Our plain-English summary of Surface reactivity in the pathogenic response to particulates, by B. Fubini (Environmental Health Perspectives, 1997).
You don't need the product names or old records. No fee unless we recover compensation for your family.
The study
- Author: B. Fubini
- Journal: Environmental Health Perspectives
- Published: 1997;105 Suppl 5(Suppl 5):1013-20
- Type of article: Review
- Cited by: 105 articles, as counted by NIH iCite
- Read it: PubMed · Publisher · Free full text
Abstract
The peculiar characteristics of dust toxicity are discussed in relation to the processes taking place at the particle-biological medium interface. Because of surface reactivity, toxicity of solids is not merely predictable from chemical composition and molecular structure, as with water soluble compounds. With particles having the same bulk composition, micromorphology (the thermal and mechanical history of dust and adsorption from the environment) determines the kind and abundance of active surface sites, thus modulating reactivity toward cells and tissues. The quantitative evaluation of doses is discussed in comparisons of dose-response relationships obtained with different materials. Responses related to the surface of the particle are better compared on a per-unit surface than per-unit weight basis. The role of micromorphology, hydrophilicity, and reactive surface cations in determining the pathogenicity of inhaled particles is described with reference to silica and asbestos toxicity. Heating crystalline silica decreases hydrophilicity, with consequent modifications in membranolytic potential, retention, and transport. Transition metal ions exposed at the surface generate free radicals in aqueous suspensions. Continuous redox cycling of iron, with consequent activation-reactivation of the surface sites releasing free radicals, could account for the long-term pathogenicity caused by the inhalation of iron-containing fibers. In various pathogenicities caused by mixed dusts, the contact between components modifies toxicity. Hard metal lung disease is caused by exposure to mixtures of metals and carbides, typically cobalt (Co) and tungsten carbide (WC), but not to single components. Toxicity stems from reactive oxygen species generation in a mechanism involving both Co metal and WC in mutual contact. A relationship between the extent of water adsorption and biopersistence is proposed for vitreous fibers. Modifications of the surface taking place in vivo are described for ferruginous bodies and for the progressive comminution of chrysotile asbestos fibers.
In plain English
This article was a review, based on a 1996 conference presentation, of how a particle's surface chemistry may shape the body's disease response to inhaled dusts. The author discussed published work on silica, asbestos, man-made vitreous fibers, coal mine dust, and hard metal mixtures of cobalt and tungsten carbide. The author also reported some laboratory measurements. The author argued that a dust's toxicity cannot be predicted from its chemical composition alone. For surface-related effects, the author held that doses are better compared per unit surface area than per unit weight. The reviewed evidence supported a role for iron-generated free radicals in asbestos toxicity, a hypothesis the author called still controversial. In the author's measurements, three man-made vitreous fibers adsorbed more water than pure silica glass. Their order was MMVF11, MMVF10, MMVF21, then silica glass. The author noted that another study found the three fibers in the same order for biopersistence in vivo. Chrysotile leached with oxalic acid adsorbed more small molecules per unit surface than unleached chrysotile. The author suggested that water adsorption might predict the biopersistence of particles or fibers close in size and shape, if validated on many more fibers.
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 based on a conference presentation, including some of the author's own laboratory adsorption measurements on fibers
- Who was studied: No people were studied. The review covered published studies on dusts and fibers. The author's own measurements used three man-made vitreous fibers (MMVF10, MMVF11, MMVF21), a ground pure silica glass (Suprasil), and original and oxalic-acid-leached chrysotile. Sample numbers were not stated.
- Exposure: Crystalline silica (quartz, cristobalite) and asbestos (chrysotile, amosite, crocidolite, amphiboles), as well as iron-free fibers such as tremolite and ceramic fibers. Also man-made vitreous fibers (glass, slag and rock wools), coal mine dust, and hard metal mixtures of cobalt and tungsten carbide.
