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PubMed2004

Asbestos induces tissue factor in Beas-2B human lung bronchial epithelial cells in vitro.

Asbestos has been implicated in the pathogenesis of interstitial lung diseases including asbestosis. Tissue factor (TF) initiates blood coagulation in vivo contributing to inflammation and tissue remodeling via extravascular fibrin deposition and signaling for profibrogenic mediators. We hypothesized that asbestos could induce TF expression by lung epithelial cells. We found that TF mRNA and TF-dependent procoagulant activity were induced in asbestos-treated Beas-2B human airway epithelial cells, which we used as a model system. The effect was increased by crocidolite and chrysotile versus control particulates, including titanium dioxide (TiO2) and Wollastonite (W). Transcription factors that bind the TF gene promoter, including NF-kappaB, AP1 and Sp1, were induced by asbestos while TF mRNA was unstable. TF mRNA was inhibited by mithramycin in asbestos-treated as well as control cells suggesting that Sp1 contributes to TF maintenance in Beas-2B cells. Sp1 knockdown with specific siRNA decreased TF antigen, which is consistent with Sp1-mediated control of TF in Beas-2B cells. The results demonstrate that asbestos induces TF expression in lung epithelial cells in vitro, representing a newly recognized potential mechanism by which asbestos may modulate epithelial cell responses germane to lung remodeling. The mechanism involves alterations in steady-state TF mRNA that do not involve posttranscriptional regulation, implicating control of TF gene expression at the transcriptional level through Sp1 or other transcription factors.

Asbestos↗

PubMed1995

Malignant mesothelioma and duration of asbestos exposure: correlation with tissue mineral fibre content.

Among 441 cases of malignant mesothelioma in the author's files, there were 324 for whom reliable information was available regarding the duration of exposure to asbestos. Included were 298 pleural and 26 peritoneal mesotheliomas. The mean duration of exposure to asbestos was 23 +/- 14 years for all cases, and was not different for the pleural and peritoneal groups. Lung tissue was available for analysis of mineral fibre content in 94 cases. Linear regression analysis showed a significant correlation between duration of exposure and asbestos bodies per gramme of wet lung as determined by light microscopy, and between duration of exposure and total uncoated fibres (5 microns or greater in length) as well as commercial amphibole fibres per gramme as determined by scanning electron microscopy (P < 0.05). Individuals with direct exposures had on average higher asbestos contents than patients with indirect exposures. Furthermore, for each duration of exposure, shipyard workers had on average higher asbestos contents than non-shipyard workers (P < 0.05). Mesotheliomas are associated with a wide range of durations of exposure to asbestos and pulmonary asbestos burdens, and there is a rough correlation between duration of exposure and pulmonary commercial amphibole content.

Adult↗

PubMed1984

Asbestos-induced chemiluminescence response of human polymorphonuclear leukocytes.

Products of the oxidative metabolism of polymorphonuclear leukocytes (PMN), namely hydrogen peroxide and superoxide, may play a role in tissue injury at sites of inflammation. Oxidant production by PMN was measured by the luminol-enhanced chemiluminescence (CL) of cells exposed in vitro to asbestos fibers. Human peripheral blood PMN were incubated with 1-1000 micrograms/ml of UICC chrysotile B asbestos fibers opsonized with either normal or heat-inactivated human serum. CL was measured over 210 min and revealed a peak response at 45 min; this response was delayed in comparison to control CL induced by Staphylococcus aureus (5-10 min) and represented approximately 50% of that of the latter. Although maximal CL was generated by asbestos concentrations of 100-500 micrograms/ml, significant CL was observed at concentrations as low as 0.5-1 micrograms/ml. Opsonization of asbestos fibers with heat-inactivated serum markedly depressed CL responses, suggesting that complement activation by asbestos fibers may be important in the generation of CL by PMN. In view of the previously reported accumulation of PMN in the lungs of asbestos-exposed animals, this study suggests that oxidant production by PMN may mediate some of the pathological effects of asbestos fibers.

