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 883 records · Page 49Linked to original sources

PubMedDate not supplied

[SV40: a possible co-carcinogen of asbestos in the pathogenesis of mesothelioma?].

BACKGROUND: The etiopathogenic role of asbestos in causing malignant mesothelioma of the pleura is clearly supported by an impressive amount of data. Despite the frequent association with previous exposure to asbestos, only a relatively small fraction of those exposed develop malignant mesothelioma. The long latency period between initial exposure and onset of the tumor suggests that human mesothelioma, like many other tumors, has a multi-stage evolution with the occurrence of many mutating events involving various tumorigenic agents, probably in part initiating and in part promoting development. Recently this has raised great interest in the scientific world, in an attempt to identify possible factors which together with asbestos may have a role in developing this rare malignant tumor. Ionizing radiations and genetic susceptibility have occasionally been identified as the culprits. A virus called SV40 has been gaining increasing scientific credibility since the mid 1990's as a potential co-carcinogen of asbestos. OBJECTIVES: The aim of this article was to examine the supposed interaction between asbestos and SV40 in the pathogenesis of mesothelioma and the way this simian virus has become a human virus. METHODS: All biomolecular and epidemiological data available from medical literature along with the results of the experiments performed during the last 7 years in our department laboratories were reviewed and compared. RESULTS: The first two pieces of experimental evidence of the presence of SV40-like DNA sequences in mesothelioma samples were obtained in 1994 in the United States, and one year later in our laboratories. After these two studies many research groups started carrying out similar experiments, obtaining comparable results in most cases. Moreover, beyond the mere detection of viral DNA sequences large amount of biomolecular data has recently been added in favour of its role in the pathogenesis of mesothelioma. Epidemiological studies published to date were unable to provide similar unanimous results. Data regarding the source of human infection are still debatable, even if the inadvertent administration of contaminated poliovaccines to millions of people in Europe and the United States between 1955 and 1963 remains one of the most reasonable hypotheses. CONCLUSIONS: On the basis of all the biomolecular data reviewed and partially on the basis of epidemiological studies, SV40 seems to be the best candidate as a cofactor with asbestos in the development of human mesothelioma.

Animals↗

PubMed2004

Asbestos in developing countries: magnitude of risk and its practical implications.

In developing countries, aggressive marketing of chrysotile asbestos continues as a result of restrictions on its use being imposed by the developed countries. In the Asian continent, China and India are emerging as the major users of asbestos. There is enough evidence to link chrysotile with pulmonary fibrosis and lung cancer in humans, even at low levels of exposure, hence the need to apply the Precautionary Principle for phasing out its use globally. Due to poor occupational health and safety systems in developing countries and difficulties in early detection of pulmonary malignancy related to asbestos, the statistics remain sketchy. This is hampering efforts to create pressure on policy makers and to counter the propaganda of the asbestos industry. The International Labour Office believes that more than 100,000 deaths a year occur from asbestos-related disease. In the view of studies published in Europe and Australia, the number of deaths due to such malignancies will peak around the year 2020 and could be anywhere between half a million to a million. That means more than a million deaths will occur in developing countries. At about the same time when asbestos-related deaths start to decrease in developed countries, their number will begin to rise in developing countries. This presents a major challenge to the international scientific community.

Asbestos↗

PubMed2003

Environmental monitoring of asbestos products manufacturing units--a case study.

Air borne asbestos dust concentration and occupational health environment of workers in a asbestos products manufacturing unit was monitored, and compared with the standards. Study reveals that overall airborne asbestos concentration in the unit is well within the limit, but the workers, which were exposed to air borne asbestos dust, showed a marked increase in deterioration of lung function as compared to the control population, which was not exposed to this dust. Further more, the population which was exposed to airborne asbestos dust along with other predisposing factors like cigarette smoking, showed a marked deterioration of lung function as compared to the population exposed only to air borne asbestos dust.

Asbestos↗

PubMedDate not supplied

The scientific basis of a total asbestos ban.

