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PubMed1988

[Asbestos-induced malignant tumors].

Asbestos had been increasingly used in many applications across numerous industries on account of its particular material properties, including resistance to heat and fire as well as to aggressive chemicals, high mechanical strength, insulation capacity, other physical parameters, and for its low price. World wide asbestos production and processing thus went up from 50 tons to 5.5 million tons per annum, in about 100 years. Widespread application of asbestos as well as of asbestos-containing materials and workpieces together with the understanding that asbestos for its fibrogenicity is capable of causing pulmonary and pleural asbestoses constitute a major challenge for thorough elucidation of related occupational diseases and their relationship with asbestos. This demand is additionally supported in urgency by the cancerogenicity of asbestos potentially leading to malignant diffuse mesotheliomas, bronchial carcinomas, and, obviously, other tumors. In the context of malignant mesotheliomas, emphasis has to be laid on characteristic morphological features, biological behaviours, and asbestos-related aetiology. As bronchial carcinomas have several aetiological backgrounds, answers will have to be found to the questions for which of them may have been fully or partially caused by asbestos and which have not. No differentiation has so far been feasible, in this context, by tumour morphology, including histological typing. After all, when it comes to malignant tumours of other organs, additional epidemiological as well as pathologico-anatomic efforts will have to be made to find out, if and where a given case of tumour growth has coincided with exposure to asbestos.

Asbestos↗

PubMed1979

Analysis of the cores of ferruginous (asbestos) bodies from the general population. III. Patients with environmental exposure.

Typical asbestos bodies visible by light microscopy were isolated from the lungs of 29 persons with fewer than 100 such bodies per gram of lung, a level that is considered indicative of environmental rather than occupational asbestos exposure. Of 144 bodies examined by electron diffraction, 143 contained an amphibole asbestos core and one contained a chrysotile asbestos core. Thirty-five bodies from 21 patients were also analyzed by electron microprobe. Of these, 21 were chemically consistent with amosite or crocidolite asbestos, 13 with anthophyllite asbestos, and one with tremolite asbestos. Certain differences in chemical fiber types between men and women became apparent. Although cores of amosite and crocidolite predominated in men (12 of 14, 86 per cent), anthophyllite and tremolite comprised 57 per cent (12 of 21) of the cores found in women, a statistically significant difference. These differences suggest that the major commerical varieties of amphibole asbestos (amosite and crocidolite) are the source of the fibers in men, whereas in women a major source may be cosmetic talc, which is often contaminated with anthophyllite and tremolite. On the basis of this study and our previous studies, we conclude that almost all typical asbestos bodies from the lungs of the general population contain an amphibole asbestos core.

Asbestos↗

PubMed1981

Asbestos and other ferruginous bodies: their formation and clinical significance.

Analyses of asbestos bodies from the general population have confirmed that these structures, like asbestos bodies from the lungs of asbestos workers, contain an asbestos core. In members of the general population this core is almost always an amphibole, whereas asbestos workers may have bodies formed on either amphibole or chrysotile. Most adults have a few bodies, and increasing numbers are seen in blue collar workers and others who handle small amounts of the fiber, with the highest levels being seen in asbestos workers. In men with minimal or extensive occupational exposure, asbestos bodies are formed on the commercial fibers, amosite and crocidolite, whereas women also form a significant number of bodies on the noncommercial fibers, anthophyllite and tremolite. These findings suggest that women may be exposed to specific asbestos-containing products, eg, cosmetic talc. The commercial fibers found in women and white collar men probably reflect atmospheric pollution with asbestos. At the highest levels of exposure, numbers of asbestos bodies correlate in a general way with the presence of asbestosis, although no precise value has been determined above which asbestosis is always found. In persons with much lower or environmental exposure, there does not appear to be any correlation between numbers of bodies and disease, in particular between numbers of bodies and carcinoma of the lung or gastrointestinal tract. The situation for mesothelioma is uncertain.

Asbestos↗

PubMed1983

[Malignant mesothelioma and asbestos].

