Disease relevance of Chrysotile

• CONCLUSIONS: We found no measurable excess risk of death due to lung cancer among women in two chrysotile-asbestos-mining regions [1].
• Chrysotile, tremolite, and mesothelioma [2].
• Letter: Serpentine supravenous fluorouracil hyperpigmentation [3].
• However, with 50 and 25 micrograms DMBA, nontumorigenic dose levels, a 15 and 23% incidence of tracheal carcinomas occurred when DMBA exposure was followed by a nontumorigenic dose of chrysotile [4].
• After transfection with chrysotile, a minor percentage of introduced plasmid DNA bearing a simian virus 40 origin of replication replicates after 24 hr [5].
• While the debate regarding chrysotile as a risk factor for mesothelioma will likely continue for some time, future research into nonlinear, threshold cancer risk models for chrysotile-related respiratory diseases appears to be warranted [6].

Psychiatry related information on Chrysotile

• Pleural mesothelioma is a malignant neoplasm which is specifically associated with asbestos exposure: the risk is linked with the cubic power of time since first exposure, after allowing for a latency period of 10 years, and depends on the fibre type, as the risk is about three times higher for amphiboles as compared to chrysotile [7].

High impact information on Chrysotile

• Rhapidosomers (cylindrical nucleoprotein rods of bacterial origin) show great structural similarity to the microfibrils of chrysotile asbestos when negatively stained and observed with the electron microscope [8].
• To determine whether asbestos inhalation induces the formation of reactive nitrogen species, three groups of rats were exposed intermittently over 2 wk to either filtered room air (sham-exposed) or to chrysotile or crocidolite asbestos fibers [9].
• Pleural mesothelial cells (rabbit or human) were exposed to asbestos (crocidolite, amosite, or chrysotile) or control particles at moderate doses (1-10 microg/cm2) over 24 h and evaluated for oligonucleosomal DNA fragmentation, loss of membrane phospholipid asymmetry, and nuclear condensation [10].
• IL-1 beta and TNF alpha mRNA transcript expression as well as IGF-1 protein synthesis were also stimulated by chrysotile asbestos [11].
• We have studied the interaction of chrysotile asbestos fibers with rat lung fibroblasts (RLF) in vitro and the consequent changes in PDGF receptor mRNA expression, PDGF binding, and mitogenic activity of PDGF isoforms [12].

Chemical compound and disease context of Chrysotile

• One month later, such treatments induced either no change (xonotlite), granuloma formation (attapulgite and short chrysotile 4T30), or fibrosis (UICC chrysotile B) [13].
• Previous studies in a rat model of asbestosis have demonstrated increased incorporation of tritiated thymidine by bronchiolar and alveolar epithelial cells 19 to 72 h after a single, 5-h exposure to chrysotile asbestos [14].
• It was also found that the metal complexes of all flavonoids were absorbed by chrysotile asbestos fibers considerably better than uncomplexed compounds and probably for this reason flavonoid metal complexes have better protective properties against asbestos induced hemolysis [15].
• The polymer poly-2-vinylpyridine-N-oxide inhibited hemolysis caused by montmorillonite, palygorskite, kaolinite, and silica, but it was less effective with chrysotile [16].
• Carboxymethyl cellulose (CMC), an agent known to blunt chrysotile-induced hemolysis and production of reactive oxygen metabolites by human PMNL, specifically inhibits chrysotile-induced release of collagenase [17].

Biological context of Chrysotile

• In vitro cytogenetic studies of amosite, chrysotile, and crocidolite asbestos have shown that these fibers may induce chromosome abnormalities and an elevated sister chromatid exchange (SCE) rate in mammalian cells [18].
• Chrysotile asbestos upregulates gene expression and production of alpha-receptors for platelet-derived growth factor (PDGF-AA) on rat lung fibroblasts [12].
• We have tested the ability of chrysotile asbestos fibers to introduce plasmid DNA into monkey COS-7 cells and the ability of this DNA to function in both replication and gene expression [5].
• Chrysotile fibers are at least as effective as calcium phosphate in standard transfection assays at optimal ratios of asbestos to DNA [5].
• Chrysotile asbestos treatment of the cells significantly induced chromosome changes in a dose-dependent manner [19].

