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PubMed1988

Results of recent experimental research on the carcinogenicity of natural and modified asbestos.

Long-term experimental bioassays were carried out on natural asbestos of different types and origin (crocidolite, chrysotile, amosite, antophyllite), on asbestos cement, and on industrially modified chrysotiles. The materials were tested on Sprague-Dawley rats by intraperitoneal and intrapleural injection. The experiments were carried out with highly standardized procedures on all materials to enable comparative evaluation of the results. The data presented confirm that asbestos of different types produces peritoneal and pleural mesotheliomas, show that asbestos cement is also mesotheliomatogenic, and demonstrate that the peritoneum is more responsive than the pleura. Furthermore, evidence is provided that the mesotheliomatogenic effects of different types of asbestos vary with the types and origin of the minerals, and that physical and chemical modifications of the natural chrysotile can lower its carcinogenic effect.

Administration, Inhalation↗

PubMed1992

Biphasic lung diffusing capacity: detection of early asbestos induced changes in lung function.

Asbestos related changes in the single breath carbon monoxide diffusing capacity (DLCO) were longitudinally analysed in 14 subjects exposed predominantly to chrysotile asbestos in an asbestos cement factory. These subjects were examined annually over the past nine years; their lung function was initially characterised with increased DLCO as the sole functional abnormality and they had normal chest radiographs. The radiological examination included a chest x ray film and, in the past two years, high resolution computed tomography (HRCT). A biphasic DLCO change was found: an initial increase followed by a relative decrease. The increase in DLCO was mainly caused by an increase in the membrane component (Dm). Indomethacin treatment applied after the sixth annual follow up significantly reduced DLCO and Dm. The decrease in DLCO correlated well with the parenchymal abnormalities found on HRCT, whereas the chest x ray film profusion score for small opacities (ILO classification) was unchanged. In conclusion, the data suggested that, as well as the absolute values of pulmonary function tests, the measurement of progression of functional parameters is essential in the assessment of pleural and parenchymal disease of the lung related to exposure to asbestos. High resolution computed tomography is suggested as the radiological method of choice in subjects with an isolated decrease in DLCO. Exposure to asbestos can be associated not only with a reduction in DLCO, but also with a temporary increase in DLCO caused by a subclinical inflammatory reaction.

Adult↗

PubMed1995

Radiological changes in asbestos cement workers.

OBJECTIVE: To explore associations between exposure to asbestos cement dust and radiographic findings in lung parenchyma and pleura. METHODS: Radiographs from 174 blue collar workers and 29 white collar workers from an asbestos cement plant formed one part of the study. Progression of small opacities was further studied in those 124 blue collar workers, for whom two radiographs taken after the end of employment were available. The median readings from five readers who used the full ILO 1980 classification were used. As exposure indices, time since start of employment, duration of employment, cumulative exposure, and average intensity of asbestos exposure were used. The influence of age and smoking was also considered in multiple logistic regression analyses. RESULTS: Small opacities (profusion > or = 1/0) were closely correlated with time related exposure variables, and showed weaker association with intensity based exposure variables. The odds ratio (OR) for small opacities was equal to 2.8 (90% CI 1.2, 6.7) in the > 30 f(fibre)-y/ml group, compared with those in the 0-10 f-y/ml group. Progression of at least two minor ILO categories after the end of employment was seen in 20%. Also, pleural thickening was closely related to time. By contrast, costophrenic angle obliterations were not associated with the time related variables, but closely associated with the intensity of asbestos exposure, and tended to occur during employment. The OR was 4.5 (90% CI 1.3, 15) in the > 2 f/ml group, compared with those in the 0-1 f/ml group. CONCLUSIONS: In these workers, exposed mainly to chrysotile but also to small amounts of amphibole, the risk of radiographically visible parenchymal abnormality was substantially increased and strongly dependent on time related exposure variables. Progression was found long after the end of exposure. The findings on costophrenic angle obliterations, supposed to be sequelae of benign pleural effusions, were consistent with an immediate reaction triggered by intense asbestos exposure.

Adult↗

PubMed1997

Analysis of cell cycle disruptions in cultures of rat pleural mesothelial cells exposed to asbestos fibers.