Malignant mesothelioma is a rare neoplasm of rapidly lethal course arising primarily in the pleura and less often in the peritoneum. In the majority of cases the disease is closely related to occupational exposure to asbestos. The latency period, calculated from the first contact with asbestos to the appearance of mesothelioma, is generally in the order of 20 years or more irrespective of the duration of exposure. A causal relationship can be established with certainty only by a careful history and positive tissue analysis for the presence of asbestos. The author's own series of 48 pleural mesotheliomas comprises 39 cases involving occupational exposure to asbestos, 6 others with asbestos demonstrable in pulmonary tissue but no discernible source in the history, and 3 where no relation to asbestos could be established at all. Although a dose-response relation may be assumed for asbestos as for all other carcinogens, the lack of data on asbestos dust concentrations at former places of work rendered determination of the minimal noxious dose difficult or impossible. It also remains unclear whether the various asbestos types, such as chrysotile and amphiboles, differ in pathogenic effect. It is hoped that careful registration and continuing study of mesotheliomas will shed further light on their relationship to asbestos and on the possible hazards of the mineral to the general population.

Adult↗

PubMed1982

Asbestos fibers and pleural plaques in a general autopsy population.

It has been claimed that symmetric lower zone pleural or diaphargmatic plaques are markers of asbestos exposure both in asbestos workers and the general population. In this study, total pulmonary asbestos burden was analyzed for 29 patients selected because pleural plaques were found at autopsy, and the results were compared with values obtained for 25 patients who had no occupational asbestos exposure. The average number of asbestos bodies in the plaque groups was 1732/g wet lung, and in the control group, 42/g wet lung. Uncoated asbestos fibers were extracted from lung and counted, measured, and identified by morphologic examination, electron diffraction, and energy-dispersive x-ray spectroscopy. The total number of fibers/per gram wet lung in the plaque group (114 x 10(3)) was similar to that in the control group (99 x 10(3), as was the number of chrysotile fibers (51 x 10(3) versus 29 x 10(3)). However, the plaque patients had a marked increase in the number of the commercially used high aspect ratio amphiboles, amosite and crocidolite (50 x 10(3) versus 1 x 10(3). A retrospective history of fairly certain asbestos exposure was obtained for 16 of the plaque patients, and such a history correlated strongly with increased numbers of commercial amphiboles in lung. It is concluded that 1) in this general autopsy population, two subgroups of patients are present. About one half of the patients appear to have developed pleural plaques as a result of asbestos exposure, while the etiology of the plaques in the other half is unclear; 2) the presence of pleural plaques correlates with a modest (50-fold) increase in numbers of long high-aspect ratio commercial amphiboles in lung tissue but does not correlate with numbers of chrysotile fibers, noncommercial amphiboles, or the total number of asbestos fibers; 3) asbestos-induced lesions are related to a complex set of mineralogic parameters and not to mere numbers of fibers in lung.

Asbestos↗

PubMed1995

[Asbestos: past, present and future].

Owing to its particular properties asbestos has been widely used for the production of insulating material, for fire proofing, and for strengthening to other materials such as cements and plastics, and thus the story of this mineral was one of progressive commercial success until the middle of this century. However, serious health hazards were realized early: around the turn of the century a progressive form of diffuse fibrosis (asbestosis) in asbestos workers was observed and in 1950 an excess risk of lung cancer, while in 1960 the causal relationship between asbestos and mesothelioma were confirmed. In view of the known potential risks of asbestos and its widespread use in the building industry, more recently asbestos has caused considerable public concern and anxiety. Based on numerous experimental and epidemiological observations, present knowledge of the pathogenic effects of asbestos is sufficient for a number of broad conclusions to be drawn. (1) The amphibole types of asbestos are too dangerous for use as industrial material, and should be banned. (2) Chrysotile can probably be used safely if there is strict control of the workers' dust exposure. (3) It is very unlikely that the general public is at any measurable risk from asbestos in buildings. Exceptions are people working regularly on maintenance tasks involving removing or cutting of asbestos in buildings; such people are properly classified as asbestos workers and should be protected accordingly.(ABSTRACT TRUNCATED AT 250 WORDS)

Asbestos↗

PubMed1996

Occupational exposure to dusts containing asbestos and chronic airways disease.

