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PubMed2006

Asbestos redirects nitric oxide signaling through rapid catalytic conversion to nitrite.

Asbestos exposure is strongly associated with the development of malignant mesothelioma, yet the mechanistic basis of this observation has not been resolved. Carcinogenic transformation or tumor progression mediated by asbestos may be related to the generation of free radical species and perturbation of cell signaling and transcription factors. We report here that exposure of human mesothelioma or lung carcinoma cells to nitric oxide (NO) in the presence of crocidolite asbestos resulted in a marked decrease in intracellular nitrosation and diminished NO-induced posttranslational modifications of tumor-associated proteins (hypoxia-inducible factor-1alpha and p53). Crocidolite rapidly scavenged NO with concomitant conversion to nitrite (NO(2)(-)). Crocidolite also catalyzed the nitration of cellular proteins in the presence of NO(2)(-) and hydrogen peroxide. Nitrated protein adducts are a prominent feature of asbestos-induced lung injury. These data highlight the ability of asbestos to induce phenotypic cellular changes through two processes: (a) by directly reducing bioactive NO levels and preventing its subsequent interaction with target molecules and (b) by increasing oxidative damage and protein modifications through NO(2) production and 3-nitrotyrosine formation.

Animals↗

PubMed1983

Asbestos and benzo(a)pyrene synergism in the transformation of Syrian hamster embryo cells.

Four varieties of asbestos fibers, crocidolite, anthophyllite, amosite, and chrysotile, induced a low rate of morphologic transformation in Syrian hamster cells. Of the four tested, chrysotile was the most lethal as reflected by colony survival. When cells were exposed to 1 microgram of benzo(a)pyrene (BP)/1 ml medium or 3 J/m2 ultraviolet irradiation and to different concentrations of the asbestos fibers, an enhancement of transformation occurred only with BP. The enhancement was dose responsive with all fiber species except for amosite which was dose independent. The synergistic activity of BP and asbestos suggests that asbestos facilitates the transport of BP to the cell site(s) critical for transformation. These results provide a basis for investigating the carcinogenic and cocarcinogenic potential of asbestos fibers in mammalian cells.

Animals↗

PubMed1992

Coexistence of a malignant fibrous histiocytoma and asbestos exposure. Brief report.

A 59-year-old male died of malignant fibrous histiocytoma. He had a history of asbestos exposure as a shipfitter in the Japanese Naval Shipyard and other shipyards for 45 years. Numerous asbestos bodies were detected in the autopsied lung and within the lesion. X-ray analysis of the asbestos fibers showed them to be crocidolite, a type of asbestos fiber commonly seen in association with mesothelioma and other types of cancer. This case adds malignant fibrous histiocytoma to the growing number of tumors that can be attributed etiologically to asbestos exposure.

Asbestos↗

PubMed1993

Pathogenesis of mesothelial reactions to asbestos fibers. Monocyte recruitment and macrophage activation.

Exposure to asbestos fibers leads to a variety of mesothelial reactions: pleural effusions, fibrotic pleural plaques, and malignant mesotheliomas. An animal model was developed to reproduce these lesions in C57B1/6 mice using weekly intraperitoneal injections of asbestos fibers. After exposure to asbestos fibers, monocytes were recruited into the abdominal cavity and acquired the characteristics of inflammatory or nonspecifically activated macrophages. Nontoxic titanium dioxide or toxic silica particles did not produce activation of the free peritoneal macrophage population. Aggregates of asbestos fibers were found on the diaphragm and other peritoneal surfaces within only 24 h after a single injection. Macrophage recruitment to these sites peaked between 3 and 5 days, while activated macrophages persisted up to 14 days. Recruitment and activation of macrophages by repeated exposures to asbestos fibers may contribute to chronic damage of the mesothelial lining caused by these mineral fibers.

Animals↗

PubMed2000

Chest pain in asbestos-exposed individuals with benign pleural and parenchymal disease.

Many asbestos-exposed individuals complain of chest pain for which there is no clear explanation. To determine whether chest pain is associated with the presence of benign pleural or parenchymal disease on chest radiograph, we studied 1,280 subjects undergoing surveillance because of prior asbestos exposure at Wittenoom, Western Australia. All subjects completed the Rose questionnaire on chest pain and this revealed 556 subjects (43%) who experienced some chest pain. A posterior-anterior chest radiograph was performed at the same clinic visit and was subsequently graded independently by two experienced readers for diffuse parenchymal disease and pleural disease. Logistic regression models adjusted for sex, age, and cumulative asbestos exposure indicated that the presence of chest pain was significantly associated with the presence of both benign pleural disease and diffuse parenchymal disease. Further analysis after stratification of chest pain into nonanginal and anginal pain showed that there was a significant association between anginal pain and the presence of pleural and parenchymal asbestos-induced radiologic abnormalities and an association of nonanginal pain with parenchymal disease. We conclude that radiographic evidence of either parenchymal or pleural disease in subjects exposed to asbestos is significantly related to the presence of chest pain, particularly anginal pain.