- Main results:
- Author's measurements: all three glass fibers adsorbed more water vapor than pure vitreous silica at the same pressure. Affinity for water per unit surface decreased in the order MMVF11, MMVF10, MMVF21, vitreous silica.
- The author noted that these fibers ranked in the same order for biopersistence in vivo, as reported in a separate cited study.
- Author's measurements on chrysotile: leached fibers adsorbed much more of small molecules (water, ammonia, tert-butanol) than unleached fibers, even per unit surface area. The author took this to mean that leaching changes the chemical reactivity of the surface.
- Reviewed literature: in vivo and in vitro data showing that antioxidants, free radical scavengers and strong iron chelators reduce or block the biological response to asbestos support the hypothesis that iron-derived reactive oxygen species play some role in asbestos toxicity. The author called this hypothesis still controversial and said it leaves unexplained the effects of iron-free fibers such as tremolite or ceramic fibers.
- Reviewed literature: unlike amphiboles, which persist in the body virtually unchanged in crystal structure, chrysotile is progressively split into fibrils and eventually cleared from the lung. The author said this can make chrysotile exposure difficult to assess.
- Author's view on dose measurement: mass is the least appropriate way to express doses, particularly when comparing materials with different specific weights or surface per unit mass.
- The authors' conclusion: The author concluded that knowledge of pathogenic minerals could be used to design safer substitute materials, and that cell-free and in vitro tests could be used to prescreen new fibers and particles. The author also suggested that, if validated, water vapor adsorption might offer a quick way to predict the biopersistence of particles or fibers close in size and shape.
- Limitations the authors state:
- The link between water adsorption and biopersistence was based on a few fibers and would need validation on a much larger number.
- The molecular mechanisms by which particles cause disease remain partly obscure, even for asbestos and crystalline silica.
- The biological significance of asbestos (ferruginous) body formation is still unclear.
Topics
Medical terms in this study, explained in our Lexicon: Surface Reactivity, Dose-response relationship, Cation, Crystalline, Redox Cycling, STEM, Reactive Oxygen Species (ROS), biopersistence.
Related studies
- Surface reactivity and cell responses to chrysotile asbestos nanofibers — F. Turci, M. Colonna, et al. (2012)
- The ability of mineral dusts and fibres to initiate lipid peroxidation. Part I: parameters which determine this ability — M. Gulumian (1999)
- Assessment of the pathogenic potential of asbestiform vs. nonasbestiform particulates (cleavage fragments) in in vitro (cell or organ culture) models and bioassays — B.T. Mossman (2008)
- Iron topochemistry and surface reactivity of amphibole asbestos: relations with in vitro toxicity — A. Pacella, G.B. Andreozzi, et al. (2012)
- Surface chemistry and surface reactivity of fibrous amphiboles that are not regulated as asbestos — M. Fantauzzi, A. Pacella, et al. (2012)
- Surface physico-chemical studies of chrysotile asbestos and related minerals — C. Jolicoeur, D. Poisson (1987)
Browse more research in Environmental Health Perspectives, or return to medical research.
Cited on this site
How to cite it
Cite the study
B. Fubini. Surface reactivity in the pathogenic response to particulates. Environmental Health Perspectives 1997;105 Suppl 5(Suppl 5):1013-20. doi:10.1289/ehp.97105s51013. PMID: 9400693.
Cite our summary
“Surface reactivity in the pathogenic response to particulates.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/surface-reactivity-in-the-pathogenic-response-to-particulates.
ACL Doc numbers and their short links never change. See how to cite the Library.
Talk with an asbestos lawyer
Start with what you remember, and we'll take it from there.
This page is provided for general informational purposes and does not constitute legal advice. Every asbestos case turns on its own facts, exposure history, diagnosis, deadlines, available evidence, and applicable law. Reviewing this page does not create an attorney-client relationship. For advice about your specific situation, call 833-4-ASBESTOS for a free case review.