Chronic inhalation of asbestos fibres has been recognized as a cause of both malignant and non-malignant diseases of lung parenchyma and pleura. The objective of this review was to examine epidemiological evidence concerning this type of occupational exposure as a risk factor for chronic disorders of airways, classified as peripheral airways disease and chronic airflow limitation. A number of published pathophysiological findings that are suggestive of the involvement of peripheral airways in workers exposed to asbestos could be supported by workforce-based assessment of simple tests of small airways function. In asbestos workers the tests' results are usually found to be lower than in reference groups and depend on cumulative exposure. The cross-sectional surveys carried out in large populations of workers exposed to asbestos document an association of both forced expiratory volume in the first second and forced vital capacity with increasing exposure. The majority of the studies reviewed show an exposure-response type of association, also documented by longitudinal studies. The presence of lung function impairment in subjects with normal chest radiographs is compatible with the view that the airway defect may be an independent outcome of exposure to asbestos. The occurrence of the obstructive ventilatory impairment is not infrequent in workforce-based cross-sectional studies, also in nonsmokers in whom the prevalence of obstruction was found to exceed the prevalence of restriction. In conclusion, the review provides evidence that peripheral airways abnormality could be a consequence of inhalation of asbestos. This association seems to be strong and exposure to mineral dust containing asbestos can be therefore regarded as one of the etiologic factors in the genesis of peripheral airways abnormalities. A number of findings favour the plausibility of causal association of chronic airflow limitation with exposure to asbestos dust. However, the insufficient epidemiological data concerning the relationships of an obstructive pattern of ventilatory defect preclude the elaboration of frequent occurrence of obstructive profile in non-smoking asbestos workers. The epidemiologic evidence on association between occupational exposure to dusts containing asbestos and chronic airways disease confirms the presence of "mineral dust airways disease" and adds credibility to the concept of "work-related chronic airflow limitation".

Asbestos↗

PubMed1995

Incorporation of bromodeoxyuridine (BrdU) in the bronchiolar-alveolar regions of the lungs following two inhalation exposures to chrysotile asbestos in strain A/J mice.

We have been studying early fibroproliferative events in the lungs of rodents exposed to aerosols of asbestos fibers. In the experiments presented here, incorporation of bromodeoxyuridine (BrdU) in the bronchiolar/alveolar (B/A) regions of the lungs in mice was assessed following two consecutive exposures to chrysotile asbestos. Six to 8-week-old male strain A/J mice, a strain with a high spontaneous incidence of B/A tumors, were exposed to inhaled asbestos fibers for two consecutive days (3 hours/day). A group of mice was also given an intraperitoneal injection of urethane, a known lung carcinogen in A/J mice, 48 h after initial inhalation exposure to asbestos. The groups of mice exposed to asbestos had significantly (p <0.05) increased incorporation of BrdU in the nuclei of epithelial and interstitial cells in the B/A regions of the lung at 48 h, 72 h, and 2 weeks after initial exposure. By 1 month, the labeling indices in mice exposed to asbestos were not statistically significantly different from the controls; however, in the regions of the first alveolar duct bifurcations (ALDB), the primary site of initial asbestos deposition, there continued to be detectable labeling of the epithelial and interstitial cells. Because of considerable variability from duct to duct, there were no statistically significant differences between the asbestos-exposed mice and control groups at 3 months. We conclude that in A/J mice the initial proliferative response observed in the B/A regions of the lung after two 3-h inhalation exposures to asbestos is significantly prolonged through 2 weeks post-exposure. In addition, there was measurable labeling above control values in the epithelial and interstitial cells of the first alveolar duct bifurcations up to 3 months after exposure. Urethane had no apparent effect on the incorporation of BrdU into any cells of the B/A regions of the lung when administered after inhalation exposure to asbestos. Furthermore, although the A/J strain is highly susceptible to lung tumor formation, the unexposed control A/J mice showed no spontaneous increases in cell proliferation.