Adolescent↗

PubMed1987

Diagnostic value of asbestos bodies in bronchoalveolar lavage fluid.

Asbestos bodies (AB) were counted by light microscopy in bronchoalveolar lavage (BAL) fluid obtained from 563 subjects. The presence of AB was found to reflect occupational exposure to asbestos and was rarely found in unexposed control subjects at concentrations above 1/ml of fluid (6.9% of white collar workers and 17.8% of blue collar workers). The overlap of results observed between subjects with definite exposure and those without underlines the difficulty in assessing exposure by questioning alone, which leads to underestimations or even overestimations of the risk. The highest counts (log mean, 120.5 AB/ml; range, 0 to 42,600) were found in patients with radiologic evidence of asbestosis, most likely reflecting the known association of this disease with retention of large amounts of long amphiboles, rather than in patients with pleural disease. A considerable overlap of results was also observed between groups with different diseases or without any apparent disease. Apart from uncertainties in the radiologic diagnosis, this may be explained by differences in latency since first exposure, in individual response to asbestos inhalation, or in pathogenic properties of different asbestos types. Because the presence of AB in BAL fluid appears to be a marker of exposure and not of disease, AB are more likely to be detected in patients presenting with asbestos-related diseases but in whom exposure is not confirmed by the occupational history (65 of 78 cases).

Adult↗

PubMed1989

Bronchoalveolar lavage cell and lymphocyte phenotype profiles in healthy asbestos-exposed shipyard workers.

The cellular and lymphocyte phenotypic composition of bronchoalveolar lavage (BAL) fluid and peripheral blood (PB) from 15 healthy, nonsmoking, asbestos-exposed shipyard workers (AEW) and 10 nonsmoking, age-matched unexposed workers (UEW) were compared. None of the AEW had clinical, radiographic, or physiologic evidence of asbestosis, but six had radiographic evidence of pleural plaques and/or thickening. The mean duration of asbestos exposure was 16.3 +/- 2.3 yr, and the mean period since exposure was 10.8 +/- 0.5 yr. All but three of the AEW and none of the UEW had asbestos bodies detected in the first 20 ml of BAL fluid recovered (0.1 to 35 asbestos bodies/ml). The AEW had a significantly higher mean percentage (19.1 +/- 2.8% versus 9.7 +/- 1.6%) and concentration (31.6 +/- 5.2 x 10(3) cells/ml versus 14.7 +/- 2.5 x 10(3) cells/ml) of BAL lymphocytes compared with that in the UEW, with an increased mean concentration of each phenotype measured. In PB, the mean lymphocyte concentration was also higher in the AEW than in the UEW (2.0 +/- 0.3 x 10(3) cells/ml versus 1.5 +/- 0.3 x 10(3) cells/ml), but the difference was not statistically significant, and there was no increase of any phenotype measured. BAL lymphocytosis did not correlate with exposure history or BAL asbestos body count, but was greater in AEW with pleural abnormality (30.1 +/- 2.9% versus 11.8 +/- 1.6%). BAL concentrations of CD-20, CD-3, and CD-4, but not of CD-8 cells were significantly increased compared with those in the AEW without pleural abnormality. Further longitudinal studies are needed to determine the prognostic significance of these findings.

Adult↗

PubMed1989

Exposure to low levels of ozone results in enhanced pulmonary retention of inhaled asbestos fibers.

Health effects associated with exposure to ozone at environmentally relevant concentrations are subject to considerable controversy. Currently, no compelling evidence exists that exposure to low levels of ozone leads to lasting impairment of pulmonary structure or function. One adverse health effect of ozone may be to change lung uptake or clearance functions for other inhaled air pollutants. As a test of this hypothesis, Fischer 344 rats were continuously exposed to 0.06 ppm ozone 7 days a week with a slow rise in ozone to a peak of 0.25 ppm and subsequent decrease to 0.06 ppm over a 9-h period five times each week for 6 wk. Three days after the end of ozone exposure, animals-were exposed to aerosolized asbestos fibers for 5 h and examined immediately after or 30 days after exposure to asbestos. Filtered air control animals were simultaneously exposed to asbestos. Immediately after the end of fiber exposure, lung asbestos fiber burden was similar in both groups. However, 1 month after exposure, fiber mass and fiber number were significantly greater (p less than 0.05) in the lungs of animals exposed to ozone than in the lungs of those exposed to air. These findings suggest that ambient levels of ozone can impair clearance of fibrogenic and carcinogenic materials such as asbestos from the lungs and represent an important adverse effect of prolonged exposure to low levels of this oxidant gas.

