Iron homeostasis in the lung following asbestos exposure

Our plain-English summary of Iron homeostasis in the lung following asbestos exposure, by A.J. Ghio, J. Stonehuerner, J. Richards, et al (Antioxidants & Redox Signaling, 2008).

The study

• Authors: A.J. Ghio, J. Stonehuerner, J. Richards, R.B. Devlin
• Journal: Antioxidants & Redox Signaling
• Published: 2008;10(2):371-7
• Type of article: News
• Cited by: 48 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Human exposure to asbestos can cause a wide variety of pulmonary diseases, including pneumoconiosis (i.e., asbestosis). This lung injury is mediated by oxidant generation which increases with the concentration of iron associated with the asbestos. Iron from host sources is complexed by the surface of these fibrous silicates following introduction into the lower respiratory tract. Using bronchoalveolar lavage from unexposed and exposed workers, we demonstrate that asbestos disrupts the normal iron homeostasis in the lungs. Based on these findings, we propose a model of oxidative stress and human lung injury after asbestos exposure.

In plain English

This short article, published as a "Forum News & Views" piece by researchers at the US Environmental Protection Agency, tested whether asbestos exposure disrupts the normal handling of iron in the lungs. The authors compared lung-washing fluid (bronchoalveolar lavage) from 10 nonsmoking unexposed people (6 males and 4 females, mean age 40.2 years) with fluid from 14 nonsmoking males (mean age 53.3 years). The males had occupational asbestos exposure lasting 10 years or longer, with or without changes on X-rays. The article did not name the fiber types the workers were exposed to. Compared with the unexposed group, the asbestos-exposed workers had significantly higher lavage protein, although the difference was small in absolute terms. Their iron was about twofold higher and their transferrin receptor two- to threefold higher, and their lactoferrin and ferritin levels were also significantly higher. Transferrin did not differ significantly between the groups. The authors concluded that asbestos disrupts normal iron homeostasis in the lungs. Based on these findings, they proposed a model of oxidative stress and human lung injury after asbestos exposure.

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: Small comparison of bronchoalveolar lavage fluid between asbestos-exposed and unexposed people, presented in a short "Forum News & Views" article that also proposes a biological model
• Who was studied: 10 nonsmoking unexposed individuals (6 males and 4 females, mean age 40.2 years) and 14 nonsmoking asbestos-exposed subjects (all males, mean age 53.3 years). Location and dates are not stated.
• Exposure: Occupational asbestos exposure for 10 years or longer, with or without radiographic findings. Fiber types, products and jobs are not specified.
• Main results:
  • Lavage total protein was significantly higher in asbestos-exposed workers than in unexposed subjects, but the difference was small in absolute value.
  • Lavage iron in asbestos-exposed workers was approximately twofold that of healthy unexposed individuals, a statistically significant difference.
  • Lavage transferrin in asbestos-exposed workers was not significantly different from that in healthy unexposed controls.
  • Lavage transferrin receptor was increased two- to threefold in those exposed to asbestos.
  • Lavage lactoferrin was significantly higher in asbestos-exposed workers than in unexposed controls.
  • Lavage ferritin in asbestos-exposed individuals was significantly higher than in the control group.
• The authors' conclusion: The authors concluded that asbestos disrupts the normal iron homeostasis in the lungs. Based on these findings, they proposed a model of oxidative stress and human lung injury after asbestos exposure.

Topics

Medical terms in this study, explained in our Lexicon: Asbestos Exposure, Pneumoconiosis, Silicate, Bronchoalveolar Lavage (BAL), Oxidative Stress.

Related studies

• 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)
• Synchrotron X-ray microscopy reveals early calcium and iron interaction with crocidolite fibers in the lung of exposed mice — L. Pascolo, G. Zabucchi, et al. (2016)
• In vivo accumulation of iron on crocidolite is associated with decrements in oxidant generation by the fiber — A.J. Ghio, A. LeFurgey, et al. (1997)
• Iron and Iron-Related Proteins in Asbestosis — A.J. Ghio, E.N. Pavlisko, et al. (2015)
• The role of iron in Libby amphibole-induced acute lung injury and inflammation — J.H. Shannahan, A.J. Ghio, et al. (2011)

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