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PubMed1999

Tissue burden of asbestos in nonoccupationally exposed individuals from east Texas.

BACKGROUND: The potential for asbestos exposure among members of the general population is appreciable, considering its widespread use in many products. This study examined tissue burden of asbestos in such a population. METHODS: A group of 33 individuals who had no work history of occupational exposure to asbestos were included in the study. Tissue sections from areas adjacent to those sites sampled for digestion were found to be without ferruginous bodies (FB) or histopathology consistent with asbestos-induced changes. All individuals had 20 or less FBs per gram of digested wet lung, a number considered to reflect general population levels. Tissue analysis of uncoated fiber burden was carried out by analytical electron microscopy. There was a trend of a higher likelihood of FB and asbestos fiber content correlated with age. RESULTS: The data are not consistent with the findings that chrysotile is readily found in lung tissue from the general population, in that none was found in 19 of the cases. It was almost as likely that one would find anthophyllite (12 of 33 cases) in this study. The commercial amphiboles (amosite and crocidolite) were occasionally found in the tissue from the general population and, when observed, were few in numbers. Twenty-six of the patients had no FBs and ten had no uncoated asbestos fibers within the limits of detectability in this study. CONCLUSIONS: The total tissue burden of asbestos in this study is much less than earlier reported observations from other general populations.

Adolescent↗

PubMed1988

Acute myelocytic leukemia after exposure to asbestos.

While the carcinogenicity of asbestos has been established in malignant mesotheliomas and lung cancers, and has recently been suspected in several other types of cancer, asbestos has not been implicated in the pathogenesis of acute leukemias. This article includes two cases of acute myelocytic leukemia in individuals with a long history of exposure to asbestos. Significant numbers of asbestos bodies were detected in specimens of their lungs and bone marrow. In addition, the kind of asbestos in both organs was crocidolite, which is implicated in carcinogenesis. No asbestos bodies were detected in the bone marrow specimens from a control group consisting of ten patients with lung cancer with similar occupational histories. The role of asbestos exposure in the development of leukemia requires further study.

Aged↗

PubMed2003

Exposing the "myth" of ABC, "anything but chrysotile": a critique of the Canadian asbestos mining industry and McGill University chrysotile studies.

BACKGROUND: Beginning in the 1930s, the Canadian asbestos industry created and advanced the idea that chrysotile asbestos is safer than asbestos of other fiber types. METHODS: We critically evaluate published and unpublished studies funded by the Quebec Asbestos Mining Association (QAMA) and performed by researchers at McGill University. RESULTS: QAMA-funded researchers put forth several myths purporting that Quebec-mined chrysotile was harmless, and contended that the contamination of chrysotile with oils, tremolite, or crocidolite was the source of occupational health risk. In addition, QAMA-funded researchers manipulated data and used unsound sampling and analysis techniques to back up their contention that chrysotile was "essentially innocuous." CONCLUSIONS: These studies were used to promote the marketing and sales of asbestos, and have had a substantial effect on policy and occupational health litigation. Asbestos manufacturing companies and the Canadian government continue to use them to promote the use of asbestos in Europe and in developing countries. Am. J. Ind. Med. 44:540-557, 2003.

Asbestos↗

PubMed1987

Asbestos exposure, cigarette smoking, and airflow limitation in long-term Canadian chrysotile miners and millers.

To investigate further the relationships of asbestos exposure, cigarette smoking, and airflow limitation, we have obtained detailed pulmonary function tests (PFT) in 331 long-term Canadian chrysotile workers, 34 of whom were lifetime nonsmokers. Three disease categories were defined on the bases of standard diagnostic criteria, gallium-67 lung uptake, and the lung pressure-volume curve. Category A was composed of workers without changes suggestive of alveolitis or asbestosis. There were eight nonsmokers (ns), among whom we found a statistically significant 30% reduction in airflow conductance (Gus) at low lung volume, which is consistent with the concept of an asbestos airway lesion. The 85 smokers (sm) of category A had reduction of Gus at both high and low lung volumes. Category B was composed of workers without asbestosis but with evidence of asbestos alveolitis. In the six ns, Gus was significantly reduced to 50% normal at low lung volume. The 59 sm had reduction of Gus at both high and low lung volumes but less severely than sm in category A. Category C was composed of workers with asbestosis. The 20 ns had restrictive pattern of lung function, and Gus was decreased to 39% normal at 50% TLC. The 153 sm in C had airflow reduction comparable to sm in B. We concluded that asbestos exposure, which leads to asbestos airway disease, asbestos peribronchiolar alveolitis, and asbestosis, causes airflow limitation at low lung volume but does not reduce the expiratory flow rates on the flow-volume curve in lifetime nonsmokers. In the smoking asbestos workers with alveolitis or asbestosis, the major component of airflow limitation is a smoking effect. In these smoking workers, rigidity of the lung lessens airflow obstruction associated with smoking at the expense of increased work of breathing.

