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PubMed2001

Non-malignant asbestos-related diseases in Brazilian asbestos-cement workers.

BACKGROUND: Production of asbestos-cement products in Brazil started in the 1940s, peaked in the 60-70s and is still an active industry. This study was designed to assess the non-malignant effects of asbestos exposure in the asbestos-cement industry in Brazil. METHODS: A group of 828 former asbestos-cement workers enrolled in a cross-sectional and cohort study of respiratory morbidity, submitted to a detailed occupational history, respiratory symptoms questionnaire, spirometry, PA chest x-ray, and high resolution computed chest tomography (HRCT). Asbestos exposure was assessed by years of exposure, cumulative exposure (a semi-quantitative method), and latency time from first exposure. Asbestosis and pleural thickening were assessed according to HRCT criteria. RESULTS: Asbestosis was present in 74 (8.9%) and pleural thickening in 246 (29.7%). Using the HRCT as the "best available evidence", it was shown that were more false negatives than false positives in the x-ray readings for parenchymal (21.6% false negatives, 4.2% false positives) and pleural (26.0% false negatives, 14.4% false positives) diseases due to asbestos. Latency time from first exposure was the best predictor for both asbestosis and pleural thickening. Subjects in the higher exposure groups presented lower levels of lung function. Obstructive defects were significantly related to smoking, shortness of breath, body mass index, and age, whereas restrictive defects were related to asbestosis, shortness of breath, and latency time. Chronic bronchitis increased with latency time in the three smoking groups and was significantly related to pleural thickening (OR 1.56 (1.00-2.42)). Shortness of breath was significantly associated with body mass index and pleural thickening (OR 1.30 (1.24-2.09)). CONCLUSIONS: Pleural thickening and asbestosis showed a significant association with latency time and exposure. FVC and FEV(1) decreased across increasing profusion with an added effect of pleural thickening. There was a significant and independent effect of exposure on lower levels of FVC and FEV(1). Obstructive defects were mainly related to smoking and restriction to asbestosis. Dust exposure and smoking were synergistic in increasing chronic bronchitis and shortness of breath report. Shortness of breath report was also related to pleural thickening and higher body mass index.

Adult↗

PubMedDate not supplied

Asbestos, asbestos-related diseases, and compensation claims in The Netherlands.

In The Netherlands the number of asbestos-related diseases is increasing. An age-cohort model predicts a steep rise in pleural mesothelioma deaths up to 490 cases per year among men, with a total death toll close over 12,000 cases during 2000-2028. In the past decade the number of compensation claims for asbestos-related diseases has more than doubled, with increasingly verdicts in favor of claimants. In addition to the medical information, information about the state of the art of preventive measures in different periods of time plays a decisive role in these claims. The use of asbestos in The Netherlands, the occurrence of asbestos-related diseases, the national asbestos regulations, and the position of the claimants in asbestos lawsuits in The Netherlands are reviewed.

Asbestosis↗

PubMed1983

[Frequency of asbestos fibers and asbestos bodies in lung sections].

100 specimens of lung resections coming from 100 patients operated on in 1980 in the thoracic surgical department were examined without any selection by turn for the presence of asbestos fibres or ferruginous asbestos bodies. Among these patients asbestos fibres were found in 65% and asbestos bodies in 46% of all cases examined. The observations were related to age, residence (town, village), occupation, and underlying diagnosis found with the surgical procedure. It could be recognized by the analysis that also the population of Slovakia is exposed to ubiquitious asbestos. An etiological relation between the frequency of asbestos fibres and the occurrence of malign tumours could not be proved. Such a relation is very complex, the cancerogenic effect of other factors (benzpyrene, smoking) has to be taken into consideration.

Adult↗

PubMed1987

Asbestos exposure dose-bronchoalveolar milieu response in asbestos workers and the sheep model: evidences of a threshold for chrysotile-induced fibrosis.

