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[Nonmalignant asbestos-related diseases].

Non malignant asbestos diseases are dominated numerically by pleural plaques. This form of circumscribed fibrosis of the parietal pleural is generally asymptomatic and its potential for evolution is weak. More rarely diffuse pleural fibrosis results from disease of the visceral pleura with a secondary fusion of the two pleural layers. Usually it follows a pleural effusion which resolves spontaneously. Its functional effects are sometimes important. The generalised practice of computerized tomographic scanning as a work up for asbestos related disease has revealed the frequent association of this diffuse pleural fibrosis with a particular form of peripheral pulmonary collapse called round atelectasis. Asbestosis or pulmonary fibrosis induced by the inhalation of asbestos has become rarer due to the improvement in working conditions in the asbestos industry. It develops following heavy exposure. The frequency of bronchopulmonary cancer is increased when asbestosis exists although it is not currently possible to say if the two disorders are independent and each is only conditioned by exposure to asbestos or if the two diseases are inextricably linked by the same physiopathological process.

Asbestos↗

[Asbestos exposure and pleuropulmonary cancer].

Pleuropulmonary cancers are recognized asbestos-related diseases. Mesothelioma occurs almost uniquely in individuals exposed to asbestos whereas lung cancer is strongly associated with smoking. If the asbestos exposure is sufficient however, the incidence of lung cancer is higher than would be expected from the smoking effect alone. For lung cancer in asbestos workers, asbestosis is not a prerequisite for recognition as an occupation related disease. The intensity and duration of exposure to asbestos are factors associated with higher risk of lung cancer. These factors can be estimated on the basis of the work history or, when necessary, by analyzing mineral dust from available lung tissues.

Asbestos↗

Asbestos management and removal in hospitals.

Asbestos has been used in a vast assortment of materials installed in hospitals since the turn of the century. While there is a perception that many regulations pertaining to asbestos have become less stringent, new regulations are continuing to be enacted that require building owners and facilities managers to implement methods of recognition and control for asbestos-containing building materials. Several states have initiated regulations on asbestos consultants and contractors that supersede federal requirements. This document is intended to summarize some of the most important management practices that hospitals should undertake when conducting work that would disturb, or have the potential to disturb, asbestos-containing building materials.

Air Pollution, Indoor↗

Health effects of asbestos exposure in humans: a quantitative assessment.

Asbestos causes four diseases in humans: Lung fibrosis (asbestosis) follows heavy exposure and, in industrialized countries, is mainly a relic of past working conditions. The risk of pleural fibrosis and plaques is likely to be linearly dependent from time since first exposure and is present for all types of asbestos fibres. The diagnostic uncertainties regarding pleural plaques and the substantial degree of misclassification make it difficult to precisely estimate the shape of the dose-response relationship. The risk of lung cancer seems to be linearly related to cumulative asbestos exposure, with an estimated increase in risk of 1% for each fibre/ml-year of exposure. All fibre types seem to exert a similar effect on lung cancer risk; a multiplicative interaction with tobacco smoking has been suggested. Pleural mesothelioma is a malignant neoplasm which is specifically associated with asbestos exposure: the risk is linked with the cubic power of time since first exposure, after allowing for a latency period of 10 years, and depends on the fibre type, as the risk is about three times higher for amphiboles as compared to chrysotile. Environmental exposure to asbestos is also associated with mesothelioma risk.

Asbestos↗

[Reporting and compensation of mesothelioma caused by occupational exposure to asbestos in Romagna (1986-1994). Work Group for Surveillance of Mesothelioma in Romagna].

A working group for the surveillance of mesothelioma was established in the Romagna Region of Italy. For the present report of the early data on compensation, 94 cases notified to the Romagna Cancer Registry between 1986 and 1994 (mean age, 66.7 years; male: female ratio, 1.8; frequency of pleural location, 76%; frequency of cyto-histologic confirmation, 79%) were considered. Information on asbestos exposure, occupational history, and compensation status was obtained from the patients or their relatives, the general practitioners, the local occupational health services, the National Institute of Social Insurance, the National Board for Insurance against Industrial Accidents (INAIL), and the Trade Unions. Asbestos exposure was associated with 42/94 cases (45%). Of these, 11 (26%) had been reported to INAIL. All such cases had cyto-histological confirmation. The greater frequency of reporting was found among cases known to the occupational health service (7/7) as well as those with definite, documented asbestos exposure (9/13). Only two cases had been reported by hospital physicians. Seven cases were compensated. In addition to cyto-histological confirmation, also the male sex, patient's age under the mean of 66, pleural location, and documented asbestos exposure were found to be prerequisites for compensation. Not only in these subgroups but also among cases known to the occupational health service as well as those diagnosed in 1990-94, most cases reported were compensated. These early data suggest that a more accurate diagnostic process as associated with prompt notification to the occupational health service for thorough assessment of asbestos exposure may improve the compensation process.