Animals↗

PubMed1983

Enhanced release of a chemoattractant for alveolar macrophages after asbestos inhalation.

Alveolar macrophage supernatants from 2 groups of asbestos-exposed rats and a group of sham-exposed rats were tested for chemoattractant activity towards rat alveolar macrophages. Enhanced chemotaxin release was observed in culture supernatants from both crocidolite and chrysotile asbestos-exposed rats when compared with supernatants from sham-exposed rats. These between-group differences persisted for as long as 15 months after exposure had ceased. Chemotactic factor release was maximal after 24 h of culture in all animal groups. Partial characterization of the chemoattractant from each of the 3 rat groups revealed that it was thermolabile, nondialyzable, and trypsin-sensitive. Separation on SDS-polyacrylamide gel electrophoresis revealed 3 major peaks of activity. The production of the chemotaxin in supernatants from asbestos-exposed rats was partially inhibited by both actinomycin D and puromycin. These agents had no appreciable effect on the production of chemoattractant in cultures from sham-exposed animals. The enhanced release of an alveolar macrophage chemoattractant after asbestos inhalation may explain why macrophages accumulate at sites of asbestos deposition in the lungs.

Aerosols↗

PubMed1985

Lymphocyte subpopulations in bronchoalveolar lavage fluid in asbestos workers.

We examined peripheral blood and bronchoalveolar lavage (BAL) fluid lymphocyte subpopulations in 29 asbestos workers, 10 with and 19 without clinical or radiologic evidence of asbestosis. Peripheral blood lymphocyte subpopulations were also measured in 13 control subjects. The mean OKT4:OKT8 (T-helper/inducer:T-suppressor/cytotoxic lymphocyte) ratio in BAL fluid in the 29 asbestos workers was 0.96 (range, not detected to 3.33), significantly less than 1.76 (1.33 to 2.67) in peripheral blood (p less than 0.001). There were no significant differences in OKT4:OKT8 ratios in peripheral blood between the 10 patients with asbestosis, the 19 asbestos workers without asbestosis, and the 13 normal control subjects or in the OKT4:OKT8 ratios in BAL fluid between patients with asbestosis and asbestos workers without asbestosis. In the group as a whole, 83% of those who had suffered more than 5 yr of exposure to asbestos showed OKT4:OKT8 ratios less than 1.2, whereas in those who had suffered fewer than 5 yr of exposure, 80% showed ratios greater than 1.2 (p less than 0.02). No other relationships between OKT4:OKT8 ratios and clinical, radiographic, or physiologic variables were observed.

Adult↗

PubMed1996

Apoptosis is observed in mesothelial cells after exposure to crocidolite asbestos.

Asbestos causes protracted, dose-dependent increases in steady-state mRNA levels of the proto-oncogenes c-fos and c-jun, and AP-1 DNA-binding activity in normal rat pleural mesothelial (RPM) cells (1). To determine the phenotypic end points of overexpression of these early response genes by asbestos, both cell proliferation and apoptosis were examined in confluent RPM cells exposed to a range of concentrations (1.25 to 10 micrograms/cm2 dish) of crocidolite asbestos for 24 and 48 h. Quantitation of RPM cells pulsed with 5-bromo-2'-deoxyuridine revealed that asbestos caused dose-dependent decreases in cells undergoing DNA synthesis. Decreases in cell proliferation were accompanied by dose-related increases in apoptosis using (1) terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (i.e., ApopTag technique), (2) 4',6-diamidino-2-phenylindole cell staining, and (3) fluorescent-activated cell sorter after incorporation of propidium iodide. Less striking but significant dose-related increases in apoptosis were observed in RPM cells exposed to H2O2 (300 microM), and no apoptosis was seen after exposure of cells to high concentrations (10 micrograms/cm2 dish) of glass beads. Our results are unique in that they demonstrate that asbestos induces apoptosis in mesothelial cells at concentrations eliciting increased expression of the proto-oncogenes c-fos and c-jun.

Animals↗

PubMed1997

Inhaled asbestos fibers induce p53 expression in the rat lung.

