Silicosis and Asbestosis

Prolonged and extensive exposure to some crystalline silicates (quartz, tridymite and cristobalite) and to silicates with a fiber structure (asbestos) cause the serious diseases silicosis and asbestosis. 

When workers inhale crystalline silica (dust), scars are developed around trapped silica particles in the lungs. For the silicosis victim, breathing becomes difficult and there is also a high risk of developing tuberculosis. 

Use of asbestos has been banned but asbestos removal is a hazardous process. If done improperly it increases the health risks to those exposed. 

North Carolina State University, Raleigh, North Carolina, U.S.A. 

Asbestos and silica are naturally occurring minerals that are mined in various forms for numerous commercial purposes (1,2). Asbestos ore breaks down into fiber forms with a crystalline backbone, while silica can be in crystalline or amorphous (noncrystal) particle form. Asbestos is divided mineralogically into the serpentine form known as chrysotile and the amphibole forms that include crocidolite and amosite. Chrysotile constitutes about 95% of the world s use, and the amphibole fibers, approximately the other 5% (1). All the asbestos varieties have been established as causative agents of all the asbestos-induced diseases (i.e., scarring, lung cancer, and mesothelioma), while it is only the crystalline form of silica that causes disease (1,2). 

The diseases asbestosis and silicosis are characterized by increased amounts of connective tissue in the lung from inhaling asbestos fibers and silica crystals, respectively (1,2). While there are relatively few new cases of either disease presenting to clinics in North America, there are numerous cases developing in countries where fewer controls and good industrial hygiene are practiced. There are excellent reasons to consider the fundamental cellular and 

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Lanza, A. J., ed. (1938). Silicosis and Asbestosis. Oxford University Press, Oxford. 

Landau, L. D., and Lifshitz, E. M., Fluid Mechanics, Pergamon Press, New York, 1959. Lanza, A. J., in Silicosis and Asbestosis, Oxford University Press, New York, 1938. Lawton, J., and Weinberg, F. J., Electrical Aspects of Combustion, Clarendon Press, Oxford, 1969. 

Erdogdu G, Hasirci V. 1998. An overview of the role of mineral solubility in silicosis and asbestosis. Environ Res 78 38-42. 

Other mineral dusts Dusts of talc, kaolinite, other clays, micas, aluminosilicates. Sources include dusts generated from industrial, commercial activities and products. Inhalation. Mineral-specilic fibrosis, such as talcosis also silicosis and asbestosis due to intermixed crystalline silica and asbestos. 

Many chemicals used in the workplace can damage the body. Effects range from skin irritation and dermatitis to chronic lung diseases such as silicosis and asbestosis or even cancer. The body may be harmed at the point where a chemical touches or enters it. This is called a local effect. When the solvent benzene touches the skin, it can cause drying and irritation (local effect). 

This volume, unique in its concept, not only covers in a comprehensive way the imaging features of the well-known coal worker s pneumoconiosis and the severe forms of silicosis and asbestosis, but also deals extensively with the effects of new organic and inorganic materials, used in the modern chemical industry as well as with the noxious effects of cigarette smoking. 

Individuals whose jobs expose them to unusually high particulate concentrations are especially susceptible to health problems from the pollutant. For example, men and women who work with the mineral asbestos are very prone to development of a serious and usually fatal condition known as asbestosis, in which fibers of the mineral become embedded in the interstices (the empty spaces within tissue) of the lung. Similar conditions are observed among coal workers who inhale coal dust (pneumoconiosis, or black lung disease) textile workers (byssinosis, or brown lung disease) those who work with clay, brick, silica, glass, and other ceramic materials (silicosis) and workers exposed to high levels of beryllium fumes (berylliosis). 

Solid Particles. Dust and fibers from coal, clay, glass, asbestos, and minerals can lead to scarring or fibrosis of the lung lining. Pneumoconiosis, a condition common among coal miners that breathe coal dust, silicosis caused by breathing silica-containing dusts, and asbestosis from asbestos fibers are all well-known industrial pollution diseases. 

The spectrum of classical pneumoconiosis has changed during the past decades in industrialized countries as a result of better control of air dust levels and reduction of workforce in large sectors of industry, the incidence of severe forms of silicosis, coal worker s pneumoconiosis and asbestosis (lung fibrosis), has decreased over time. Most incident cases of disabling pneumoconiosis result from exposures dating back several decades ago. 

Total frequencies of environmental illness are difficult to measure. When causes can be identified, however, scientists observe that frequencies of occurrence of a particular illness vary directly with the severity and extent of exposure. Particularly frequent in the workplace are skin lesions from many different causes and pulmonary diseases related to the inhalation of various dusts, such as coal dust (black lung), cotton dust (brown lung), asbestos fibers (asbestosis), and silica dust (silicosis). Environmental agents can also cause biological effects without overt clinical illness (for example, chromosome damage from irradiation). 

PNEUMOCONIOSIS A group of lung diseases of a chronic fibrotic character due to the inhalation and retention in the lungs of a variety of industrial dusts. The main diseases are asbestosis, silicosis, coalworkers pneumoconiosis and mixed-dust pneumoconiosis less common pneumoconioses are associated with talc, clay or aluminium. 

Hucpcr, W. C. (1955a). Silicosis, asbestosis and cancer of the lung. Am. J. Clin. Pathol. 25 1388. 

Asbestosis is much less common but more senous than silicosis, since once contracted it is more rapidly fatal, and is associated with a liability to lung cancer. 

Bissonnette E, Bubois C, Rola-Pleszczynski M. 1989. Changes in lymphocyte function and lung histology during the development of asbestosis and silicosis in the mouse. Res Commun Chem Pathol Pharmacol 65 211-227. 

Mossman BT, Churg A. 1998. Mechanisms in the pathogenesis of asbestosis and silicosis. Am J Resp CritCare Med 157 1666-1680. 

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