The control of DNA integrity in mammalian cells is important to maintain the cell homeostasis and prevent neoplastic transformation. Control of cell division and cell death permits repair or elimination of damaged cells. Since asbestos fibers can produce DNA damage, chromosome alterations and apoptosis in several sorts of cells, including mesothelial cells, it was interesting to investigate cell cycle disturbances in rat pleural mesothelial cells (RPMC) treated with asbestos fibers. Cell cycle analyses were performed in RPMC exposed to crocidolite (10 and 20 microg/cm2) and chrysotile (5 and 10 microg/cm2) for different times (4 to 48 h). Both fiber types entailed a G2/M accumulation in agreement with a delay in the mitosis course. Chrysotile fibers produced a G0/G1 accumulation associated with a time-dependent p53 and p21 expression. Crocidolite exposure resulted in a delay in the G1/S transition paralleling a low rate of p53 expression. These results are in agreement with a DNA damaging potential of asbestos fibers since similar results were found following RPMC exposure to gamma rays. In asbestos-treated RPMC, a low rate of apoptosis was found suggesting that RPMC may follow a DNA repair pathway that could contribute to the formation of DNA lesions. In addition, the cell cycle disturbances at the G2/M checkpoint suggest that genetically altered cells have progressed through the cycle and support the already published findings on the ability of asbestos fibers to impair cell division.

Animals↗

PubMed1993

Chrysotile asbestos upregulates gene expression and production of alpha-receptors for platelet-derived growth factor (PDGF-AA) on rat lung fibroblasts.

PDGF isoforms have been postulated to serve as mediators of fibroblast proliferation and chemotaxis during lung fibrogenesis induced by asbestos inhalation. 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. Northern blot analysis revealed that mRNA for the PDGF-receptor alpha subtype (PDGF-R alpha) on RLF was upregulated after a 24-h exposure to asbestos in culture (0.5-15 micrograms fibers/cm2). [125I]PDGF-BB receptor assays showed that normal RLF possess mainly PDGF-R beta and a paucity of PDGF-R alpha. In agreement with the Northern data, saturation binding of [125I]PDGF-BB to RLF exposed to asbestos demonstrated an approximately 40% increase in binding sites accompanied by a twofold decrease in receptor affinity. Treating asbestos-exposed RLF with PDGF-AA, which binds only PDGF-R alpha, blocked the PDGF binding sites that were upregulated by fiber exposure. PDGF-AA had increased mitogenic potency for fiber-exposed RLF, but PDGF-BB was a less potent mitogen for these RLF. Nonfibrogenic carbonyl iron spheres induced similar changes in PDGF growth responses. These data show that inorganic particulates alter the PDGF-R alpha population on RLF without significant change in PDGF-R beta.

Animals↗

PubMed1983

Interactions of chrysotile asbestos with erythrocyte membranes.

Chrysotile asbestos causes lysis of red blood cells. It has been proposed that the mechanism of hemolysis is mediated through interactions between asbestos and cell membrane glycoproteins. Our studies support this concept and the following results are reported. Electron microscopy shows that asbestos fibers distort red blood cells and bind to cell membranes which may become wrapped around the fibers. This reaction is prevented by pretreatment of the cells with neuraminidase. The distribution of lectins which bind to membrane glycoproteins is altered by treating the cells with asbestos. Cell distortion and membrane deformation consequent to asbestos treatment correlate with a clear increase in the ratio of intracellular Na+:K+ ions.

Animals↗

PubMed1987

A possible mechanism of chrysotile asbestos toxicity.

In vitro evaluations of heat treated and/or irradiated chrysotile asbestos indicate the importance of electron transfer in determining the biological outcome of asbestos exposure. Regardless of the assay system used, all show the same trends. Namely, heat treatment reduces cytotoxicity while heat treatment in combination with irradiation increases activity over heat treatment alone. Furthermore, studies of BSA and DNA binding consistently indicate a lower molecular adsorption for heated asbestos. BSA and DNA adsorption are similar for untreated, irradiated and heated or irradiated samples. Physical and chemical analyses indicate that the size and elemental composition are unaffected by the treatment processes. X-ray diffraction indicates no change in the crystal structure of chrysotile asbestos. IR spectroscopy suggests that heat treatment affects the external hydroxyl group population while heat treatment and irradiation may repopulate this functional group. A proposed mechanism consistent with the biological and physical characterization is based upon electron transfer from the chrysotile asbestos matrix to biological receptors.

Adsorption↗

PubMed1990

Increases in endogenous antioxidant enzymes during asbestos inhalation in rats.

Although the pathogenesis of asbestos-induced pulmonary damage is still not completely understood, an important role has been attributed to active oxygen species. In the present paper we present results of a study investigating the effect of crocidolite asbestos inhalation on different lung antioxidant enzymes in rats. During the development of pulmonary fibrosis induced by crocidolite asbestos, lung superoxide dismutase, catalase and selenium-dependent glutathione peroxidase activities increased, indicating an adaptive response to increased pulmonary oxidant stress. However, this adaptive response obviously is not sufficient to protect the lung from asbestos-induced pulmonary damage. Considering the role of active oxygen species in both the fibrotic process and tumor promotion, it is hypothesized that antioxidants may also protect the lung from chronic asbestos-induced pulmonary damage such as bronchogenic carcinoma.