Asbestos↗

PubMed1984

Asbestos-activated peritoneal macrophages release a factor(s) which inhibits lymphocyte mitogenesis.

Intraperitoneal asbestos injection in mice has previously been reported to elicit an activated macrophage population. In the present study supernatants from such macrophages were tested for their effect on thymocyte mitogenesis in response to concanavalin A; control supernatants were obtained from saline- and latex-elicited macrophages. Supernatants from asbestos-elicited macrophages were significantly inhibitory to thymocyte mitogenesis while saline- and latex-elicited macrophages did not release significant amounts of such activity. Asbestos-activated macrophage supernatants were inhibitory in a dose-dependent way and the activity was not secreted by macrophages from mice which had received asbestos in the long term. The inhibitory activity was partially dialysable. Supernatants prepared by treating macrophages in vitro with a lethal dose of asbestos were not inhibitory suggesting that the inhibitory activity in the supernatants of asbestos-activated macrophages did not leak from dead or dying cells. The asbestos macrophage supernatant was also significantly inhibitory to mature T-cell-enriched spleen cells but had no effect on fibroblasts, suggesting that the inhibitory effect could be lymphoid cell specific.

Animals↗

PubMed1989

On the cytotoxicity of chrysotile asbestos fibers toward pulmonary alveolar macrophages. II. Effects of nicotinamide on the cell metabolism.

Since it was recently shown that the addition of nicotinamide (NAM) to pulmonary alveolar macrophages (PAM) cell monolayers significantly altered their ATP pools (Nadeau and Lane, 1988), the effects of the vitamin on the metabolism of the cells, exposed or not to very short chrysotile asbestos fibers (VSF), were evaluated. First, it was found that the addition of NAM to the culture medium caused a dose-dependent (5-30 mM) decrease in the extracellular liberation of lactate and pyruvate by PAM. This is suggestive of a direct effect of NAM on the metabolism of glucose. A decrease in extracellular lactate was also observed when control PAM were exposed to 50 micrograms of VSF asbestos. This latter effect was however progressively abolished when the NAM was added to the asbestos-exposed cell monolayers. Second, contrary to the lactic acid production, the exposure to chrysotile caused an increase in the extracellular liberation of pyruvate by PAM. This cell response to the asbestos fibers could represent an antioxidative defense mechanism. Yet, interestingly enough, this effect of the VSF on PAM was not suppressed by the presence of the vitamin. The NAM also induced a dose-dependent decrease in the total lactate dehydrogenase content of PAM monolayers. By comparison, 3-aminobenzamide (up to 5 mM) did not appreciably modify these parameters. After an 18-hr incubation period with 20 mM NAM, the NAD+ pools of control PAM increased by approximately 300% comparatively to a approximately 40% increase for the NADP+ content. The exposure to the VSF asbestos caused a dose-dependent depletion of the cellular NAD+ and NADH pools. However, for the latter, the vitamin prevented the depletion effect of the asbestos fibers. Comparatively, the NADP(H) pools increased. This shift toward the phosphorylated pyridine nucleotide forms could also represent a defense of the cell against the oxygen radicals produced during the ingestion of the fibers. Overall, it is shown that changes in the energy metabolism could be implicated in the toxicity of chrysotile asbestos fibers toward PAM, and that the cells seem to be able to respond to an oxidant stress. Although not fully elucidated at the present time, these data tend nonetheless to point out that the protective effect of NAM could involve some modifications of the host defenses against prooxidants.

Animals↗

PubMed1984

Evaluation by electron microscopy techniques of asbestos contamination in industrial, cosmetic, and pharmaceutical talcs.

Talc powders from national and international markets were analyzed in order to assess their fiber contents and the proportion of asbestos in the fibrous material. Samples of talc powders used as excipients in pharmaceutical and cosmetic preparations demonstrated fiber contents up to 30% of total particles. About a half of the talc powders revealed the presence of asbestos: in five samples chrysotile (a serpentine asbestos) was present, in the other ones tremolite and anthophyllite (an amphibole asbestos). The amounts of asbestos vary up to 90% in the different samples of the fibrous fraction. About 75% of observed asbestos fibers were thinner than 0.4 micron, i.e., below the resolving power of light microscopy which until now was the most utilized technique for evaluating the environmental pollution due to asbestos.

