Asbestos lung fibre concentrations in South African chrysotile mine workers.
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Mesothelioma has not been found in South African chrysotile miners and millers despite decades of producing about 100000 tons of the mineral per year. One possible explanation for the scarcity or absence of the cancer may be a relative lack of contaminating fibrous tremolite, an amphibole that variably occurs with chrysotile ores. The fibre content in the lungs of nine former chrysotile mine workers was ascertained by transmission electron microscopy. Despite fairly long service in most cases (median 9.5 yr; range 32-4 yr) the concentrations of chrysotile fibres were relatively low: only two cases exceeded 1.14 million fibres/g dried lung. Tremolite fibre levels were even lower: less than 1 million fibres/g dried lung in all but one case. Tremolite fibre concentrations exceeded those of chrysotile in only two cases. These results support the contention that South African chrysotile is not heavily contaminated by tremolite. (+info)
Analysis of p16 and p21(Cip1) expression in tumorigenic human bronchial epithelial cells induced by asbestos.
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Although asbestos is carcinogenic to humans, the mechanism(s) by which it induces cancer is unknown. Using tumor cell lines generated previously by asbestos treatment of immortalized human bronchial epithelial (BEP2D) cells, we examined alterations in p16 and p21(Cip1) genes together with their protein levels. Results were compared with untreated BEP2D cells, normal human bronchial epithelial cells (NHBE), as well as non-tumorigenic fusion cell lines generated by fusing tumor cells with BEP2D cells. No deletion in the p16 gene was found in any of the tumor cell lines examined. Although p16 protein was expressed at a similar level in tumor and BEP2D cells, there was a fourfold decrease in its expression among NHBE cells. In contrast, both the protein and mRNA expression levels of p21(Cip1) were decreased by about threefold in tumor cell lines when compared with either BEP2D or NHBE cells, which had a similar expression level. Expression of p21(Cip1) mRNA was restored to the control level in all the fusion cell lines examined. The results suggested that down regulation of p21(Cip1) expression is linked to the tumorigenic conversion of BEP2D cells by asbestos. (+info)
Community health risk assessment after a fire with asbestos containing fallout.
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BACKGROUND: A factory fire in Tranmere, Merseyside, England, deposited asbestos containing fallout in an urban area. There was considerable community anxiety for months after the incident. Therefore an assessment of the long term health risks of this acute environmental incident were requested by the local health authority. METHODS: The facts of the incident were gathered and appraised from unpublished and press reports, involved personnel, and further analysis of material collected at the time of the incident. The literature on the long term health risks of asbestos was reviewed, and combined with evidence on asbestos exposure to estimate community health risk. RESULTS: Risk was almost entirely from exposure to fire fallout of chrysotile in asbestos bitumen paper covering the factory roof. Amosite was only detected in a few samples and in trace amounts. The number of people who lived in the area of fallout was 16 000 to 48 000. From a non-threshold model with assumptions likely to overestimate risk, the lung cancer risk is estimated to be undetectably small. Risk of mesothelioma from chrysotile exposure, and risks of lung cancer and mesothelioma from amosite exposure were based on observational studies and were estimated to be even lower than that of lung cancer risk from chrysotile exposure. Academically, there are assumptions that while reasonable cannot be proven, for example, the validity of extrapolating observed risk from much higher exposures to lower exposures, estimates of individual exposure, and that there is no threshold for asbestos to cause cancer. CONCLUSIONS: The author is unaware of a similar study on long term health risks in a community exposed to asbestos in a fire. It is concluded that, using methods that do not underestimate risk, risk is undetectably small. Practical lessons from this methodology and approach to health risk assessment are discussed. (+info)
Present status of asbestos mining and related health problems in India--a survey.
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At present in India more than thirty mines are in operation. It produces 2800 tones of asbestos per month (mainly chrysotile and tremolite) and in recent years substantial quantity (-70%) is imported from Canada. The quality of asbestos produced in India is very poor. The mining and milling and other related processes expose the people to cancer and related diseases. Women are more affected by their exposure in processing unit compared to male who are generally working in mines. Direct and indirect employment in asbestos related industry and mine is around 100,000 workers. Latency period (length of the time between exposure and the onset of diseases) in India is estimated to be 20-37 yr. The causes for lung and breathing problem are mainly due to obsolete technology and direct contact with the asbestos products without proper precaution, because in India asbestos are sold without statutory warning. This paper reviews health effects (such as fibrosis, sequelae, bronchogenic cancer, and malignant mesothelioma) on the Indian mine workers caused due to asbestos mining related activities with respect to their present day condition. (+info)
The combination of effects on lung cancer of cigarette smoking and exposure in quebec chrysotile miners and millers.