Administration, Inhalation↗

PubMed1997

Inhibition of protein kinase C prevents asbestos-induced c-fos and c-jun proto-oncogene expression in mesothelial cells.

Asbestos and the phorbol ester tumor promoter, 12-O-tetradecanoylphorbol-13-acetate (TPA), increase c-fos and c-jun mRNA levels and AP-1 DNA binding activity in rat pleural mesothelial (RPM) cells, a target cell of asbestos-induced mesotheliomas (N. H. Heintz et al., Proc. Natl. Acad. Sci. USA, 90: 3299-3303, 1993). Because protein kinase C (PKC) is the intracellular receptor of phorbol ester tumor promoters and asbestos is a putative tumor promoter in the respiratory tract, we hypothesized that PKC might play a critical role in asbestos-induced cell signaling pathways associated with regulation of proto-oncogenes. Using a panel of PKC antibodies, we identified PKC alpha as the major PKC isozyme in RPM cells. We then pretreated cells with phorbol ester dibutyrate to down-modulate PKC or with calphostin C, a specific PKC inhibitor, to determine if depletion of PKC alpha could block asbestos-induced c-fos/c-jun expression. Quantitation of Northern blots showed that fiber-associated c-fos/c-jun mRNA levels were significantly lower either after PKC alpha down-modulation or pretreatment with calphostin C. In addition, to determine whether tyrosine kinases also were involved in proto-oncogene activation by asbestos, tyrphostin AG82 or herbimycin A was added to RPM cells before exposure to asbestos. These inhibitors decreased crocidolite-induced c-fos but not c-jun levels, suggesting that tyrosine kinases have different regulatory roles in asbestos-induced c-fos versus c-jun signaling pathways. The ability to block induction of asbestos-induced proto-oncogene expression using pharmacological intervention may be important in prevention and treatment of asbestos-induced proliferative diseases including lung cancers, mesothelioma, and pulmonary fibrosis.

Animals↗

PubMed1981

Asbestos and drinking water in Canada.

Samples of raw, treated and distributed tap water were collected from 71 municipalities across Canada and analyzed for asbestos content by transmission electron microscopy. Chrysotile asbestos was identified as the major asbestos type present in drinking water with some 5% of public water supplies containing asbestos at concentrations greater than 10 million fibres per litre. Improvement factors of up to 300 were observed for the removal of chrysotile fibres from drinking water during treatment, indicating that coagulation/filtration treatment is efficient for this purpose. In certain cases there is evidence to suggest that erosion of asbestos from pipe material is taking place. Age-standardized mortality rates for gastro-intestinal cancers were calculated for each city for the period of 1966 to 1976. Rates for the 2 localities with the highest (congruent to 10(8)/L) concentrations of asbestos fibres in treated drinking water were compared with the weighted average of the rates for the 52 localities with asbestos concentrations not significantly greater than zero. Eleven localities had intermediate concentrations of asbestos and six were too small for meaningful statistical analysis. Relatively high mortality rates were apparent amongst males in city 1 for cancer of the large intestine except rectum, and in both sexes in city 1 and males in city 2 for stomach cancer. It is felt that these findings are probably related to occupational exposure to asbestos. Further statistical analyses are required, however, before the significance of these observations can be fully assessed.

Asbestos↗

PubMed1993

Persistent induction of c-fos and c-jun expression by asbestos.

To investigate the mechanisms of asbestos-induced carcinogenesis, expression of c-fos and c-jun protooncogenes was examined in rat pleural mesothelial cells and hamster tracheal epithelial cells after exposure to crocidolite or chrysotile asbestos. In contrast to phorbol 12-myristate 13-acetate, which induces rapid and transient increases in c-fos and c-jun mRNA, asbestos causes 2- to 5-fold increases in c-fos and c-jun mRNA that persist for at least 24 hr in mesothelial cells. The induction of c-fos and c-jun mRNA by asbestos in mesothelial cells is dose-dependent and is most pronounced with crocidolite, the type of asbestos most pathogenic in the causation of pleural mesothelioma. Induction of c-jun gene expression by asbestos occurs in tracheal epithelial cells but is not accompanied by a corresponding induction of c-fos gene expression. In both cell types, asbestos induces increases in protein factors that bind specifically to the DNA sites that mediate gene expression by the AP-1 family of transcription factors. The persistent induction of AP-1 transcription factors by asbestos suggests a model of asbestos-induced carcinogenesis involving chronic stimulation of cell proliferation through activation of the early response gene pathway that includes c-jun and/or c-fos.