Asbestos↗

PubMed1989

Asbestos hazards in the city of Rome, Italy.

A review is made of asbestos as a health hazard, and attention is drawn to possible dangers due to exposure to asbestos in the city of Rome in and outside the work place. The exposure to asbestos of workers of the ATAC company (the public concern of urban passenger transport of Rome) is examined. This is particularly dangerous for workers who repair equipment with asbestos components, such as brake linings. Exposure to asbestos may also occur in inhabitants who live and work close to where asbestos fibres collect. The study evaluates the contamination of asbestos fibres in both work and urban environment among people directly or indirectly exposed to this pollutant.

Air Pollutants↗

PubMed2004

Genotoxic effects of asbestos in humans.

Risks of carcinogenic and non-carcinogenic effects from asbestos continue owing to the persistence of the fibres in building materials and other products. For this reason, epidemiological and mechanistic research on the toxic effects of asbestos and mineral fibres is still needed. The present molecular epidemiological study was conducted in a former asbestos cement plant in Slovakia. Altogether 82 subjects were investigated, 61 exposed subjects (24 smokers and 37 non-smokers), and 21 factory controls (8 smokers and 13 non-smokers). Workers were exposed to asbestos for between 5 and 40 years. Though the exposure to asbestos during past 40 years was relatively high, at the time of sampling the concentrations of asbestos in the production hall exceeded the Slovak occupational limit (0.001 fibre/cm3) by a factor of only 3-5. The office area levels were below this limit. Biomarkers of exposure, effect and individual susceptibility were measured, including DNA damage (strand breaks [SBs], base oxidation and alkylation, using the comet assay); cytogenetic parameters; and individual DNA repair capacity (incision at 8-oxoguanine measured using a modified comet assay). Oxidised pyrimidines were significantly higher in exposed men compared with non-exposed (P = 0.04). There was also a positive association between SBs (P = 0.04) and age, and alkylation damage to DNA (P = 0.04) and age. Moreover, oxidised pyrimidines (P = 0.01) and alkylated bases (P = 0.001) strongly correlated with years of occupational exposure. Micronucleus frequency did not differ between exposed and control subjects. Repair capacity overall did not show any effect of exposure, though female controls had higher incision rates than did female exposed subjects. However, exposed asbestos workers had significantly higher numbers of chromosomal aberrations (P = 0.01) compared with control group. This finding is consistent with the known association of chromosome aberrations with cancer-risk.

Asbestos↗

PubMed2005

Immunological monitoring in workers occupationally exposed to asbestos.

Occupational exposure to asbestos is strongly associated with pulmonary diseases, cancer and immunotoxic effects. Both systemic and local immunity may play an important role in the pathogenesis of these events. Immune cells appear to be influenced by asbestos exposure, either through direct effects or as a result of the host's protective response to exposure. In this study several immune system parameters were assessed in workers (n = 61) with at least 5 years' exposure to asbestos at an industrial plant. Workers exposed to asbestos fibres had significantly increased levels of immunoglobulin E and concentrations of interleukin-6 and -8 in comparison with two sets of controls (in-plant and town control groups). The levels of soluble adhesion molecule ICAM-1 were higher in the exposed group compared to the town control group. Significantly increased levels of IgA were found in asbestos-exposed group in comparison to the town control. Evaluation of the expression of adhesion molecules on lymphocytes, monocytes and granulocytes by flow cytometry showed significant increases in the class of selectins CD62L on monocytes and granulocytes. Moreover, significantly increased expression of markers CD69 and CD66b on eosinophils was found among workers exposed to asbestos. In conclusion, exposure to asbestos fibres was found to have several effects on immune system. Alterations of these immune parameters may indicate hypersensitivity (increased levels of IgE, increased expression of activation markers CD66b and CD69 on eosinophils) and an elevated inflammatory status (increased levels of interleukins--IL-6, IL-8) in exposed workers.

