Pulmonary toxicology of silica, coal and asbestos

Our plain-English summary of Pulmonary toxicology of silica, coal and asbestos, by A.G. Heppleston (Environmental Health Perspectives, 1984).

The study

• Author: A.G. Heppleston
• Journal: Environmental Health Perspectives
• Published: 1984;55:111-27
• Type of article: Review
• Cited by: 48 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Mineral particles are customarily inhaled as mixtures, though one component may predominate and determine the response. Although the lesions often possess a characteristic structure, according to the main type of particle deposited, morphology affords little indication of pathogenesis. Being a major element in the evolution of dust lesions, macrophage behavior has been examined extensively in vitro after treatment with mineral particles, attention being directed to membrane and biochemical changes; however, no clear lead to the origin of the lesions has emerged. Pulmonary fibrosis, as one of the ultimate consequences of dust accumulation, required a direct in vitro approach in which the products of the macrophage-particle interaction were utilized to provoke collagen formation by fibroblasts in a two-phase system. By this means, silica and asbestos stimulated connective tissue formation and application of the technique to coal dusts appears promising. Coal workers may develop a peculiar type of emphysema in relation to lesions whose fibrous content is comparatively small. Type II alveolar epithelium is also stimulated by inhaled particles and lipid accumulation follows. Alveolar lipidosis interferes with the fibrotic response by preventing contact between macrophage and particles. This phenomenon may account in part for anomalies, apparent in coal workers, between epidemiological findings and dust composition. Carcinogenesis is a well-recognized feature of asbestos exposure, but, as with fibrosis, risk prediction on the basis of in vitro tests of cytotoxicity is premature and may not be valid.

In plain English

This article was a review by a single author, not a new study. It surveyed published work on how inhaled silica, coal mine dust and asbestos damage the lung. The author described a cell-culture system in which extracts from quartz-treated macrophages raised hydroxyproline (collagen) formation by fibroblasts. The review also described quartz-exposed rats in which fat-like material built up in the air sacs and fibrotic nodules failed to develop. The author argued that the simple lung lesion of coal workers is best seen as a nonspecific reaction to heavy dust accumulation. In red-blood-cell tests, chrysotile was strongly hemolytic while amphiboles were relatively inactive, but the author cautioned that test-tube and whole-body effects may not be comparable. All main UICC asbestos types caused lung fibrosis when inhaled by rats, with significant differences in severity. In its discussion of cancer, the review stated that smoking combined with asbestos exposure had a multiplicative effect. Fiber shape and size were stressed for mesothelioma. The author concluded that judgment should be reserved on whether short-term laboratory tests can identify particles harmful to people.

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: Narrative review of published experimental (animal and cell-culture), pathological and epidemiological literature
• Who was studied: No single study population. The review covered published work on human lung material and workers (coal miners, asbestos-exposed people), rats, guinea pigs, mice and rabbits, and cultured cells such as macrophages, fibroblasts and erythrocytes.
• Exposure: Crystalline and other forms of silica (quartz, tridymite, cristobalite, coesite, stishovite), coal mine dusts of different rank, and asbestos: chrysotile and the amphiboles crocidolite, amosite, anthophyllite and tremolite. Man-made fibers such as glass fiber were also covered.
• Main results:
  • In a two-phase cell-culture system, extracts from the macrophage-quartz reaction repeatedly and significantly raised hydroxyproline formation by fibroblasts. Quartz applied directly to fibroblasts had no such effect.
  • In rats inhaling quartz, lipid accumulated in the alveoli and macrophages were few. The macrophage-quartz reaction was prevented and fibrotic nodules failed to develop.
  • The author interpreted the simple dust lesion of coal workers as a nonspecific reaction to excessive dust accumulation. The author held that human studies minimize a necessary role for quartz.
  • In red-blood-cell (hemolysis) tests, chrysotile, like silica, was strongly hemolytic, while the amphiboles were relatively inactive.
  • The hemolytic activity of amphiboles rose in the presence of serum while that of chrysotile and silica did not. The author took this to suggest that test-tube (in vitro) and whole-body (in vivo) effects may not be comparable.
  • All main types of UICC asbestos samples induced lung fibrosis in rats by inhalation, with significant differences in severity. Amosite was the least fibrogenic in sacrificed animals.
  • In the section on carcinogenicity, the review stated that all types of asbestos fiber are potentially carcinogenic.
  • In the same cancer discussion, the combination of cigarette smoking and asbestos exposure was described as having a multiplicative effect.
  • The review stated there is no reliable evidence of increased lung cancer prevalence in men with silicosis or coal workers' pneumoconiosis.
  • From experiments applying fibers to the pleura, it was concluded that the major factor in both cancer formation and fibrosis was a durable fibrous shape in a narrow size range.
• The authors' conclusion: The author concluded it seems prudent to reserve judgment on whether short-term in vitro tests can identify particles that may prove harmful to people by inhalation.
• Limitations the authors state:
  • The author cautioned that certain rodents tend to develop tumors after solid particles are introduced by injection or implantation. Such results need care before being applied to human disease.
  • The author judged stable cell lines to be of dubious value for predicting fibrogenicity.

Topics

Medical terms in this study, explained in our Lexicon: Macrophage, Pulmonary Fibrosis, Collagen, Fibroblast, Emphysema, Epithelium, Carcinogenesis, Asbestos Exposure.

Related studies

• Particle toxicology: from coal mining to nanotechnology — P.J. Borm (2002)
• Respiratory symptoms and functional status in workers exposed to silica, asbestos, and coal mine dusts — X.R. Wang, D.C. Christiani (2000)
• Some investigations into the nature and cause of massive fibrosis (MF) in the lungs of South African gold, coal, and asbestos mine workers — M.C. Leibowitz, B. Goldstein (1987)
• Relationship of inflammatory cell cytokines to disease severity in individuals with occupational inorganic dust exposure — W.N. Rom (1991)
• An update on the detoxification processes for silica particles and asbestos fibers: successess and limitations — M. Gulumian (2005)
• Chest pain in asbestos and silica-exposed workers — E.K. Park, P.S. Thomas, et al. (2011)

Browse more research in Environmental Health Perspectives, or return to medical research.