SEARCH · PubMed Health

Results for “ASBESTOS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,801 records · Page 100Linked to original sources

PubMed2004

[Use of a job-exposure matrix for the screening of occupational exposure to asbestos].

BACKGROUND: According to a recent French legislation (1995), retired people who have been exposed to an occupational carcinogen can benefit from a specific post-occupational medical follow-up program, supported by the "Caisse Primaire d'Assurance-Maladie" (CPAM), the French health insurance system. However, only very few people presently take access to this social measure. The ESPACES project developed and evaluated a procedure to identify retirees who have been exposed to asbestos during their career, and to inform them about the post-occupational medical follow-up program. METHODS: This pilot study was performed within the health centers ("Centres d'examens de santé" (CES)) of the health insurance system in a random sample of men who have retired from the six main French administrative divisions between 1994 to 1996. A probability of exposure to asbestos was attributed through a job exposure matrix. Subjects were interviewed in the CES to validate their exposure data. Retired subjects with confirmed exposure to asbestos were referred to their CPAM, to apply for the medical follow-up. The whole process was evaluated through a comparison with control CPAMs, and simulations were performed to assess its sensitivity and specificity, as well as the total number of persons in France who could potentially benefit. RESULTS: Among the 737 persons classified as exposed by the matrix who came to the CES, the exposure was confirmed for 53.8%, and 143 benefited from the medical follow-up, 17 times more than in a sample of control CPAMs. Based on an annual number of about 250,000 new retirees, simulations showed that a low detection threshold, taking into account the probability and duration of exposure, would yield approximately 25,000 persons coming to the CES, more 6,000 of them benefiting from the follow-up. CONCLUSION: The proposed detection threshold would allow for a feasible and ethically acceptable generalization, due to the optimization of the false negative and false positive rate.

Asbestos↗

PubMed2002

Crocidolite asbestos inhibits pentose phosphate oxidative pathway and glucose 6-phosphate dehydrogenase activity in human lung epithelial cells.

The cytotoxicity of asbestos has been related to its ability to increase the production of reactive oxygen species (ROS), via the iron-catalyzed reduction of oxygen and/or the activation of NADPH oxidase. The pentose phosphate pathway (PPP) is generally activated by the cell exposure to oxidant molecules. Contrary to our expectations, asbestos (crocidolite) fibers caused a dose- and time-dependent inhibition of PPP and decreased its activation by an oxidative stress in human lung epithelial cells A549. In parallel, the intracellular activity of the PPP rate-limiting enzyme, glucose 6-phosphate dehydrogenase (G6PD), was significantly diminished by crocidolite exposure. This inhibition was selective, as the activity of other PPP and glycolysis enzymes was not modified, and was not attributable to a decreased expression of G6PD. On the opposite, the incubation with glass fibers MMVF10 did not modify PPP and G6PD activity. PPP and G6PD inhibition did not correlate with the increased nitric oxide (NO) production elicited by crocidolite in A549 cells. Experiments with the purified enzyme suggest that crocidolite inhibits G6PD by directly interacting with the protein. We propose here a new mechanism of asbestos-evoked oxidative stress, wherein fibers increase the intracellular ROS levels also by inhibiting the main antioxidant pathway of the cell.

Asbestos, Crocidolite↗

PubMed1995

High-resolution computed tomography sampling for detection of asbestos-related lung disease.

RATIONALE AND OBJECTIVES: We determined whether a limited number of high-resolution computed tomography (HRCT) scans will effectively screen for interstitial lung disease (ILD) in a population of individuals exposed to asbestos. METHODS: We retrospectively reviewed the computed tomography studies of 49 patients exposed to asbestos. HRCT in the supine and prone positions had been performed at specifically preselected levels. Two teams of thoracic radiologists evaluated, on separate occasions: (1) all images, (2) prone images only, and (3) a single prone image through the lung bases for the presence of diffuse ILD. RESULTS: A relatively high level of accuracy was obtained with a single prone scan. However, improvement to 95% or better was found when additional prone images were used. CONCLUSION: A screening study for ILD, in this case patients exposed to asbestos, may be performed by preselected prone HRCT images only. The ease and decreased time of performing the procedure make screening relatively large patient groups for ILD more feasible.

Asbestos↗

PubMed2003

Cell signaling and transcription factor activation by asbestos in lung injury and disease.