Adult↗

PubMed2004

Reduction of chrysotile asbestos-induced genotoxicity in human peripheral blood lymphocytes by garlic extract.

Asbestos fibers are well known environmental carcinogen, however, the underlying mechanisms of their action have still not clearly been identified. Asbestos is capable of depleting glutathione and generating reactive oxygen species (ROS), which are important mediators of damage in biological system. Asbestos-induced mutagenecity, may be mediated by the generation. It is known that a number of scavengers and antioxidants attenuate asbestos-induced ROS release. Furthermore, it is known that garlic, contains numerous sulfur compounds and glutathione precursors which act as antioxidants and also demonstrate anticarcinogenic properties. The aim of this study was to investigate whether garlic extract has any influence on asbestos-mediated genotoxicity. As an assay system, we applied the micronucleus assay, sister chromatid exchanges, and chromosomal aberrations with human peripheral blood lymphocytes, which has already been used to analyze the genotoxicity of asbestos fibers. Our results indicate that garlic extract, when administered to the lymphocytes cell culture simultaneously with chrysotile reduced the rates of micronucleus formation, sister chromatid exchanges, and chromosomal aberrations significantly. We conclude that garlic extract may be an efficient, physiologically tolerable quencher of asbestos-mediated genotoxicity.

Asbestos, Serpentine↗

PubMed2004

Asbestos exposure from gaskets during disassembly of a medium duty diesel engine.

Diesel engines have historically used asbestos-containing gaskets leading to concerns of fiber release and mechanic exposure. Other published studies regarding asbestos fiber release during gasket removal have reported on short-duration events; were conducted under simulated work conditions; or had other limitations. There are no comprehensive studies relating to diesel engine gaskets under conditions similar to those reported herein, evaluating asbestos fiber release from gaskets during all facets of a complete disassembly and cleaning of a medium duty diesel engine in a busy repair and service shop by a journeyman mechanic. Asbestos content of all gaskets was identified; all disassembly tasks were described and timed; and personal and area air monitoring was conducted for each task. Twenty seven of thirty three gaskets contained chrysotile asbestos in concentrations that ranged from 5 to 70%. All but one air monitoring sample reported results below the limit of reliable detection even though plumes of visible dust were evident during various removal, cleaning, and buffing procedures. The detection limit for airborne asbestos fibers in this investigation was influenced by the presence of other shop dust in the air. Our investigation demonstrates that using shop-standard procedures in an established repair facility, a journeyman mechanic has very little potential for exposure to airborne asbestos fibers during disassembly of an engine, approximately 10% or less than that currently considered to be acceptable by OSHA.

Air Pollution, Indoor↗

PubMed1986

Effects of asbestos fibers on alveolar macrophage-mediated lymphocyte cytostasis.

Prolonged asbestos inhalation results in pulmonary inflammation and fibrosis. Since alveolar macrophages are active in regulation of immune responses in lung and appear to be involved in the pathogenesis of asbestosis, we evaluated the effects of asbestos exposure on the ability of these cells to regulate lymphocyte function. Alveolar macrophages obtained by lung lavage from BALB/C mice were treated in vitro with either UICC amosite or chrysotile asbestos and the effects on lymphocyte cytostasis compared with those of macrophages incubated with latex beads or zymosan. Macrophages (10%) incubated either alone or with latex beads for 48 hr effectively inhibited lymphocyte mitogenesis. However, alveolar macrophages incubated with either amosite or chrysotile asbestos did not demonstrate intact cytostatic activity. Decreased viability of chrysotile asbestos-treated macrophages correlated with loss of cytostatic effects, but alveolar macrophages exposed to amosite remained viable. We conclude, therefore, that exposure of alveolar macrophages to asbestos can result in loss of their ability to down-regulate lymphocyte proliferation, a finding which may be important in the pathogenesis of asbestos-related disease.

Animals↗

PubMed2004

Asbestos exposure as a risk factor for retroperitoneal fibrosis.

