Asbestos: Foe or Friend?

Asbestos is grouped into two serpentine and amphibole. Serpentine group, which includes only chrysotile fibre, while amphibole covers actinolite, amosite, anthophyllite, crocidolite and tremolite.

Asbestos is characterized as long, thin, flexible, separable with high tensile strength, heat resistant and of course crystalline in nature. It is well known that the asbestos exposure threatens the normal life of occupational workers, neighbors, pets etc.

Across the globe, asbestos is being used for the manufacturing of more than 3000 different kinds of asbestos-based products including asbestos-cement pipes, asbestos-cement sheets, brake-shoes, brake linings, electric heater plates etc. (Ramanathan and Subramaniam, 2001).

In India alone more than 30 mines are operational in Andhra Pradesh and Rajasthan. About 2500 tonnes of chrysotile (Serpentine) and 36,500 tonnes of tremolite (Amphibole) asbestos are annually mined in India. Asbestos production at present is about 2000 tonnes per month from their own mines in Andhra Pradesh, Rajasthan and Bihar. In addition, India imports asbestos worth Rs 40 – 50 crores annually, without mentioning any remarks of hazardous product (Govt. of India., 1997,1999). The tremolite asbestos variety of amphibole group mined accounts 58% in Rajasthan. Tremolite and Anthophyllite are the largest amphibole deposits in Rajasthan known so far (Mansinghka and Ranawat, 1996).

In India asbestos mining and milling is concentrated to the mainly small-scale sector. Asbestos deposits in Rajasthan are primarily located in Beawar, Deogarh and Jharol ultramafic belts (Mansighka and Ranawat; 1996).

Occupational exposure though inhalation is the most hazardous to industrial workers. During the asbestos-based industrial activities whether related to mining, milling or manufacturing, asbestos fibers get airborne at the work places. The people living in the vicinity of asbestos mines and asbestos related industries might be exposed to higher levels of asbestos (Case and Sebastein, 1987).

Epidemiological surveys and experimental studies have confirmed that asbestos acts as carcinogen as well as co-carcinogen. Its prolonged exposure causes progressive pulmonary fibrosis (asbestosis), pleural diseases (pleural plaques and effusion), malignancies as mesothelioma and bronchogenic carcinoma (Rahman et al, 1993, Rahman and Athar, 1994, Mossman et al, 1996). This article is focused on the unorganized units of grinding and milling processes of Beawer, Deogarh in Rajasthan. Most of the units are not registered by any Government agencies. These units presently exist in these areas mainly producing asbestos cement pipes and pillars as mentioned above. These unorganized small-scale units consuming asbestos depend on the indigenous asbestos supply from local sources. Mostly these units exist in the corner or far distance from central village or public place; such units are running by only very small number of workers. Further it seems that these workers are not aware about the hazardous nature of asbestos and the children, infants of workers were found to be playing along with pets like goats, dogs etc were also present in the vicinity premises. Goats grazing in asbestos contaminated fields inhale an asbestos fibre, which causes parietal and pleural plaques (Dumortier P., 2002). People living in the vicinity of these units are also at higher risk. (Selikoff et al; 1980).

Asbestos hazards: Asbestosis It is the diffuse interstitial fibrogenesis caused by the inhalation of asbestos fibre (Billing and Howard et al., 2000). The features supported asbestosis are changes in the nail beds of the fingers and toes (Clubbing), increased dyspnea on exertion, and diffuse interstitial fibrosis with honey combing, decreased total lung capacity and force vital capacity, restrictive type of lung disease (Belis et al., 1989 and Rom et al., 1991).

Pleural Plaque Thickening of areas of the surface membrane of the lungs (the pleural) is found quite frequently in asbestos exposed persons. Pleural plaques are circumscribes areas of pleural thickening that are the most common x-ray finding with chronic exposure to asbestos. The plaque often become calcified and is the visible on chest radiograph (Selikoff et al., 1968). These plaques are calcified deposits that may cause pain and shortness of breath. Hyaline pleural plaque is discrete, white to yellow white, irregular shaped, frequently calcified, raised structure involving the parietal pleura in persons exposed to asbestos.