Signaling pathways initiated at the external cell surface or within the cytoplasm regulate transactivation of transcription factors and gene expression that are causally related to a number of critical cellular outcomes including proliferation, apoptosis, cell survival, and production of inflammatory cytokines. Asbestos, a ubiquitous pathogenic group of mineral fibers, can stimulate gene expression in a variety of cell types in the lung via intracellular signaling pathways. These cell signaling cascades may be initiated through receptor-mediated events or integrins. Alternatively, they may be stimulated by oxidants generated both during phagocytosis of minerals and/or by redox reactions on the mineral surface. Once initiated, these pathways can lead to promotion of gene expression critical to cellular injury, proliferation and inflammation-events leading to the development of fibroproliferative diseases of the lung and pleura. The elucidation and relevance of critical signaling cascades to lung injury or repair following asbestos exposure could aid in developing strategies to prevent or treat asbestos-associated lung and pleural diseases.

Animals↗

PubMed2000

Modulation of cell and DNA damage by poly(ADP)ribose polymerase in lung cells exposed to H(2)O(2) or asbestos fibres.

Poly(ADP)ribose polymerase (PARP) may participate in cell survival, apoptosis and development of DNA damage. We investigated the role of PARP in transformed human pleural mesothelial (MeT-5A) and alveolar epithelial (A549) cells exposed from 0.05 to 5mM hydrogen peroxide (H(2)O(2)) or crocidolite asbestos fibres (1-10 microg/cm(2)) in the presence and absence of 3-aminobenzamide (ABA), a PARP inhibitor. The cells were investigated for the development of cell injury, DNA single strand breaks and depletion of the cellular high-energy nucleotides. Compared to H(2)O(2), fibres caused a minor decrease in cell viability and effect on the cellular high-energy nucleotide depletion, and a marginal effect on the development of DNA strand breaks when assessed by the single cell gel electrophoresis (the Comet assay). Inhibition of PARP transiently protected the cells against acute H(2)O(2) related irreversible cell injury when assessed by microculture tetrazolium dye (XTT) assay and potentiated oxidant related DNA damage when assessed by the Comet assay. However, PARP inhibition had no significant effect on fibre-induced cell or DNA toxicity with the exception of one fibre concentration (2 microg/cm(2)) in MeT-5A cells. Apoptosis is often associated with PARP cleavage and caspase activation. Fibres did not cause PARP cleavage or activation of caspase 3 further confirming previous results about relatively low apoptotic potential of asbestos fibres. In conclusion, maintenance of cellular high-energy nucleotide pool and high viability of asbestos exposed cells may contribute to the survival and malignant conversion of lung cells exposed to the fibres.

Asbestos↗

PubMed2002

Modulation of DNA single-strand breaks by intracellular glutathione in human lung cells exposed to asbestos fibers.

We investigated the role of glutathione and nitric oxide synthase (NOS) in fiber-induced cell and DNA toxicity using alkaline (pH 13) single-cell gel electrophoresis (the Comet assay). Transformed cultured human pleural mesothelial (MeT-5A) cells and alveolar epithelial cells (A549) were exposed to crocidolite asbestos fibers (1-10 microg/cm(2)) in the presence of buthionine sulfoximine (BSO) or L-arginine-methyl ester (L-NAME). BSO inhibits gamma-glutamylcysteine synthetase (gamma-GCS) and causes glutathione depletion, and L-NAME inhibits nitric oxide generation. Studies were also conducted to assess the expression of the heavy and light subunits of gamma-GCS in human pleural mesothelium and bronchial epithelium in vivo and the induction of inducible NOS (iNOS) by asbestos fibers. Asbestos fibers caused DNA single-strand breaks, and the process was significantly enhanced by BSO (69% compared to the non-treated cells). A549 cells had a 3.5-fold glutathione content compared to MeT-5A cells, which was consistent with the higher resistance of these cells against oxidants and fibers. Flow cytometry of iNOS showed no change of iNOS by the fibers in either cell type in vitro. L-NAME had no effects on the DNA single-strand breaks in the Comet assay, either. Studies on lung biopsies showed that the immunoreactivities of both gamma-GCS subunits were very low in healthy human mesothelium in vivo. We conclude that glutathione may play an essential role in protecting intact cells against fiber-induced oxidative DNA alterations, and low gamma-GCS reactivity in pleural mesothelium may be associated with the high sensitivity of mesothelial cells to fiber-induced toxicity.