Worldwide, in the new millennium, standards for the protection of workers and the general population from as-bestos risks are not equally stringent in all countries. The present review analyzes some arguments which in recent years have been proposed as a rationale for the reconsideration of the scientific background of a total asbestos ban, such as that adopted in the European Union. The conclusion is that in order to ensure adequate protection, there is no alternative to a total ban. The evidence for carcinogenicity of chrysotile is as good as for the amphiboles, the carcinogenic potency of chrysotile is lower than that of the amphiboles, but risk estimates must also be based on extent of exposure (nowadays chrysotile represents 95% of asbestos used worldwide). The fact that induction of mesothelioma by asbestos results from the interaction of environmental exposure and genetic factors reflects a general phenomenon in carcinogenesis and does not warrant any re-consideration of the role of asbestos. The role of SV40 as yet is unclear: even assuming that current risk estimates are correct (which is debatable), this agent would interact with asbestos in only a faction of mesothelioma cases. The effectiveness of protocols suggested for "controlled use" has not been tested with a scientfiic approach: they seem hardly practicable, particularly in the countries which are currently the major consumers of asbestos.

Animals↗

PubMedDate not supplied

[Lung cancer in a female non-smoker with occupational exposure to asbestos: a case report].

BACKGROUND: Until recently, asbestos was widely used in a variety of industrial processes. Workers exposed to asbestos may develop lung and pleural diseases such as asbestosis, lung cancer, benign pleural effusion, pleural plaques and mesothelioma. OBJECTIVE: To describe a clinical case of lung cancer in a female non-smoker with occupational exposure to asbestos. METHODS: The clinical and occupational history was based on the information kindly provided by the Occupational Unit of the National Health Service and on the case history of a hospital admittance in 2001, when the patient underwent surgery for lung cancer. RESULTS: The patient worked for 6 years in an asbestos manufacturing industry where she was exposed to high concentrations of asbestos, and then worked for 14 years in a sugar refinery only during the summer. She had benign pleural effusion, pleural plaques, asbestosis and lung cancer. CONCLUSIONS: We concluded that a six-year exposure to high doses of asbestos may induce lung cancer and asbestosis in a female non-smoker.

Asbestos↗

PubMed1991

[Small-airway lesions induced by inhalation of asbestos dust in dogs--pathological and aetiological studies].

This paper presents the pathological changes of the small airways of dogs inhaling asbestos dust in the workshop of Xin Kong Asbestos Mine for 1 to 3 years. Dogs of the experimental group showed that variable degrees of dust deposition and fibrous tissue reaction were found in all the three types of the small airways-respiratory bronchioles, alveolar ducts and membranous bronchioles of both lungs. The lesions in the lung increased with the duration of exposure. These changes in the canine small airways resulting from asbestos dust were very much similar to those of the humans. In addition, deposited dust collected from the workshop of the asbestos mine, and 50 dust particles selected randomly in foci were identified in situ by energy dispersive X-ray analysis. Findings demonstrated that the majority of the dust particles in the foci was principally mixed silicate dust. Among them asbestos dust predominated absolutely, and there were more amphiboles than chrysotiles. Therefore, it is concluded that the small airway lesions induced in the dogs are mainly due to mixed asbestos dust, and that there appears to exist a dose-response relationship.

Animals↗

PubMed1991

Role of asbestos and active oxygen species in activation and expression of ornithine decarboxylase in hamster tracheal epithelial cells.

Induction of ornithine decarboxylase (ODC) enzyme activity occurs after exposure of hamster tracheal epithelial (HTE) cells to asbestos and the soluble tumor promoter 12-O-tetradecanoylphorbol-13-acetate. Since active oxygen species are implicated as mediators of asbestos-induced biological responses studies here were designed to examine whether active oxygen species generated by asbestos or oxidants caused increased ODC activity. In confluent HTE cells, significant blockage of chrysotile or crocidolite asbestos-stimulated ODC activity occurred with simultaneous addition of catalase, but not superoxide dismutase, to medium. The addition of xanthine plus xanthine oxidase caused a dose-dependent increase in ODC activity, which was inhibited significantly after addition of catalase or mannitol, indicating that H2O2 was the principal oxidant produced in that reaction. Addition of phenazine methosulfate, a redox reagent used to generate superoxide, resulted in significant elevation of ODC, which was inhibited by addition of superoxide dismutase but not catalase. Hydrogen peroxide added to culture medium also caused a potent increase in ODC activity inhabitable by catalase. Hypochlorous acid caused increases in ODC activity, although the magnitude of this response was less than that observed with other oxidants. Therefore, although all active oxygen species examined triggered ODC, less reduced species (O2- and H2O2) were more proficient than OH or a halogenated oxidant. All oxidants, except HOCl, caused a significant increase in [3H] thymidine incorporation at 24 or 48 h after their addition to HTE cells. In comparative studies, exposure of HTE cells to either asbestos or xanthine plus xanthine oxide increased the level of ODC mRNAs proportionate to oxidant concentration and the extent of enzyme induction. Thus, data indicate that H2O2 plays a major role in asbestos-stimulated ODC induction and proliferation of epithelial cells of the respiratory tract by altering the regulation of a gene critical to proliferation.

