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Relative Intrinsic Potency of Asbestos and Erionite Fibers: Proposed Mechanism of Action

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Mechanisms in Fibre Carcinogenesis

Part of the book series: NATO ASI Series ((NSSA,volume 223))

Abstract

Data from human exposure to naturally occurring mineral fibers indicates extreme variability in the rate of mesothelioma between various asbestos varieties and erionite. Experiments on rats have confirmed these differences even where dose responses are based on the number, size and shape of the fibers. In vitro parameters of cytotoxicity and chromosomal aberrations follow the same trend. In such studies the zeolite fiber erionite, which possesses unique internal voids in the crystal lattice, ranks as several orders of magnitude more potent than any asbestos. The data suggests that an intrinsic physicochemical phenomenon is superimposed on the known length/width factor which is responsible for the variability in mesothelioma induction.

Tumorigenesis by asbestos has been ascribed to induction by free radicals. It has been shown that free radical effects are associated with exposure to asbestos and that these can be quenched by free radical scavengers. A mechanism is proposed here based on the co-ordination of endogeous ferric iron with surface silanol groups and formation of hydroxy radicals via the Fenton reaction. It is postulated that the greater activity of erionite is due to a sheltering of the reaction from free radical scavengers within the internal voids of the mineral. A possibility also exists that prolongation of the half-life of the radicals would result from such sequestration. Additionally this activity of the radical effect may be enhanced by proximity to the chromatin material after penetration of the cellular nucleus by long thin fibers following pinocytosis by the mesothelial cells.

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© 1991 Plenum Press, New York

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Coffin, D.L., Ghio, A.J. (1991). Relative Intrinsic Potency of Asbestos and Erionite Fibers: Proposed Mechanism of Action. In: Brown, R.C., Hoskins, J.A., Johnson, N.F. (eds) Mechanisms in Fibre Carcinogenesis. NATO ASI Series, vol 223. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-1363-2_8

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  • DOI: https://doi.org/10.1007/978-1-4684-1363-2_8

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