Animals↗

PubMed2002

Does asbestos exposure cause non-Hodgkin's lymphoma or related hematolymphoid cancers? A review of the epidemiologic literature.

Asbestos exposure has been linked to non-Hodgkin's lymphoma (NHL) and other types of hematolymphoid cancer (HL-CA) in several case reports and epidemiologic studies. This review covers the scientific and medical literature on the issue of whether asbestos exposure is a cause of NHL or other HL-CAs. Studies of animals exposed to asbestos have not shown an increase in NHL or other types of HL-CA. Although some patients with asbestosis have mild immunologic abnormalities, 32 of 35 epidemiologic studies of asbestos exposure in humans are negative for NHL or other HL-CAs. Therefore, it can be concluded that there is no increased risk of NHL or other HL-CAs associated with asbestos exposure.

Adult↗

PubMed1998

Radiographic abnormalities among Finnish construction, shipyard and asbestos industry workers.

OBJECTIVES: The prevalence of asbestos-related radiographic abnormalities was surveyed among Finnish construction, shipyard, and asbestos industry workers. METHODS: The radiographic screening focused on active and retired workers who were under the age of 70 years and had been employed for at least 10 years in construction or for at least 1 year in shipyards or in the asbestos industry. In 1990-1992, 18,943 people participated in an X-ray examination of the lungs and an interview on work history and exposure. The criteria for a positive radiological finding were (i) small irregular lung opacities clearly consistent with interstitial pulmonary fibrosis (ILO 1/1 or higher), (ii) lung opacities indicating mild pulmonary fibrosis (ILO 1/0) with unilateral or bilateral pleural plaques, (iii) marked adhesions with or without thickening of the visceral pleura, or (iv) findings consistent with bilateral pleural plaques. RESULTS: Fulfilling the criteria were 4133 workers (22%) (22% from construction, 16% from shipyards, and 24% from the asbestos industry). The radiological findings included signs of pulmonary fibrosis (3%), changes in the visceral pleura (7%), bilateral plaques (17%), and unilateral plaques (10%). Occupational disease was diagnosed according to the Finnish insurance regulations for three-fourths of those referred for further examinations, 96% being abnormalities in the pleura and 4% being asbestosis. CONCLUSIONS: Exposure to asbestos dust has been common in ordinary construction work, and, consequently, radiographic abnormalities (mostly pleural) occur frequently among active and retired construction workers.

Adult↗

PubMedDate not supplied

[Sanitary characteristics of the production of asbestos membranes].

The paper presents preliminary results of sanitary assessment of the production of asbestos membranes. The production may emit highly disperse asbestos-containing aerosols of disintegration with low levels of filamentous particles and respirable fibers of chrysotile-asbestos into the air of working areas. It is concluded that latest chrysotile-asbestos processing is not a significant source of air pollution in the working areas where asbestos-containing and related noxious substances are present.

Aerosols↗

PubMed1992

Increased manganese superoxide dismutase protein in type II epithelial cells of rat lungs after inhalation of crocidolite asbestos or cristobalite silica.

Manganese-containing superoxide dismutase (Mn-SOD) is a mitochondrial enzyme implicated in cellular defense from oxidative damage. We investigated the immunocytochemical distribution and protein concentration of Mn-SOD in rat lungs in response to aerosolized crocidolite asbestos or cristobalite silica, fibrogenic minerals eliciting generation of oxidants by cellular and acellular pathways. Rats were exposed to 7-10 mg/m3 dust for 6 hours a day for 10 days. Experimental and sham control rats were euthanized 10 days after cessation of exposure, and lungs prepared for immunocytochemistry and determination of amounts of Mn-SOD protein. Quantitation of Western blots showed that the amount of immunodetectable Mn-SOD increased in lungs exposed to asbestos or silica by approximately 1.3- and 2.4-fold, respectively, when compared with sham controls. Immunoelectron microscopy using the protein A-gold technique showed that Mn-SOD was located predominantly in mitochondria of type II epithelial cells. Fibroblasts contained little immunodetectable Mn-SOD, whereas type I epithelial cells, polymorphonuclear leukocytes (PMNs), and endothelial cells contained no detectable protein. Some alveolar macrophages (AMs) were found with labeled mitochondria, whereas most interstitial macrophages had no detectable protein. Quantitative analysis of type II cells showed that the number of immunogold particles per unit of mitochondrial area increased in the terminal airways of lungs exposed to asbestos or silica by 2.2-fold and 3.6-fold, respectively, over controls. Morphometric analyses indicated that the size of type II cells, as well as the number of interstitial macrophages and PMNs, increased in the terminal respiratory tissue of silica-exposed lungs. Less pronounced histopathologic changes were evident in asbestos-exposed lungs. These results indicate that the relative concentration of Mn-SOD increases preferentially in type II epithelial cells subsequent to inhalation of silica or asbestos. The magnitude of induction of Mn-SOD protein in these cells and whole lung correlated with the inflammatory potential of these minerals.