Animals↗

PubMed2006

Exposure of UK industrial plumbers to asbestos, Part I: Monitoring of exposure using personal passive samplers.

Epidemiological data suggest that there has been and may continue to be a significant risk to maintenance workers, who through their work may disturb asbestos-containing materials (ACM). The sampling and assessment of maintenance workers' exposure is a particular problem because they may not know that they are working with ACM. A strategy to monitor their true exposure has been developed and applied to one group of workers. The asbestos exposure of industrial plumbers was measured using personal passive samplers developed at the Health and Safety Laboratory (HSL). The light-weight samplers, which collect particles by electrostatic attraction, are simple to use and do not require prior knowledge that asbestos is to be disturbed as does conventional sampling. The samplers were issued by post and analysed, after return, using transmission electron microscopy (TEM). The strategy was found to be a reasonably efficient and cost-effective way to obtain data on maintenance worker's exposure to asbestos. The results of the TEM analysis of the passive samplers showed that the percentage of workers exposed to >5 microm long asbestos fibres was 62% in Round 1 and 58% in Round 2. For phase contrast microscopy equivalent (PCME) asbestos fibres, the values were 46 and 29%, respectively. The three samples with the highest numbers of fibres were followed up and were associated with plumbers working in areas which had supposedly been stripped of asbestos just prior to their starting work, suggesting that poor removal, clean-up and clearance practice presents a significant part of the risk to plumbers. Although flow rates will vary with conditions and time, an approximate average sampling rate from previous comparisons was used to calculate the concentration. This gave an average exposure to regulated PCME fibres of 0.009 f ml-1 for amphibole asbestos and 0.049 f ml-1 for chrysotile. The calculate risk based on the PCME fibre types collected and their estimated concentrations, showed that the risk from airborne amphibole fibres was approximately 6 times greater than from chrysotile fibres. If representative, the estimated lifetime risk of death from an asbestos related cancer for an exposure from age 20 for 40 years would be 68 per 100,000, which equates to an annual risk of death of the order of 10 per million.

Air Pollutants, Occupational↗

PubMed1997

[Cancer risk in asbestos-cement industry workers in Poland].

A cohort study was carried out in order to evaluate the cancer risk in the asbestos-cement industry workers. The cohort consisted of workers employed in four asbestos-cement plants. One of those plants was established in 1924, the other three in the 1960s and 1970s. Currently only two of these plants continue their production. The plants used mainly chrysotile asbestos as well as crocidolite and amosite. Amphibolite asbestos was used before the mid-nineteen eighties in production of pressure pipes utilising about 15% of the total quantity of asbestos used. The measurements of the asbestos fibre concentration at work-sites have been taken occasionally since the mid 1980s, thus, the determination of a cumulative dose for individual persons in the cohort and the evaluation of the dose-effect relationship were not feasible. It could only be supposed that the concentrations at the preparatory work-site during first years of the plants' operation accounted for several tens fibres/cm3 in the production that employed the dry method. The cohort consisted of workers employed in the plant for at least three months between beginning of the plant during the post-war period, and 1980, that is during the period when amphibolite asbestos was in use. The retrospective observation was completed on 31 December 1991. The analysis of the death risk by causes was based on a standardized mortality ratios (SMRs) calculated using the person-years method. Statistical significance of SMRs was assessed by means of Poisson distribution one-sided test. The general population of Poland was used as the reference population to estimate the death risk. The cohort comprised 4,712 persons (3,563 males and 1,149 females). Of this number 4,500 persons (3,405 males and 1,095 females) were followed. The cohort availability were 95.5%. Male mortality, both total (473 deaths; SMR = 83) and due to malignant neoplasms (108 deaths; SMR = 86) was lower than in the general population. An excess of deaths from neoplasm of the pleura was by about 23 times higher (5 deaths; SMR = 2,288) and from neoplasm of the large intestine by two times higher (7 deaths; SMR = 214). Among females (41 deaths; SMR = 50) death risk was lower than in the reference population. At a low level of total mortality from neoplasms (13 deaths; SMR = 52) a statistically significant excess of deaths from neoplasm of the pleura (2 deaths; SMR = 2,112) was observed. In the plants investigated the analysis revealed a considerably diversified mortality from asbestos-related neoplasms. The incidence of pleura mesothelioma should be attributed to the use of considerable quantities of crocidolite asbestos and high concentrations of fibres in the air in plants II and IV, particularly during the first years after their establishment. In view of a long period of latency the excess of this neoplasm can be expected till 2020.

