Translocation pathways for inhaled asbestos fibers

Our plain-English summary of Translocation pathways for inhaled asbestos fibers, by G. Miserocchi, G. Sancini, F. Mantegazza, et al (Environmental Health, 2008).

The study

• Authors: G. Miserocchi, G. Sancini, F. Mantegazza, G. Chiappino
• Journal: Environmental Health
• Published: 2008;7:4
• Type of article: Review
• Cited by: 119 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

We discuss the translocation of inhaled asbestos fibers based on pulmonary and pleuro-pulmonary interstitial fluid dynamics. Fibers can pass the alveolar barrier and reach the lung interstitium via the paracellular route down a mass water flow due to combined osmotic (active Na+ absorption) and hydraulic (interstitial pressure is subatmospheric) pressure gradient. Fibers can be dragged from the lung interstitium by pulmonary lymph flow (primary translocation) wherefrom they can reach the blood stream and subsequently distribute to the whole body (secondary translocation). Primary translocation across the visceral pleura and towards pulmonary capillaries may also occur if the asbestos-induced lung inflammation increases pulmonary interstitial pressure so as to reverse the trans-mesothelial and trans-endothelial pressure gradients. Secondary translocation to the pleural space may occur via the physiological route of pleural fluid formation across the parietal pleura; fibers accumulation in parietal pleura stomata (black spots) reflects the role of parietal lymphatics in draining pleural fluid. Asbestos fibers are found in all organs of subjects either occupationally exposed or not exposed to asbestos. Fibers concentration correlates with specific conditions of interstitial fluid dynamics, in line with the notion that in all organs microvascular filtration occurs from capillaries to the extravascular spaces. Concentration is high in the kidney (reflecting high perfusion pressure and flow) and in the liver (reflecting high microvascular permeability) while it is relatively low in the brain (due to low permeability of blood-brain barrier). Ultrafine fibers (length < 5 mum, diameter < 0.25 mum) can travel larger distances due to low steric hindrance (in mesothelioma about 90% of fibers are ultrafine). Fibers translocation is a slow process developing over decades of life: it is aided by high biopersistence, by inflammation-induced increase in permeability, by low steric hindrance and by fibers motion pattern at low Reynolds numbers; it is hindered by fibrosis that increases interstitial flow resistances.

In plain English

This article was a review: the authors used the physics of body fluids to discuss how inhaled asbestos fibers might move from the lung to other parts of the body, and reported no new measurements. They proposed that fibers can cross the lining of the air sacs with water absorbed into lung tissue, be carried by lung lymph into the blood (which they called "primary translocation"), and then spread to other organs ("secondary translocation"). They suggested that lung inflammation, by raising pressure in lung tissue, could also push fibers into lung capillaries and toward the pleural space. Citing earlier studies, they reported that about 93% of asbestos fibers in malignant human mesothelioma tissue, most of them chrysotile, were narrower than 0.25 micrometres. They also cited an earlier study that found the lowest fiber concentrations in the brain and pleural space. The authors concluded that fiber movement can be interpreted as a water-flow-driven process. They said it is aided by inflammation and by the fibers' persistence, is hindered by fibrosis, and develops slowly over decades. They noted that this process is difficult to monitor directly.

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 and theoretical discussion based on lung and pleural fluid physiology; no original data collected
• Who was studied: No study population of its own; the review drew on published experimental (animal) studies and studies of human tissue
• Exposure: Inhaled asbestos fibers in general, with discussion of chrysotile, amphiboles (including crocidolite and amosite) and fiber size (ultrafine fibers under 5 µm long and under 0.25 µm in diameter)
• Main results:
  • The authors proposed that fibers are carried from lung tissue into lung lymphatics (primary translocation) and, once in the blood, can be distributed to all organs (secondary translocation)
  • The authors proposed that primary translocation of fibers to the pleural cavity requires inflammation to raise lung interstitial pressure to about 5 cm H2O
  • Citing an earlier study (their reference 3), the authors reported that in malignant human mesothelioma tissues about 93% of asbestos fibers, most of them chrysotile, were smaller than 0.25 µm in width
  • Citing an earlier study (their reference 56), the authors reported that the lowest fiber concentrations were in the brain and pleural space, and that fiber deposition was relevant in the kidney and liver. They interpreted this as reflecting the permeability and blood flow of these organs
  • Citing earlier work, the authors reported that the residence half time of amphiboles in the lung ranges from years to decades. For chrysotile, the half time was much shorter: 16 days for 20 µm fibers and 107 days for fibers under 5 µm
• The authors' conclusion: The authors concluded that translocation of asbestos fibers within the body can be interpreted as a water-flow-driven process aided by high biopersistence and inflammation, hindered by fibrosis, and developing slowly over decades of life
• Limitations the authors state:
  • The authors stated that the translocation process is difficult to monitor because it takes place over decades of life
  • The authors stated that differences in drift and translocation between curly, flexible chrysotile and rigid, rod-like amphiboles were not specifically modelled on physical grounds

Topics

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

Medical terms in this study, explained in our Lexicon: Translocation, Interstitial, Visceral Pleura, Inflammation, Parietal Pleura, Mesothelioma, biopersistence, Fibrosis.

Related studies

• Asbestos causes translocation of p65 protein and increases NF-kappa B DNA binding activity in rat lung epithelial and pleural mesothelial cells — Y.M. Janssen, K.E. Driscoll, et al. (1997)
• Translocation of inhaled dust to the pleura — P.F. Holt (1983)
• Pulmonary and pleural leukocytes from F344 rats produce elevated levels of fibronectin following inhalation of refractory ceramic fibers — T.R. Gelzleichter, J.B. Mangum, et al. (1996)
• Deposition pattern and clearance pathways of inhaled chrysotile asbestos — A.R. Brody, L.H. Hill (1981)
• Exposure to low levels of ozone results in enhanced pulmonary retention of inhaled asbestos fibers — K.E. Pinkerton, A.R. Brody, et al. (1989)
• Human and experimental data on translocation of asbestos fibers through the respiratory system — J. Bignon, G. Monchaux, et al. (1979)

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