Radiographic abnormalities in asbestos insulators: effects of duration from onset of exposure and smoking. Relationships of dyspnea with parenchymal and pleural fibrosis

Our plain-English summary of Radiographic abnormalities in asbestos insulators: effects of duration from onset of exposure and smoking. Relationships of dyspnea with parenchymal and pleural fibrosis, by R. Lilis, A. Miller, J. Godbold, et al (American Journal of Industrial Medicine, 1991).

The study

• Authors: R. Lilis, A. Miller, J. Godbold, E. Chan, I.J. Selikoff
• Journal: American Journal of Industrial Medicine
• Published: 1991;20(1):1-15
• Cited by: 38 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. 004915).

Abstract

Chest radiographs and spirometry were evaluated in 2,907 active and retired asbestos insulators; most (86.8%) had greater than or equal to 30 years from onset of asbestos exposure. Testing was performed in 19 cities in the United States during 1981-1983. Complete demographic, smoking, clinical, and radiologic data were obtained for 2,790 workers. This is the largest single group of insulators that has been studied. Five hundred forty-eight (19.7%) had never smoked cigarettes, 942 (33.9%) were current cigarette smokers, and 1,300 (46.6%) were ex-smokers. Only 439 (15.7%) workers had no radiographic evidence of asbestos-related disease (normal chest X-ray); 668 (23.9%) had pleural fibrosis only, 325 (11.6%) had parenchymal fibrosis alone, and 1,358 (48.7%) had both parenchymal and pleural fibrosis. The prevalence of radiographic parenchymal changes increased significantly (p less than .001) from 38.6% (DURONSET less than 30 years) to 70% (greater than or equal to 40 years). For pleural changes the comparative prevalences were 55% and 82%. Those with no history of cigarette smoking were more likely to have normal films than those with a history of smoking (19.2% versus 14.4% for current smokers and 15.2% among ex-smokers), and were less likely to have parenchymal fibrosis (44.5% versus 69.7% for current smokers and 60.2% of ex-smokers). Dyspnea, MRC grade 3 and higher, was more prevalent when pleural fibrosis was associated with interstitial pulmonary fibrosis (at all profusion levels of small opacities) than when pleural fibrosis was absent. Logistic regression analysis of factors contributing to such dyspnea showed that the presence of combined parenchymal and pleural abnormalities was a significant explanatory variable, in addition to age, smoking, and body mass (Quetelet index); the presence of parenchymal changes only or of pleural changes only, as factors contributing to dyspnea, did not reach the level of statistical significance in the regression analysis. The results of these examinations show that pleural fibrosis is a frequent finding in asbestos-exposed groups with long-term follow-up and that its functional significance is not negligible. The contribution of cigarette smoking to prevalence and severity of interstitial fibrosis is an additional reason for smoking cessation among asbestos-exposed individuals.

In plain English

This cross-sectional study examined chest X-rays and shortness of breath in U.S. asbestos insulation workers from a union-based cohort. Examinations took place in 19 U.S. cities from November 1981 to November 1983; complete data were available for 2,790 of 2,907 workers examined. Of these, 15.7% had normal X-rays. Another 23.9% had pleural fibrosis only (scarring of the lung lining), 11.6% had parenchymal fibrosis only (scarring of lung tissue), and 48.7% had both. Parenchymal changes rose from 38.6% in workers under 30 years from first exposure to 69.7% in those at 40 years or more. Pleural changes rose from 55.4% to 82.4%. Never-smokers had parenchymal fibrosis less often than current smokers (44.5% versus 69.7%, though one table prints 69.1%). Smoking was not found to affect how often pleural changes appeared on X-ray. In a regression analysis, shortness of breath (MRC grade 3 or higher) was significantly linked with having both kinds of change together, along with age, smoking and body mass. It was not significantly linked with either kind alone. The authors concluded that pleural fibrosis contributes to shortness of breath.