BACKGROUND: Retroperitoneal fibrosis (RPF) is an uncommon disease with unknown causation in most cases. The pathognomonic finding is a fibrous mass covering the abdominal aorta and the ureters. Our aim was to clarify the possible role of asbestos exposure in the development of RPF. The hypothesis was based on the ability of asbestos to cause fibrosis in pulmonary and pleural tissue. METHODS: We undertook a case-control study of 43 patients with the disease (86% of eligible cases) treated in three university hospital districts of Finland in 1990-2001. For every patient, five population-based controls were selected, matched by age, sex, and central hospital district. We assessed asbestos exposure and medical history using a postal questionnaire and a personal interview. Of the 215 eligible controls, 179 (83%) participated in the study. FINDINGS: The age-standardised incidence of RPF was 0.10 (95% CI 0.07-0.14) per 100?000 person-years. The disease was strongly associated with asbestos exposure. The odds ratio (OR) was 5.54 (1.64-18.65) for less than 10 fibre-years of asbestos exposure and 8.84 (2.03-38.50) for 10 or more fibre-years, the attributable fraction being 82% and 89%, respectively. Other risk factors were previous use of ergot derivates (OR 9.92 [1.63-60.26]), abdominal aortic aneurysm (OR 6.73 [0.81-56.08]), and smoking for more than 20 pack-years (OR 4.73 [1.28-17.41]). INTERPRETATION: Our results show that occupational asbestos exposure is an important causal factor for RPF. For patients with work-related asbestos exposure, RPF should be considered an occupational disease.

Aged↗

PubMed2004

Asbestos exposure among Seoul metropolitan subway workers during renovation of subway air-conditioning systems.

Air quality in underground spaces has seldom been evaluated in Korea. Accordingly, the current study recently evaluated asbestos exposure among Seoul metropolitan subway workers during the renovation of the subway's air-conditioning system. To identify possible routes of asbestos exposure, suspected sources, including gaskets, ceiling boards, ceiling materials, and dust settled inside ducts, were all sampled. Personal air samples were also taken to evaluate any asbestos exposure during the renovation. The asbestos fibers found in the samples were analyzed using a transmission electron microscope (TEM) equipped with an energy dispersive X-ray analyzer (EDX). Twelve out of eighteen bulk samples contained asbestos, the majority of which was chrysotile fibers. Asbestos was detected in 9 out of 72 personal air samples and the level ranged from 0.003 to 0.02 fibers/cm(3). While asbestos levels were below Korean occupational limit of 2 fibers/cm(3), they were still detectable and therefore further monitoring would be appropriate.

Air Conditioning↗

PubMed2003

Airborne asbestos concentration from brake changing does not exceed permissible exposure limit.

The use in the past, and to a lesser extent today, of chrysotile asbestos in automobile brake systems causes health concerns among professional mechanics. Therefore, we conducted four separate tests in order to evaluate an auto mechanic's exposure to airborne asbestos fibers while performing routine brake maintenance. Four nearly identical automobiles from 1960s having four wheel drum brakes were used. Each automobile was fitted with new replacement asbestos-containing brake shoes and then driven over a predetermined public road course for about 2253 km. Then, each car was separately brought into a repair facility; the brakes removed and replaced with new asbestos-containing shoes. The test conditions, methods, and tools were as commonly used during the 1960s. The mechanic was experienced in brake maintenance, having worked in the automobile repair profession beginning in the 1960s. Effects of three independent variables, e.g., filing, sanding, and arc grinding of the replacement brake shoe elements, were tested. Personal and area air samples were collected and analyzed for the presence of fibers, asbestos fibers, total dust, and respirable dust. The results indicated a presence in the air of only chrysotile asbestos and an absence of other types of asbestos. Airborne chrysotile fiber exposures for each test remained below currently applicable limit of 0.1 fiber/ml (eight-hour time-weighted average).

Air Pollutants, Occupational↗

PubMed1998

GRP78, HSP72/73, and cJun stress protein levels in lung epithelial cells exposed to asbestos, cadmium, or H2O2.

