Asbestos lung residue and asbestosis risk

Our plain-English summary of Asbestos lung residue and asbestosis risk, by A. Rogers (The Annals of Occupational Hygiene, 2005).

The study

• Author: A. Rogers
• Journal: The Annals of Occupational Hygiene
• Published: 2005;49(4):363-4; author reply 364-5
• Type of article: Comment, Letter
• Cited by: 1 article, as counted by NIH iCite
• Read it: PubMed · Publisher

In plain English

This item is a letter to the editor, not a research study, followed by the first part of a reply. The letter's author criticised a 2005 article by Howie that applied a lung clearance model, in a court case, to a plaintiff's lung fibre count. The letter stated that amphiboles stay in the lungs in excess quantities decades after exposure, while chrysotile is cleared relatively rapidly. It also stated that more than 50 published case series report tens to hundreds of millions of fibres per gram of dry tissue in the lungs of people with asbestosis. The letter pointed out that Howie's model needed 2000 fibre-years per ml of amosite over 1943 to 1979 to produce 0.61 million amosite fibres per gram, and said this showed the absurdity of the model. In the reply, the author of the original article accepted that such lungs can hold many millions of fibres per gram. That author argued, from Churg and Vedal (1994) data, that the plaintiff's amosite level lay within the statistical range for asbestosis and airway fibrosis. The reply text is cut off.

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: letter to the editor (commentary on a published article), with the start of a reply from the original article's author; not an original study
• Who was studied: No study population. The letter discusses a single plaintiff in a court case, whose lung fibre content was analysed by a UK laboratory and modelled by Howie (2005).
• Exposure: Amosite, chrysotile, tremolite, amphiboles generally and mixed asbestos types. The letter centres on the modelled cumulative airborne amosite exposures in Howie's clearance model. The reply refers to a plaintiff exposure of 40 fibre-years per ml.
• Main results:
  • The letter's author stated, citing Churg (1991), that excess amphiboles remain in the lungs decades after exposure ends, while chrysotile is cleared relatively rapidly, though a few long fibres and fibrils remain.
  • The letter's author stated that more than 50 published case series report tens of millions to hundreds of millions of asbestos fibres per gram of dry tissue in the lungs of asbestotics, even many decades after exposure.
  • According to the letter, the UK laboratory in the case reported that asbestosis is generally associated with lung fibre levels above 50 million fibres per gram of dry tissue. The letter's author said this is well above the plaintiff's value.
  • According to the letter, Howie's model required 2000 fibre-years per ml of amosite for 1943 to 1979 to produce 0.61 million amosite fibres per gram of lung tissue. The letter equated this to 55.5 fibres per ml time-weighted average for 36 years. The letter's author said this result is just slightly above the level in the normal population.
  • The letter cited the author's earlier report (Rogers, 1984) on an asbestos cement manufacturing worker with 24 years of heavy exposure to mixed asbestos types. Some 20 years after exposure ended, the worker's lung burden was 78 million fibres per gram of dry tissue. Of these, 14 million were chrysotile, and tremolite was less than 0.2 million.
  • In the reply, the author of the original article cited Churg and Vedal (1994). That study gave geometric mean amosite levels of 10 million fibres per gram of dry tissue in shipyard workers and insulators with asbestosis, and 4.3 million in those with airway fibrosis. The plaintiff's amosite level of 0.61 million fibres per gram was 1.5 SD below the first mean and 0.8 SD below the second.
  • From those data, the reply's author concluded that the plaintiff's amosite residue lay within the statistical range for both asbestosis and airway fibrosis.
• The authors' conclusion: The letter's author concluded that, given the gap between measured lung fibre results and theoretically modelled exposures, the American Industrial Hygiene Association recommendations on validating predictive exposure models should be taken into account. The author also hoped the court exercised caution.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Lung cancer, Mesothelioma.

Related studies

• Asbestos lung residue and asbestosis risk — R. Howie (2005)
• Is asbestos or asbestosis the cause of the increased risk of lung cancer in asbestos workers? — K. Browne (1986)
• Risk of asbestosis in crocidolite and amosite mines in South Africa — L.M. Irwig, R.S. du Toit, et al. (1979)
• Absence of radiographic asbestosis and the risk of lung cancer among asbestos-cement workers: Extended follow-up of a cohort — M.M. Finkelstein (2010)
• The additional risk of malignant mesothelioma in former workers and residents of Wittenoom with benign pleural disease or asbestosis — A. Reid, N. de Klerk, et al. (2005)
• Asbestos-related cancer risk in patients with asbestosis or pleural plaques — J. Ameille, P. Brochard, et al. (2011)

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