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PubMed1989

Airborne mineral fibre concentrations in an urban area near an asbestos-cement plant.

Ambient air concentrations of asbestos and total mineral fibres were measured during the period June-July 1985 at several locations near a large asbestos-cement factory located in the proximity of a northern Italian town. Measurements of the number and type of fibres were made by means of analytical scanning electron microscopy and energy-dispersive X-ray analysis (SEM-EDXA), essentially according to the RTM2 reference method of the Asbestos International Association. Total mineral fibre concentrations (longer than 5 microns) ranged from below detection limit (D.L., i.e. 0.4 fibres per litre (f/1] to 227 f/1 (single value); mean values ranged from 1.3 to 74.0 f/1. However, elemental microanalysis (EDXA) showed that about 65% of fibres were sulfate fibres, 20% were aluminium silicates or other silicates, and only 15% were asbestos fibres (mainly chrysotile and tremolite-group amphiboles). Asbestos concentrations (fibres more than 5 microns in length) were in the range of less than D.L. to 19.1 f/1, mean values ranging from less than D.L. to 11.1 f/1. The results obtained showed large differences in day-to-day concentrations, suggesting that they were affected by the rate of production in the plant and by weather conditions. In particular, wind direction and distance from the source appeared to be of major importance since the highest asbestos fibre concentrations were mostly found at points closer to the source and downwind. When the distance from the source was increased, other local factors appeared to be determining. In addition, the large proportion of non-asbestos mineral fibres and elongated sulfate (or sulfur-containing) particles clearly indicates major contributions from other sources, such as local pollution and natural soil erosion.

Air Pollutants↗

PubMed1989

Estimations of risk from environmental asbestos in perspective.

Because very recent data on asbestos in the environment are available, some fairly firm conclusions can now be drawn regarding current exposure to asbestos fibres. If account is taken of occupational exposure data (where past exposure levels were very high indeed, leading to a very significant risk to workers at the time), it is possible to make some reasoned estimates of the risk from ambient air. In the past, there was considerable confusion regarding the degree of risk for both occupational and environmental conditions. In estimating the risk, account needs to be taken, in particular, of the fact that: (a) occupational exposures in the past were frequently higher than reported; (b) asbestosis (a disease only associated with very heavy occupational exposures) would seem to be mechanistically involved in the development of lung cancer associated with asbestos exposure; (c) chrysotile asbestos is now the commonest form of fibre used unlike in the past, when greater quantities of crocidolite and amosite were used, the latter types being much more closely associated with mesothelioma than chrysotile; (d) overall levels of asbestos in environmental ambient air are lower than they used to be; (e) ingested asbestos seems to be associated with a negligible degree of risk as indicated by animal and human studies. The estimated values of risk provided here are smaller than those published some years ago but are similar to those given in very recent key publications. The level of environmental lifetime risk from exposure to airborne asbestos would appear to be about 1 in 100,000 or even lower. Such a level of risk is exceedingly low, and bearing in mind the criteria of both WHO and the Royal Society of London, it would appear to represent an acceptable 'rare-event' extremely low-level risk, like the cancer risk from the cosmic radiation adsorbed when flying across the Atlantic or from eating charcoal broiled meat, or the risk of being killed by lightning.

Air Pollutants↗

PubMed1988

[Measurement of the fibrous dusts in West Germany. Fiber concentration in the vicinity of objects and buildings with asbestos-containing building materials].

Ambient air concentrations of fibrous dusts were measured in the vicinity of buildings with weathered and corroded asbestos-cement (AC)-products during 1983-1985. The concentrations of the total dust (TSP) were higher (mean value of 150 micrograms/m3) than the background concentrations. The mean value of ambient air asbestos concentrations lay at 750 fibers/3 for long asbestos fibers (longer than 5 microns). The maximum values were in the range of 10(3) fibers/m3. About 37% of the measured asbestos fiber concentrations (long fibers) were in the range above 500 fibers/m3; 12% of all long asbestos fiber concentrations were higher than 1000 fibers/m3. In the case of a proposed preventive concentration limit of 400 long asbestos fibers/m3, the asbestos fibers released from the corroded surfaces of AC-products on buildings, mean additional health risk not only for the house residents but in some cases also for the general population.