Epidemiological studies of asbestos workers have proposed a linear dose-response relationship between asbestos cumulative exposure indices and the incidence of asbestos-related lung diseases. However, for chrysotile, several studies have not observed such a linear relationship in low exposure workers. To further study the relationship of chrysotile exposure dose - lung tissue response, we designed in the sheep model one experiment of one exposure at variable intensity and one experiment with variable rates of individual exposures. In the first study, 6 groups of 6 sheep were exposed to either 0, 1, 10, 25, 50 or 100 mg chrysotile in 100 ml saline and lung lavage analyses carried out at day 0, 12, 24, 40 and 60 after. Histopathology was done at day 60. In the second experiment, 4 groups of 12 sheep were exposed to 100 ml saline every week or every two weeks, 100 mg chrysotile in 100 ml saline every week or every two weeks. In the second experiment, lung damage was assessed by changes in vital capacity (VC), lung compliance (Cst) and profusion of chest radiographic opacities (PO). On BAL in the control sheep, there were small and transient early increases in total cells/ml, macrophages/ml, neutrophils/ml, lactate dehydrogenase (LDH)/ml, alkaline phosphatase (AK)/ml, beta-glucuronidase (beta G)/ml and procollagen lll/ml. In the 1, 10, 25, and 50 mg asbestos sheep groups, there were no significant differences. However, in the 100 mg asbestos sheep, there were significant sustained increases in total cells/ml (3-6 times controls), macrophages/ml (2-6 times controls), neutrophils/ml (60-600 times controls), LDH/ml (5-10 times controls), AK/ml (1.5-2 times controls), beta G/ml (3-5 times controls), procollagen lll/ml (2 times controls) and IgG (1.5-3 times controls). These data were correlated with histopathological findings. In the sheep exposed weekly to chrysotile, significant changes in VC, Cst and PO occurred at mean cumulative exposure dose of 1.2 g whereas in the sheep exposed every 2 weeks, similar changes in VC, Cst and PO occurred at the cumulative exposure dose of 3.6 g (P less than 0.05). In conclusion, our data suggest that there is a threshold for chrysotile-induced fibrosis. This level cannot be considered adequately in term of cumulative exposure dose but must take into account intensity and rate of individual exposures.

Animals↗

PubMed1977

Asbestos and lung cancer: an analysis of the epidemiological evidence on the asbestos-smoking interaction.

Three simple models for the asbestos-smoking interaction on human lung cancer production are considered. In the first model the excess incidence of lung cancer independently due to asbestos and to smoking adds together when both agents are present (additive model). In the second the addition of each one of the two agents produces an effect (increase in lung cancer incidence) which is proportional to the effect of the other (multiplicative model). In the third, asbestos can only increase lung cancer incidence in the presence of smoking. As previously found by other investigators, the additive model appears the least plausible in the light of the data from two published epidemiological studies. A discrimination between the other two models is attempted through a detailed analysis of the five published epidemiological studies today available which provide information on occupational asbestos exposure, smoking habits and lung cancer risk. Although the data do not allow a definitive discrimination, the multiplicative model appears to be more plausible, being also consistent with a multi-stage carcinogenic mechanism and with evidence from animal (rat) experiments. It is relevant both for biology and for public health that in this model asbestos and smoking are regarded as independently capable of producing lung cancer in humans and that they act synergistically when exposure to both occurs.

Air Pollutants↗

PubMed1996

A study of personal and area airborne asbestos concentrations during asbestos abatement: a statistical evaluation of fibre concentration data.

Data were collected and analysed on airborne concentrations of asbestos generated by abatement of different asbestos-containing materials using various removal practices. Airborne concentrations of asbestos are dramatically variable among the types of asbestos-containing material being abated. Abatement practices evaluated in this study were removal of boiler/pipe insulation in a crawl space, ceiling tile, transite, floor tile/mastic with traditional methods, and mastic removal with a high-efficiency particulate air filter blast track (shot-blast) machine. In general, abatement of boiler and pipe insulation produces the highest airborne fibre levels, while abatement of floor tile and mastic was observed to be the lowest. A comparison of matched personal and area samples was not significantly different, and exhibited a good correlation using regression analysis. After adjusting data for outliers, personal sample fibre concentrations were greater than area sample fibre concentrations. Statistical analysis and sample distribution of airborne asbestos concentrations appear to be best represented in a logarithmic form. Area sample fibre concentrations were shown in this study to have a larger variability than personal measurements. Evaluation of outliers in fibre concentration data and the ability of these values to skew sample populations is presented. The use of personal and area samples in determining exposure, selecting personal protective equipment and its historical relevance as related to future abatement projects is discussed.

Air Pollutants, Occupational↗

PubMed2006

Assessment of airborne asbestos exposure during the servicing and handling of automobile asbestos-containing gaskets.