Asbestos, Crocidolite↗

PubMed2004

Role of asbestos in etiology of malignant pleural mesothelioma.

The evidence presented in this article demonstrates that asbestos fibers may be genotoxic to mesothelial cells through their distinctive structure and chemistry and through their interactions with complex cellular response mechanisms. Reactive oxygen and nitrogen species play a key role. Understanding the balance between these complex mechanisms that permit neoplastic transformation and facilitate the proliferation of tumor cells is the focus of current investigation in the development of mesothelial malignancy. In human disease, the persistence of asbestos fibers in the lung and pleural tumor is a critical feature that links the exposure to asbestos with the development of disease.

Asbestos↗

PubMed2000

Environmental exposure to asbestos and risk of pleural mesothelioma: review and meta-analysis.

A number of epidemiological studies have addressed the risk of pleural mesothelioma from environmental (household and neighborhood) exposure to asbestos, but no overall risk estimate is available. We reviewed the epidemiological studies on risk of pleural mesothelioma and household or neighborhood exposure to asbestos. We identified eight relevant studies; most were conducted in populations with relatively high exposure levels. We combined the risk estimates in a meta-analysis based on the random-effects model. The relative risks (RRs) of pleural mesothelioma for household exposure ranged between 4.0 and 23.7, and the summary risk estimate was 8.1 (95% confidence interval [CI]: 5.3-12). For neighborhood exposure, RRs ranged between 5.1 and 9.3 (with a single RR of 0.2) and the summary estimate was 7.0 (95% CI: 4.7-11). This review suggests a substantial increase in risk of pleural mesothelioma following high environmental exposure to asbestos; however, the available data are insufficient to estimate the magnitude of the excess risk at the levels of environmental exposure commonly encountered by the general population in industrial countries.

Asbestos↗

PubMed1998

The release of iron from different asbestos structures by hydrogen peroxide with concomitant O2 generation.

Treatment of aqueous suspensions of different asbestos fibers (amosite, anthophyllite, chrysotile, and crocidolite) at 0-4 degrees C and pH 7.2 with H2O2 results in the consumption of H2O2 with concomitant release of iron and production of O2. During incubations, [H2O2] decreased in proportion to the mass of the suspended fiber, the duration of incubation, and the initial [H2O2]. The consumption of H2O2, production of O2 and release of iron all vary synergistically with the structure of the asbestos fiber. Release of silicon during the incubation was small relative to the decrement in [H2O2], reflecting a lack of dissolution of the fiber. The data are consistent with a redox process for the release of surface bound iron and it is significant that iron release occurs in the absence of a Fe(II) or Fe(III) chelator. The implications of iron release from the asbestos surface may be important in inflammatory disorders in which both silicate bound iron and H2O2 accumulate.

Asbestos↗

PubMed2002

Cytotoxic effects of macrophages and asbestos on transformed rat mesothelial cells.

Asbestos produced a cytotoxic effect on transformed cells of rat pleural mesothelium and on IAR2 epithelial cells and Rat1 fibroblasts transformed by ras oncogene, but not on normal cells of these strains under conditions of coculturing with peritoneal macrophages. Contact of mesothelioma cells, but not macrophages with asbestos was necessary and sufficient for attaining the cytotoxic effect. Macrophage-conditioned medium potentiated asbestos cytotoxicity for transformed mesothelial cells, but not for IARS-ras and Rat1-ras.

Animals↗

PubMed2002

Downregulation of Betaig-h3 gene is causally linked to tumorigenic phenotype in asbestos treated immortalized human bronchial epithelial cells.

Although Betaig-h3 gene has been suggested to modulate cell adhesion and tumor formation, its physiological functions are not well understood. Using human papillomavirus immortalized human bronchial epithelial (BEP2D) cells, we found that Betaig-h3 expression was markedly decreased in asbestos-induced tumorigenic cells. Fusion of tumorigenic and control BEP2D cells resulted in the recovery of Betaig-h3 gene expression to control level and the loss of tumorigenic phenotype. Furthermore, ectopic expression of Betaig-h3 gene in asbestos-induced tumorigenic cells inhibited cell growth in vitro, anchorage independent phenotype, as well as tumorigenicity in nude mice. Betaig-h3 gene is ubiquitously expressed in various normal human tissues, with the exception of the brain, where there is little or no expression. In contrast, there was a decrease or absence in expression of the Betaig-h3 gene in 14 human tumor cell lines of diverse histological types examined, when compared with normal human cells or tissues. The result strongly suggests that loss of Betaig-h3 expression is a frequent event in human cancer and causally related to acquisition of tumorigenic phenotype in asbestos-treated BEP2D cells.

