The relation between lung dust and lung pathology in pneumoconiosis

Our plain-English summary of The relation between lung dust and lung pathology in pneumoconiosis, by G. Nagelschmidt (British Journal of Industrial Medicine, 1960).

The study

• Author: G. Nagelschmidt
• Journal: British Journal of Industrial Medicine
• Published: 1960;17(4):247-59
• Cited by: 51 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. 001602).

Abstract

Methods of isolation and analysis of dust from pneumoconiotic lungs are reviewed, and the results of lung dust analyses for different forms of pneumoconiosis are presented. A tentative classification separates beryllium, aluminium, abrasive fume, and asbestos, which cause interstitial or disseminated fibrosis from quartz, coal, haematite, talc, kaolin, and other dusts, which cause a nodular or focal fibrosis which may change to forms with massive lesions. The data suggest that in the first, but not in the second, group the dusts are relatively soluble; only in the second group do amounts of dust and severity of fibrosis go in parallel for a given form of pneumoconiosis. In classical silicosis the quartz percentage is higher and the amount of total dust much lower than in coal-miners' pneumoconiosis. Mixed forms of both groups occur, for instance, in diatomite workers. The need for more research, especially in the first group, is pointed out.

In plain English

This 1960 paper was a review of how dust is sampled, separated and analysed from the lungs of people with pneumoconiosis. It combined published lung dust analyses with work from the author's laboratory in Sheffield. It compared the amount and make-up of lung dust in classical silicosis, coal-miners' pneumoconiosis, lungs with almost no quartz (such as kaolin and talc workers), iron oxide lungs, berylliosis, aluminosis, Shaver's disease and asbestosis. In classical silicosis the lungs held about 1 to 3 g of quartz and 4 to 10 g of total dust. Colliers with massive fibrosis averaged 40 to 50 g of dust. The author called lung dust analyses in asbestosis surprisingly rare. Citing Knox and Beattie's 27 cases, the paper reported mineral dust averaging 0.4% of dried lung, with no clear increase as fibrosis became more severe. In one severe asbestosis case analysed in the author's laboratory, no asbestos mineral or fibres were identified in the dust. The author suggested that slowly dissolving breakdown products of chrysotile and hornblende asbestos might cause asbestosis fibrosis, but called this hardly more than a speculation.

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: Review of lung dust analysis methods and of published lung dust analyses, combined with analyses from the author's own laboratory
• Who was studied: Lungs of people with various forms of pneumoconiosis, taken from earlier studies and from the author's laboratory. The groups included South African gold-miners, Australian metal miners, tunnel workers and coal-miners, Cornish tin miners and granite workers, South Wales coal-miners, kaolin, talc, mica and electrode workers, haematite miners, foundry workers, an ochre grinder, and cases of berylliosis, aluminosis, Shaver's disease and asbestosis.
• Exposure: Inhaled dusts including quartz, coal, kaolin, talc, mica, iron oxide (haematite), beryllium, aluminium, abrasive fume (Shaver's disease) and asbestos. The paper describes asbestos as covering chrysotile and several hornblende varieties.
• Main results:
  • In classical silicosis, lungs contained from 1 to 3 g of quartz and from 4 to 10 g of total dust, with amounts rising with the degree of fibrosis.
  • In colliers with massive fibrosis, the lungs held on average 40 to 50 g of dust, of which over 80% was coal.
  • In lungs that contained almost no quartz (kaolin, talc, mica, and coke and coal cases), the average dust was about 74 g, or 20% of dried lung weight.
  • In asbestosis, as reported by Knox and Beattie (1954) for 27 cases, mineral dust averaged 0.4% of dried lung. Dust did not clearly increase with more severe fibrosis, and it decreased with longer time between the end of exposure and death.
  • In one case of severe asbestosis (X5747) analysed in the author's laboratory, very little dust was found (0.8% of dried lung). No asbestos mineral could be identified by x-ray diffraction, and no fibres were seen by optical or electron microscopy in the isolated dust.
  • The author stated that, as far as was known, no positive identification of chrysotile in a human lung with asbestosis had been published. A footnote added that Knox and Beattie (1960) had recently observed chrysotile in asbestosis bodies from human lungs.
• The authors' conclusion: The author proposed a tentative split into two groups. Dusts causing interstitial fibrosis (beryllium, aluminium, abrasive fume, asbestos) appeared relatively soluble. Dusts causing nodular fibrosis appeared insoluble, and in that group the amount of dust and the severity of fibrosis went together. The author suggested that breakdown products of chrysotile and hornblende, rather than mechanical damage by larger fibres, might cause asbestosis. The author called the link between slow dust solubility and interstitial fibrosis hardly more than a speculation that needs more lung dust analyses and laboratory support.
• Limitations the authors state:
  • Lung dust analyses in asbestosis were few, and the author stated that present information was clearly insufficient.
  • The proposed link between dust solubility and interstitial fibrosis rests on scanty data and needs more lung dust analyses, physico-chemical studies and animal experiments.
  • Sampling only part of the lungs (half of each lung, or one whole lung) may lead to some error.

Topics

Medical terms in this study, explained in our Lexicon: Pathology, Pneumoconiosis, Interstitial, Fibrosis, Talc, Silicosis.

Related studies

• Dusts causing pneumoconiosis generate .OH and produce hemolysis by acting as Fenton catalysts — T.P. Kennedy, R. Dodson, et al. (1989)
• Experimental infective pneumoconiosis: effect of asbestos dust and Candida albicans infection on the lungs of rhesus monkeys — S.H. Zaidi, R. Shanker, et al. (1973)
• Pulmonary mineral dust. A study of ninety patients by electron microscopy, electron microanalysis, and electron microdiffraction — J.P. Berry, P. Henoc, et al. (1976)
• Relationship between chest X-ray findings and pulmonary function tests in dust workers — Y. Tonori, M. Niitsuya, et al. (2005)
• WHO/ILO work-related burden of disease and injury: Protocol for systematic reviews of occupational exposure to dusts and/or fibres and of the effect of occupational exposure to dusts and/or fibres on pneumoconiosis — D. Mandrioli, V. Schlünssen, et al. (2018)
• Talc dust pneumoconiosis — A. Berner, B. Gylseth, et al. (1981)

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