Adult↗

PubMed1998

Expression and activity of urokinase and its receptor in endothelial and pulmonary epithelial cells exposed to asbestos.

An elongated endothelial cell phenotype, which demonstrated increased ICAM-1-dependent neutrophil adherence, was induced when these cells were exposed to noncytotoxic concentrations of asbestos (Treadwell et al., Toxicol. Appl. Pharmacol. 139, 62-70, 1996). The present study examined mechanisms underlying this phenotypic change by investigating the effects of asbestos on transcription factor activation and expression of urokinase-type plasminogen activator (uPA) and its receptor uPAR. In situ zymography was used to compare the effects of these fibers on the activity of uPA. Cultures incubated with chrysotile or crocidolite asbestos, but not refractory ceramic fiber 1 (RCF-1), demonstrate localized cleavage of plasminogen, which was inhibited by amiloride. Immunocytochemistry showed that chrysotile-stimulated uPA activity was associated with a time-dependent augmentation of uPAR protein levels. RT-PCR analysis was used to investigate molecular mechanisms for these increases. Chrysotile asbestos, but not RCF-1, increased endothelial cell uPA message, relative to changes in beta-actin mRNA. This response to asbestos was not limited to endothelial cells, since both uPA and uPAR mRNA levels increase in human bronchial epithelial BEAS-2B cells exposed to chrysotile fibers. Finally, both types of asbestos, but not RCF-1, increased nuclear levels of nuclear factor-kappaB (NF-kappa B), a transcription factor common to increased expression of ICAM-1 and uPA. These data demonstrate that asbestos caused fiber-specific activation of endothelial and pulmonary epithelial cells, resulting in phenotypes capable of facilitating tissue remodeling.

Animals↗

PubMed1989

The involvement of ionic interactions during asbestos-induced enzyme release from polymorphonuclear leukocytes.

Chrysotile asbestos permeabilizes the plasma membrane of rabbit polymorphonuclear leukocytes (PMNs) which is evident from the release of the cytoplasmic enzyme lactate dehydrogenase (LDH) from the cell. When Ca2+ is present in the medium exocytosis is observed, evident from the release of the granule associated enzyme lysozyme which is not liberated in the absence of Ca2+. Asbestos-induced enzyme release is inhibited by polyanions or by removal of positive charges on asbestos, and resembles enzyme release induced by synthetic polycations. Pretreatment of PMNs with neuraminidase does not affect the ability of asbestos to induce enzyme release from these cells. Asbestos induces release of glucose from glucose-loaded liposomes, and this effect can be inhibited by the polyanion poly-D-glutamic acid. The results are compatible with the view that positive charges play a decisive role in the interaction between PMNs and asbestos, and that the primary target of asbestos could be the lipid bilayer of the membrane. The interaction results in a permeabilized plasma membrane. When Ca2+ is present in the medium it moves into the cell and causes exocytosis of the granule enzyme lysozyme. Inhibition of cytotoxicity by polyanion may cause a diminished Ca2+-influx and hence inhibition of lysozyme release.

Animals↗

PubMed1994

Use of asbestos, health risks and induced occupational diseases in the former East Germany.

In the period from 1960 to 1990 about 1.4 million tons of asbestos were imported and mainly processed into asbestos-cement products for the building industry. The production was concentrated in the former countries of Magdeburg and Dresden. In the past asbestos was primarily used as insulation and fire prevention material, etc. in the large-scale chemical industry. The asbestos was imported from the former Soviet Union, smaller amounts came from Canada. In the German Federal State of Saxony-Anhalt, approximately 600 asbestoses, almost 2700 pleural changes caused by asbestos, 843 asbestos-induced mesotheliomas and 787 bronchial and laryngeal carcinomas were recorded in the period from 1960 to 1990. A considerable percentage of the mesotheliomas are solely due to exposure to chrysotile asbestos.

Asbestos↗

PubMed1986

Asbestos bodies and the diagnosis of asbestosis in chrysotile workers.

