Asbestos is a family of crystalline hydrated silicates that form fibers. Based on epidemiologic studies, occupational exposure to asbestos is linked to

Localized fibrous plaques or , rarely, diffuse pleural fibrosis
Pleural effusions
Parenchymal interstitial fibrosis ( asbestosis)
Bronchogenic carcinoma
Mesotheliomas
Laryngeal and perhaps other extrapulmonary neoplasms including colon carcinomas.

An increased incidence of asbestosis- related cancer in family members of asbestos workers has alerted the general public to the potential hazards of asbestos in the environment. The proper public health policy toward lo-level exposures that might be encountered in old buildings or schools is controversial, with some experts questioning the wisdom of expensive asbestos abatement programs for environments with airborne fiber counts that are up to 100 fold lower than allowed by occupational standards.

Pathogenesis. Concentration, size , shape, and solubility of the different forms of asbestos dictate, whether disease cocurs. There are two distinct geometric forms of asbestos: sepentine (curly and flexible fibers) and amphibole (stright, stiff, and brittle fibers) The serpentine chrysotile chemical form accounts for most of the asbestos used in industry. Amphiboles include crocidolite, amosite, tremolite, anthophyllite, and actinolyte. This confusing array of terms is important because amphiboles, even though less prevalent, are more pathogenic than chrysotiles, particularly with respect to induction of malignant pleural tumers ( mesotheliomas). Some studies of mesotheliomas have shown the link is almost always to amphibole exposure. The relatively few cases of mesotheliomas arising in chrysotile workers are in all likelihood due to contamination of chrysotile with the amphibole tremolite.

The greater pathogenicity of straight and stiff amphiboles is apparently related to their aerodynamic properties and solubility. Chrysotiles, with their more flexible, curled structure, are likely to become impacted in the upper respiratory passages and removed by the mucociliary elevator. Furthermore, once trapped in the lungs, crysotiles are gradually leached from the tissues because they are more soluble than amphiboles. In contrast, the straight , stiff amphiboles may align themselves in the airsteam and thus be delivered deeper into the lungs, where they can penetrate epithelial cells and reach the interstitium. The length of amphibole fibers also plays a role in pathogenicity, those longer than 8 mm and thinner than 0.5 mm being more injurious than shorter, thicker ones. Nevertheless, both amphiboles and serpentines are fibrogenic, and increasing doses are associated with a higher incidence of all asbestos related disease except that only amphibold exposure correlates with mesothelioma. In contrast to other inorganic dusts, asbestos can also act as both a tumor initiator and a tumor promoter. Potentially toxic chemicals absorbed onto the asbestos fibers however undoubtedly contribut to the oncogenicity of the fibers. For example, the adsorption of carcinogens in tobacco smoke on to asbestos fibers may well be important in the remarkable synergy between tobacco smoking and the development of bronchogenic carcinoma in asbestos workers. One study of asbestos workers found a 5 fold increase of bronchogenic carcinoma for asbestos exposure alone, while asbestos exposure and smoking together led to a 55 fold increase in the risk of lung cancer.

Asbestosis, similar to the other pnumoconioses, depends on the interaction of inhaled fibers with lung macrophages and other parenchymal cells. The initial injury occurs at bifurcations of small airways and ducts, where the stiff fibers land and penetrate. Macrophages both alveolar and interstitial attempt to ingest and clear the fibers and are activated to release chemotactic factors and fibrogenic mediators that amplify the response. Chronic deposition of fibers and persistent release of mediators eventually leads to generalized interstitial pulmonary inflammation and interstitial fibrosis. It is not completely understood why silicosis is a nodular fibrosing disease and asbestosis a difuse interstitial process. The more diffuse distribution may be related to the ability of asbestos to reach alveoli more consistently or its ability to penetrate epithelial cells, or to both.