Administration, Inhalation↗

PubMed1990

Cytotoxicity of long and short crocidolite asbestos fibers in vitro and in vivo.

Fiber length and diameter are important factors in the pathogenicity of asbestos. We examined the relative toxicity of long and short crocidolite asbestos fibers in vitro and in vivo. Both long and short crocidolite asbestos fibers were toxic to elicited macrophages in vitro. Similar to native crocidolite asbestos, long and short fibers stimulated the release of reactive oxygen metabolites from elicited macrophages in vitro. We evaluated whether in vitro cytotoxicity was dependent on the production of reactive oxygen metabolites. In the presence of the reactive oxygen metabolite scavenging enzymes, superoxide dismutase or catalase, the toxicity of long and short crocidolite fibers to macrophages was prevented. Furthermore, macrophages were not killed when either long or short fibers were soaked in the iron chelator, deferoxamine. Native, long, and short crocidolite fibers also caused depolarization of the mitochondrial membrane potential prior to cell death. In vivo, a single i.p. injection of long crocidolite fibers stimulates an intense inflammatory reaction, release of reactive oxygen metabolites near sites of fiber deposition, and cell death. In contrast, these events were minimal after a single injection of short fibers due to the removal of fibers from the peritoneal cavity. After five daily injections of short fibers, however, fibers were present on the surface of the mesothelium and provoked an inflammatory response. Cell death was observed on the surface of the mesothelium. Reactive oxygen metabolites were also produced near accumulations of short fibers. Our results suggest that both long and short crocidolite asbestos fibers are toxic to macrophages in vitro via an oxidant and iron-dependent mechanism. In vivo, short fibers are cytotoxic when the clearance of these fibers is prevented.

Animals↗

PubMed1989

Cytotoxicity and carcinogenicity of chrysotile fibres from asbestos-cement products.

Fibres from weathered asbestos-cement products have little or no haemolytic activity, as compared with UICC chrysotile; this is probably the result of magnesium leaching during the weathering process. Weathered samples of asbestos cement are cytotoxic, but the release of lactic dehydrogenase (LDH) by guinea-pig alveolar macrophages caused by low and intermediate dust concentrations of UICC chrysotile is greater than that of such samples. The influence of serum is different as between UICC chrysotile and asbestos cement. In the former, LDH release by macrophages is enhanced, whereas it is reduced in the latter. Cytotoxicity is length-dependent in respect of LDH release from macrophages and proliferating cells, as well as cell proliferation. In all test systems, the sample from the unweathered core of an asbestos-cement plate is less toxic; only in the haemolysis system using an unbuffered solution can erythrocyte destruction be observed. This may be because this sample contains fewer single fibres than the others and because the specific surface of those fibres is smaller. The carcinogenicity of the weathered asbestos-cement chrysotile fibres is comparable to that of standard chrysotile fibres following intraperitoneal (i.p.) application.

Animals↗

PubMed1989

Brief inhalation of chrysotile asbestos induces rapid proliferation of bronchiolar-alveolar epithelial and interstitial cells.

Inhalation of asbestos fibres causes a progressive interstitial pulmonary fibrosis. To understand the basic cellular mechanisms which lead to this disease, we have studied the earliest proliferative events at the bronchiolar-alveolar regions of rats and mice exposed to chrysotile asbestos for 5 h. Animals were injected with tritiated thymidine 4 h prior to sacrifice at varying times ranging from immediately after cessation of exposure to one month post exposure. Light microscopic autoradiography showed that air-exposed control animals never had more than 1% of cells labelled. Rats and mice studied immediately after exposure also had normal numbers of labelled cells. However, between 12 and 48 h post exposure, asbestos-exposed animals exhibited up to 4-fold increases in the percentages of labelled epithelial and interstitial cells. Normal labelling returned by 8 days after exposure and was maintained through the one-month period studied. We conclude that inhalation of chrysotile asbestos induces rapid and highly significant increases in proliferation of epithelial and interstitial cells of the bronchiolar-alveolar regions where asbestos fibres were initially deposited.