It has been suggested that because chrysotile asbestos forms asbestos bodies poorly, use of the traditional histologic requirements (diffuse interstitial fibrosis plus asbestos bodies) for the diagnosis of asbestosis, may lead to an underdiagnosis of this condition in workers exposed only to chrysotile. We examined lungs from 25 chrysotile miners with diffuse interstitial fibrosis. Asbestos bodies were found easily in histologic section using hematoxylin and eosin stains in all cases. Mineralogic analysis of four cases showed that 46 of 72 (64%) bodies isolated and examined contained chrysotile cores, and 21 of 72 (29%) bodies contained cores of the amphiboles tremolite and actinolite. By contrast, tremolite and actinolite constituted the majority of uncoated fibers in these cases. The mean length for bodies formed on chrysotile was 35 micron, and for bodies formed on tremolite or actinolite, 36 micron. We conclude that (1) the usual histologic criteria for the diagnosis of asbestos are applicable to chrysotile-exposed workers; (2) in workers with occupational chrysotile exposure, bodies form readily on this mineral; and (3) asbestos bodies in these lungs reflect the presence of long asbestos fibers.

Asbestos↗

PubMed1982

Indoor airborne asbestos pollution: from the ceiling and the floor.

Electron microscopic measurements of the concentrations of airborne asbestos were carried out inside and outside an office building having ceilings sprayed with a crocidolite-containing material and floors covered with vinyl-chrysotile tiles. Under normal conditions in this building, constructed 10 years ago, the two asbestos-containing materials released fibers into the air. This is the first measurement of elevated (up to 170 nanograms per cubic meter) concentrations of indoor airborne asbestos associated with the weathering of asbestos floor tiles during their service life. Asbestos flooring is used in a large number of buildings and represents the third largest use of asbestos fibers in the United States and in Europe, ranking after roofing and asbestos-cement pipe.

Air Pollutants↗

PubMed1993

Production of interleukin 1 by rat pleural leucocytes in culture after intratracheal instillation of crocidolite asbestos.

This study was undertaken to investigate the production of interleukin 1 (IL-1) by pleural leucocytes in culture and to evaluate the influence of intratracheal instillation of crocidolite asbestos on this production. Normal pleural leucocytes spontaneously released IL-1 in culture and stimulation with lipopolysaccharide (LPS) dramatically increased production. Intratracheal instillation with crocidolite asbestos induced recruitment of pleural leucocytes in the longer term and changed IL-1 production by the leucocytes. Reduced production of IL-1 was found by one day after instillation of asbestos and this was correlated with the dose of asbestos. With increasing time after instillation, however, release of IL-1 by pleural leucocytes gradually recovered to normal until, one month after asbestos injection, the leucocytes produced augmented IL-1 in culture compared with control pleural leucocytes. Our data show that pleural leucocytes possess the potential to produce IL-1 in vitro and this capability is altered by intratracheal instillation of crocidolite asbestos. This may be relevant to development of pleural diseases associated with inhalation of asbestos.

Animals↗

PubMed1983

Benign asbestos pleurisy in the rabbit. A model for the study of pathogenesis.

Benign asbestos pleurisy is a manifestation of asbestos-induced disease that is not uncommon but often ignored. We developed an animal model to study the pathogenesis of this syndrome. Crocidolite asbestos injected into the rabbit pleural space resulted in the appearance of chemotactic activity in an exudative effusion, characterized by a polymorphonuclear leukocyte (PMN) response that peaked 4 h after the injection. The chemotactic activity and the PMN responses occurred equally in normal animals and in animals that had been depleted of complement with cobra venom. Neutropenia, induced with vinblastine, did not alter the appearance of chemotactic activity but abrogated the PMN response. Treatment with colchicine failed to block the release of chemotactic activity into the pleural fluid, but decreased the PMN response without affecting the ability of peripheral blood PMN to respond to pleural fluid chemotactic activity. When pleural fluid containing chemotactic activity was injected into the pleural space of another rabbit, a PMN response was observed. These studies suggest that the acute exudative response seen in the rabbit model of benign asbestos pleurisy results from the release of chemotactic activity from sources other than complement. The response probably depends on interaction between the asbestos and the pleural tissue. Asbestos-PMN interaction may release chemotactic factors that amplify the response secondarily. Colchicine blocked the acute response to intrapleural asbestos by a mechanism yet to be understood.

Animals↗

PubMed1989

IgG specifically enhances chrysotile asbestos-stimulated superoxide anion production by the alveolar macrophage.

