Asbestos, white is a white asbestos is a slender, fine, flaxy fiber. Long term occupational exposure to the dust can result in lung cancer. Asbestos is resistant to fire and most solvents. The primary hazard is the threat to the environment. Immediate steps should be taken to limit its spread to the environment. It is used as a heat resistant material, in cement, furnace bricks, and brake linings.
颜色/状态：
Crystal system: monoclinic (pseudoorthorhombic); usually white to grayish green; may have tan coloration
Asbestos fibers are not metabolized in the true sense of the word; however, a number of animal studies indicate that chrysotile fibers are physically altered in the lung after intratracheal injection. Following phagocytosis, chrysotile fibers were observed to decrease in size, become transparent, and, in some cases, break into fragments. ... These changes in fiber shape and size may directly impact fiber clearance and toxicity in the lung.
Asbestos fibers are not metabolized in the normal sense of the word, and amphibole fibers that are retained in the lung do not appear to undergo any major changes. However, chrysotile fibers appear to undergo some type of breakdown or alteration in the lung. Some of the fibers will be deposited in the air passages and on the lung cells. Most fibers are removed from the lungs by being carried away or coughed up in a layer of mucus to the throat, where they are swallowed into the stomach. Fibers that are deposited in the deepest parts of the lung are removed more slowly. In fact, some fibers may move through the lungs and can remain in place for many years and may never be removed from the body. Longer fibers that are retained in the lung may undergo a number of processes including translocation, dissolution, fragmentation, splitting, or protein encapsulation. Long fibers that reside in the lung can become encapsulated in protein, forming what is often referred to as an "asbestos body". In response to asbestos fibers, alveolar macrophages produce reactive oxygen species in an attempt to digest the fiber. The reactive oxygen species include hydrogen peroxide and superoxide radical anion (O2-). Fibers that have been swallowed (those present in water, or those moved to the throat from the lungs) almost all pass along the intestines within a few days and are excreted in the feces. (L222)
Asbestos fibers are not metabolized in the normal sense of the word, and amphibole fibers that are retained in the lung do not appear to undergo any major changes. Some of the fibers will be deposited in the air passages and on the cells that make up your lungs. Most fibers are removed from the lungs by being carried away or coughed up in a layer of mucus to the throat, where they are swallowed into the stomach. Fibers that are deposited in the deepest parts of the lung are removed more slowly. In fact, some fibers may move through the lungs and can remain in place for many years and may never be removed from the body. Longer fibers that are retained in the lung may undergo a number of processes including translocation, dissolution, fragmentation, splitting, or protein encapsulation. Long fibers that reside in the lung can become encapsulated in protein, forming what is often referred to as an "asbestos body". In response to asbestos fibers, alveolar macrophages produce reactive oxygen species in an attempt to digest the fiber. The reactive oxygen species include hydrogen peroxide and superoxide radical anion (O2-). Fibers that have been swallowed (those present in water, or those moved to the throat from the lungs) almost all pass along the intestines within a few days and are excreted in the feces. (L222)
