Asbestos Bodies

Asbestos bodies or Ferruginous bodies are classically asbestos fibers. The term asbestos originated from the Greek word, which means “indestructible or inextinguishable”, which represents the longer durability of the material. Asbestos is a naturally occurring hydrated mineral silicate comprised of two groups: serpentine and amphibole (Mossman et al. 1990). Serpentine includes only one type of asbestos that is white colour and mostly 95% used as commercial asbestos known as chrysotile [3MgO.2SiO₂.2H₂O], while amphibole contains amosite [(FeMg) SiO₃], actinolite [CaO. 3(MgFe) O.4 SiO₂, anthophyllite [(MgFe)7.Si₈O₂₂.(OH)2, crocidolite [NaFe (SiO₃).FeSiO₃.H₂O) and tremolite [Ca₂Mg₅Si₈O₂₂.(OH)2] (ATSDR, 2001).

Both the groups have different fibrous structures as chrysotile is curly stranded whereas amphiboles are straight and rod-like (Kamp and Weitzman, 1999). Asbestos is typically used in asbestos-cement sheets and pipes, jointing, brake lining, brake shoes, clutch facing, fireproof suits etc. Literature reveals that asbestos bodies have become layered with an iron-rich substance, which is supposed to be derived from proteins such as ferritin and hemosiderin (Pooley, 1972). Asbestos bodies are golden yellow, rod-like coated fiber, elongated, golden brown structurally 10 – 60 µ length and 0.5 – 2.5 µ wide beaded or pear or round shape appearance with many segments. These also may appear as 1 – 6 µ in thickness and 10 – 60 µ in length beaded structure along with its length and often clubbed on one or both the ends to resemble a dumble and their color varies from yellow to dark brown. Asbestos bodes are usually formed on straight fibers and are always found to occur by all the commercial types of asbestos but less frequently on chrysotile asbestos fibers. Asbestos body have a crystalline component which is structurally similar to the extract of ferritin, an inorganic iron-containing core, covered by a shell of protein, this protein is iron free and composed of approx 20 – 24 peptide chains per ferritin molecule, which forms a hollow sphere with a radius 60 – 70 Å, the ferritin core may be ferricoxyhydroxides. The fericoxyhydroxide core of ferritin is variable in shape with maximum dimensions of approximately 60Å produced from animal and human organs. Issues associated to asbestos-induced disorders caught more concentration worldwide in the last couple of decades (Skinner, 2003; Lange, 2004).

Extensive sustainable efforts have been made by several workers and came to the conclusion through experimental studies that chronic exposure to asbestos may lead to several mutagenic disorders including, progressive pulmonary fibrosis (asbestosis), pleural diseases (pleural plaques and effusion), and malignancies as mesothelioma and bronchogenic carcinoma (Mossman et al, 1990, Rahman et al, 1993, Rahman and Athar, 1994, Mossman et al, 1996). Asbestos bodies (AB) are suggestive to interstitial pulmonary fibrosis, these are considered the hallmark of past exposure to asbestos (Dumortier, 1990).

Exposure to asbestos bodies can examine in the sputum or bronchoalveolar lavage (BAL) of the workers. Asbestos bodies are also rarely seen in plaques, though they can usually be detected for the underlying pulmonary parenchyma (Roberts, 1971). A higher incidence of asbestos bodies may be due to heavy exposure and poor unhygienic condition of asbestos processing or product use. Asbestos bodies are also significantly related to radiographic findings of interstitial pulmonary disease and pleural fibrosis and to Spirometric findings of restrictive lung disease.

References:

1. Agency For Toxic Substances and Disease Registry, ATSDR. (2001). Toxicological profile for asbestos. Update (Final Report). Public Health Service, U.S. Department of Health and Human Services Atlanta, GA: 146 pp.NTIS Accessories No. PB/2001/109/01, USA.
2. Dumortier, P., De Vuyst, P., Stranss, P., and Yernault, J.C., (1990). Brit. J. Ind. Med. 47: 91.
3. Kamp, D.W. and Weitzman, S.A., (1999). Occasional review: The molecular basis of asbestos-induced lung injury. Thorax, 54 (2): 638 – 652.
4. Lange, JH (2004). Asbestos-containing floor tile and mastic abatement: is there enough exposure to cause mesothelioma, lung cancer or asbestosis? Indoor Built Environ. (in press).
5. Mossman, B.T., Bignon. J., and Corn, M., et al. (1990). Asbestos: scientific developments and implications for public policy. Science; 247:294-301.
6. Mossman, B.T., Kamp, D.W., and Weitzman, S.A., (1996). Mechanisms of carcinogenesis and clinical features of asbestos-associated cancers. Cancer Invest: 14: 464 – 78.
7. Pooley, F.D., (1972). Asbestos Bodies, Their Formation, Composition and Character. Environ. Res. 5: 363 – 369.
8. Rahman, Q., and Athar, M., (1994). Asbestos-induced carcinogenesis: An Update. Advances in Biosciences. (Review).
9. Rahman, Q., Arif, J.M., Mahmood, N., and Khan, S.G., (1993). Asbestos and lung diseases: A mechanistic approach II. In “Sourcebook of asbestos diseases” Ed. G. A. Peters and B. J. Peters, Vol. 8, Butter worth Legal Pub. USA.
10. Roberts, G.H., (1971). The pathology of parietal pleural plaques. J. Clin. Pathol. May. 24 (4): 348 – 53.
11. Skinner, HCW (2003). Mineralogy of asbestos minerals. Indoor Built Environ 12: 385-389.

Furquan Ahmad Ansari and Qamar Rahman
Industrial Toxicology Research Centre,
Post Box – 80, M. G. Marg Lucknow-226 001

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