Adult↗

[Bronchiolitis obliterans-organizing pneumonia (BOOP) containing asbestos bodies: clinico-pathological study of a case].

We describe a case of bronchiolitis obliterans-organizing pneumonia (BOOP) with asbestos bodies. A 65-year-old man, treated in the past for gastric lymphoma and with an history of asbestos exposure, presented with fever and two nodular opacities in the lower lobe of the left lung. Histologic examination revealed a BOOP pattern; in the inflammatory tissue some asbestos bodies were present. Patients exposed to asbestos may rarely present with localized inflammatory pulmonary lesions. In these cases, the possible etiopathogenetic role of asbestos needs further studies.

Aged↗

[K-ras gene mutations of asbestos and welding-fumes related human lung cancer].

UNLABELLED: To investigate the K-ras gene mutations in asbestos and welding-fumes related human lung cancer (hLC), comparing with the mutational spectrum of K-ras gene in non-occupational hLC, 8 cases of non-occupational hLC, 9 cases of asbestos-related hLC and 4 cases of welding-fumes related hLC were collected. The techniques of genomic DNA extraction, nested-polymerase chain reaction (PCR), polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP), polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) and DNA direct sequencing were employed. THE RESULTS: showed the mutation frequencies of K-ras gene were 25% in non-occupational hLC and welding-fumes related hLC, whereas 44.4% in asbestos-related hLC. Mutations mainly occurred in codons 12 and 15. A mutation of codon 13 was detected in welding-fumes related hLC. The type of base substitution was principally G-->T transversion in non-occupational hLC, whereas mainly G-->A transition in asbestos and welding-fumes related hLC. THE RESULTS suggested there were obvious differences of K-ras gene mutations among non-occupational hLC, asbestos and silica related hLC. Therefore, different mechanisms of carcinogenesis were implicated among them. However, no speific spectrum of K-ras gene mutation can be derived from welding-fumes related hLC because of the limitation of samples.

Asbestos↗

[Effects of asbestos on P53 protein expression in V79 cells].

OBJECTIVE: To explore the effects of physical and chemical properties of asbestos on mutagenesis/carcinogenesis. METHODS: The P53 protein expression in V79 cells exposed to asbestos suspension and filtrate was studied using immunohistochemical method. RESULTS: After asbestos suspension and filtrate treatment of V79 cells, the value of hue for indicating P53 protein expression was significantly lowered, and such abnormal expression was especially observed in binucleate cells and polykaryocytes. CONCLUSION: The above data demonstrated that abnormal accumulation of P53 protein in V79 cells was related to asbestos exposure and that asbestos suspension and filtrate had even greater effect on the cells at the segmentation period.

Animals↗

Interconvertibility of asbestos fibre count concentrations recorded by three most frequent methods.

Simultaneous airborne chrysotile asbestos fibre samples were collected with three types of instruments, namely, the konimeter, the thermal precipitator and the membrane filter, in four asbestos plants (textile manufacturing, asbestos cement production, mining, milling). Linear regression analyses were performed of the membrane filter on the konimeter and thermal precipitator count concentrations, respectively. Sampling was performed at 24-35 locations in each of the processes studied. In order to linearize the relationships and to stabilize the sample variances the data were transformed using the transformation ln(x+1) for both the predictor and the response variables. Eight linear regression equations were developed. The slope coefficients of regressions differed significantly (P < 0.05 or < 0.01) between all the asbestos processes except for the differences of coefficients in mining and milling (P > 0.05). It is concluded that no single conversion factor can be used to reliably convert the konimeter or thermal precipitator to membrane filter asbestos fibre concentrations; a separate conversion factor must be derived for each technological process. In this case the confidence limits of estimates are acceptable for practical occupational hygiene purposes.

Air Pollutants, Occupational↗

[The role of oxygen free radicals in asbestos cytotoxicity].

