Inhaled particles in human disease and animal models: use of electron beam instrumentation

Our plain-English summary of Inhaled particles in human disease and animal models: use of electron beam instrumentation, by A.R. Brody (Environmental Health Perspectives, 1984).

The study

• Author: A.R. Brody
• Journal: Environmental Health Perspectives
• Published: 1984;56:149-62
• Type of article: Review
• Cited by: 15 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

The mineral pneumoconioses (lung disease caused by inhalation of inorganic dust) have been an important disease entity for centuries. In the last several decades, the electron microscope has been used to elucidate the distribution and identification of inhaled minerals, to aid in establishing etiologic factors, and less commonly, to determine the basic biologic mechanisms through which inhaled minerals cause lung disease. In this section, I review the instrumentation and tissue preparation currently used to address some modern problems in particle-induced lung disease. For example, human pneumoconioses of undetermined etiology can be clarified by electron microscopy and X-ray energy spectrometry. In addition, the initial deposition patterns of asbestos and silica are demonstrated in animal models, and the contributions of electron microscopy in establishing the initial lesions of asbestosis are described.

In plain English

This 1984 book chapter reviewed how electron microscopes, combined with X-ray analysis of what chemical elements particles contain, are used to study lung disease caused by inhaled mineral dust. It described instruments and tissue preparation, then gave three human case examples. In a talc miner, particles of magnesium and silicon were associated with lung scarring. In sandblasters, silicon-containing particles strongly suggested silica caused the scarring. In a 55-year-old heating duct insulator with severe lung fibrosis, the techniques yielded what the author described as sufficient evidence of significant exposure to amosite asbestos. The chapter also described rat experiments from the author's laboratory. After rats inhaled chrysotile asbestos for 1 hour, fibers that passed through the conducting airways landed mainly at branch points of alveolar ducts, especially those nearest the terminal bronchioles that lead into these ducts. Some fibers were taken up by lining cells and passed into the underlying tissue. Scavenger cells gathered at those same spots. Inhaled chrysotile also changed in elemental makeup. The author concluded these methods are powerful tools for studying dust-related lung disease.

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 / book chapter on electron microscopy methods, with illustrative case reports and descriptions of animal experiments from the author's laboratory
• Who was studied: Three human case examples: a 30-year-old man from a talc mine; four tombstone sandblasters, with lung tissue from three of them at autopsy; and a 55-year-old heating duct insulator. Also white rats exposed to quartz or to chrysotile asbestos.
• Exposure: Human cases: talc, silica sandblasting dust, and suspected asbestos as a heating duct insulator. Rats: pure quartz for 3 hours (the concentration is lost in the scan), or aerosolized chrysotile asbestos for 1 hour at a concentration printed as 10 mg/m3, preceded by a garbled symbol.
• Main results:
  • Talc mine case: the author reported that SEM and X-ray analysis showed a clear association of talc particles (magnesium and silicon) with interstitial lung lesions
  • Sandblaster cases: particles in the connective tissue gave clear silicon peaks in all tissues studied, which the author said strongly suggested the fibrosis was caused by silica
  • Heating duct insulator case: asbestos bodies and small asbestos fibrils were found, which the author said gave sufficient evidence of significant exposure to amosite asbestos
  • Silica-exposed rats: the number of silica particles per square micron of alveolar duct surface was reduced significantly 24 hours after the 3-hour exposure
  • Silica-exposed rats: the percentage of lavaged macrophages containing silica rose to about 60% over the first 24 hours and stayed near that level for 4 weeks
  • Chrysotile-exposed rats: immediately after exposure, fibers small enough to pass through the conducting airways deposited primarily at the bifurcations of alveolar ducts
  • Chrysotile-exposed rats: most fibers deposited on the alveolar duct bifurcations closest to terminal bronchioles; the farther a bifurcation was from its terminal bronchiole, the less asbestos was observed
  • Chrysotile-exposed rats: fibers taken up by epithelial cells passed through basement membranes into interstitial connective tissue
  • Chrysotile-exposed rats: the initial lesion was an accumulation of macrophages at the same alveolar duct bifurcations where the fibers first landed
  • Chrysotile's elemental content (magnesium to silicon ratio) was altered in vitro by acid treatment, and inhaled chrysotile also changed in elemental character after inhalation
• The authors' conclusion: The author concluded that scanning and transmission electron microscopy together with X-ray energy spectrometry are powerful tools for enhancing knowledge of dust-related lung disease
• Limitations the authors state:
  • When particles are separated from tissue by ashing or digestion, they lose their relationship to anatomic structures and lesions, and some particles may be partially dissolved or elementally altered
  • With mixed dust exposures, the diagnostic problem is often insurmountable and no definitive diagnosis can be made

Topics

Medical terms in this study, explained in our Lexicon: Etiology, Deposition.

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