Development of radiological and clinical evidence of parenchymal fibrosis in men with non-malignant asbestos-related pleural lesions

Our plain-English summary of Development of radiological and clinical evidence of parenchymal fibrosis in men with non-malignant asbestos-related pleural lesions, by G.H. McMillan, C.E. Rossiter (British Journal of Industrial Medicine, 1982).

The study

• Authors: G.H. McMillan, C.E. Rossiter
• Journal: British Journal of Industrial Medicine
• Published: 1982;39(1):54-9
• Cited by: 30 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text
• In J-M's library: Johns-Manville's company medical library held a copy (J-M no. 000694).

Abstract

After assessment of radiographs taken in 1966, 201 men employed at HM Dockyard, Devonport, were judged to have pleural abnormalities due to exposure to asbestos but to be free from small opacities (ILO U/C 1971 category 1/1 or more), mesothelioma, or bronchial carcinoma. By 1976, 32 of these men had died. Of the survivors, 155 were re-examined to determine the attack rates of parenchymal fibrosis or malignant disease, or both. In 1976, 16 (10.3%) of the survivors had radiographs showing small opacities of category 1/1 or more. When additional clinical criteria had to be satisfied before a diagnosis of parenchymal fibrosis was made the attack rate in the survivors was 4.5%. These attack rates were substantially higher than those observed in a sample of men with no initial pleural abnormality but were unrelated to age, smoking habit, occupation, duration of exposure to asbestos, or type of pleural abnormality. The number of cases of malignant disease was too small to allow any reliable conclusions.

In plain English

The authors followed men at HM Dockyard, Devonport, whose 1966 X-rays showed asbestos-related pleural plaques or diffuse pleural thickening but no small opacities of category 1/1 or more, mesothelioma or bronchial carcinoma. Of 201 such men, 155 survivors were re-examined in 1976. Another 20 who died had been examined within 12 months before death. Exposure was assessed from job histories, not measurements. By 1976, 16 (10.3%) of the 155 survivors showed small opacities of category 1/1 or more. Counting the dead, the figure was 23 of 175 (13.1%). Seven (4.5%) survivors met stricter fibrosis criteria. These added persistent basal crackles and gas transfer below 75% of predicted, without significant airway obstruction. This contrasted with 0.6% among 971 dockyard men with neither pleural nor parenchymal lesions in 1966, though the authors cautioned the groups differed in important ways. Lesion type, age, smoking and occupation did not appear to determine who developed opacities. Among the dead, three had mesothelioma (2 pleural, 1 peritoneal) and one bronchial carcinoma, too few for conclusions. The authors concluded that pleural lesions may identify men at greatest risk of parenchymal fibrosis.

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: 10-year follow-up study comparing 1966 and 1976 chest radiographs, with clinical examination and lung function tests in 1976. Results were compared with a separate, earlier-studied sample of dockyard men without pleural or parenchymal lesions.
• Who was studied: 201 men employed at HM Dockyard, Devonport, whose 1966 radiographs showed asbestos-related pleural lesions without small opacities of category 1/1 or more, mesothelioma, or carcinoma. By pleural lesion type: 133 uncalcified pleural plaques, 27 calcified plaques, 13 diffuse pleural thickening, 28 diffuse thickening with plaques. Of the 169 alive in 1976, 155 (92%) were re-examined. Twenty of the 32 who had died had an examination within 12 months before death, so 175 men were analysed.
• Exposure: Occupational exposure to asbestos dust at the dockyard, assessed from a detailed occupational history. No actual exposure measurements were available and no fiber type is specified. Survivors were grouped by occupation, from group 1 (greatest risk, for example laggers and asbestos sprayers) to group 3 (lowest risk).
• Main results:
  • In 1976, 16 (10.3%) of the 155 surviving men had radiographs showing small opacities of category 1/1 or more.
  • Including men who died with a pre-death examination, 23 (13.1%) of 175 reached small opacities of category 1/1 or more (16 survivors, 7 dead).
  • Seven (4.5%) of the 155 responders met strict criteria for asbestos-induced parenchymal fibrosis. The criteria were small opacities 1/1 or more agreed by at least two readers, persistent basal crackles, and gas transfer below 75% of predicted value in the absence of significant airway obstruction.
  • In a separate large random sample from the same dockyard (971 men with neither pleural nor parenchymal lesions in 1966), the attack rate of clinically confirmed parenchymal fibrosis was 0.6%.
  • Small opacities 1/1 or more by 1966 pleural lesion type: 15 (12.8%) of 117 men with simple plaques; 6 (23.1%) of 26 with calcified plaques; none of the 9 with diffuse thickening only; 2 (8.7%) of 23 with diffuse thickening and plaques.
  • Twenty (87%) of the 23 men who developed small opacities had a smoking history, compared with 85% of the 152 who did not. The authors reported this difference as not statistically significant.
  • Among survivors, small opacities occurred in 5.5% of exposure group 1, 9.1% of group 2 and 15.8% of group 3. The authors attributed the low group 1 rate to selection: many heavily exposed men already had small opacities by 1966 and were excluded.
  • No mesothelioma or bronchial carcinoma was found among the responders. Among the dead, three had mesothelioma (2 pleural, 1 peritoneal) and one died from bronchial carcinoma.
• The authors' conclusion: The authors concluded that asbestos-related pleural lesions may not be merely markers of previous exposure but may identify those at greatest risk of developing parenchymal fibrosis. They also stated that type of pleural lesion, time since first exposure, occupation, age and smoking habit did not appear to determine which men were affected.
• Limitations the authors state:
  • The authors said the comparison with men without pleural lesions strengthens but does not confirm their view. The two groups differed in occupational mix, proportion of non-smokers, and duration of exposure (about four years shorter in the larger sample).
  • The comparison sample was screened with 100-mm radiographs, so some cases of small opacities were likely missed, though the authors thought it unlikely these included any of category 1/1 or more.
  • There was significant inter-reader variation in reading small opacities: reader 2 read significantly more cases. The authors therefore used the agreed reading of at least two of the three readers.
  • Actual exposure measurements were not available.
  • No firm conclusions could be drawn for the diffuse thickening only group, which had only nine men.
  • The numbers of mesothelioma (3) and bronchial carcinoma (1) were too small to establish a relationship with benign pleural lesions.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis, Pleural plaques and thickening.

Medical terms in this study, explained in our Lexicon: Parenchymal Fibrosis, Mesothelioma, Carcinoma, Habit.

Related studies

• Comparison of independent randomised reading of radiographs with direct progression scoring for assessing change in asbestos-related pulmonary and pleural lesions — G.H. McMillan, C.E. Rossiter, et al. (1982)
• Effect of smoking on attack rates of pulmonary and pleural lesions related to exposure to asbestos dust — G.H. McMillan, R.J. Pethybridge, et al. (1980)
• Parenchymal and pleural fibrosis in construction workers — P. Oksa, H. Koskinen, et al. (1992)
• Development, radiological zone patterns, and importance of diffuse pleural thickening in relation to occupational exposure to asbestos — H. Bohlig, A. Calavrezos (1987)
• Radiological characteristics, histological features and clinical outcomes of lung cancer patients with coexistent idiopathic pulmonary fibrosis — K.A. Khan, M.P. Kennedy, et al. (2015)
• Radiological changes in asbestos cement workers — K. Jakobsson, U. Strömberg, et al. (1995)

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