Despite numerous experiments, the cytotoxicity of asbestos is still far from being well understood. There is an increasing evidence which supports the contribution of free oxy-radicals resulting from the phagocytosis of asbestos fibres concerning macrophages neutrophils, pulmonary epithelial and endothelial cells. Both in vitro and in vivo studies revealed an asbestos-induced generation of hydrogen peroxide, hydroxyl radical and superoxide anion. The intensity of the process varies with the physico-chemical properties of the asbestos fibres. Oxygen free radical activity accounts for the lipid peroxidation of cell membranes as well as for the damage of structural proteins and DNA. However, the cells contain antioxidant enzymes such as catalase, superoxide dismutase, etc., which prevent the toxic effect of oxidants. Their activity increases when the cells are exposed to asbestos.

Asbestos↗

A preliminary study of biochemical changes in the rat small intestine following long-term ingestion of chrysotile asbestos.

Changes are reported in the DNA, RNA, protein and brush border enzymes in the small intestine mucosal lining cells and gut lumen, induced by maintaining rats on a diet containing chrysotile asbestos for 10 months. Intracellular levels of RNA, DNA and protein remained unchanged but significant alterations, consistent with a mineral-induced cytotoxicity, were found in the lumen level of DNA (increased) and RNA (decreased) in asbestos-treated rats. Most intracellular enzyme levels were consistently, but not significantly, elevated in animals maintained on diets containing asbestos whilst the activities within the lumen were significantly higher than those found in normal animals. The presence of cigarette smoke alone in the diet induced changes in intracellular RNA and lumen ATPase but the combined effect of cigarette smoke and asbestos was rarely different from the alterations induced by asbestos alone on the majority of parameters studied.

Adenosine Triphosphatases↗

[Assessment of asbestos exposure via mineralogical analysis of bronchoalveolar lavage fluid].

BACKGROUND: Mineralogical analysis of bronchoalveolar lavage fluid (BALF) by electron microscopy could be the most suitable method for assessing asbestos exposure. However, it has been claimed that there is not a standardized or systematic approach to the subject of mineralogical analysis. OBJECTIVES: The aim of the study was to evaluate mineralogical analysis of BALF by transmission electron microscopy (TEM) as biomarker of asbestos fibre load. METHODS: BALF was examined in 193 exposed workers (189 men and 4 women) and in 84 patients (65 men and 19 women) who underwent diagnostic fibreoptic bronchoscopy for various clinical purposes. Asbestos bodies (AB) in BALF were counted with a phase contrast microscope, while fibres were counted and analysed by TEM. RESULTS: Fibre counting by TEM showed a significant difference in the two populations (two tailed Mann-Whitney U test, p=0.0044), since it was positive in all exposed subjects. Only 75.1% of the exposed population was positive for asbestos bodies (AB). Subjects who had been exposed over a long time period had higher concentrations of fibres than subjects who had been exposed more recently probably because of higher exposure in the past. CONCLUSIONS: The study confirms the results of a previous study on a limited number of subjects. Fibre concentrations in BALF can be considered as a reliable biomarker of past asbestos exposure even after many years after cessation of exposure.

Adult↗

The risk of lung cancer and mesothelioma after cessation of asbestos exposure: a prospective cohort study of shipyard workers.

A prospective cohort study of 3,893 shipyard workers, mainly exposed to chrysotile, indicated no increased risk of lung cancer 7-15 yrs after exposure to asbestos had ceased. The shipyard workers, however, had an increased risk of pleural mesotheliomas with 11 observed cases versus 1.5 expected. An explanation for these observations may be that asbestos may have different carcinogenic mechanisms in causing lung cancer and mesothelioma. A non-increased risk of lung cancer some years after exposure to asbestos has stopped is in accordance with asbestos acting as a promotor. The high risk of mesothelioma, on the other hand, may indicate that asbestos acts as a complete carcinogen in developing this disease.

Adult↗

[The role of macrophages in asbestos-induced carcinogenesis].

Data available on the pathways of asbestos (fibrous) carcinogenesis still leaves much to be desired. Asbestos is regarded as a non-genotoxic substance by most researchers. There is insufficient evidence on the interaction of fibres, target-cells and macrophages. Macrophages secreted proteins (ca. 450 kD) to inhibit proliferation of intact mesothelium and cytoxine (3-5 kD) which stimulated the cellular sensitivity of intact mesothelium and mesotheliomas to the toxic influence of asbestos. It was suggested that the effect was due to the triggering of intrinsic causation of cell death. Like any other fibres, carcinogenic effect of asbestos could be accounted for by such significant factor as active oxygen radicals. When exposed to asbestos, both intact mesothelial and mesothelioma cells and macrophages synthesized those substances. Free radical-like substances in conjunction with macrophage-conditioned media produced toxic effect on mesothelial cells. The role of active oxygen radicals in fibre-induced carcinogenesis is discussed.