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Although it is well known that both cigarette smoke and microscopic airborne asbestos fibres can cause lung cancer, evidence as to how these two agents combine is nebulous. Many workers have believed in the multiplicative theory, whereby asbestos increases the risk in proportion to the risk from other causes. However, evidence against this theory is mounting: a recent review concluded that the multiplicative hypothesis was untenable, and that the relative risk of lung cancer from asbestos exposure was about twice as high in non-smokers as in smokers, a finding largely independent of type of asbestos fibre. The criteria for entry to the current study were met by 7279 men in the 1891-1920 birth cohort of Quebec chrysotile miners and millers. The data consisted of date of birth, place of employment, smoking habit, asbestos exposure accumulated to age 55 and, for those 5527 who died between 1950 and June 1992, date and cause of death; 533 of the deaths were from lung cancer. For the principal analyses, ex-smokers were excluded from the study cohort, which comprised 5888 men, of whom 473 died of lung cancer. The conventional form of analysis is simply of the double dichotomy: non-smokers of cigarettes, 'unexposed' and exposed; all others, 'unexposed' and exposed. The respective standardized lung cancer mortality ratios (SMRs) were 0.29 and 0.62; and 1.37 and 1.72. Thus, the differences in relative risk, due to exposure, were closely similar, 0.33 and 0.35. On the other hand, the effects of asbestos measured by the corresponding ratios, 2.12 and 1.25, did differ, being 1.7 times as high in non-smokers as in others. The principal analysis was much more penetrating: the method was to fit models to a 'disaggregated' 6 x 10 array, by smoking habit (excluding ex-smokers) and asbestos exposure, of lung cancer SMRs. Both linear and log-linear models were fitted: the former included the additive and linear-multiplicative; the latter embraced the more conventional multiplicative form. The additive model fitted much the best. The fit of each multiplicative model was improved by the introduction of an interaction term that implied a less than multiplicative relationship. Thus smoking and exposure to chrysotile appear to have acted independently in causing lung cancer, with 10 cigarettes a day having an effect roughly equivalent to exposure amounting to 700 million particles per cubic foot x years. The refutation of the multiplicative hypothesis in these data reinforces its inapplicability in general; but the additive hypothesis is not generally applicable either. Indeed, there seems to be no good reason to believe that interactions conform to any simple theory. The implications are important. (+info)
Chrysotile and tremolite asbestos fibres in the lungs and parietal pleura of Corsican goats.
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BACKGROUND AND AIMS: Environmental exposures to chrysotile and tremolite from the soil cause pleural plaques and mesothelioma in northeast Corsica. Goats grazing in the contaminated areas inhale asbestos fibres. We used this natural animal model to study whether these exposures actually result in increased fibre burdens in the lungs and parietal pleura. METHODS: Ten goats from areas with asbestos outcrops and two from other areas were slaughtered. Fibre content of lung and parietal pleural samples was determined by analytical transmission electron microscopy. RESULTS: Both chrysotile and tremolite fibres were detected. In the exposed goats, the geometric mean concentrations of asbestos fibres longer than 1 microm were 0.27 x 10(6) fibres/g dry lung tissue and 1.8 x 10(6) fibres/g dry pleural tissue. Asbestos fibres were not detected in the lungs of the two control goats. Chrysotile fibres shorter than 5 microm were predominant in the parietal pleura. Tremolite fibres accounted for 78% and 86% of the fibres longer than 5 microm in lung and parietal pleural samples, respectively. CONCLUSIONS: Environmental exposure in northeast Corsica results in detectable chrysotile and tremolite fibre loads in the lung and parietal pleura of adult goats. Tremolite fibres of dimensions with a high carcinogenic potency are detected in the parietal pleura. (+info)
Cancer incidence among workers in the asbestos-cement producing industry in Norway.
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OBJECTIVES: The incidence of cancer among employees of a Norwegian asbestos-cement factory was studied in relation to duration of exposure and time since first exposure. The factory was active in 1942-1968. Most of the asbestos in use was chrysotile, but for technical reasons 8% amphiboles was added. METHODS: For the identification of cancer cases, a cohort of 541 male workers was linked to the Cancer Registry of Norway. The analysis was based on the comparison between the observed and expected number of cancer cases. Standardized incidence ratios (SIR) and 95% confidence intervals (95% CI) were estimated. Period of first employment, duration of employment, and time since first employment were used as indicators of exposure. Poisson regression analysis was used for the internal comparisons. RESULTS: The standardized incidence ratio was 52.5 (95% CI 31.1-83.0) for pleural mesothelioma, on the basis of 18 cases. The highest standardized incidence ratio was found for workers first employed in the earliest production period (SIR 99.0, 95% CI 51.3-173). No peritoneal mesothelioma was found. The standardized incidence ratio for lung cancer was 3.1 (95% CI 2.14.3), but no dose-response effect was observed. The ratio of mesothelioma to lung cancer cases was 1:2. CONCLUSIONS: This study showed a high incidence of mesothelioma and a high ratio of mesothelioma to lung cancer among asbestos-cement workers. The high incidence of mesothelioma was probably due to the fact that a relatively high proportion of amphiboles was used in the production process. (+info)
Evaluation of the catalytic activity of lipases immobilized on chrysotile for esterification.
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In the present work, the ester synthesis in organic media catalyzed by lipases immobilized on chrysotile was studied. Lipases of different sources (Mucor javanicus, Pseudomonas cepacia, Rhizopus oryzae, Aspergillus niger and Candida rugosa) were immobilized on chrysotile, an inexpensive magnesium silicate, and used for esterification of hexanoic, octanoic and lauric acid with methanol, ethanol, 1-butanol and 1-octanol at 25 C in hexane as solvent. The best results were obtained with Mucor javanicus lipase and lauric acid giving yields of 62-97% of ester. (+info)