Asbestosis

Our plain-English summary of Asbestosis, by R.T. Johnstone (1948).

The study

• Author: R.T. Johnstone
• Published: Occupational Medicine And Industrial Hygiene, St. Louis: C.V. Mosby, Pp. 368-372 (1948)
• Type of article: Book excerpt
• Our copy: from Johns-Manville's own medical library, J-M no. 002853.

In plain English

This is a chapter on asbestosis from an occupational medicine textbook dated 1948 in the citation. It is a descriptive overview, not a study, and much of it reports other researchers' work. It described exposure in packing, insulating, fireproofing and textile trades. It stated that the first sign is shortness of breath (dyspnea), with a usually dry cough. It said the lung scarring is diffuse and basal, unlike the nodular upper-lung scarring of silicosis, and that the pleura is thickened. It quoted Gardner of the Saranac Laboratory, who concluded that asbestos irritates the lungs mechanically as stiff fibres. In Gardner's inhalation experiments, very finely ground chrysotile produced no fibrosis, while long-fibre dust at one-third the concentration produced fibrosis after about two years. Citing Pendergrass, the chapter said X-ray changes lie mostly in the lower lungs and that early asbestosis cannot be reliably diagnosed by X-ray. It estimated ("it is felt") that asbestosis takes on average seven to nine years to develop at fairly high concentrations and fifteen to twenty at lower ones, and that it progresses even after exposure ends.

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: Textbook chapter: a descriptive overview of asbestosis that draws on other authors' work. No original study is reported.
• Who was studied: No specific study population. The chapter describes the disease in exposed workers in general.
• Exposure: Asbestos, described as a hydrated magnesium silicate, in packing, insulating, fireproofing and textile trades. Chrysotile is discussed in the experimental work cited.
• Main results:
  • The chapter stated that, as in silicosis, the first sign is dyspnea (shortness of breath) and the cough is usually dry.
  • The chapter stated that tuberculosis as a complication is far less frequent than in silicosis.
  • The chapter described the lung fibrosis of asbestosis as diffuse, peribronchial and basal, in contrast to the nodular upper-lung fibrosis of silicosis.
  • The chapter stated that the pleurae, especially in the basal regions, are thickened.
  • The chapter quoted Gardner (Saranac Laboratory), who concluded that inhaled asbestos fibres irritate the lungs because they are stiff fibres, not because they are silicates.
  • In Gardner's experiments, chrysotile ground so finely that few fibres were longer than 2 microns produced no fibrosis over several years of inhalation at an average of 125 million particles per cubic foot of air. Long-fibre asbestos dust at one-third this concentration produced well-marked fibrosis after about two years.
  • The text, in the passage on Gardner's experiments, stated that there was no clinical asbestosis at the Thetford Mills even though the air there had been very dusty. It explained this by the mill dust being serpentine and extremely short chrysotile fibres, while spinning and weaving mill dust contains many more long fibres.
  • The chapter stated that asbestosis bodies, first described by McDonald, are scattered throughout the lung in both diseased and healthy parts.
  • Citing Pendergrass, the chapter stated that X-ray findings are largely limited to the lower half or two-thirds of the lung fields.
  • Citing Pendergrass, the chapter stated that X-ray diagnosis of early asbestosis is unreliable.
  • The chapter estimated that asbestosis takes on average seven to nine years to develop at fairly high concentration, and fifteen to twenty years at less severe concentration.
  • The chapter gave the allowable concentration as 10,000,000 particles per cubic foot of air, for particles between 0.5 and 5 in size. The unit of size is not printed.
  • The chapter stated that once established, the disease is progressive even after exposure stops. The cited experimental passage separately says that in animals the change was not progressive after exposure ceased.
• The authors' conclusion: The chapter states no overall conclusion. It ends with medicolegal points on time to develop disease, the allowable concentration, and progression after exposure ends.

Topics

Medical terms in this study, explained in our Lexicon: Dyspnea, Silicosis, Pleura, Saranac Laboratory, Chrysotile, Fibrosis.

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