Royal Naval dockyards asbestosis research project: nine-year follow-up study of men exposed to asbestos in Devonport Dockyard

Our plain-English summary of Royal Naval dockyards asbestosis research project: nine-year follow-up study of men exposed to asbestos in Devonport Dockyard, by C.E. Rossiter, J.R. Heath, P.G. Harries (Journal of the Royal Society of Medicine, 1980).

The study

• Authors: C.E. Rossiter, J.R. Heath, P.G. Harries
• Journal: Journal of the Royal Society of Medicine
• Published: 1980;73(5):337-44
• Cited by: 15 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. 000857).

Abstract

Progression of asbestos-related disease was assessed in a group of 253 dockyard workers examined in 1966 and 1975. Despite the almost complete protection from exposure to asbestos since 1966, radiographic parenchymal abnormalities increased and occurred more frequently during the next 9 years in those men who had been more heavily exposed to asbestos. Lung function values were lower in those most heavily exposed and were declining at a faster rate than in those with less dust exposure. The most sensitive lung function index was the transfer factor.Those men with persistent crackles in 1966 exhibited a restrictive pattern of lung function, whereas an obstructive pattern was seen in men with wheezes in 1966. The men with irregular small opacities of category 1/1 or more or with diffuse pleural change in 1966 and who survived to 1975 had worse lung functions than any other groups.Progression of disease was greater for smokers than non-smokers, with those who gave up smoking between 1966 and 1975 suffering the greatest changes. This latter group showed most increase in small opacities and included almost all new cases of diffuse pleural changes. They also showed the greatest declines in forced expiratory volume and forced vital capacity.

In plain English

This follow-up study re-examined Devonport Dockyard workers first studied in 1966, who had been effectively removed from further asbestos exposure from then. Of 369 men analysed in 1966, 43 died, 268 were re-examined in 1975, and 253 had complete data. Men were grouped by job, from asbestos sprayers and laggers to trades intermittently exposed near asbestos work. Small lung opacities on X-ray (category 1/1 or more) rose from 2% to 11% of all men, and from 7% to 33% among sprayers. Diffuse pleural thickening also increased, almost entirely among the 27 men who stopped smoking between the surveys (7% to 30%). Lung function was lowest in sprayers and laggers, and the transfer factor showed the largest differences. In 1975, 62% of sprayers had breathlessness of MRC grade 3 or worse (breathless walking with people of the same age on level ground), against 8% of the intermittently exposed group. Among all 420 originally selected men, 49 died between the surveys, 3 of them from mesothelioma, and more deaths than expected occurred in the three most exposed groups. The authors said these numbers were too small for firm conclusions. The authors reported that disease progressed more in smokers than in non-smokers.

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: Follow-up study: the same men were examined in 1966 and again in 1975, after exposure had largely stopped. Each examination included chest X-rays, a questionnaire, a physical examination and lung function tests.
• Who was studied: Men at Devonport Dockyard (Plymouth, UK). 420 were selected in 1966 and 369 were analysed in 1966. Of the 326 still alive by 1975, 268 (82%) were re-examined and 253 had complete data. The 253 were 29 sprayers (group I), 72 laggers (group II), 28 asbestos storemen, sailmaker laggers and asbestos masons (group III), and 124 men in various trades intermittently exposed (group IV).
• Exposure: Asbestos dust from spraying, lagging, asbestos stores, asbestos cloth used by sailmaker laggers, asbestos cement and flooring material used by masons, and intermittent exposure near these workers. Fiber types are not named. The men were effectively removed from further exposure from the 1966 survey onward.
• Main results:
  • Small opacities of category 1/1 or more rose among all 253 men from 2% (1966) to 11% (1975). The rise was 7% to 33% among sprayers and 3% to 19% among laggers (Table 5).
  • The rise in small opacities was greatest among the 27 men who gave up smoking between 1966 and 1975 (4% to 33%). It also rose among continuing smokers (2% to 12%), but not among the remaining men (Table 6).
  • Diffuse pleural thickening rose most among sprayers (3% to 17%) and laggers (1% to 10%). The increase was almost exclusively among the 27 men who gave up smoking after 1966 (7% to 30%).
  • Pleural plaques did not increase much overall, but 7 of the 35 men with plaques in 1966 developed diffuse pleural changes by 1975. Among smokers, plaque prevalence rose from 10% to 23%.
  • In 1975, breathlessness of MRC grade 3 or worse was reported by 62% of sprayers, 26% of laggers, 11% of group III and 8% of group IV. Grade 3 means being breathless when walking with people of the same age on level ground. Crackles were recorded in 48% of sprayers. Breathlessness, crackles and finger clubbing were most common in groups I and II.
  • Wheezes did not follow the exposure pattern. They were significantly related to smoking (p less than 0.05): wheezes were found in 13% of smokers and in no non-smokers.
  • The transfer factor showed greater differences than any other lung function index. It was lowest in group I (8.28 in 1966 and 7.69 in 1975, mmol/min/kPa) and highest in group IV (9.30 and 8.94).
  • The 7 men with both persistent crackles and wheezes in 1966 showed a decline in forced vital capacity of over 90 ml per year, four times the expected decline.
  • The 6 men with diffuse pleural thickening in 1966 had the greatest reduction in lung function: reduced transfer factor, raised residual volume, and low total lung capacity and forced vital capacity.
  • Among all 420 men in the original study, 49 died between 1966 and 1975. Deaths included 6 from asbestosis, 3 from mesothelioma and 8 from lung cancer (Table 8). Table 8 gives expected deaths of 9.7, 9.7, 4.9 and 19.2 for groups I to IV. More deaths than expected occurred in groups I to III, while group IV had 14 deaths against 19.2 expected. Among laggers, 7 of 14 deaths were associated with asbestos.
• The authors' conclusion: The authors concluded that, despite almost complete protection from exposure since 1966, X-ray abnormalities increased more in the more heavily exposed men. They found that lung function was lower and declining faster in those men. They also concluded that disease progressed more in smokers than non-smokers, with the largest changes in men who gave up smoking between the surveys.
• Limitations the authors state:
  • Death numbers were small and the 9-year period too short for firm conclusions about the pattern of deaths.
  • Observer variation and the intermittent nature of crackles and wheezes probably explained why these signs appeared and disappeared between the surveys.
  • Several men who had symptoms or signs in 1966 died before 1975 and were not included in the comparison.
  • There were too few men with diffuse pleural thickening (6) to draw firm conclusions about their residual volume to total lung capacity ratio.

Topics

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

Medical terms in this study, explained in our Lexicon: Obstructive Lung Disease.

Related studies

• UK Naval Dockyards asbestosis study: survey of the sample population aged 50-59 years — C.E. Rossiter, P.G. Harries (1979)
• UK Naval Dockyards Asbestosis Study: radiological methods in the surveillance of workers exposed to asbestos — G. Sheers, C.E. Rossiter, et al. (1978)
• The health of welders in naval dockyards. The risk of asbestos-related diseases occurring in welders — G.H. McMillan (1983)
• Protection of dockyard workers against asbestosis — P.G. Harries (1970)
• Correlation between fibre content of the lungs and disease in naval dockyard workers — J.C. Wagner, C.B. Moncrieff, et al. (1986)
• Asbestos-associated disease in employees of Devonport Dockyard — G. Sheers (1979)

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