Air Pollution↗

PubMedDate not supplied

The biomedical and epidemiological characteristics of asbestos-related diseases: a review.

The purpose of this paper is to provide the reader with an overview of the biomedical and epidemiological characteristics of asbestos-related disease based upon currently available information. Epidemiological and experimental data developed over the past 20 years have greatly added to our knowledge of the biological effects of asbestos, particularly in relation to clinical disease. This information has substantially strengthened the evidence linking asbestos to specific health effects. Lung cancer and mesothelioma are clearly the most important asbestos-related causes of death among exposed individuals, although the accumulated data is suggestive of the existence of an excess risk of gastrointestinal and a variety of other neoplasms. Animal studies confirm the human epidemiological results and indicate that all commercially available fiber types are capable of producing lung cancer and mesothelioma. Experimental implantation and injection studies also show that the carcinogenicity of mineral fibers (including asbestos) is directly related to their dimensionality and not their chemical composition. Although the asbestos-related medical and scientific literature is voluminous, many issues related to the biological activity of asbestos fibers are as yet unresolved. Due to experimental and analytical limitations, questions concerning risk at low-level exposure, dose-response relationships, and individual susceptibility remain problematic.

Animals↗

PubMed1985

[The diagnostic value of asbestos bodies in mesotheliomas].

The exposure of asbestos was studied in 31 cases of mesothelioma from case histories and by microscopic mineralogical analysis of the broncho-alveolar lavage fluid (BAL) (31 cases) and of pulmonary tissue (5 cases). When definite exposure had occurred the lavage contained asbestos bodies in every case, except one patient with severe airflow obstruction. The most positive lavages, probably reflecting exposure to industrial amphiboles, were found in patients presenting with radiological evidence of asbestosis. Two patients had positive lavages 50 years after exposure had ceased. The lavage confirmed exposure in 6 out of 11 suspected cases and revealed contamination by asbestos in a further 4 cases, in a group of 6 not known to have been exposed. In 19.3% of cases there was a low concentration of asbestos bodies (less than 1AB/ml of BAL), comparable to what is found in 16.2% of controls from an urban population. An analysis of lung tissue confirmed massive exposure (greater than 20 000 AB/g) in two cases and in particular revealed a significant dust load (greater than 250 AB/g) in patients presenting with a weak positive BAL. Thus it seems that all the positive results should be taken into account. Of the 31 cases, 8 had a BAL without asbestos bodies. These were either mesotheliomas not linked to the inhalation of asbestos, or were the result of false negatives on account of artefacts related either to the BAL technique itself or linked to the technique of mineral analysis. Indeed the microscopic counts of asbestos bodies probably underestimate certain exposures, notably environmental exposure to chrysotile.

Adult↗

PubMed1977

Correlation of quantitative asbestos body counts and occupation in urban patients.

Asbestos bodies were quantified in digests of lung from 252 urban patients who were over 40 years of age. Patients were assigned to six occupational categories that had been determined without knowledge of asbestos body counts. Asbestos bodies were present in the lungs of 96% of the total population. Fewer than 12% of the white-collar men and the blue- and white-collar women had more than 100 asbestos bodies per gram of lung, whereas 32% of the blue-collar men not working in steel mills or construction, 45% of steelworkers, and 65% of construction workers had more than 100 asbestos bodies per gram lung. This distribution suggests that almost everyone in our population has some exposure to asbestos, and certain persons are subject to an additional occupational exposure. Whether asbestos bodies in low concentration are related to disease remains to be determined.

Adult↗

PubMed1982

Influence of asbestos fibers on collagen and prostaglandin production in fibroblast and macrophage co-cultures.

