Literature DB >> 9400693

Surface reactivity in the pathogenic response to particulates.

B Fubini1.   

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.

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Year:  1997        PMID: 9400693      PMCID: PMC1470126          DOI: 10.1289/ehp.97105s51013

Source DB:  PubMed          Journal:  Environ Health Perspect        ISSN: 0091-6765            Impact factor:   9.031


  53 in total

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2.  Variation of properties of chrysotile asbestos subjected to milling.

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3.  The effect of crystal structure on mouse lung inflammation and fibrosis.

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4.  Comparative clearance of quartz and cristobalite from the lung.

Authors:  D R Hemenway; M P Absher; L Trombley; P M Vacek
Journal:  Am Ind Hyg Assoc J       Date:  1990-07

5.  Production of oxygen radicals by the reduction of oxygen arising from the surface activity of mineral fibres.

Authors:  H Pezerat; R Zalma; J Guignard; M C Jaurand
Journal:  IARC Sci Publ       Date:  1989

6.  Man-made mineral fibers and lung cancer: an hypothesis.

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7.  Detection of surface free radical activity of respirable industrial fibres using supercoiled phi X174 RF1 plasmid DNA.

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8.  Iron mobilization from crocidolite asbestos greatly enhances crocidolite-dependent formation of DNA single-strand breaks in phi X174 RFI DNA.

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Journal:  Carcinogenesis       Date:  1992-04       Impact factor: 4.944

Review 9.  Experimental research into the pathogenesis of cobalt/hard metal lung disease.

Authors:  D Lison; R Lauwerys; M Demedts; B Nemery
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10.  Chemical characterization and reactivity of iron chelator-treated amphibole asbestos.

Authors:  J Gold; H Amandusson; A Krozer; B Kasemo; T Ericsson; G Zanetti; B Fubini
Journal:  Environ Health Perspect       Date:  1997-09       Impact factor: 9.031

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  29 in total

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10.  Mesothelioma: Do asbestos and carbon nanotubes pose the same health risk?

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