Asbestos and Iron

Our plain-English summary of Asbestos and Iron, by A.J. Ghio, M. Stewart, R.G. Sangani, et al (International Journal of Molecular Sciences, 2023).

The study

• Authors: A.J. Ghio, M. Stewart, R.G. Sangani, E.N. Pavlisko, V.L. Roggli
• Journal: International Journal of Molecular Sciences
• Published: 2023;24(15)
• Type of article: Review
• Cited by: 8 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Theories of disease pathogenesis following asbestos exposure have focused on the participation of iron. After exposure, an open network of negatively charged functional groups on the fiber surface complexes host metals with a preference for iron. Competition for iron between the host and the asbestos results in a functional metal deficiency. The homeostasis of iron in the host is modified by the cell response, including increased import to correct the loss of the metal to the fiber surface. The biological effects of asbestos develop in response to and are associated with the disruption of iron homeostasis. Cell iron deficiency in the host following fiber exposure activates kinases and transcription factors, which are associated with the release of mediators coordinating both inflammatory and fibrotic responses. Relative to serpentine chrysotile, the clearance of amphiboles is incomplete, resulting in translocation to the mesothelial surface of the pleura. Since the biological effect of asbestos is dependent on retention of the fiber, the sequestration of iron by the surface, and functional iron deficiency in the cell, the greater clearance (i.e., decreased persistence) of chrysotile results in its diminished impact. An inability to clear asbestos from the lower respiratory tract initiates a host process of iron biomineralization (i.e., asbestos body formation). Host cells attempt to mobilize the metal sequestered by the fiber surface by producing superoxide at the phagosome membrane. The subsequent ferrous cation is oxidized and undergoes hydrolysis, creating poorly crystalline iron oxyhydroxide (i.e., ferrihydrite) included in the coat of the asbestos body.

In plain English

This article was a review, not a new study. The authors examined published research on how asbestos interacts with iron in the body. It covered the five amphibole types (actinolite, amosite, anthophyllite, crocidolite and tremolite) and chrysotile, and it reported no new data on people. The review noted that standard samples of amosite and crocidolite contained 28% and 27% iron, compared with 0–2% in chrysotile. However, the authors argued that the evidence does not support iron built into the fiber's structure as the source of asbestos's biological effects. Instead, they proposed that the fiber surface binds iron taken from the body's own cells, leaving those cells short of usable iron. In their account, the cells' responses to this shortage include inflammation and fibrosis (scarring). The review also described asbestos bodies, the iron-coated fibers found in lungs. Most inhaled fibers stay uncoated (95–97%), and the coats are made mainly of an iron mineral called ferrihydrite. The authors concluded that because chrysotile is cleared from the lungs more readily than amphiboles, its biological effect is diminished.

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 research (no new data collected)
• Who was studied: Not a study of a defined group of people. The article reviewed published laboratory, animal and human lung-tissue research on asbestos and iron.
• Exposure: Asbestos in general: five amphibole minerals (actinolite, amosite, anthophyllite, crocidolite, tremolite) and the serpentine mineral chrysotile, with a focus on how their fiber surfaces interact with iron
• Main results:
  • The review cited measurements of standard reference asbestos samples. Iron made up 28% of amosite and 27% of crocidolite, compared with 0–2% of chrysotile.
  • The authors stated that current evidence does not support iron built into the fiber's crystal structure as the driver of asbestos's biological effect.
  • The authors proposed that the fiber surface binds the host's iron and that the resulting functional iron deficiency in cells is the critical event producing a biological effect.
  • Of all inhaled asbestos fibers, 95–97% remain uncoated, meaning they do not form asbestos bodies.
  • Asbestos bodies with a chrysotile core are a very small share of all asbestos bodies: usually less than 1 to 3%, with a mean of 0.14%.
  • In adults without occupational fiber exposure, asbestos bodies were found in 21% to 100% of lung tissues examined at autopsy (median 90%).
  • The coat of asbestos bodies is mainly ferrihydrite. More crystalline iron forms such as hematite are often absent or make up well below 5%.
  • The review stated that most chrysotile does not persist in the lungs.
• The authors' conclusion: The authors concluded that the biological effect of asbestos depends on the fiber surface binding iron, and that the greater clearance of chrysotile diminishes its biological effect relative to amphiboles.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis, Chrysotile.

Medical terms in this study, explained in our Lexicon: Asbestos Exposure, Serpentine Group, Chrysotile, Amphibole Group, Translocation, Pleura, Asbestos Body Formation, Superoxide.

Related studies

• Iron and Iron-Related Proteins in Asbestosis — A.J. Ghio, E.N. Pavlisko, et al. (2015)
• Disruption of iron homeostasis in mesothelial cells after talc pleurodesis — A.J. Ghio, J.M. Soukup, et al. (2012)
• The biological effect of asbestos exposure is dependent on changes in iron homeostasis — A.J. Ghio, J.M. Soukup, et al. (2016)
• Iron homeostasis in the lung following asbestos exposure — A.J. Ghio, J. Stonehuerner, et al. (2008)
• The role of iron in Libby amphibole-induced acute lung injury and inflammation — J.H. Shannahan, A.J. Ghio, et al. (2011)
• Essential metals--case study on iron — E.S. Gurzau, C. Neagu, et al. (2003)

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