Animals↗

PubMed1991

AIHA position statement on the removal of asbestos-containing materials (ACM) from buildings.

The health risks associated with asbestos exposure for building occupants has been demonstrated to be very low. The decision to remove asbestos-containing materials (ACM) in undamaged, intact condition that are not readily accessible to occupants should be made only after assessing all other options. Both technical and financial issues should be fully explored by a team of trained specialists, including industrial hygienists, architects, and engineers. The optimal solution will vary from building to building, based on factors unique to each situation. One important consideration is the use of a well-designed air-monitoring program to identify changes in airborne levels of asbestos. Special training and maintenance programs are needed to ensure the safety and health of building and contract workers who may encounter asbestos or who may disturb it during routine or nonroutine activities. Each building owner who has ACM in a building should identify an in-house asbestos manager, and it is also necessary to provide appropriate resources, including professional consultants, to develop and manage a responsible and effective in-place management program throughout the life of a building containing asbestos.

Asbestos↗

PubMed1991

Iron-catalyzed reactions may be responsible for the biochemical and biological effects of asbestos.

The most carcinogenic forms of asbestos contain iron to levels as high as 36% by weight and catalyze many of the same biochemical reactions that freshly prepared solutions of iron do, i.e. oxygen consumption, generation of reactive oxygen species, lipid peroxidation and DNA damage. The participation of iron from asbestos in these reactions has been demonstrated using the iron chelator desferrioxamine B which inhibits iron-catalyzed reactions. Iron appears to be redox active on the asbestos fiber, but chelation and subsequent iron mobilization from asbestos by a variety of chelators, e.g. citrate, EDTA or nitrilotriacetate, makes the iron more redox active resulting in greater oxygen consumption and production of oxygen radicals in the presence of reducing agents. Iron also appears to be important for some of the asbestos-dependent biological effects on tissues or cells in culture, such as phagocytosis, cytotoxicity, lipid peroxidation and DNA damage. Therefore, redox cycling of iron to generate oxygen radicals at the surface of the fiber and/or in solution, as mobilized, low molecular weight chelates, may be very important in eliciting some of the biological effects of asbestos in vivo.

Animals↗

PubMed1990

Asbestos-related radiographic abnormalities in public school custodians.

A cross-sectional prevalence study of 120 public school custodians was carried out to investigate the prevalence of asbestos-related disease and to determine the proportion with disease attributable to asbestos exposures in school buildings. Medical and occupational histories, flow-volume loops, and posterior-anterior, lateral, and anterior oblique (AO) chest radiographs were obtained. Single breath DLCO was measured and chest auscultation performed. The present report describes radiographic abnormalities and associations with exposure. Mean age of subjects was 57 years and mean duration of work as a custodian, 27 years. Fifty-seven (47.5%) had no known or likely exposure to asbestos outside of their work as a school custodian (NOE). Pleural plaques (PP) occurred in 40 (33%) of the total group and 12 (21%) of the group with NOE. Multivariate analysis revealed significant associations (p less than 0.05) between PP and duration of asbestos exposure. The proportion with PP increased PP detection by a factor of 1.9. Our results reveal PP prevalence in excess of background in the study population and indicate that PP are attributable to asbestos exposure in schools in a subset with NOE. Prudent management of asbestos in buildings is indicated for the prevention of related disease.

Adult↗

PubMed1990

Asbestos bodies in pulmonary hilar lymph nodes.

