films together by consensus under the ILO scheme, without knowledge of smoking habits or plant.
• Who was studied: Men aged 40 or over employed at two asbestos products manufacturing plants: 40 in Plant A and 48 in Plant B. Chest films and smoking histories came from the 1975 annual survey. The plants' location is not stated.
• Exposure: Plant A used only chrysotile asbestos. Plant B used chrysotile plus amosite, with the amosite limited to 1950-64. Products included asbestos papers, millboard, textiles, sheet packing, molded thermal insulation and asbestos cement boards. Exposure was also analysed by cigarette smoking habit. No fiber counts were made before 1972; recent counts were generally under 2 fibers per cubic centimetre.
• Main results:
  • Pulmonary disease was found in 25% of men in Plant A and 33% of men in Plant B.
  • Pleural thickening was found in 18% of men in Plant A and 35% of men in Plant B.
  • The differences between the two plants were not statistically significant at the 0.05 level, because of small numbers.
  • In Plant A there was no discernible relationship between smoking and disease.
  • In Plant B, pulmonary disease was absent in the ten nonsmokers but occurred in one-third of exsmokers and almost half of current smokers. This relationship was statistically significant (chi square 6.92, P less than 0.05).
  • In Plant B, pleural thickening was seen in only one of the nonsmokers and in 42% of the exsmokers and current smokers combined. This difference was not quite statistically significant (P = 0.074 by Fisher's exact test).
  • Pleuropulmonary disease occurred mainly in men who had worked at the plants 20 years or more. Only nine men with disease had worked less than 20 years. All nine were aged 42 or over and might have been exposed elsewhere before hire.
• The authors' conclusion: The authors concluded that their data suggest amosite may be more potent than chrysotile in producing both pleural and pulmonary asbestos-related disease. They also concluded that smoking must be seriously considered as an etiologic (causal) or confounding factor in the prevalence of disease due to amosite exposure, but perhaps not chrysotile. Elsewhere they raised the possibility that smoking merely produces disease that is confused with asbestos-related disease.
• Limitations the authors state:
  • Small numbers of employees, which the authors said makes the conclusions tentative.
  • No quantitative exposure measurements were available for the years when dust levels were high, because fiber counts began only in 1972.
  • On X-ray it was not possible to tell fibrosis caused by smoking from fibrosis caused by asbestos. The question of whether the two act independently or jointly therefore could not be answered.

Topics

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

Medical terms in this study, explained in our Lexicon: Habit, Chrysotile, Amosite, Pleural Thickening.

Related studies

• Insulation, asbestos, smoking habits, and lung cancer cell types — J.E. Muscat, S.D. Stellman, et al. (1995)
• Smoking and duration of asbestos exposure in the production of functional and roentgenographic abnormalities in shipyard workers — J.L. Pearle (1982)
• Pleural plaques and cigarette smoking in asbestos workers — W. Weiss, R. Levin, et al. (1981)
• Cigarette smoking, asbestos, and pulmonary fibrosis — W. Weiss (1971)
• Combined effect of asbestos exposure and smoking on mortality from lung cancer in factory workers — G. Berry, M.L. Newhouse, et al. (1972)
• Lung function and exercise performance in smoking and nonsmoking asbestos-exposed workers — D.Y. Sue, A. Oren, et al. (1985)

Browse more research in Journal of Occupational Medicine., or return to medical research.