Asbestos↗

PubMed1977

Changes in pulmonary surfactant and phosphatidylcholine metabolism in rats exposed to chrysotile asbestos dust.

1. Pulmonary surfactant was isolated from rats that had been exposed to chrysotile asbestos dust for from 3 days to 15 weeks. 2. Asbestos-treated rats showed a progressive increase in amounts of surfactant. After 15 weeks, treated animals contained 4 times as much as non-treated. 3. No significant change was seen in the total protein or total fatty acid composition of surfactant with exposure. 4. The increase in surfactant phosphatidylcholine normally seen on maturation of rat lung was accelerated by exposure of animals to asbestos. 5. An increase in the activity of phosphorylcholine glyceride transferase in lung homogenates and free cell populations was found. 6. Lysosomal phospholipase A was relatively unaffected by dust exposure. 7. It is suggested that the increase in surfactant amounts could be due to an increase in its synthesis without a corresponding alteration in its degradation.

Animals↗

PubMed2000

Primary malignant gonadal mesotheliomas and asbestos.

AIMS: The clinicopathological, immunohistochemical and aetiological aspects, with respect to asbestos, of seven primary gonadal mesotheliomas (three intratesticular, four ovarian) are described and compared. These tumours are extremely rare, poorly described and the knowledge of their natural history is very limited. METHODS AND RESULTS: The cases were collated from the UK Health and Safety Executive Mesothelioma Register over a 24-year period (1968-91). Primary mesotheliomas of the tunica vaginalis and ovary comprised 0. 09% (10 cases) and 0.03% (three cases) of mesothelioma deaths, respectively. No primary intratesticular (non-tunica vaginalis) malignant mesotheliomas have been described. In this study, we present seven (three intratesticular, four ovarian) primary malignant gonadal mesotheliomas. In both genders the tumours show a similar age distribution (with median onset in the sixth decade), a similar association with asbestos (in approximately 50% cases), a diverse histological spectrum (with predominantly tubulopapillary epithelial subtype tumours) and an immunophenotype that is comparable with malignant pleural and peritoneal mesothelioma. The clinical course appears variable (mean, 26 months; range, 9-50 months). All tumours in the study presented as localized masses and their prognosis appeared more favourable than that of diffuse pleural and peritoneal cases. CONCLUSIONS: An awareness of the existence of these rare forms of malignant mesothelioma is important to prevent misdiagnosis. Immunohistochemistry has an important role in confirmation of the diagnosis. The accurate diagnosis of primary gonadal mesothelioma has potentially important medicolegal compensation considerations as a significant proportion of these cases are associated with asbestos.

Adult↗

PubMed2003

Desmoplastic malignant mesothelioma of the pleura: autopsy reveals asbestos exposure.

Desmoplastic mesothelioma is a rare subtype of diffuse malignant mesothelioma, and is often difficult to distinguish from reactive pleural fibrosis because of associated extensive collagen fibrosis. An 82-year-old woman with a severe cough was revealed to have pleural effusion and diffuse pleural thickening on the right side. Antibiotics were ineffective, and a compression fracture of the ninth and tenth thoracic vertebral bodies was recognized on X-ray. Autopsy revealed a diffuse pleural thickening with hyalinized collagen tissue in the central part of the pleura. However, the peripheral part of the fibrous tissue was composed of spindle and polygonal cell proliferation that were immunohistochemically positive for antibodies against cytokeratin and vimentin. In addition, the ninth and tenth thoracic spines were infiltrated by similar cells. The condition was diagnosed as desmoplastic mesothelioma with bone metastases. Asbestos bodies were detected in the thickened pleura and fibrosed alveolar septa, and it was suggested retrospectively that the patient had been exposed to asbestos. Thus, autopsy analyses of fibrous pleurisy are necessary to detect a desmoplastic variant of mesothelioma of the pleura and its association with asbestos exposure.

