silicon and Asbestosis

Consideration of the human epidemiology of diseases arising from exposure to naturally occurring and man-made mineral fibers encompasses the several forms of asbestos (chrysotile, crocidolite, amosite, anthophyllite, tremolite-actinolite), other naturally occurring silicates (talc, sepiolite, erionite, attapulgite, vermiculite, and wollastonite), and man-made mineral fibers (glass continuous filament, glass/rock/slag insulation wools, ceramic and other refractory fibers, and glass microfibers). The diseases arising from exposures to some of these fibers include pleural thickening (plaques, diffuse pleural thickening, and calcification), pulmonary fibrosis, lung cancers, mesothelioma of the pleura and peritoneum, and other cancers). Risk factors important in assessing these diseases include assessment of latency, duration of exposure, cumulative exposure, fiber origin and characteristics (length and diameter), other possible confounding occupational or environmental exposures, and smoking. Methodological issues commonly presenting problems in evaluation of these data include assessment of the adequacy of environmental exposures, particularly in regard to fiber identification, distribution, and concentration over the duration of exposure, and the adequacy of study design to detect health effects (disease frequency, latency, and cohort size). Research priorities include further assessment and standardization of pleural thickening relative to fiber exposure, uniform mesothelioma surveillance, further epidemiological assessment of certain silicate and man-made mineral fiber cohorts with emphasis given to assessment of tremolite and small diameter glass and ceramic fibers. Further assessment of possible health risks of the general public should await improved definition of relevant fiber exposure in ambient air.

Topics: Asbestos; Asbestosis; Humans; Lung Neoplasms; Mesothelioma; Minerals; Neoplasms; Pleural Diseases; Respiratory Tract Diseases; Silicon

To further study the pathogenic mechanism of crocidolite, the imperceptible changes of crocidolite surface in rat were observed.. The animal model was established and the changes in the rat infected with dust were observed by use of microscopy, SEM, differential thermal analysis and IR spectroscopy.. In the course of interaction between organism protein and crocidolite, the protein symmetry decreased and structure loosened. The silicon of crocidolite was bonded with the alkyl, amido- of protein. New absorption bands of Si-O-C(N), Si-R clearly appeared. The organism cleared the dust by means of dissolution, enwrapping, winding or in the way of biochemical dissolution, and the fibre became shortened, broken, bifurcated, ends-rounded, and also it could dissolve, transfer and chemically react on surface.. The results showed that the surface radicals of asbestos fibre reacted with some albumen in tissue and hence formed new surface mediator. It is a new form of dissolution and reaction of fibre in vivo that fibres in alveoli transform to carbonate. The residual substances of crocidolite are mainly Si-O. Tissue membrane is the retardation cingulum of dust transference in vivo.

Topics: Animals; Asbestos, Crocidolite; Asbestosis; Dust; Microscopy, Electron, Scanning; Mineral Fibers; Pleural Diseases; Pulmonary Fibrosis; Rats; Silicon

The physical and microchemical alterations of chrysotile and amosite asbestos (Union International Contre le Cancer standard samples) in the hamster lung and in vitro following acid treatments were studied by scanning electron microscopy (SEM) and x-ray energy-dispersive spectrometry (XEDS). Following intratracheal instillation, the ratio of short chrysotile fibers (less than 5 microns in length) decreased initially from 38% to 13% in the hamster lung, but increased again to 56% 2 years after the instillation. The majority of these new short chrysotile fibers had diameters less than 0.05 micron. Contrary to this, short amosite fibers (less than 5 microns in length) decreased from 41% initially to 4% 2 yr after instillating into the hamster lung. The diameters of amosite fibers appeared much less altered than that of chrysotile during the same time period. After 2 yr in the hamster lung, 33% of chrysotile and 68% of amosite found were asbestos bodies. The Si/Mg ratios of chrysotile fibers with diameters less than 0.2 micron were significantly higher than those with diameters between 0.2 and 0.6 micron in all groups: this relationship was reversed in all amosite groups. The Si/Mg ratios of the instillated and acid-treated chrysotile fibers were both higher than that of the same-sized control fibers. Acid treatments of chrysotile fibers in asbestos bodies from the hamster lung further altered their Si/Mg ratio. The Si/Mg ratios of the instillated amosite fibers were lower than that of the same-sized control fibers, but the difference between them disappeared following acid treatments. The hamster lung disposed of both chrysotile and amosite fibers smaller than 5 microns efficiently. Chrysotile and its asbestos bodies appeared to lose Mg ions and to fragment continuously in the hamster lung, and also in vitro with acid treatments. Amosite appeared also to fragment but lose more silicon than magnesium ions, at a much slower rate than that of chrysotile, presumably from the difference in their basic structures.

Topics: Acids; Animals; Asbestos; Asbestosis; Cricetinae; Lung; Magnesium; Mesocricetus; Microscopy, Electron, Scanning; Silicon; Time Factors

Topics: Animals; Asbestosis; Guinea Pigs; Humans; Lipids; Macrophages; Magnesium; Microscopy; Microscopy, Electron, Scanning; Osmium; Pulmonary Alveoli; Silicon; Silicosis; Spectrophotometry

Topics: Aluminum; Animals; Asbestos; Asbestosis; Carbon; Carbon Compounds, Inorganic; Dust; Environmental Exposure; Lung; Rats; Silicon; Silicon Dioxide; Silicosis; Time Factors

Topics: Aluminum Silicates; Animals; Asbestosis; Cricetinae; Dust; Ferritins; Injections; Lung; Pneumoconiosis; Silicon; Silicon Dioxide; Staining and Labeling