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 study (chest X-rays, respiratory questionnaire and spirometry; spirometry results reported in a separate paper)
• Who was studied: Active and retired asbestos insulation workers from a cohort of insulation workers union members in the United States and Canada established January 1, 1967. 2,907 were examined in 19 U.S. cities from November 15, 1981 to November 24, 1983, and 2,790 had complete data for analysis. Of these, 548 had never smoked, 942 were current smokers and 1,300 were ex-smokers. Most had reached 30 years from onset of exposure. Another 384 who were under 30 years from onset, and so had not been invited, also took part.
• Exposure: Occupational asbestos exposure as insulation workers. Fiber types are not specified. Analyses used time since onset of exposure (less than 30, 30 to 39, and 40 or more years), years exposed, and cigarette smoking (pack-years).
• Main results:
  • Of all 2,790 workers, 439 (15.7%) had a normal chest X-ray, 325 (11.6%) had parenchymal changes only, 668 (23.9%) had pleural changes only, and 1,358 (48.7%) had both. In total, 72.6% had pleural abnormalities and 60.3% had parenchymal abnormalities.
  • Total parenchymal abnormalities rose with time from onset: 38.6% in workers under 30 years (N = 368), 61.1% at 30 to 39 years (N = 1,712) and 69.7% at 40 years and over (N = 710). Total pleural abnormalities rose from 55.4% to 72.3% to 82.4%. The test for trend gave p less than .001.
  • Normal chest X-rays were seen in 19.2% of non-smokers (105 of 548), 14.4% of current smokers (136 of 942) and 15.2% of ex-smokers (198 of 1,300). Parenchymal fibrosis was seen in 44.5% of non-smokers, 69.7% of current smokers and 60.2% of ex-smokers. The article gives two figures for current smokers. Its opening summary gives 69.7%, and the same figure can be worked out from Table V's component counts (154 parenchymal only plus 503 both = 657 of 942). Table V's total row prints 651 (69.1%).
  • Among workers with parenchymal abnormalities, profusion grade 2 or 3 (more advanced fibrosis) was compared between those with and without a smoking history. At 30 to 39 years from onset, it was found in 24.0% of those with a smoking history versus 3.9% of never-smokers (p less than .001). At 40 or more years, it was 32.2% versus 13.9% (p less than .001). The difference was not significant at under 30 years.
  • The prevalence of pleural abnormalities on X-ray did not differ significantly by smoking history. In regression analysis, smoking made no contribution to the prevalence of pleural abnormalities. Duration from onset of exposure was significant even with age in the model.
  • Among workers without radiologically detectable interstitial fibrosis, 60.3% (668 of 1,107) had pleural fibrosis.
  • Dyspnea of MRC grade 3 or higher was found in 24.0% (326 of 1,358) of workers with both parenchymal and pleural changes, versus 18.2% (59 of 325) of those with parenchymal changes only. By profusion category, the figures were 19.4% versus 17.7% (category 1), 34.5% versus 22.2% (category 2) and 49.4% versus 14.3% (category 3).
  • In logistic regression of dyspnea, age, pack-years of smoking and Quetelet index (body mass) were significant explanatory variables. Combined parenchymal and pleural abnormalities were also significant (p = .01). Parenchymal abnormalities only (p = .54) and pleural abnormalities only (p = .29) were not statistically significant.
• The authors' conclusion: The authors concluded that pleural fibrosis was a very frequent result of asbestos exposure, more frequent than parenchymal abnormalities even in this group. They concluded that cigarette smoking resulted in higher prevalence of interstitial fibrosis but had no effect on the prevalence of radiologically evident pleural fibrosis. They also concluded that pleural fibrosis contributes to dyspnea.
• Limitations the authors state:
  • The authors noted possible selection bias from non-participation. They checked it in two ways: by questioning a sample of 1,393 invited non-participants about their reasons, and by comparing mortality of participants and non-participants (reported elsewhere; no significant difference).
  • Duration from onset of exposure was very closely correlated with age (r = .79). Its effect on parenchymal changes appeared in the regression only after age was removed from the model.

Topics

Medical terms in this study, explained in our Lexicon: Insulator, Dyspnea, Fibrosis, Chest X-Ray, Spirometry, Asbestos Exposure, Parenchymal Fibrosis, Interstitial.

Related studies

• Spirometric impairments in long-term insulators. Relationships to duration of exposure, smoking, and radiographic abnormalities — A. Miller, R. Lilis, et al. (1994)
• Pulmonary function and pleural fibrosis: quantitative relationships with an integrative index of pleural abnormalities — R. Lilis, A. Miller, et al. (1991)
• Interaction of asbestos, age, and cigarette smoking in producing radiographic evidence of diffuse pulmonary fibrosis — K.H. Kilburn, R. Lilis, et al. (1986)
• Comparative quantitative evaluation of pleural fibrosis and its effects on pulmonary function in two large asbestos-exposed occupational groups--insulators and sheet metal workers — R. Lilis, A. Miller, et al. (1992)
• Relation of spirometric function to radiographic interstitial fibrosis in two large workforces exposed to asbestos: an evaluation of the ILO profusion score — A. Miller, R. Lilis, et al. (1996)
• Asbestosis: interstitial pulmonary fibrosis and pleural fibrosis in a cohort of asbestos insulation workers: influence of cigarette smoking — R. Lilis, I.J. Selikoff, et al. (1986)

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