IDENTIFICATION AND USE: Chrysotile asbestos forms monoclinic crystals, which are usually white to grayish green, but may have tan coloration. Chrysotile, the most abundant form of asbestos in industrial applications, occurs naturally in fiber bundle lengths ranging from several millimeters to over 10 cm. Chrysotile was the predominant fiber type in use in buildings. Other uses include paper products, paint and caulking, textiles and plastics. HUMAN STUDIES: Most airborne chrysotile fibers are considered respirable because their fiber diameters are less than 3 um. Analyses of human lungs of workers exposed to chrysotile asbestos indicate much greater retention of tremolite, an amphibole asbestos commonly associated with commercial chrysotile in small proportions, than of chrysotile. In humans commercial grades of chrysotile have been associated with an increased risk of lung cancer in epidemiological studies of exposed workers. Mesothelioma and digestive-tract cancer were observed in workers occupationally exposed to chrysotile. An excess of laryngeal cancer was reported in studies of chrysotile miners. Cytogenetic study of workers in the chrysotile asbestos industry demonstrated that chromosome type aberrations were presented by paired fragments and centromere rupture, those of chromatide type - by deletions, single fragments and chromatide ruptures. ANIMAL STUDIES: In laboratory rats, chrysotile fibers are deposited primarily at the alveolar duct and bifurcations. In the nasopharyngeal and tracheobronchial regions, chrysotile fibers are cleared via mucociliary clearance. At the alveolar duct bifurcations the fibers are taken up by epithelial cells. Fiber length is an important determinant of alveolar clearance of chrysotile fibers. Short fibers (less than 5 um long) are cleared more rapidly than long fibers. Chrysotile is more rapidly cleared from the lung than are ampohiboles including crocidolite and amosite. Experimental samples of chrysotile fibers have been shown in long term inhalation studies to cause fibrogenic and carcinogenic effects in laboratory rats. These effects include interstitial fibrosis and cancer of the lung and pleura. Fibrogenic and carcinogenic effects have also been found in long term studies in rats using other modes of administration (intratracheal instillation and intrapleural or intraperitoneal injection.) When filter material containing chrysotile was added to the diet of rats, the overall incidence of malignant tumors (including kidney, lung, and liver tumors) was increased. Oral administration of chrysotile did not cause tumors in hamsters. Dietary administration of chrysotile asbestos fibers of short or intermediate lengths did not cause tumors in female rats, but dietary exposure to the intermediate-length fibers resulted in a low incidence of benign adenomatous polyps of the large intestine in male rats. Placental transmission of chrysotile asbestos fibers from mother to fetus with reliable increased incidence of neoplasma in first generation was demonstrated in rats. Chrysotile demonstrated fetotoxicity and teratogenicity in mice. Chinese hamster cells exposed to 0.01 ng/mL chrysotile had a significantly increased number of chromosome abnormalities. Chrysotile induced unscheduled DNA synthesis in rat hepatocytes. Chrysotile did not induce micronuclei in bone-marrow cells of mice or chromosomal aberrations in bone-marrow cells of rhesus monkeys treated in vivo. Based on the broad surface area of asbestos fibers and their ability to enter the cytoplasm and nuclei of cells, it was hypothesized that proteins that adsorb onto the fiber surface play a role in the cytotoxicity and carcinogenesis of asbestos fibers. Chrysotile directly interact with chromatin structure through different mechanisms. Furthermore, RNA-binding proteins preferably interacted with chrysotile, suggesting that chrysotile may also interfere with transcription and translation. ECOTOXICITY STUDIES: L. gibba plants were exposed to four concentrations (0.5, 1.0, 2.0, and 5.0 ug/mL) of chrysotile asbestos under laboratory conditions. Chrysotile exposure caused a decrease in total and reduced glutathione and an enhancement in the oxidized glutathione as well as the reduced/oxidized glutathione ratio. An increase in ascorbate pool size, and reduced as well as oxidized ascorbate was found to be accompanied by a decrease in the ratio of reduced/oxidized ascorbate.