Aged↗

PubMed1988

B cell neoplasms and occupational asbestos exposure.

To evaluate the etiologic role of asbestos exposure in B cell neoplasms, we compared the estimated level of occupational exposure to asbestos of cases with chronic lymphocytic leukemia (CLL; N = 429) and multiple myeloma (MM; N = 698) with that of controls (N = 1,683). Cases were identified through four population-based cancer registries in the U.S. and controls were randomly selected from the same geographic areas. Exposure to asbestos was assessed by classifying each job held by a subject into one of four categories, based on the estimated intensity of exposure to asbestos. Evidence was found for a modest increasing risk of CLL with increasing asbestos exposure. Relative to persons with no known occupational exposure to asbestos, the risk for CLL was 1.1 (95% confidence interval (CI) = 0.8-1.6) for low, 1.2 (CI = 0.8-1.8) for medium, and 1.4 (CI = 0.8-2.3) for high peak asbestos exposure (p value for trend = 0.13). The association was strongest in white study subjects and in those individuals exposed 10 to 19 years prior to the interview. No association was observed between MM and occupational exposure to asbestos in the entire study population or within specific subgroups. Given the pattern of immunologic abnormalities that occur with increased frequency in asbestos-exposed persons, our observation of an association between occupational asbestos exposure and CLL deserves attention in subsequent studies.

Aged↗

PubMed1995

Finnish Institute of Occupational Health Asbestos Program 1987-1992.

In 1987-1992, the Finnish Institute of Occupational Health (FIOH) implemented a nationwide asbestos program aimed at preventing asbestos-related risks in good cooperation with governmental authorities, industry, trade unions, the health care and insurance systems, and mass media. The goals were to minimize all exposure to asbestos, identify people exposed at work, and improve the diagnostics of asbestos diseases, especially cancers. The program entailed several concrete actions and extensive dissemination of information, training, services, and scientific research. As proposed by the State Asbestos Committee, new use of asbestos products was banned and strict regulations were applied to renovation and inspection of old buildings. The screening study of asbestos-induced diseases included 18,943 current and retired workers from house building, shipyard, and asbestos industries. Pleural and parenchymal changes were found in 4,133 persons (22%), who were referred to further clinical examinations as suspected cases of an occupational disease. It was estimated that past exposure of asbestos among the Finnish population of 5 million causes > 150 mesotheliomas and lung cancers annually, totalling > 2,000 asbestos-induced cancer deaths by the year 2010. Although several major control actions were made or started during the program, the bulk of the preventive work still lies ahead.

Asbestosis↗

PubMed2001

[Frequency and risk of bronchopulmonary neoplasia related to asbestos].

