Toxicity asbestos

Goodlick, L.A. and Kane, A.B. (1986). Role of reactive oxygen metabolites in crocidolite asbestos toxicity to mouse macrophages. Cancer Res. 46, 5558-5566. 

Carbon nanotubes (CNTs) currently attract intense interest because of their unique properties which make them suitable for many industrial applications.28 Carbon nanotubes exhibit some of the properties implied in asbestos toxicity. Carbon nanotubes share with asbestos the fibrous habit - long fibers with a diameter of a few nanometers -and a very high biopersistence. On this basis they are suspected to be hazardous and indeed the first studies in vivo14,29,30 have shown an inflammatory response followed by some evolution towards fibrosis. When inhaled, CNTs may thus constitute a possible hazard to human health. The inflammatory and fibrotic responses elicited by CNTs is similar to that caused by other toxic particles which might be the result of oxidative stress caused by particle- and/or cell-derived free radicals. There is no direct experimental evidence of a capacity of carbon nanotubes to generate free radicals similar to silica asbestos and nano sized iron oxide particles. 

A number of physical and chemical properties such as fiber size, durability, and iron content are important determinants of asbestos toxicity. The dependence of toxicity on these fiber properties is discussed below. 

Fisher GL, Mossman BT, McFarland AR, et al. 1987. A possible mechanism of chrysotile asbestos toxicity. Drug Chem Toxicol 10 109-131. 

Reiss B, Millette JR, Williams GM. 1980a. The activity of environmental samples in a cell culture test for asbestos toxicity. Environ Res 22 315-321. 

Rosenthal GJ, Simeonova P, Corsini E. 1999. Asbestos toxicity An immunologic perspective. Rev Environ Health 14(1) 11-20. 

What are the molecular events involved in the development of asbestos-induced respiratory and pleural effects and how are they influenced by fiber dimensions and mineral type Identification of the molecular and cellular events of asbestos-induced disease has been the subject of extensive research within the past two decades (see Mechanisms of Asbestos Toxicity Overview section). However, much remains unknown, and the precise steps in pathogenic pathways are not frilly established. 

Important determinations of asbestos toxicity include exposure concentration, duration, fiber dimensions, and fiber durability. There is animal and human evidence that long fibers are retained in the lungs for longer periods than short fibers and that amphibole fibers, such as tremolite asbestos, are retained longer than chrysotile fibers. Short and long fibers may contribute to the pathogenesis of inflammation, fibrosis, and cancer in humans, but their relative importance is uncertain. 

Asbestos produces its toxic effects by direct contact with lung tissue or by stimulating an acute or chronic inflammatory reaction in the tissue (via active oxygen mechanism or other cell-mediated mechanisms). The important determinants of asbestos toxicity are fiber size, fiber durability, and iron content. 

Mechanisms based on electron transfer and active oxygen species have been proposed to explain asbestos-induced toxicity and lung disease. Fisher et al. (1987) studied the effect of heat treatment on chrysotile asbestos toxicity. The in vitro study showed that heat treatment reduced cytotoxicity. Infra red spectra indicated a reduction of external hydroxyl group population, which repopulated after irradiation. There is, apparently, an electron transfer from the asbestos matrix to biological receptors. In an earlier study, Fisher and coworkers (1985) reported that irradiation of chrysotile samples heated to 400°C (752°F) restored the biological activity to near-control values. X-ray diffraction pattern showed no change in the crystal structure. Brucite, present as a surface contaminant, was removed by heating. 

J. Marsh, A. R. McFarland, and W. R. Hart. 1985. Investigations into the mechanisms of asbestos toxicity. NATO ASI Ser. G3 31-38 cited in Chem. Abstr. CA 104(15) 124419d. 

Kane, A. B. 2003. Asbestos bodies clues to the mechanism of asbestos toxicity Human Pathol. 34 735-36. 

Inert airborne dust with TLV lOmg/m Harmful substance with TLV 0.1-10mg/m (except for asbestos) Toxic substance with TLV <0.1mg/m Asbestos Human carcinogens Spores, bacteria, viruses, proteolytic enzymes... 

Nitric oxide pathway also engaged in asbestos toxicity... 

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