Humans and rodents exposed to an aerosol of asbestos fibers develop lung injury that can lead to a fibroproliferative response culminating in excessive scarring and impaired lung function. To define the early events that precede asbestos-induced fibrotic lung disease, rats were exposed to an aerosol of chrysotile asbestos fibers for 5 h. At various times after exposure, the lungs of the asbestos-exposed animals were evaluated immunohistochemically for expression of the p53 tumor suppressor protein, a growth regulatory protein. p53 became detectable by immunostaining at the predicted sites of fiber deposition (the bronchiolar-alveolar duct bifurcations) by 24 h after exposure. The number of cells positive for p53 immunostaining increased to a maximal level at 8 days after exposure, decreased by 14 days and returned to a low basal level at the 30-day time point. Control groups of rats that were unexposed or exposed to an aerosol of iron beads were negative for p53 immunostaining throughout the 30-day assessment period. Simultaneous detection of the proliferating cell nuclear antigen (PCNA) at the sites of fiber deposition in the asbestos-exposed animals agrees with our previous finding that p53 binds and regulates the PCNA promoter.

Administration, Inhalation↗

PubMed2001

Different accumulation of activated extracellular signal-regulated kinases (ERK 1/2) and role in cell-cycle alterations by epidermal growth factor, hydrogen peroxide, or asbestos in pulmonary epithelial cells.

The extracellular signal-regulated kinase (ERK) pathway is induced by cytokines and oxidative stress. In this study we examined the patterns of localization of phosphorylated ERK proteins in relationship to subsequent phenotypic responses by the mitogenic agent epidermal growth factor (EGF) (5 ng/ ml); hydrogen peroxide (H(2)O(2)) (100 to 300 microM), an inducer of apoptosis; and crocidolite asbestos (5 microg/cm(2) dish) in a nontransformed murine alveolar type II epithelial cell line (C10). Laser scanning cytometry and flow cytometry were used to determine: (1) whether expression of phosphorylated ERKs was cell cycle-related; and (2) whether cell-cycle alterations by agents could be modified after addition of the mitogen-activated protein kinase/ERK kinase (MEK) 1 inhibitor PD98059. In contrast to other stimuli which induced transient increases in phosphorylated ERKs, asbestos caused fiber-associated localization of phosphorylated ERKs that were elevated from 1 to 24 h (P < or = 0.05), and striking apoptosis followed by increased numbers of cells in the S phase at 72 h. In both control and asbestos-exposed cells, the percentage of phosphorylated ERK-positive cells was greatest in cells in the G(2)/M and S phases of the cell cycle. All stimuli caused increased proportions of cells in G(2)/M at 24 h that were inhibited by PD98059 (30 microM). Increases in G(2)/M cells by H(2)O(2) and asbestos also were decreased at 48 h by the MEK1 inhibitor. In addition, PD98059 abrogated elevations in S-phase cells by EGF and H(2)O(2) at 24 h and by asbestos at 72 h. Our results suggest that ERKs mediate cell-cycle alterations during the development of epithelial cell apoptosis or proliferation by diverse ERK stimuli.

Animals↗

PubMed2004

Fibroblast growth factor-10 prevents asbestos-induced alveolar epithelial cell apoptosis by a mitogen-activated protein kinase-dependent mechanism.

Asbestos induces alveolar epithelial cell (AEC) DNA damage and apoptosis by the mitochondria-regulated death pathway and oxidative stress. Fibroblast growth factor-10 (FGF-10), an alveolar epithelial type II cell mitogen that is required for the lung development, prevents H(2)O(2)-induced AEC DNA damage by a mitogen activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK)-dependent mechanism. In this study, we show that FGF-10 attenuates asbestos-induced AEC DNA strand break formation and apoptosis. MAPK/ERK kinase (MEK) inhibitors, U0126 or PD98059, each blocked the protective effect of FGF-10 against asbestos-induced DNA damage and apoptosis, whereas a p38-MAPK inhibitor had a negligible effect, suggesting a crucial role for MEK/ERK activation in mediating the protective effects of FGF-10. Further, we show that FGF-10 attenuates asbestos-induced change in AEC mitochondrial membrane potential and caspase 9 activation, both of which are blocked by U0126. We conclude that FGF-10 decreases asbestos-induced AEC DNA damage and apoptosis in part by mechanisms involving MEK/ERK-dependent signaling that affects the mitochondria-regulated death pathway.

Animals↗

PubMed2005

Oxidant generation promotes iron sequestration in BEAS-2B cells exposed to asbestos.

