Investigative techniques in the laboratory study of coal workers' pneumoconiosis: recent advances at the cellular level

Our plain-English summary of Investigative techniques in the laboratory study of coal workers' pneumoconiosis: recent advances at the cellular level, by J.S. Harington (Annals of the New York Academy of Sciences, 1972).

The study

• Author: J.S. Harington
• Journal: Annals of the New York Academy of Sciences
• Published: 1972;200:816-34
• Type of article: Review
• Cited by: 13 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Summary of the article

This paper set out problems and priorities for laboratory research on coal workers' pneumoconiosis, focusing on how coal dust behaves towards macrophages in cell culture. The author noted that few such studies had been done and drew on earlier silica and asbestos work. Two laboratory-milled coal dusts were tested, one from a South Wales colliery (SWS 3) and one from a Nottinghamshire colliery (NT 1). Both were tested native and after benzene extraction, which removed 1.5% and 0.7% organic material respectively. Hemolytic activity was measured on human and sheep erythrocytes. Cytotoxicity was assessed in hamster peritoneal macrophages, with Fransil silica and UICC chrysotile as cytotoxic standards and rutile as a control dust. Native NT 1 was strongly hemolytic to human erythrocytes (70%), falling to 29% after extraction. Fresh serum increased hemolysis, but not significantly. SWS 3 was weakly hemolytic, and the extracts alone were inactive on sheep erythrocytes. Neither coal was toxic to macrophages, whereas silica and chrysotile caused marked degeneration. The author then reviewed how methods varied between laboratories: animal species, type of macrophage, culture media, incubation conditions, measures of cytotoxicity and dusts. He reported conflicting published results for asbestos. He concluded that coal itself is the most variable factor and recommended international working parties to standardize coal samples and techniques, as the 1965 UICC asbestos working parties had done.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

In plain English

This 1972 paper from a South African cancer research unit discussed problems and priorities in laboratory research on coal workers' pneumoconiosis. It reviewed how other studies had tested silica and asbestos on cells, and it reported the author's own tests on two laboratory-milled coal dusts: one from a South Wales colliery (SWS 3) and one from a Nottinghamshire colliery (NT 1). Native NT 1 coal released 70% of the hemoglobin from human red blood cells. After its organic matter was removed with benzene, this fell to 29%. Native and extracted SWS 3 were weakly hemolytic. In cultured hamster macrophages, neither coal, native or extracted, was found toxic. Silica and chrysotile asbestos, used as toxic standards, damaged and destroyed the cells. Because airborne dust was not used, the author did not relate the results to miners. He described published cell-culture results on asbestos as somewhat confusing. He concluded that working parties should study the many variables, with international agreement on criteria and standard coal samples.

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: Discussion and review of laboratory (cell culture) methods for studying coal workers' pneumoconiosis, including the author's own laboratory experiments on two coal dusts
• Who was studied: Two laboratory-milled coal samples, one from colliery SWS 3 (South Wales) and one from colliery NT 1 (Nottinghamshire). They were tested on washed human and sheep red blood cells and on peritoneal macrophages from young adult male golden hamsters. The work was done at the Cancer Research Unit, National Cancer Association of South Africa, Johannesburg.
• Exposure: Native and benzene-extracted coal dusts SWS 3 and NT 1, plus the benzene-extracted organic matter. Fransil (amorphous) silica and UICC chrysotile asbestos were used as toxic standards, and rutile (titanium dioxide) as a control dust. The dose was 300 micrograms of dust per million macrophages.
• Main results:
  • Benzene-extractable organic material made up 1.5% of SWS 3 coal and 0.7% of NT 1 coal.
  • Native NT 1 coal released 70% of the hemoglobin from human red blood cells. After benzene extraction this fell to 29%. Adding fresh serum raised hemolysis somewhat, but not enough to be regarded as significant. SWS 3, native and extracted, was weakly hemolytic.
  • On sheep red blood cells, all coals and extracts were weakly hemolytic except native NT 1 (39% in Table 2). The extracted organic matter alone was inactive.
  • The organic matter removed by benzene did not cause hemolysis on its own, even though removing it from the coal reduced hemolysis. The author suggested it contributes to hemolysis when it remains attached to the coal.
  • Up to 42 hours after taking up the coal dusts, hamster macrophages looked no different from those given rutile. Cells given silica or chrysotile showed marked degenerative changes and were eventually destroyed.
  • Neither coal, native or benzene-extracted, was toxic to macrophages in culture. With native SWS 3, 87% of the cells remaining at the end of the experiment were viable. The author attributed the loss of cells to cells falling away from the dish after heavy phagocytosis, not to toxicity.
  • In reviewing other studies, the author described published results on the effects of asbestos on cells in culture as somewhat confusing. Some workers found no toxic effect of chrysotile and other types, while others found marked effects.
• The authors' conclusion: The author concluded that coal itself is the greatest source of variation. He proposed that working parties study the many variables, aiming for international agreement on test criteria and standard coal samples, as had been done for asbestos.
• Limitations the authors state:
  • The tests used laboratory-milled coal rather than airborne dust samples, so the author made no attempt to relate the results to possible effects on miners.

Topics

Medical terms in this study, explained in our Lexicon: Pneumoconiosis, Macrophage, UICC, Chrysotile.

Related studies

• Molecular basis for differences in susceptibility to coal workers' pneumoconiosis — P.J. Borm, R. Schins, et al. (1992)
• A battle for compensation for Welsh coal miners: JS Haldane v "Sericite" Jones, 1932-1934 — M. Greenberg (1997)
• Respiratory symptoms and functional status in workers exposed to silica, asbestos, and coal mine dusts — X.R. Wang, D.C. Christiani (2000)
• Ventilatory function after exposure to various respirable hazards in a population of former coal miners — G.M. Calvert, M. Moore, et al. (1991)
• Respiratory impairments due to dust exposure: a comparative study among workers exposed to silica, asbestos, and coalmine dust — X. Wang, E. Yano, et al. (1997)
• The classic pneumoconioses: new epidemiological and laboratory observations — A.S. Laney, D.N. Weissman (2012)

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