Asbestos bodies (AB) have long been recognized in light microscopic (LM) sections of pulmonary hilar lymph nodes (LN) from patients with asbestos-related diseases, but the presence of AB on LM has not been correlated with the lung AB burden. The purpose of the present study was to determine whether AB in histologic sections of LN are indicative of heavy lung asbestos burdens. Twenty cases (17 with asbestosis, 15 with carcinoma of the lung, and two with malignant pleural mesothelioma) with at least one AB on a hilar LN section were identified. Bleach digestion of lung tissue in 15 cases demonstrated a median of 24,000 AB/g by LM and 44,000 AB/g by scanning electron microscopy. Digestion of hilar nodes demonstrated 21,800, 15,500, and 3,200 AB/g by LM in three cases which had lung burdens of 22,000, 481,000, and 5470 AB/g, respectively. A fourth LN specimen contained 322,000 AB/g in a case with no lung available to digest. Mean AB lengths in the LN in three cases were 48, 45, and 27 microns. Fourteen control cases of men over 50 without known asbestos exposure or asbestos-related disease had no AB in LN sections even after staining for iron. Among fourteen patients with parietal pleural plaques and an elevated lung asbestos body content, AB were observed in iron-stained LN sections in only two cases. These two patients had 3240 and 610 AB/g lung tissue, respectively (normal range 0 to 20 AB/g). We conclude that the finding of AB on a histologic section of hilar LN is generally indicative of a heavy lung AB burden.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1990

[Observer variation of the radiographic assessment of pulmonary changes caused by asbestos].

Assessment was undertaken of 165 x-ray photographs of the thorax originating from 165 men with varying degrees of exposure to asbestos: 37 were workers in an eternite factory, 65 insulation workers, 42 were plumbers and 21 were patients from the Lung Clinic in Bispebjerg Hospital. Assessment of the x-rays was carried out according to the directives established by the International Workers' Organisation (ILO) by three experienced specialists who had no knowledge of the individual person's exposure to asbestos or smoking habits. In order to investigate not only inter- but also intra observer variation, the three medical specialists described the material on two occasions with an interval of several days. Analysis of the descriptions revealed that there was considerable inter- and intra-observer variation in assessment of the changes caused by asbestos. Description of the parenchymatous changes was associated with slightly greater variation than description of the pleural changes. A partial analysis of smokers who had not had occupational exposure to asbestos showed a not inconsiderable occurrence (5-33%) of parenchymatous changes which could not be differentiated from changes caused by asbestos. It is concluded, that the diagnosis of pulmonary disease caused by asbestos should not be based on radiographic examination alone.

Adolescent↗

PubMed1989

[Health damage caused by asbestos and other mineral fibers].

Occupational exposure to asbestos is associated with malignant tumors in the lung and malignant mesothelioma in the pleura and peritoneum. Tumors at other sites have also been reported. The benign asbestos-related disorders are asbestosis and pleural fibrosis, effusion and plaques. Chronic bronchitis may be associated with previous asbestos exposure. Fiber dimensions and durability are main factors for carcinogenicity. For practical reasons, long and thin fibers like asbestos should be considered carcinogenic. The diagnosis of asbestos-related disease is based upon information on occupational exposure. Analysis of lung fiber burden supports information given by the occupational history and gives valuable information on dose-response and dose-effect relationships. Building materials with good maintainance of the surfaces do not release asbestos fibers, whereas materials subject to mechanical stress should be replaced by nonasbestos-containing materials to avoid the stipulated very low increase in cancer risk.

Asbestos↗

PubMed1988

[On the analysis of actual state of contamination with asbestos in the autopsy cases in Hokkaido].

The exposure of asbestos was surveyed in the 92 autopsy cases, including 60 cases of lung cancer with the digestion method of lung tissue. More or less asbestos body was found in 94.6% of cases examined. There was no correlation between numbers of asbestos bodies and histological types of lung cancer. In the group of pulmonary fibrosis, the pleural adhesion was more intense in the cases with increased number of asbestos bodies. More than 80 asbestos bodies per 1g of wet lung tissue were found in 4 cases, but there was no significant relation between occupation and the grade of asbestos contamination.

Aged↗

PubMed1988

A comparison of asbestos burden in non-urban patients with and without lung cancer.

