Chest Radiography Remains the Mainstay of Imaging in Benign Asbestos-Related Diseases

There are a myriad of ways one can be exposed to asbestos as the mineral is ubiquitous and found in thousands of everyday products.  One interesting study is called, “Computed tomography in the evaluation of benign asbestos-related disorders.” Radiol Clin North Am. 1992 Nov;30(6):1191-207.  Department of Radiology, University of British Columbia, Vancouver, Canada.  Here is an excerpt: “Abstract – High-resolution CT is more sensitive than chest radiography and conventional CT in the detection and assessment of benign asbestos-related pleural and parenchymal diseases. The HRCT features of asbestosis correlate with clinical and functional restriction. The specificity of HRCT findings of asbestosis needs further evaluation. Given its low cost and availability, chest radiography remains the mainstay of imaging in benign asbestos-related diseases. CT (conventional or high-resolution) is not recommended as a universal screening test in asbestos-exposed workers. It has a useful role in identifying and quantitating pulmonary fibrosis distinct from emphysema and pleural disease, in distinguishing pleural disease from normal extrapleural soft tissues, and in clarifying the confusing chest radiograph or conflicting pulmonary function data. CT is useful in excluding a mass that may be obscured by extensive pleural and parenchymal fibrosis and is helpful in the follow-up of benign fibrotic masses or in the direction of their biopsy.”

Another interesting study is called, “Src-dependent ERK5 and Src/EGFR-dependent ERK1/2 activation is required for cell proliferation by asbestos” by Luca Scapoli, Maria E Ramos-Nino, Marcella Martinelli and Brooke T Mossman – Department of Pathology, University of Vermont College of Medicine, Burlington, VT 05405, USA.  Here is an excerpt: “Abstract – Crocidolite asbestos elicits oxidative stress and cell proliferation, but the signaling cascades linked to these outcomes are unclear. To determine the role of mitogen-activated protein kinases (MAPK) in asbestos-induced cell signaling, we evaluated the effects of crocidolite asbestos, EGF and H2O2, on MAPK activation in murine lung epithelial cells (C10 line). In contrast to rapid and transient activation of extracellular signal-regulated kinase 5 (ERK5) by EGF or H2O2, asbestos caused protracted oxidant-dependent ERK5 activation that was inhibited by an Src kinase inhibitor (PP2), but not by an inhibitor of epidermal growth factor receptor (EGFR) phosphorylation (AG1478). ERK1/2 activation by asbestos was inhibited by either PP2 or AG1478. To confirm the involvement of Src in ERK1/2 and ERK5 activation, a dominant-negative Src construct was used. These experiments showed that Src was essential for ERK1/2and also ERK5 phosphorylation by asbestos. Time frame studies indicated immediate activation of Src by asbestos fibers, whereas EGFR phosphorylation occurred subsequently. Data suggest that asbestos causes activation of ERK5 through an EGFR-independent pathway, whereas ERK1/2 activation is dependent on Src through a mechanism involving phosphorylation of the EGFR. Furthermore, Src, ERK1/2 and ERK5 activation are essential for cell proliferation by asbestos. The use of a dominant-negative ERK5 construct caused selective downregulation of c-jun expression, whereas inhibition of Src by PP2 or MEK1 by PD98059 caused decreases in c-fos, fra-1 and c-jun expression in asbestos-exposed C10 cells. These observations may have broad relevance to cell proliferation by carcinogenic mineral fibers and oxidants.”

Another interesting study is called, “Variation of properties of chrysotile asbestos subjected to milling” by A. M. Langera; M. S. Wolffa; A. N. Rohla; and I. J. Selikoffa
- Journal of Toxicology and Environmental Health, Part A, Volume 4, Issue 1 1978 , pages 173 – 188.  Here is an excerpt: “Abstract – Mechanical milling is commonly used to produce short chrysotile asbestos for experimental purposes. Such manipulation also decreases fiber crystallinity, alters Si-O and Mg-O interlayer bonding, induces coordination changes in the brucite layer, diminishes the ability of fiber to reduce specific free radicals and physisorb organic molecules, and decreases hemolytic potency and antagonist sorption capabilities. The degree of alteration is related to the time of milling. Results of biological experimentation with these materials must be interpreted with caution. Interaction mechanisms in the biological setting are suggested for chrysotile fiber.”

We all owe a debt of gratitude to these researchers.  If you found any of these excerpts interesting, please read the studies in their entirety.

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