Occupational exposure to crocidolite asbestos is associated with the development of nonmalignant and malignant pulmonary disease. Considerable evidence indicates that the mechanisms of asbestos-induced toxicity involve the production of active oxygen species (AOS). Production of AOS in excess of cellular defenses creates an environment of oxidative stress and stimulates the expression of a number of different genes whose products may be involved in mediating responses from oxidant injury. To further investigate the mechanisms of asbestos-induced pathogenicity, we have examined by Western blot analyses the induction of the stress response proteins GRP78 and HSP72/73 in rat lung epithelial cells (RLE) exposed to crocidolite asbestos. In comparative studies, we also examined GRP78, HSP72/73, and cJun expression in RLE cells exposed to equitoxic concentrations of cadmium chloride (CdCl2) and hydrogen peroxide (H2O2). Our results demonstrate that asbestos and H2O2 do not alter GRP78 or HSP72/73 protein levels in RLE cells, but do increase levels of cJun protein. Increases by asbestos and H2O2 were not accompanied by alterations in cellular glutathione levels in this cell type, but asbestos caused elevations in protein levels of manganese-containing superoxide dismutase (MnSOD), an indirect indicator of oxidant stress. In contrast, exposure of cells to CdCl2 led to no changes in MnSOD protein levels, but increases in GRP78, HSP72/73, and cJun proteins as well as significant increases in oxidized and reduced thiol pools. Results suggest that environmental agents causing oxidative injury to lung epithelium elicit different patterns of stress responses.

Animals↗

PubMed2001

p53, p21 and metallothionein immunoreactivities in patients with malignant pleural mesothelioma: correlations with the epidemiological features and prognosis of mesotheliomas with environmental asbestos exposure.

The aim of this study is to investigate immunoreactivity for p53, p21 and metallothionein in diffuse malignant pleural mesothelioma (DMPM) and to determine the relationships between the age, sex, asbestos exposure time, survival of DMPM patients with environmental asbestos exposure and immunoreactivity to p53, p21 and metallothionein. Sixty-seven histopathologically-confirmed DMPMs, 38 of whom had environmental and 29 had occupational asbestos exposure, were included. The tumour tissue samples were immunostained with antibodies against p53, p21 and metallothionein. Epidemiological data and the survival times for the DMPM patients with environmental asbestos exposures were obtained from hospital records. Thirty-three per cent of the DMPMs were positive for p53, 35% for p21 and 52% for metallothionein. There was no statistical difference between the histological subtypes of DMPM in terms of immunoreactivity for p53, p21 and metallothionein. For p21 and metallothionein there was a statistically significant difference between the exposure characteristics: patients with environmental asbestos exposure had shown more immunopositivity. There were statistically significant differences between age groups and between asbestos exposure times for metallothionein, and between asbestos exposure times and p21. The patients with positive immunostaining had longer exposure times and were older than those having negative immunostaining. The differences between survival of the patients were not statistically significant in terms of the immunohistochemical results for p53, p21 and metallothionein.

Age Factors↗

PubMed1984

[Mesothelioma as an index tumor of the occupational hazard of asbestos dust].

Mesothelioma arises from the cover epithelia of the serous body cavities and is a most malignant and fatal tumour. Since 1978 42 cases of diffusely growing mesothelioma have been observed. An extreme difference in the expected frequency of mesothelioma among previously severely asbestos-dust-exposed persons and the rest of the population is characteristic. Accordingly, death from mesothelioma does not only show a predominantly high occupational asbestos-dust-risk association but also to environmental exposition by neighborhood and household contact. Thus in production and use of asbestos-containing products a risk must be expected. Due to the great likelihood of asbestos-induced mesothelioma in the individual case it is justified to consider this tumour as signal for asbestos exposition decades ago. In the German Federal Republic "pleural and peritoneal mesothelioma caused by asbestos" is a notifiable occupational disease since 1977. Each diagnosis of mesothelioma initiates the suspicion and thus the medical duty of notification of an occupational disease. Following the large increase of asbestos consumption in the GFR over the last 30 years an increase of medically confirmed mesotheliomas can be expected.

Adult↗