Five test sessions were conducted to assess asbestos exposure during the removal or installation of asbestos-containing gaskets on vehicles. All testing took place within an operative automotive repair facility involving passenger cars and a pickup truck ranging in vintage from late 1960s through 1970s. A professional mechanic performed all shop work including engine disassembly and reassembly, gasket manipulation and parts cleaning. Bulk sample analysis of removed gaskets through polarized light microscopy (PLM) revealed asbestos fiber concentrations ranging between 0 and 75%. Personal and area air samples were collected and analyzed using National Institute of Occupational Safety Health (NIOSH) methods 7400 [phase contrast microscopy (PCM)] and 7402 [transmission electron microscopy (TEM)]. Among all air samples collected, approximately 21% (n = 11) contained chrysotile fibers. The mean PCM and phase contrast microscopy equivalent (PCME) 8-h time weighted average (TWA) concentrations for these samples were 0.0031 fibers/cubic centimeters (f/cc) and 0.0017 f/cc, respectively. Based on these findings, automobile mechanics who worked with asbestos-containing gaskets may have been exposed to concentrations of airborne asbestos concentrations approximately 100 times lower than the current Occupational Safety and Health Administration (OSHA) Permissible Exposure Limit (PEL) of 0.1 f/cc.

Air Pollutants, Occupational↗

PubMedDate not supplied

Asbestos-related mesothelioma: epidemiological evidence for asbestos as a promoter.

A series of 144 cases of mesothelioma among asbestos workers indicated important divergences from the epidemiological pattern shown to exist for asbestos-related lung cancer. Consideration of exposure duration and intensity and the latent period between first exposure and death suggests that asbestos does not act as a complete carcinogen, but as a promoter. A threshold seems probable for both duration and intensity of exposure in the induction of mesothelioma. This threshold may, in part, be related to the passage of fibers from the lungs to the pleura or peritoneum, and would, in any case, be masked in lung cancer by the retention of asbestos in the lungs. Reported cases of mesothelioma in immediate family members indicate the existence of an additional factor in mesothelioma induction, acting earlier in life than the first asbestos exposure.

Asbestos↗

PubMed1988

Direct enhancement by cigarette smoke of asbestos fiber penetration and asbestos-induced epithelial proliferation in rat tracheal explants.

Tracheal explants from Sprague-Dawley rats were briefly exposed to cigarette smoke or air (control) and then to amosite asbestos. Asbestos fibers in or under the tracheal epithelium were counted and extent of hyperplastic lesions was ascertained at 24 hours, 72 hours, and 1 week after exposure. Smoke-exposed cultures showed significantly greater numbers of fibers in the epithelium and greater proliferative activity compared to findings in cultures not exposed to smoke. These observations indicate that very short exposure to cigarette smoke can directly affect the response of the epithelium to asbestos fibers and that smoke exposure need not be concurrent with asbestos exposure for such event to occur. These reactions may play a role in the greater incidences of lung cancer and asbestosis seen in asbestos-exposed workers who smoke.

Animals↗

PubMed1999

Mutations of p53 gene and SV40 sequences in asbestos associated and non-asbestos-associated mesotheliomas.

AIM: To examine mesotheliomas for a possible relation between p53 immunostaining, p53 gene mutation, simian virus 40 (SV40), and asbestos exposure. METHODS: Paraffin sections from 11 mesotheliomas were used for p53 immunostaining and also to extract DNA. This was analysed for the presence of mutations in exons 5 to 8 of the p53 gene using a "cold" single strand conformational polymorphism method, together with sequencing. The DNA from the paraffin sections was also used to search for SV40 sequences. A 105 base pair segment at the 3' of the SV40 large T antigen (Tag) was targeted and any PCR amplification products were sequenced to confirm that they were of SV40 origin. EDAX electron microscopic differential mineral fibre counts were performed on dried lung tissue at a specialist referral centre. RESULTS: The fibre counts showed that seven of the mesotheliomas were associated with abnormally high asbestos exposure. Of these, two showed p53 immunostaining, none showed p53 gene mutation, and five showed SV40. Of the four other mesotheliomas, three showed p53 immunostaining, one showed a (silent) p53 mutation, and none showed SV40. The difference in frequency of SV40 detection was significant at the p < 0.05 level. CONCLUSIONS: Immunostaining for the p53 gene was relatively common but p53 mutations were rare in this series. SV40 virus sequence was detected in five of seven asbestos associated mesotheliomas but in none of the non-asbestos-associated mesotheliomas. This suggests there may be a synergistic interaction between asbestos and SV40 in human mesotheliomas. A study with a larger number of cases is needed to investigate these observations further.

Asbestos↗

PubMedDate not supplied

Expression of the T cell receptor Vbeta repertoire in a human T cell resistant to asbestos-induced apoptosis and peripheral blood T cells from patients with silica and asbestos-related diseases.