Mesothelioma is a cancer arising in the pleural and peritoneal cavity of the lung. Development of human malignant mesothelioma is strongly associated with asbestos exposure and around 5% of individuals exposed to heavy doses of asbestos over an extended period of time finally will develop this malignancy (Craighead and Mossman 1982). Mesothelioma has strong association with crocidolite and weak with chrysotile and Crocidolite asbestos (Szeszenia et al., 2000) and amosite appers to be the type of asbestos fibre with the highest potential for inducing mesothelioma. Diffused malignant mesothelioma is a fatal tumor arising from mesothelial cells or underlining mesenchymal cells in the pleura, peritoneum and pericardium. Approximate 80% of diffused malignant mesotheliomas occur in men exposed to mineral fibres in the work place and sometimes their family members also.

Safety control and measures:

• Workers should avail the proper safety documentary procedure in regional languages to each worker and encourage following the same.
• Label all asbestos containing containers/bags in regional language showing it is hazardous to the health.
• The processing of asbestos should be in wet mode.
• Workers should use ventilatory mask, safety shoes, gloves etc.
• Wear separate clothes for work area and change them before leaving for house.
• Always use covered trolley to transfer the asbestos to prevent the emission and accident to spread into the environment.
• Management should organize educational training to educate the workers how to handle and process the asbestos keeping its dispersion into the environment.
• Do not try to touch or smell or taste asbestos.
• Smoking should be strictly banned in the working environment because it accelerates the asbestos related diseases.
• Do permit to eat the liquid or solid at the place of working.
• Provision should be there for taking bath after leaving work place area.

References:

1. Belis, D., Andrion, A., Desedime, L., (1989). Mineral pathologic changes of the lungs and asbestos exposure. Human Pathol. 20; 102 – 106.
2. Billing, C. G., and Howard, P., (2000). Asbestos exposure, lung cancer and asbestosis. Monaldis Arch.Chest. Dis. 55:151 – 156.
3. Case, B.W., and Sebastien, P., (1987): Environmental and occupational exposure to chrysotile asbestos: A comparative analytic study. Arch. Environ. Health. 42: 185 – 191.
4. Craighead, J. E., and Mossman, B. T., (1982). The pathogenesis of asbetsos associated diseases. N. Engl. J. Med. 306: 1446 – 1455.
5. Dumortier, P. F. Rey, J. R. Viallat, I., Broucke, C., Boutin, P., Vuyst, De., (2002).Chrysotile and tremolite asbestos fibres in the lungs and parietal pleura of Corsican goats. Occup. Environ. Med. 59: 643 – 646.
6. Government of India., (1997). Statistics of mines in India Vol. II (non-coal). Published by the Director General of Mines. Dhanbad, Government of India.
7. Government of India., (1999). Abstract of Statistics. Central Statistical Organization, Department of Statistics, Ministry of planning, New Delhi.
8. Mansingha, B. K., and Ranawat, P. S., (1996). Mineral economics and occupational health hazards of the asbestos resources of Rajasthan. J. Geol. Soc. (India) 47; 375 – 382.
9. 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 – 30.
10. Rahman, Q., and Athar, M., (1994). Asbestos-induced carcinogenesis. An Update. Advances in Biosciences (Review).
11. 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 8, Butter worth Legal Pub. USA.
12. Rom, W. N., Travis, W. D., Brody, A. R. (1991). Cellular and molecular basis of asbestos related disease. Am. Rev. Res. Dis. 143: 408 – 422.
13. Selikoff, I. J., Hammond, E. C., and Churg, J., (1968). Asbestos exposure, smoking & neoplasia. JAMA (204) 106 – 112.
14. Selikoff, I. J., Sedman, H., and Hammond, E., (1980). Mortality effects of cigarette smoking among amosite asbestos factory workers. J. N. C. I. 65: 507 – 513.
15. Szeszenia., Dabrowska, N., Wilczynska, U. S., Zymeczak, W., (2000). Mortality of workers at two asbestos – cement plants in Poland. Int. J. Occup. Med. Env. Health. 13: 121 – 130.

Furquan Ahmad Ansari, Iqbal Ahmad, and Qamar Rahman
Fibre Toxicology Division Industrial Toxicology Research Centre,
Post Box – 80, M. G. Marg Lucknow-226 001
E-mail: [email protected]

Mohd. Yunus,
Dean, Department of Environmental Sciences Babasaheb Bhimrao Ambedkar University (A Central University)

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