When asbestos fibers are inhaled, many are deposited on the epithelial surface of the respiratory tree. Fibers that are retained in the lung or mesothelium for long periods of time are capable of producing chronic inflammation and fibrotic and tumorigenic effects. These effects may be mediated by direct interactions between the fiber and key cellular macromolecules, or they may be mediated by the production of reactive oxygen species and other cellular factors originating from alveolar macrophages. In addition, the physical-chemical nature of the fiber appears to be an important determinant of toxicity. It is generally agreed that exposure to amphibole fibers can produce mesothelioma, and that the potency of amphibole fibers to produce mesothelioma is greater than that of chrysotile. Asbestos fibers can adsorb to a variety of cellular macromolecules (e.g., proteins,membrane lipids, RNA, DNA). The coulombic forces between the asbestos fiber and some of these macromolecules may induce conformational changes, and these changes could affect protein function and chromosomal fidelity. Chrysotile fibers were found to bind to cytochrome P-450, thereby decreasing mono-oxygenase activity. Chrysotile and crocidolite fibers were also found to bind to artificial lipid membranes in vitro, thereby increasing membrane rigidity. Fibers found to be translocated near the nucleus can interact with the cytoskeleton and interfere with chromosome segregation. (L222)
When asbestos fibers are inhaled, many are deposited on the epithelial surface of the respiratory tree. Fibers that are retained in the lung or mesothelium for long periods of time are capable of producing chronic inflammation and fibrotic and tumorigenic effects. These effects may be mediated by direct interactions between the fiber and key cellular macromolecules, or they may be mediated by the production of reactive oxygen species and other cellular factors originating from alveolar macrophages. In addition, the physical-chemical nature of the fiber appears to be an important determinant of toxicity. It is generally agreed that exposure to amphibole fibers can produce mesothelioma, and that the potency of amphibole fibers to produce mesothelioma is greater than that of chrysotile. Asbestos fibers can adsorb to a variety of cellular macromolecules (e.g., proteins,membrane lipids, RNA, DNA). The coulombic forces between the asbestos fiber and some of these macromolecules may induce conformational changes, and these changes could affect protein function and chromosomal fidelity. Fibers found to be translocated near the nucleus can interact with the cytoskeleton and interfere with chromosome segregation. (L222)
There is sufficient evidence in humans for the carcinogenicity of all forms of asbestos (chrysotile, crocidolite, amosite, tremolite, actinolite, and anthophyllite). Asbestos causes mesothelioma and cancer of the lung, larynx, and ovary. ... There is sufficient evidence in experimental animals for the carcinogenicity of all forms of asbestos (chrysotile, crocidolite, amosite, tremolite, actinolite and anthophyllite). All forms of asbestos (chrysotile, crocidolite, amosite, tremolite, actinolite and anthophyllite) are carcinogenic to humans (Group 1).
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
石棉及其所有商业形式根据基于人类研究的致癌性充分证据被认为是一种人类致癌物。/石棉/
Asbestos and all commercial forms of asbestos are known to be human carcinogens based on sufficient evidence of carcinogenicity from studies in humans. /Asbestos/
.../After/ chrysotile /was fed/ to rats... the presence of fibers of the material /was noted/ in many sites in colonic epithelium and lamina propria... .
In studies in which chrysotile, labelled intrinsically with radioactive trace metals by neutron irridation, was injected intrapleurally into rats. ... Evidence for passage of a small amount of the fiber from the pleural cavity & lungs into such other organs as the liver /was found/; after the intrapleural inoculation ... into rats, as much as 22% of the admin dose was found later in the liver. In a similar expt ... /it was/ reported that a population of radionuclides, consistent with that expected on the basis of the labelled chrysotile, was found in the heart, lungs, diaphragm & chest muscles.
In cases of lung cancer without lung fibrosis, a higher concentration of asbestos fibers, mostly of the chrysotile type, was clearly demonstrated in peripheral areas of the lung. Optical and transmission electron microscopic study of lung and pleura revealed a preferential accumulation of chrysotile versus amphibole fibers in pleura; the mean length of the fibers was greater in the lung and visceral pleura than in the parietal pleura, this being particularly the case for the amphiboles. There was no relationship between the numerical concentration of fibers in lung parenchyma and that in parietal pleura. Generally, the concentration was always less in pleura than in parenchyma; however, the distribution of chrysotile microfibrils in the pleura was not homogenous, and in some areas high concentrations identical to those in the parenchyma could be observed.
The retention of different types of asbestos in rats following exposure to the same concentration of respirable dusts... /has been described/. For the amphiboles, there was a similar pattern with an almost proportional increase of lung dust with dose. Much less dust was found for the chrysotiles, and no increase of dust content was shown in the lungs. Dust in the lungs of animals with 6 months' exposure had been partially cleared 18 months after the inhalation period. About 74% of the amosite and crocidolite and 41% of the anthophyllite were eliminated. The elimination rate of chrysotiles could not be determined exactly, because of their low occurrence in the lung.
