Studies of Mineral Content and Particle Size Distribution

Our plain-English summary of Studies of Mineral Content and Particle Size Distribution, by J. Beattie, J.F. Knox (1967).

The study

• Authors: J. Beattie, J.F. Knox
• Published: Inhaled Particles and Vapors II, Pergamon Press. Presented September 28 - October 1st 1965 (1967)
• Type of article: Conference paper
• Our copy: from Johns-Manville's own medical library. The article is still under copyright, so we describe it here rather than post it.

In plain English

The authors measured mineral content in lung, hilar lymph node and pleural tissue from autopsies of 50 asbestos textile workers at one factory, and particle sizes in the lung. They had reported 27 of these cases in 1954. Exposure ranged from 3 months to 46 years. The lungs of six unexposed people were also examined. Asbestosis was present in 33 of the 50. Mineral built up at a mean of 0.26 mg per gram of dry lung per year in 13 workers who died within 6 months of last exposure. In 12 who survived 5 to 8 years the rate was 0.25, not a significant difference. Lung mineral content was not correlated with asbestosis severity. Moderate and severe asbestosis occurred only after 20 years from first exposure. The share of fibres longer than 15 microns was significantly lower in severe asbestosis than with no asbestosis. The authors concluded that their findings pointed to a fibrogenic agent released from breaking-down asbestosis bodies under conditions unfavourable to its disposal, and that once fragmentation occurs, asbestotic changes are likely to be progressive.

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: Autopsy tissue study (case series). It measured mineral content in lung, hilar and pleural tissue and particle size distribution in lung tissue, with a small comparison group of unexposed lungs.
• Who was studied: 50 deceased workers (42 men and 8 women) from the asbestos textile industry who had all worked in the same factory: 27 previously reported in 1954 plus 23 new cases. Lungs from 6 people never exposed to asbestos dust were also examined.
• Exposure: Asbestos dust in asbestos textile work. Exposure time ranged from 3 months to 46 years, and time from last exposure to death ranged from less than one year to 25 years. 34 of the 50 had some exposure to conditions before 1932, when dust controls led to a great improvement in working conditions. The chemical checks assumed the lung mineral was chrysotile.
• Main results:
  • Asbestosis was present in some degree in 33 of the 50 cases.
  • In the 13 cases who died within 6 months of last exposure, the average rate of mineral accumulation was 0.26 mg per gram dry weight of lung per year.
  • In 12 cases who survived 5 to 8 years after last exposure, the mean rate was 0.25 mg per gram dry lung per year. The authors found no significant difference from the group who died within 6 months.
  • Mineral matter in the lung appeared to increase with exposure time, but it was not correlated with the degree of asbestosis.
  • Moderate and severe asbestosis found at death occurred only after 20 years from first exposure to asbestos dust.
  • The mineral concentration in the hilar lymph nodes was never more than 6 times that in the lung tissue.
  • After 13 years of survival since last exposure, no fibres longer than 36 microns were present in the lung.
  • The percentage of fibres longer than 15 microns was significantly different (lower) in the cases with severe asbestosis than in the cases with no asbestosis.
  • Fewer long fibres in recent cases led the authors to suggest that fewer long fibres were present in the factory dust sometime after 1953.
  • All cases with moderate or severe asbestosis had been exposed for several years to pre-1932 conditions.
• The authors' conclusion: The authors concluded that the mass of mineral in the lungs is not what determines asbestosis. They considered that their findings pointed to a fibrogenic agent being liberated from the breakdown of asbestosis bodies under conditions unfavourable to its disposal, and that when such fragmentation occurs, asbestotic changes are likely to be progressive. They also said the effect of the improved working conditions introduced in 1932 could not be expected to appear until after 1963.
• Limitations the authors state:
  • Particles smaller than 0.75 microns are very hard to count, so counts in the smallest size range (up to 5 microns) are underestimates.
  • The series is heavily weighted toward workers exposed under the dustier pre-1932 conditions.
  • The grading of asbestosis may have been uneven, and some cases may belong in a different severity group.
  • The finding on hilar node mineral content in 5 cases who died of cardiovascular conditions rests on a very small number of cases.
  • In the 12 lung cancer cases, findings on hilar and pleural mineral content were equivocal because 9 also had asbestosis.
  • In the published discussion, a discussant argued that expressing dust per weight of dried lung can be misleading. The author replied that only lung fragments were available, so whole-lung weights could not be measured.

Topics

Medical terms in this study, explained in our Lexicon: Fibrogenic.

Browse return to medical research.