The interaction of chrysotile asbestos with alveolar macrophages in vitro is known to stimulate cellular superoxide anion production. However, it is likely that particulates in the respiratory tract are present together with components of the pulmonary surfactant, and it is not known how these components may alter the bioactivity of the particulate. We now show that guinea pig immunoglobulin G, a surfactant protein, causes a significant, dose-dependent enhancement of superoxide anion production by nonadherent guinea pig alveolar macrophages in response to chrysotile asbestos. This enhancement could not be mimicked by other particulates or proteins, including IgG fragments, implying that the interaction between IgG, cell, and chrysotile is relatively specific. The enhancing effect of IgG in solution could be reproduced by pretreating the chrysotile asbestos with IgG. The fact that IgG specifically enhances chrysotile asbestos-stimulated superoxide anion production, in turn, leads to a proposal for a molecular mechanism by which asbestos may stimulate the guinea pig macrophage, namely, by crosslinking cell-surface immunoglobulin Fc receptors. In view of the submicromolar concentrations at which IgG was effective in enhancing macrophage stimulation by chrysotile asbestos in vitro, these results also suggest that IgG adsorption may play a role in the progression of asbestos-induced pulmonary fibrosis.

Animals↗

PubMed1990

Alveolar type II cell responses to chronic inhalation of chrysotile asbestos in rats.

The effects of chronic exposure to chrysotile asbestos on alveolar type II cells were examined in the lungs of Fischer 344 rats. Morphometric and three-dimensional analyses were used to characterize the alveolar type II cell and to determine the relationship of asbestos fiber localization to ultrastructural change in these cells. During the 2-yr period of study, type II cell number and volume increased to values more than 4 times those seen in controls. Ultrastructurally, cisternal dilations of the rough endoplasmic reticulum (RER) composed 12% of the total cell volume after 12 mo of exposure to asbestos and was still 15% of the total cell volume 1 yr after fiber exposure had ended compared to less than 1% in control cells. Asbestos fiber density surrounding these cells was directly proportional to the degree of cisternal dilatation in the cell; however, lamellar body volume and number in these cells were not different from that found in control type II cells. The incidence of a subset of type II cells with large lamellated inclusions was 10-fold greater in regions near bronchiolar-alveolar duct junctions, compared to more distal gas exchange regions of the lungs. Normal-sized lamellar bodies were fused to these large lamellated inclusions. These cells also contained significantly greater numbers of lamellar bodies and multivesicular bodies than those type II cells in more distal lung regions. These ultrastructural changes observed in type II cells may be a simple dose response to inhaled asbestos or the manifestation of two distinct populations of cells in the lungs that respond to asbestos in different ways. Asbestos fiber dose, cellular microenvironment, and aberrations of the cell plasma membrane and/or cell cytoskeleton (i.e., microtubules and filaments) are discussed as potential factors in the changes noted in type II cells.

Administration, Inhalation↗

PubMed2004

Role of iron in inactivation of epidermal growth factor receptor after asbestos treatment of human lung and pleural target cells.

Although the mechanism by which asbestos causes cancer remains unknown, iron associated with asbestos is thought to play a role in the pathogenic effects of fibers. Here, we examined the effects of asbestos on the epidermal growth factor receptor (EGFR) in human lung epithelial (A549) cells, human pleural mesothelial (MET5A) cells, and normal human small airway epithelial (SAEC) cells. Treatment of A549, MET5A, and SAEC cells with asbestos caused a significant reduction of EGFR tyrosine phosphorylation. This was both time- (15 min to 24 h) and concentration-dependent (1.5, 3, and 6 mug/cm(2)) in A549 cells. Also, treatment with 6 mug/cm(2) crocidolite for 24 h diminished the phosphorylation levels of human EGFR 2 (HER2). Exposure of A549 cells to 6 mug/cm(2) crocidolite for 3-24 h resulted in no detectable Y1045 phosphorylation and no apparent degradation of the EGFR. Inhibition of fiber endocytosis resulted in a considerable inhibition of EGFR dephosphorylation. Removal of iron from asbestos by desferrioxamine B or phytic acid inhibited asbestos-induced decreases in EGFR phosphorylation. 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. These results strongly suggest that iron plays an important role in asbestos-induced inactivation of EGFR.

Asbestos↗

PubMed1998

Asbestos inhalation induces reactive nitrogen species and nitrotyrosine formation in the lungs and pleura of the rat.