To explore the effects of asbestos and silica on the human immune system, an experimental model of low-dose and long-term exposure was established using a human HTLV-1-immortalized polyclonal T cell line, MT-2 (MT-2Org). MT-2 cells were continuously exposed to asbestos at a concentration (10 microg/ml) which does not induce complete cell death during short-term exposure. After acquiring resistance to CB-induced apoptosis (designated MT-2Rst), an immunological comparison was made between the MT-2Org and MT-2Rst lines in terms of T cell receptor-Vbeta (TcR-Vbeta) expression. MT-2Rst cells showed excess expression of various TcR-Vbeta, although TcR-Vbeta-overpresenting cells were characterized as undergoing apoptosis due to first contact with CB. Patients with asbestos-related diseases (ARD), such as asbestosis and malignant mesothelioma, were compared with silicosis (SIL) patients as a disease control and with healthy donors (HD). SIL and ARD not only differed in their causative materials, silica and asbestos as mineral silicates, but also in terms of complications; autoimmune disorders in SIL and tumors in ARD. ARD patients showed a restricted overpresentation of TcR-Vbeta without clonal expansion, whereas SIL patients revealed significant overpresentation of TcR-Vbeta 7.2. These experimental and clinical analyses indicate the superantigenic and dysregulation of autoimmunity-inducing effects of asbestos and silica, respectively.

Adult↗

PubMedDate not supplied

Asbestos in the sputum, crackles in the lungs, and radiologic changes in women exposed to asbestos.

In a rural community in South Africa historically exposed to asbestos environmentally and occupationally, 200 women who had worked with asbestos and applied for medical examination to determine compensable asbestos disease were evaluated. Clinical and radiologic evaluation, sputum collection, and microscopic analysis were done. A questionnaire elicited type of exposure, duration, decade of first work exposure, and environmental exposure. Crackles were present in the lungs of 166 women and asbestos fibers and ferruginous bodies were present in 122. Asbestosis was identified in 26 and plural plaques in 62. Auscultation for crackles (rales) is useful in the initial examination of former asbestos workers in rural communities of developing countries.

Age Distribution↗

PubMed1993

[Estimation of asbestos exposure among workers repairing asbestos cement pipes used for conduits].

Asbestos cement pipes (ACPs) containing 15 to 20% chrysotile or crocidolite have been used for underground conduits. Even today 16.2% of all conduits in Japan are ACPs, though the production of ACPs was suspended in 1985. When such a conduit is accidentally damaged the workers belonging to the Waterworks Bureau of a local government cut off the damaged conduit using a high-speed disk cutter and replace it with a new conduit. This operation develops a cloud of dust and the workers involved run the risk of asbestos exposure. It was the aim of the present study to estimate asbestos exposure levels among these workers. First, in the experiment, we established the typical working conditions and requested an experienced worker to cut an ACP using a high-speed disc cutter in a hole dug in the ground as he routinely does. The experiment was repeated three times. During a bout of each experiment, dust was sampled at several points both inside and outside the hole. Second, a self-administered questionnaire survey was conducted to obtain information from the workers regarding their working conditions in cutting ACPs. The subjects of the survey were 1,048 men belonging to conduit repair sections of the Waterworks Bureau of 119 local governments. The results obtained can be summarized as follows. 1) Each bout of cutting ACPs required about five minutes. The concentration of asbestos fibers longer than 5 microns with 3:1 aspect ratio ranged from 48 to 170 fibers/ml (92 fibers/ml on an average) inside and 1.7 to 15 fibers/ml outside the hole. The concentration inside the hole exceeded the ceiling limit (10 fibers/ml) recommended for asbestos by the Japanese Association of Industrial Health. A concentration of 92 fibers/ml is equivalent to 0.96 fibers/ml as 8-h time-weighted average. 2) The number of subjects with experience of cutting ACPs was 849 (81.0%). The average length of service in conduit repair section was 14.2 yr. Based on the information obtained from each subject regarding the average working days per yr for each decade from 1946, the cumulative days to date expended in cutting ACPs was estimated to average 235 d, that is, 17 d per yr. Only 18.1% of the subjects used a protective respiratory device.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed2004

Navy Asbestos Medical Surveillance Program (1984-1990): linear regression analysis for effect of asbestos exposure on pulmonary function testing.