Aged↗

PubMed1998

Computed tomographic findings of environmental asbestos-related malignant pleural mesothelioma.

Malignant pleural mesothelioma (MPM) is not an infrequent fatal neoplasm. It is endemically present in some regions of Turkey due to its aetiological relationship to exposure to environmental fibrous minerals. The aim of this study was to determine the thorax computed tomographic (CT) features of environmental asbestos-related MPM. In this study, we examined retrospectively the CT scans of 46 untreated patients with pathological diagnosis of environmental asbestos-related MPM among 151 patients with malignant pleural mesothelioma in the Izmir Chest Disease and Surgery Hospital. The CT scans were interpreted by consultation of four observers. Malignant pleural mesothelioma was unilateral in 45 (97.2%) of the patients. Pleural effusions were found in 42 (91%) of the patients, pleural calcifications in 12 (26%), contracted hemithorax in 14 (30%), interlobar fissure involvement in 25 (54%) and mediastinal pleural involvement in 26 (57%). A contracted hemithorax was significantly correlated with pleural rind configuration. Pleural thickenings were found in 45 (99%) of the patients. Pleural thickenings were in the form of nodularity in 10 (22%) cases, regular in 12 (27%) cases, as a focal mass in 3 (7%) cases and as a pleural rind in 20 (44%) cases. Pleural thickening was greater than 1 cm in 32 (71%) cases. The most common CT findings in our series were unilateral circumferential pleural thickening, nodular pleural thickening, pleural thickening greater than 1 cm and mediastinal pleural involvement. Generally, pleural effusion was accompanied by this. There was interlobar fissure involvement in half of the patients. There was no pathognomonic CT finding in environmental asbestos-related MPM. But CT was useful in suggesting the diagnosis of malignant pleural disease in the cases with MPM.

Adult↗

PubMed2000

Protective effects of green tea catechins against asbestos-induced cell injury.

Green tea extract was found to provide a strong protective effect against asbestos-induced injury of peritoneal macrophages and red blood cells in vitro. The main polyphenolic constituents of green tea extract, (-)-epicatechin gallate (ECG) and (-)-epigallocatechin gallate (EGCG), were also efficient in preventing injury of cells following exposure to asbestos fibers. The protective efficacies of EGCG and ECG expressed as IC50 values were, respectively, 10 microM and 12 microM if peritoneal macrophages were injured by chrysotile and 4 microM and 5 microM in the case of crocidolite-induced cell injury. Antiradical and chelating properties of ECG and EGCG were evaluated and it was concluded that the protective effect of catechins against asbestos-induced injury may be related to both scavenger properties towards to superoxide anion and the ability to chelate iron ions.

Animals↗

PubMed1986

[Occupational cancer study of asbestos: possibilities and limits of epidemiologic studies on the causes of death in West Germany].

The study is based on 3990 men and women exposed to asbestos dust for at least three years at their place of work, and prospectively and epidemiologically examined since 1 January, 1977. By 31 December, 1983, 336 had been registered as having died. Calculation of standard mortality rates indicates that the incidence of malignant tumour as cause of death was much higher than in the general population of the FRG, that of fatal mesothelioma about 100 times as high. Standard mortality rate for lung cancer was increased by 48% and 175%, respectively, depending on whether exposure to asbestos dust had ended after (subgroup I) or before (subgroup II) 1 January, 1972. Proportional mortality rate of 43% of tumours at all locations, with about 14% lung cancer and about 9% fatal mesothelioma cases in subgroup II, approaches the internationally recognized frequency of asbestos-associated tumours.

Adult↗

PubMed2000

Human mesothelial cells are unusually susceptible to simian virus 40-mediated transformation and asbestos cocarcinogenicity.

Mesothelioma, a malignancy associated with asbestos, has been recently linked to simian virus 40 (SV40). We found that infection of human mesothelial cells by SV40 is very different from the semipermissive infection thought to be characteristic of human cells. Mesothelial cells are uniformly infected but not lysed by SV40, a mechanism related to p53, and undergo cell transformation at an extremely high rate. Exposure of mesothelial cells to asbestos complemented SV40 mutants in transformation. Our data provide a mechanistic explanation for the ability of SV40 to transform mesothelial cells preferentially and indicate that asbestos and SV40 may be cocarcinogens.

Asbestos↗

Refine your search to explore more results.