BACKGROUND: The goal of this study was to determine the prevalence of asbestos-related lung cancer and the importance of the occupational exposure to this inorganic fibre as a risk factor. PATIENTS AND METHODS: We performed a cross-sectional study of 82 patients with lung cancer (mean age 62 SD 9 years) and 53 patients without pleuropulmonary disease (63 SD 13 years). The occupational exposure to asbestos was determined by a questionnaire. We determined the concentration of asbestos bodies (AB) in bronchoalveolar lavage (BAL) (93 patients) or lung tissue (42 patients) after chemical digestion, with the results being expressed as AB/mL BAL or AB/g dry lung, respectively. A concentration higher than 1 AB/mL or 1,000 AB/g was considered as marker of high asbestos burden in lung tissue, which could be potentially responsible for pleuropulmonary disease. The importance of asbestos occupational exposure as a risk factor for lung cancer was determined using logistic regression models. RESULTS: 25 patients with lung cancer reported occupational exposure to asbestos (30%) and in 13 out of them AB were detected in BAL or lung tissue (24%), at high concentrations in 3 cases (4%). Six patients from the group without pleuropulmonary disease reported occupational exposure to asbestos (11%) and in 13 out of them AB were found in some samples (24%), with no case having high concentrations. In the univariate logistic regression analysis, diagnosis of bronchial neoplasia was associated with both smoking (OR 10.10, 95% CI 3.50-29.13) and occupational exposure to asbestos (OR 3.69, 95% CI 1.39-9.77). The association between asbestos exposure and lung cancer persisted statistically significant after adjustment for smoking (OR 2.80, 95% CI 1.00-7.84). CONCLUSION: In Spain, lung cancer was related to occupational exposure to asbestos in 4% of cases, and it appeared to exist a synergistic effect of smoking. Occupational exposure to this inorganic fibre doubles the risk of suffering from lung cancer.

Asbestosis↗

PubMed2002

[Prophylactic examinations of former workers of asbestos processing plants: the Amiantus project].

Prophylactic examinations of the former workers of asbestos plants are performed by virtue of the Law of 19 June 1997 on a prohibition against the use of asbestos-containing products. Periodical examinations allow to detect pathological changes in the pre-symptomatic or early-symptomatic period, which permits to apply an appropriate treatment and slows down considerably the progress of morbid processes. The main objectives of the surveillance and coordination are as follows: (1) to assure good quality of prophylactic examinations through the uniform methods of medical examinations and the detection of pathology resulting from the exposure to asbestos dust, based on international criteria for diagnosing asbestos-related diseases (the Helsinki criteria, 1997); (2) to monitor the respiratory health effects among persons occupationally exposed to asbestos dust; and (3) to keep the database on persons examined and subjected to periodical prophylactic examinations throughout the country. The program of prophylactic examinations of persons occupationally exposed to asbestos dust includes mass screening. For the purpose of this program, a unified strategy of mass screening, including documentation (questionnaires on clinical, radiological and spirometric examinations) and instructions for persons responsible for performing these examinations has been worked out. Each center involved in the implementation of the program has been provided with binding criteria elaborated on the basis of the world standards (the Helsinki criteria, 1977) of clinical, radiological, spirometric and histological examinations aimed at detecting asbestos-related diseases: asbestosis, fibrous mesothelioma and lung cancer. The data obtained will serve as a basis for assessing the morbidity and incidence of asbestos-related diseases among persons occupationally exposed to asbestos dust in asbestos processing plants.

Asbestosis↗

PubMedDate not supplied

Asbestos bodies in a general hospital/clinic population.

The presence of asbestos bodies in the sputum of individuals with known occupational asbestos exposure has been well documented. However, their prevalence and clinical implications in sputum and bronchial washings from patients not clinically known to have asbestos exposure remains controversial. From 1974 to 1979, 31,353 sputum and bronchial washing specimens were processed in the course of evaluating various pulmonary complaints of approximately 11,000 patients from the outpatient clinics and hospitals of the Harris County Hospital District in Houston, Texas. Asbestos bodies were incidentally found in five patients, and, in retrospect, each of them was discovered to have had significant occupational exposure to asbestos dust. Asbestos lung disease was also subsequently proven in four of the five patients and was felt, retrospectively, to have contributed to their presenting complaints and clinical course. It is concluded that asbestos bodies in sputum and bronchial washing specimens are highly specific markers for past asbestos exposure and reflect the presence of a significant asbestos load within the lungs. Sputum cytology is both painless and inexpensive and is recommended as a supplemental procedure to document clinically significant asbestos exposure.

Adolescent↗