Asbestos is a recognized carcinogen which is widely available for environmental exposure. Since all members of our society are exposed to asbestos containing environments and, indeed, have asbestos fibres in their lungs, the concern exists as to its significance in contributing to the incidence of lung cancer in such populations. The asbestos burden was compared in lung tissue from control and lung cancer patients who had resided in a non-urban environment. There were no significant differences between the asbestos burdens in both age matched groups; however, the proportions of amphiboles to chrysotile were different from those reported in previous urban based studies. This difference was suggested to be attributable to chrysotile exposure in urban air. All patients had appreciable non-asbestos fibres within their lungs. The results indicate that when comparing any dust burden in lungs, it is necessary to have data from regional control populations before attempting to explore causal-disease relationships.

Adult↗

PubMed1986

[Neoplasm risk in men occupationally exposed to asbestos dust].

To evaluate the magnitude of cancer risk in those occupationally exposed to asbestos dust, a historically prospective cohort has been investigated. The observation covered 2403 men employed for at least 3 months, within 1945-1973, in a factory producing various asbestos products--including chrysotile. The cohort availability on 31 Dec. 1981 was 91.3%. The risk analysis was based on the standardized mortality ratio (SMR) calculated by the man-years method. The reference group was composed of general men population in Poland. Totally, in the test cohort 401 deaths were certified, in this 73 due to malignant tumours and 31 due to the respiratory system cancer. The total standardized mortality ratio (SMR) came to 85, for malignant tumours, SMR = 104.8 for the respiratory system cancer SMR = 144.7, lung cancer-139.5%. Those values were not statistically significant. In the cohort of those employed during 1945-1955, selected due to a very high concentration of asbestos dust at this time and long observation time from the first contact with asbestos dust, the total SMR was 90.7, the one for malignant tumours-136.2 (p less than 0.05). In this cohort 21 deaths for the respiratory system cancer were observed, the total SMR = 191.1 (p less than 0.01), in this 18 for the lung cancer, SMR = 187.1 (p less than 0.05). The other cancer groups did not exhibit any statistically significant standardized mortality rate. The analysis points to a considerable lung cancer risk in those occupationally exposed to asbestos dust at the time of high non-controlled asbestos dust concentrations.

Asbestos↗

PubMed1986

Airway branching patterns influence asbestos fiber location and the extent of tissue injury in the pulmonary parenchyma.

The degree to which various anatomic components of the lung influence the distribution of inhaled particles is not entirely clear. Therefore, we have studied the role intrapulmonary airways play in the localization of respired asbestos fibers and have correlated local asbestos fiber burden with tissue injury in rats following exposure to aerosolized chrysotile asbestos for 7 hours per day, 5 days per week for 12 months. Tissues arising from anatomically distinct pathways of the tracheobronchial tree were isolated by using microdissection. Adjacent tissue blocks from regions immediately distal to the last dissected airway were prepared for light microscopic evaluation or digested in hypochlorite solution to determine alveolar septal tissue density and asbestos fiber concentration respectively. These studies demonstrated regional differences in asbestos fiber number, size, and mass which were inversely related to airway pathlength and to bifurcation number along each airway path. Fiber burden within each region was found to be proportional to the relative degree of tissue injury present. These findings suggest that differences in tissue injury from region to region in the lungs following exposure to asbestos are a result of regional differences in the deposition and retention of these substances in the lungs. These airway characteristics which influence fiber deposition may also play an important role in the deposition and subsequent lung injury caused by other particulates and environmental pollutants.

Animals↗

PubMed1979

The asbestos industry and statutory control of its hazards.

The difficulties of balancing the possible hazards of asbestos against its useful properties, the cost of control measures and the availability of adequate substitutes are described. The history of the asbestos industry, of recognition of the association between asbestos and respiratory disease and of the develpment of control regulations in the UK are outlined. The present provisions for inspection of work places, for medical services to workers and for environmental control within and outside the workplace have been reviewed and a Health and Safety Commission set up to implement them; their work is described. Although the regulations are being implemented, however, public anxiety has increased. Justification for such anxiety comes from reports of still-existing hazards and from the fact that the current standard was established on faulty grounds. Three studies are described which indicate that a dose-response relationship may exist in relation to the carcinogenicity of asbestos; however, there is still not enough evidence to set standards. Further studies have shown that the different types of asbestos incur different degrees of risk. The UK Asbestos Standards are thus undergoing revision, this time in consultation not only with physicians and hygienists, but also with members of industry, trades union members, academics and local authorities.

Asbestos↗