Animals↗

[Two cases of pleural mesothelioma following unusual and unrecognized exposure to asbestos. The role of Occupational Health and Safety Service in identifying past occupational exposure].

BACKGROUND: In Italy there was a wide use of asbestos in various manufacturing sectors and for many different uses, some of which are still partly or completely unknown. A detailed reconstruction of the work histories of mesothelioma patients made it possible, in some cases, to identify ignored circumstances of asbestos exposure. Moreover, the identification of cluster of cases takes on special significance in suggesting a possible previous asbestos exposure, where the information collected on single cases do not imply as much. OBJECTIVES: This report concerns two cases of malignant mesothelioma that occurred in two workers employed in the same processes in a small factory that manufactured and repaired electric motors for hand tools. METHODS AND RESULTS: In the Province of Brescia (one million inhabitants) a Mesothelioma Register is in operation. The first case was classified, according to Re.Na.M.1996 criteria (National Mesothelioma Register) as "unknown" occupational exposure. The identification of a second case, that was discovered thanks to the surveillance system of the Mesothelioma Register, encouraged the local Occupational Health and Safety Service to perform a more detailed investigation that revealed, for both subjects, previously unknown occupational exposure. This consisted of grinding, in a damp setting, electric motor parts bushed with phenolic thermosetting resins reinforced with chrysotile asbestos. Moreover, weekly cleaning of the plants could have been an occasion for dust dispersion. It is likely that this exposure did not last long and was limited in extent. Other similar reports of such circumstances of occupational exposure were not available in the literature. CONCLUSIONS: The results confirm the high information value of systematic collection of incidental cases in the population, which is feasible thanks to the disease register, and the significant role of the local Occupational Health Services in demonstrating past asbestos exposure.

Adult↗

Compensation of asbestos victims in France.

The alarming development of pathologies linked to asbestos led to the creation in France of two funds to indemnify the victims of asbestos-related illnesses: the FCAATA (Fund for asbestos workers who take early retirement), which compensates for their reduced life expectancy, and the FIVA (Indemnification fund for asbestos victims) which ensures full compensation for harm suffered by asbestos victims.

Asbestos↗

Genetic predisposition and health effect of occupational exposure to asbestos.

OBJECTIVES: As asbestos presents a direct genetic hazard for humans, a small-scale molecular epidemiological study was conducted to monitor 61 subjects long-term exposed to asbestos in comparison with 49 town controls and 21 control subjects from administration of the same factory. RESULTS: Asbestos exposed workers had significantly higher numbers of chromosomal aberrations compared with both control groups (P=0.003). Clinical examination showed that 44.3% of exposed workers developed symptoms of asbestosis. We were interested in the relationship between the risk of asbestos-coupled diseases and individual variability in biotransformation enzymes, especially in glutathione S-transferases and microsomal epoxide hydrolase. GSTP1*105Val allele appeared less in the group of workers with asbestosis compared to those without asbestosis (18.5% vs 34.7%, P=0.044), and in subjects with developed asbestosis coupled with bronchitis compared to those without bronchitis (0% vs 25%, P=0.048). Similarly, the genotype corresponding to low activity of microsomal epoxide hydrolase was significantly decreased in workers with fibrotic plaques compared to those without plaques (26.7% vs 56.3%, P=0.045). CONCLUSIONS: Our results suggest that GSTP1*105Val allele and low EPHX1 activity genotype may be protective for people occupationally exposed to asbestos. However, more extensive studies are needed to confirm our results.

Asbestos↗

Chrysotile asbestos-induced membrane damage in human erythrocytes.

Chrysotile asbestos causes the release of K+ and hemoglobin from erythrocytes. At short incubation times K+ release is slightly higher than hemoglobin release but for incubation times of 10 min or longer the percentage K+ release, and the percentage hemolysis are the same. The results suggest that asbestos causes a sudden and complete disruption of the membrane permeability for K+, which is probably followed by colloid osmotic hemolysis. Polyanions inhibit asbestos-induced hemolysis completely. Leaching of asbestos diminishes its hemolytic potency, as does a decrease in pH. The results support the view that positive charges, probably of magnesium, play a predominant role in asbestos-induced hemolysis.

Asbestos↗