Anatomical context of Chrysotile

• Four weeks after the start of DMBA exposure (when all carcinogen had been released from the pellets), the spent pellets were removed, and 200 micrograms chrysotile, a nontumorigenic dose of asbestos, was introduced into the lumina of the preexposed tracheas [4].
• To investigate the mechanisms of asbestos-induced carcinogenesis, expression of c-fos and c-jun protooncogenes was examined in rat pleural mesothelial cells and hamster tracheal epithelial cells after exposure to crocidolite or chrysotile asbestos [20].
• Although xrs-5 cells did not show any increase in sensitivity to chrysotile fibers in short-term (4-h) treatment when compared with wild-type CHO cells, longer-term exposure (24 h) gave significantly lower cell survival accompanied by a cell growth delay as well as a higher DNA DSB induction in this mutant cell line [21].
• These results demonstrate that a brief exposure to chrysotile asbestos causes a rapid response that involves an influx of macrophages to the first alveolar duct bifurcations and alterations in the alveolar epithelium [22].
• Pleural mesothelial cells (PMC) from the parietal pleura of rats were incubated in culture with UICC A chrysotile fibers [23].

Associations of Chrysotile with other chemical compounds

• In these studies, cloned diploid hamster tracheal epithelial cells were examined in a number of short term (3-24 h) and long term (greater than 24 h) biological assays for their responsiveness to crocidolite asbestos in comparison to other fibers (chrysotile asbestos, Code 100 fiberglass) and particulates (riebeckite, antigorite, glass beads) [24].
• Simultaneously, moderate dosages of chrysotile and other agents increasing ROS levels (hydrogen peroxide, H2O2 and ethyl-methanesulfonate, EMS) inhibited cell cycle progression, in particular G1-to-S transition, in fibroblasts, but not in mesothelial cells [25].
• Alveolar macrophages stimulated with titanium dioxide, chrysotile asbestos, and residual oil fly ash upregulate the PDGF receptor-alpha on lung fibroblasts through an IL-1beta-dependent mechanism [26].
• Furthermore, crocidolite, chrysotile, and alpha-cristobalite stimulated pleural mesothelial cell fibronectin synthesis [27].
• Tritiated thymidine incorporation by epithelial cells of bronchioles in peripheral regions of the lungs was significantly increased, as much as 20-fold, 33 h after chrysotile exposure [14].

Gene context of Chrysotile

• We have investigated the mitogenic and chemotactic role of platelet-derived growth factor (PDGF) in pulmonary fibrogenesis induced by chrysotile asbestos [28].
• Suspensions of amosite, chrysotile, or crocidolite asbestos in concentrations as low as 5 micrograms/ml enhanced release of IL-8 from HPMC during 6 h of incubation at 37 degrees C. Electron microscopy of asbestos-treated HPMC showed that the cells avidly engulfed each of the different types of asbestos fibers [29].
• The effects of crocidolite, amosite, and chrysotile on the EGFR phosphorylation state appeared to be directly related to the amount of iron mobilized from these fibers [30].
• The expression of IL-1 alpha by fibers (crocidolite, chrysotile, TW, and RCF) may be a good indicator of the pathologic potential of fibers [31].
• Rats exposed by inhalation to either chrysotile or crocidolite asbestos fibers also had greater amounts of MCP-1 protein in their pleural lavage fluid than did sham-exposed rats [32].

Analytical, diagnostic and therapeutic context of Chrysotile

• The intrathoracic administrations of pulverized chrysotile, of cigarette smoke condensate and crocidolite, and of coarse cotton lint, and of intravenous injections of air particulate extract were associated with endocardial tumor in 1 of 15 rats each [33].
• Here, we show that inhaled chrysotile asbestos fibers cause increased myeloperoxidase activity in bronchoalveolar lavage fluids (BALF) and myeloperoxidase immunoreactivity in epithelial cells lining distal bronchioles and alveolar ducts, sites of initial lung deposition of asbestos fibers [34].
• Rat pleural mesothelial cells (PMCs) in culture at the exponential growing phase were exposed to 5 micrograms/ml of chrysotile (CH) or crocidolite (CR) asbestos fibers: the cells and their chromosomes were studied 48 hours thereafter by light, scanning, and transmission electron microscopy (LM, SEM, TEM) [35].
• The total number of fibers/per gram wet lung in the plaque group (114 x 10(3)) was similar to that in the control group (99 x 10(3), as was the number of chrysotile fibers (51 x 10(3) versus 29 x 10(3)) [36].
• An extensive review of the epidemiological cohort studies was undertaken to evaluate the extent of the evidence related to free chrysotile fibers, with particular attention to confounding by other fiber types, job exposure concentrations, and consistency of findings [37].

References