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. The rats were killed at 1 or 6 wk after exposure. At 1 wk, significantly greater numbers of alveolar and pleural macrophages from asbestos-exposed rats than from sham-exposed rats demonstrated inducible nitric oxide synthase protein immunoreactivity. Alveolar macrophages from asbestos-exposed rats also generated significantly greater nitrite formation than did macrophages from sham-exposed rats. Strong immunoreactivity for nitrotyrosine, a marker of peroxynitrite formation, was evident in lungs from chrysotile- and crocidolite-exposed rats at 1 and 6 wk. Staining was most evident at alveolar duct bifurcations and within bronchiolar epithelium, alveolar macrophages, and the visceral and parietal pleural mesothelium. Lungs from sham-exposed rats demonstrated minimal immunoreactivity for nitrotyrosine. Significantly greater quantities of nitrotyrosine were detected by ELISA in lung extracts from asbestos-exposed rats than from sham-exposed rats. These findings suggest that asbestos inhalation can induce inducible nitric oxide synthase activation and peroxynitrite formation in vivo, and provide evidence of a possible alternative mechanism of asbestos-induced injury to that thought to be induced by Fenton reactions.

Animals↗

PubMed1991

Biological activity of synthetic amphibole asbestos.

The carcinogenic and fibrogenic activity of four samples of synthetic amphibole asbestos with different chemical structure was examined in white rats. Pleural mesotheliomas were found: in 11 out of 27 rats (37.8%) treated with magnesium asbestos; in 4 out of 24 animals (6.7%) for nickel asbestos; 13 out of 22 (59.1%) for cobalt asbestos; and in the experiment with asbestos where germanium was substituted for silicon pleural mesotheliomas were observed in 2 out of 55 rats (3.6%). No tumours of this kind were found in the control group. As revealed by the study results, all the examined samples of synthetic amphibole asbestos exhibited carcinogenic potentials. Correlation between the carcinogenic and fibrogenic activity could also be observed. The replacement of silicon with germanium produced considerable decrease in the carcinogenic and fibrogenic potentials of asbestos.

Animals↗

PubMed1986

The endocytosis of asbestos by mouse peritoneal macrophages and its long-term effect on iron accumulation and labyrinth formation.

The effect of a single intraperitoneal injection of crocidolite asbestos fibres on the peritoneal cell population were studied. Attention was paid to the changes in the proportions taken by the various types of cell in this population after peritoneal stimulation as well as the handling of asbestos fibres by the peritoneal cells and the formation of asbestos bodies. Intraperitoneal administration of crocidolite led to an influx of inflammatory cells into the peritoneal cavity. The asbestos fibres were phagocytosed and gradually cleared from the peritoneal cavity. Long before this clearance was completed, the peritoneal cell population had returned to the steady state. The stimulated peritoneal macrophages showed increasing concentrations of iron in both lysosomes and the cytoplasm. At later time points, residual bodies containing iron and asbestos fibres were seen frequently in macrophages, but asbestos bodies were not found. As a reaction to the administration of crocidolite asbestos, macrophages from the peritoneal cavity develop tubular systems (labyrinths) that increase in number and size.

Animals↗

PubMed1994

Asbestos and nonasbestos fiber content in lung tissue of Japanese patients with malignant mesothelioma.

BACKGROUND: Pulmonary fiber content of both asbestos and nonasbestos types were evaluated in Japanese patients with malignant pleural mesotheliomas. METHODS: Pulmonary fiber content was analyzed in 16 patients and 16 case-matched control subjects by transmission electron microscopy with energy-dispersive X-ray analysis using a low-temperature ashing procedure. RESULTS: The geometric mean content of total asbestos was significantly higher in the patients (22.0 x 10(6) fibers/g dry lung) than in the control subjects (2.24 x 10(6) fibers/g dry lung) (P < 0.01). When the asbestos content was analyzed by fiber type, the geometric means were also consistently and significantly higher among the patients compared with the control subjects (P < 0.01). Results were as follows: (1) amosite: patients 3.94 times 10(6) versus control subjects 0.23 x 10(6); (2) crocidolite: patients 3.56 times 10(6) versus control subjects 0.35 times 10(6); (3) total amphiboles: patients 16.0 times 10(6) versus control subjects 0.77 times 10(6); and (4) chrysotile: patients 3.76 times 10(6) versus control subjects 1.01 times 10(6). However, when individual total asbestos content was considered, 7 of the 16 patients (44%) had levels lower than the highest value noted among the control subjects. Pulmonary fiber content of patients and control subjects also revealed the presence of nonasbestos fibers. The geometric mean of nonasbestos fibers was significantly higher in the patients (87.3 x 10(6)) than in control subjects (33.8 x 10(6)) (P < 0.01). The major type of nonasbestos fibers in both groups was aluminum silicates. The mean of ratios of nonasbestos fiber contents to total asbestos contents in the patients and control subjects was 7.0 and 17.3, respectively. CONCLUSIONS: The results were mainly in agreement with the findings of earlier investigations, but fiber content of both chrysotile and nonasbestos fiber as well as those of amphibole asbestos were significantly higher in the patients than in the control subjects.

Adult↗