This study examined records from the Navy Asbestos Medical Surveillance Program for 1984 through 1990 for Caucasian men (N = 129,598) using a population-based, cross-sectional, linear regression model. Continuous dependent variables were forced expiratory volume in 1 s and forced vital capacity (FVC), and continuous independent variables were age, height, weight, and tobacco use. A mid-period estimate of asbestos exposure was used because those values were reported as categorical variables. With asbestos exposure, forced expiratory volume in 1 s changed -3.2 cm3/year (t = -8.6, p = 0.000), and forced vital capacity changed -5.1 cm3/year (t = -11.8, p = 0.00). Those with more than 5 years of asbestos exposure demonstrated impairment over those with less exposure, and those with more than 15 years of exposure demonstrated even more impairment. These findings support the association of pulmonary function impairment with asbestos exposure for workers studied during this period.

Adult↗

PubMed2000

[A case of pulmonary fibrosis with many asbestos bodies in bronchoalveolar lavage fluid after exposure to asbestos and man-made mineral fibers].

We report a case of severe pulmonary fibrosis in a patient exposed to asbestos and other natural and man-made mineral fibers (MMMF) over a period of time. A 63-year-old man was admitted to our hospital because of progressive dyspnea and severe hypoxemia with hypercapnea. Mineral fibers recovered by bronchoalveolar lavage were analyzed by scanning electron microscope (SEM) and energy-dispersive x-ray spectroscopy (SEM-EDS). The bronchoalveolar lavage fluid (BALF) included a large number of asbestos bodies (116,000/ml). The cores of the asbestos fibers were crocidolite, and no vitreous fibers nor other kinds of man-made mineral fibers (MMMFs) were identified. To our knowledge, the number of asbestos bodies per ml of this patient's BALF is the greatest ever reported. Insufficient personal protection of the airways, high concentrations of inhaled fibers, co-exposure to cigarette smoke, and prolonged biopersistence of crocidolite asbestos fibers are presumed to be the causes of such severe asbestosis.

Asbestos↗

PubMed1991

[Occupational exposure to asbestos-containing dust at the plants manufacturing and using asbestos products during the years 1986-1989].

During 1986-1989, dust levels at workplaces in 19 plants manufacturing or using asbestos products in Poland were measured. Total dust concentrations were determined by the gravimetric method and respirable asbestos fibre concentrations were determined by the phase contrast optical microscope method (PCOM). Air was sampled at the breathing zones of the workers by using Casella personal air samplers. Average respirable asbestos fibre concentrations at the workplaces were from 0.06 fibre/cm3 (control desk operator) to 2.25 fibre/cm3 (spinning machine operator), and the average total dust concentrations were from 0.7 mg/m3 (technicians) to 2.3 mg/m3 (preparatory department workers). Compared with the 1980-1985 period, total dust concentrations were 1.5 times, and respirable asbestos fibre concentrations 2.9 times lower. Considering the obtained data and the analysis of the occupational diseases in workers exposed to asbestos dust during 1983-1988, the national expert group for industrial dusts has suggested that the MAC values for chrysotile dusts be lowered to 1.0 mg/m3 (total dust) and 0.5 fibre/cm3 (respirable fibre).

Air Pollutants, Occupational↗

PubMed1984

The effect of asbestos-cement, cement and asbestos dusts on the lungs of rats.

Experimental coniosis was induced by intratracheal administration to rats of 25 mg or 50 mg of Portland cement, asbestos-cement, as well as chrysotile and crocidolite asbestos. The rats were sacrificed 90, 165 and 180 days after dust administration. The weight of wet lungs and hydroxyproline content in lungs were determined. Statistically significant lower values of fibrogenic effects indices following cement dust administration, as compared to those indices for the other dusts, were found. On the other hand, no significant differences were found between fibrogenic effects indices for asbestos-cement containing approx. 13% of asbestos and pure asbestos dusts (chrysotile or crocidolite). Furthermore, it seems that the duration of dust action is more important than the dust dose in the development of fibrogenic asbestosis.

Animals↗

PubMed1994

Third wave of asbestos-related disease from secondary use of asbestos. A case report from industry.

An occupational health survey conducted in a workshop in which asbestos cement was used showed initial atmospheric asbestos levels ranging from 1.9 to 27.5 fibres per millilitre of air. Radiological changes suggestive of asbestos-related pleural disease were found in 2 workers (2.5%), while 3 (3.8%) had borderline features of asbestosis. The survey confirmed that uncontrolled and hazardous use of asbestos continues in industry despite public awareness of its dangers and the Asbestos Regulations of 1987.

Asbestos↗