Studies On Experimental Pneumoconiosis: Vi. Inhalation Of Asbestos Dust; Its Effect Upon Primary Tuberculous Infection

Our plain-English summary of Studies On Experimental Pneumoconiosis: Vi. Inhalation Of Asbestos Dust; Its Effect Upon Primary Tuberculous Infection, by L.U. Gardner, D.E. Cummings (1931).

The study

• Authors: L.U. Gardner, D.E. Cummings
• Published: Journal Of Industrial Hygiene 13(2):65-81, February And 13(3):97-114, March (1931)
• Type of article: Journal article
• Our copy: from Johns-Manville's own medical library, J-M no. 003062. The article is still under copyright, so we describe it here rather than post it.

In plain English

This is the concluding part of a two-part animal study. Guinea-pigs breathed Canadian chrysotile asbestos dust (about thirty-five million particles per cubic foot, counting particles 1.5 microns or less in diameter) eight hours daily for up to two and one-third years. Two groups of them were also infected by inhalation with an attenuated strain of tubercle bacilli. In one group, 40 infected animals entered the dusting room; 23 infected controls stayed in normal air. Of the 31 dusted animals dead by the report, seven of them killed, 32.2 per cent showed spread of tuberculosis. In 40 per cent of these, it later healed more or less completely by fibrosis. One of the 23 controls died of generalized tuberculosis. In a second group of 12 infected after two years of exposure, nine died or were killed within forty-eight days. Their earliest tubercles appeared in the chest lymph nodes; those dying on or after the thirty-third day had very extensive spleen tuberculosis. Their final outcome was not yet known. Dust and infection together produced more fibrosis than either alone. The authors concluded that inhaled asbestos influenced primary tuberculous infection only to a limited degree.

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: Animal experiment (guinea-pigs exposed to inhaled asbestos dust and infected by inhalation with attenuated tubercle bacilli, compared with infected undusted controls)
• Who was studied: Guinea-pigs at the Saranac Laboratory, Saranac Lake, New York. Group 1: 63 normal animals were infected; 40 of them were then placed in the dusting room and 23 were kept in normal air as controls. Group 2: 12 guinea-pigs were infected after two years of asbestos exposure, and 12 normal animals were infected at the same time as controls. Rabbits and albino rats were also exposed to dust for 330 days.
• Exposure: Inhaled Canadian chrysotile asbestos dust at approximately thirty-five million particles per cubic foot, counting particles 1.5 microns and less in diameter. Exposure was eight hours daily for up to two and one-third years. This was combined with inhalation infection by the attenuated R strain of tubercle bacilli.
• Main results:
  • Group 1 (infected at the start of dust exposure): of the 40 dusted guinea-pigs, 31 were dead at the time of the report.
  • Group 1 causes of death: seven animals were killed, four died of generalized tuberculosis, seventeen died with more or less extensive epizootic pneumonia, and the rest died from accidental causes. Nine were alive two years and three months after infection.
  • Group 1: some spread of tuberculosis was seen in ten animals. In six it was confined to the lungs, and in four it also involved the abdominal organs. Lung cavities developed in four animals.
  • Group 1: among the 31 animals dead at the time of the report (seven of them killed), spread of tuberculous infection had occurred in 32.2 per cent.
  • Group 1: among the animals with spread of tuberculosis, 40 per cent had subsequently healed more or less completely by fibrosis.
  • Undusted infection controls for Group 1: 20 of 23 were dead. One died after 595 days of generalized chronic tuberculosis. The other nineteen died of other causes, twelve of them of pneumonia.
  • Group 2 (infected after two years of dust exposure): of the 12 guinea-pigs, six died and three were killed during the following forty-eight days.
  • Group 2: the animals dying on or after the thirty-third day showed very extensive tuberculosis of the spleen and hepatic lymph nodes.
  • Group 2: the earliest tubercle formation appeared in the tracheobronchial (chest) lymph nodes rather than in the lung. The authors said this had not been seen before in experimental inhalation infection.
  • In dusted, infected animals, asbestos dust and tubercle bacilli together in the lung produced more fibrosis than either agent alone.
  • In guinea-pigs exposed to asbestos dust, fibrosis in the walls of the respiratory bronchioles was first seen after 500 days of exposure.
  • Comparison drawn by the authors: in similarly infected guinea-pigs exposed to quartz dust, every exposure longer than five months resulted in generalized chronic tuberculosis.
• The authors' conclusion: The authors concluded that inhaled asbestos influenced primary tuberculous infection only to a limited degree. In their view, the dust appeared to have some temporary stimulating effect on the attenuated tubercle bacilli when dust and bacilli were in close contact, and the new disease tended to heal by fibrosis. They contrasted this with quartz.
• Limitations the authors state:
  • Undusted control animals infected with the same strain had recently shown more disseminated tuberculosis: eleven of 148 in the last three years, compared with three of 251 from 1920 to 1928. The cause was not determined.
  • Many animals in Group 1 died prematurely from accidental causes, including epizootic pneumonia, which limited how far the course of the infection could be followed.
  • The final outcome of infection in the group infected after two years of dust exposure had not yet been observed.

Topics

Medical terms in this study, explained in our Lexicon: Pneumoconiosis, Chrysotile, Million Particles per Cubic Foot (mppcf), Fibrosis.

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