Administration, Inhalation↗

PubMed1989

Chrysotile asbestos-induced cytotoxicity and calcium-dependent exocytosis in polymorphonuclear leukocytes.

Chrysotile asbestos is cytotoxic for rabbit polymorphonuclear leukocytes (PMNs) which is evident from the release of the cytoplasmic enzyme LDH. In the presence of Ca2+, but not in its absence, a strong lysozyme release occurs. High concentrations of Ca2+ are required for exocytosis. In the presence of the stable guanine nucleotide GTP gamma S exocytosis occurs at lower Ca2+ concentrations. The results suggest that the plasma membrane is permeabilized by asbestos, allowing the influx of extracellular Ca2+ which causes exocytosis. At high Ca2+ concentrations asbestos-induced cytotoxicity is strongly reduced. The cytotoxic LDH release and, to a lesser degree, the exocytotic enzyme release are inhibited by Co2+, Mn2+ and La3+. Cytochalasin B and the glycolytic inhibitors 2-deoxyglucose and iodoacetate inhibit asbestos-induced cytotoxicity, indicating that microfilaments and glycolytic energy are required for the membrane-damaging actions of asbestos.

Animals↗

PubMed1988

Progressive lung cell reactions and extracellular matrix production after a brief exposure to asbestos.

Inhaled chrysotile asbestos fibers have been shown to deposit initially on the first alveolar duct bifurcations. In brief accidental exposure to asbestos, this would be the most likely site of a significant cellular or fibrotic reaction. The characteristics and progression of tissue reactions occurring at first alveolar duct bifurcations after a single brief asbestos exposure was defined using morphometric techniques. Seven-week-old rats were exposed, nose only, for 1 hour to chrysotile asbestos fibers. After the exposure, the animals were kept in air for 2 days or 1 month, and then their lungs were fixed by vascular perfusion or by intratracheal instillation of 2% glutaraldehyde. The first bifurcations of seven alveolar ducts in each animal were isolated from plastic-embedded tissue and thin-sectioned for electron-microscopic analysis. Two days after exposure, the volume of epithelium and interstitium in the duct bifurcations had increased by 78% and 28%, respectively (P less than 0.05). The total number and volume of alveolar macrophages on the bifurcations increased about 10 times (P less than 0.05), whereas the number and volume of interstitial macrophages increased threefold (P less than 0.05). Statistically significant increases in the numbers of Type I (82%) and Type II (29%) epithelial cells also occurred. One month after the 1-hour exposure, the volume of epithelium and the number of Type I and Type II cells were still greater than control values, but these differences no longer achieved statistical significance. The volume of the interstitium, on the other hand, increased 67% (P less than 0.05), and this was accompanied by a persistently high number of interstitial macrophages, accumulation of myofibroblasts/smooth muscle cells, and an increased volume of interstitial matrix. 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. These acute structural changes are followed by a progressive response manifested by increased numbers of interstitial cells and localized interstitial fibrosis.

Aerosols↗

PubMed1986

Immunoregulation of lung fibroblast growth: alteration in asbestos-induced pulmonary fibrosis.

Initial studies on mononuclear cell-fibroblast interactions have shown that stimulated human lymphocytes produced a fibroblast growth inhibitory factor and that asbestos, a fibrogenic dust, interferes with this process in vitro. To investigate the role of these interactions in pathologies characterized by pulmonary fibrosis, we used a rat model of asbestos-induced fibrosis. Rats received a single intratracheal instillation of either saline or 10 mg of chrysotile asbestos fibres. Three months after treatment, peripheral blood mononuclear leucocytes (PBML) supernatant fractions were prepared and their effects on lung fibroblast growth measured. As for human PBML, rat PBML stimulated with Concanavalin A (Con A) produced 24 h after initiation of the cultures a soluble factor which inhibits lung fibroblast DNA synthesis and growth in a dose-dependent fashion. By contrast, Con A-stimulated PBML from rats exposed to asbestos failed to produce significant levels of fibroblast growth inhibitory activity. No significant change of total PBML number or in the proportion of circulating mononuclear cell populations was observed. Furthermore, upon stimulation with lipopolysaccharide (LPS), monocytes from asbestotic animals retained their capacity to produce interleukin (IL-1), a mediator required for lymphokine production. Our study demonstrates that suppression of FGIF production by circulating PBML occurs in animals with lung fibrosis and suggests that mechanisms other than impairment of IL-1 production may be responsible for the suppressive effect of asbestos on the production of such fibroblast regulatory lymphokine.

Animals↗