Lung injury after asbestos exposure is associated with an oxidative stress that is catalyzed by iron in the fiber matrix, complexed to the surface, or both. We tested the hypothesis that the cellular response to asbestos includes the transport and sequestration of this iron through (1) generation of superoxide for ferrireduction, (2) up-regulation of divalent metal transporter-1 (DMT1) for intracellular transport of Fe2+, and (3) increased production of cellular ferritin where the metal is stored in a catalytically less reactive state. BEAS-2B cells with normal and elevated Cu,Zn superoxide dismutase (SOD) expression were employed for in vitro investigations. After exposure of these cells to asbestos, we demonstrated by fluorescence methodology a significantly increased generation of SOD with ferrireductive capacity. Fiber exposure also increased DMT1 protein and mRNA expression in the BEAS-2B cells. Incubation with asbestos elevated cellular iron and ferritin concentrations, and these responses were diminished in cells with an enhanced expression of SOD. Finally, fiber exposure increased supernatant concentrations of interleukin 8, but this inflammatory mediator was actually increased in cells with elevated SOD expression. We conclude that the response of respiratory epithelial cells to asbestos includes oxidant-mediated mechanisms to sequester catalytically active iron associated with the fiber.

Asbestos, Crocidolite↗

PubMed1981

Asbestos exposure in the Monfalcone area. A social and pathological study of 100 autopsy cases.

Monfalcone is a coastal town with important shipyards. In the present investigation hyalin pleural plaques, lung asbestos bodies, and occupational history were studied in 100 consecutive autopsy cases, collected at the hospital of Monfalcone. Pleural plaques were observed in 72% of males and in 33% of females. Asbestos bodies were found after chemical digestion of pulmonary tissue in 94 cases, and an approximate estimation of their amount showed high or very high numbers in 39 cases. Occupational history, obtained from patients' relatives, was suggestive of occupational asbestos exposure in 60 cases, with 37 subjects having worked in the shipyards. Thirteen other patients had had a probable domestic exposure to asbestos. The severity of asbestos exposure in the Monfalcone area is emphasized.

Adult↗

PubMed1985

Assessing the power and quality of epidemiologic studies of asbestos-exposed populations.

This paper briefly discusses criteria for evaluating epidemiologic studies for risk assessment purposes, using asbestos as an example. Asbestos is one of the few carcinogens for which substantial data exist on exposures to humans. However, there are major difficulties in using these data for conducting risk assessments. In particular, exposure data are often incomplete, and risk assessments usually involve extrapolating from the higher exposures of the occupational environments to the lower levels typically encountered in the nonoccupational environment. The term "asbestos" refers to the fibrous form of several minerals, and levels of exposures to these fibers are not easily assessed. Criteria for evaluating epidemiologic studies used in an Ontario Royal Commission report on asbestos are discussed. The importance of considering the statistical power of studies to detect an excess risk is examined using as examples major cohort studies of asbestos-exposed workers, as summarized in a report by the U.S. National Research Council.

Asbestos↗

PubMedDate not supplied

Mesotheliomas following exposure to asbestos used in railroads: the Italian cases.

The available knowledge on the oncogenic risks of asbestos, the data on the uses of asbestos in railroads, with particular regard to the Italian State Railroads (Ferrovie dello Stato = FS), and the groups at risk due to the exposure to asbestos used in railroads were briefly reviewed. The available data on the pathological effects of such exposure, and in particular on the onset of mesotheliomas among machinists and other railroad workers, were also summarized. Eighty-five cases of mesothelioma (80 pleural, 4 peritoneal, and 1 pericardial), related to the exposure to asbestos used in railroads, observed in various Italian regions, were then reported. Twenty-eight of these cases (among which 27 reported in the Emilia-Romagna Region) were submitted to a detailed study at the Bologna Institute of Oncology. Fifty cases of mesothelioma occurred among FS workers, in particular machinists; 30 cases occurred among machinists of rolling-stock workshops not belonging to the FS; 3 cases occurred among travelling workers of rolling-stock not belonging to the FS; and 2 cases were found in family members (a daughter and a wife) of FS workers. This series of cases, together with similar data from the literature, proves the existence of an actually health risk due to asbestos used in railroads, and indicates its gravity. On the basis of the available data, the following steps are considered necessary: the adoption of preventive measures, the performance of medical oncological surveillance, the promotion of systematic epidemiological investigations, and, finally, more emphasis on basic research, aimed at generating information on the biological events taking place during the incubation period of the tumors, to be used for reducing the effect of exposure, and therefore for contrasting the onset of the disease in those who, having been exposed, although healthy, are potentially at high risk.

Adult↗