The interaction of fibroblasts, macrophages, and crocidolite asbestos fibers was studied in cell culture. We determined the effects of co-cultivation and asbestos fibers on collagen, total protein, and PG production. The co-cultivation of guinea pig alveolar macrophages and fetal lung fibroblasts resulted in a 155% increase in protein and a 31% increase in collagen production above fibroblast controls. The collagen was derived exclusively from the fibroblasts. Although total protein production was derived predominantly from the fibroblasts, the macrophages in co-culture also contributed to the protein levels. The addition of asbestos fibers to fibroblast cultures resulted in a decrease in collagen and total protein production. The addition of asbestos fibers to fibroblast and macrophage co-cultures prevented the enhancement of collagen production and limited the increase in protein production above fibroblast controls. PGE2, PGI2, and TXA2 were measured in macrophage and fibroblast cultures. Very low, almost undetectable PG production was observed under basal conditions by either cell type alone or in co-culture. Bradykinin induced release of these PGs in fibroblast but not macrophage cultures. This release was enhanced in co-cultures. Asbestos fibers, when added to the co-cultures caused a significant increase in the release of PGs, particularly PGE2. PGE2 is known to inhibit collagen and total protein production by fibroblasts. The increased release of PGs in asbestos-treated co-cultures may have contributed to the described asbestos suppression of collagen production

Animals↗

PubMed1993

Is chrysotile asbestos exposure a significant health risk to the general population?

The main unresolved issues concerning environmental exposure to chrysotile asbestos of the general population are discussed. A review of the results of the measurement of airborne chrysotile fibres in buildings is presented showing that the results have been consistently low with the exception of buildings with damaged friable asbestos-containing material. Quantitative risk assessments are presented indicating that the lifetime risk is small compared to many other environmental risks. Possible adverse health effects of paraoccupational exposures in the case of high domestic airborne asbestos levels cannot be excluded. Both on the basis of electron microscopy analyses of asbestos exposures at locations with heavy traffic, and the very shallow slopes in the exposure-response relationships for increased lung cancer risk, the conclusion is drawn that exposure to airborne asbestos-containing friction materials has not been proven to pose a significant health risk to the general population. Reviewing animal ingestion studies published and all the available epidemiological studies related to asbestos in drinking water, the conclusion is drawn that the carcinogenic risk in the general population is low even in the case of drinking water containing elevated concentrations of chrysotile asbestos.

Asbestos, Serpentine↗

PubMed1995

Transcriptional activation of the proto-oncogene c-jun by asbestos and H2O2 is directly related to increased proliferation and transformation of tracheal epithelial cells.

Asbestos causes persistent increases in c-jun mRNA and AP-1 DNA binding activity in hamster tracheal epithelial (HTE) cells, the progenitor cell type of asbestos-induced bronchogenic carcinoma. Studies here were designed to determine mechanisms of c-jun induction by asbestos and the phenotypic consequences of Jun expression in HTE cells. To examine whether asbestos or H2O2 induced transcription of c-jun, we transiently transfected HTE cells with a plasmid containing a fragment of the c-jun promoter coupled to a luciferase reporter gene. In addition, c-jun was overexpressed in cells using a full-length human c-jun construct, and effects on proliferation and transformation were examined. HTE cells transfected with the jun-luciferase construct showed increased luciferase activity when exposed to crocidolite asbestos or H2O2. These results demonstrate that asbestos and H2O2 activate AP-1-dependent gene transcription. Overexpression of c-jun led to increased proliferation and enhanced ability of HTE cells to grow in soft agar, an indication of cellular transformation. Data suggest that overexpression of c-jun may contribute to asbestos and oxidant-induced proliferation and carcinogenesis.

Animals↗

PubMed1993

Asbestos related pleural plaques in retired boiler room workers.

Occupational disease is often underestimated and only a few formal reports have been published in Taiwan. This study reports of a group of workers with asbestos-induced-disease, pleural plaque in Taiwan. Pleural plaque is a marker of exposure to asbestos. The disease was found in chest radiographs of five boiler room workers in a sugar refining factory. The chest radiographs of 248 current workers in that plant were reviewed, and none of them was found to have pleural plaques. The storage of asbestos and the long-time use of mixed asbestos cement for insulation of the inner wall of the stove and pipes were found in the factory. The authors believe that the pleural plaques might be resulted from occupational exposure to asbestos. It is suggested that the use of asbestos should be prohibited, step by step, and regular follow-up of the workers with an asbestos exposure history is required.

Aged↗

PubMed1995

[Assessment of lung cancer risk due to environmental asbestos dust exposure in the general population].

Assessment of lung cancer risk due to environmental asbestos dust exposure in the general population was based on the model of risk extrapolation from the occupational (in asbestos-cement plant) to the environmental concentrations. 24-h determinations of asbestos fibre concentrations in the air varied considerably, from 0.4 f/l to 4.6 f/l. The lung cancer risk due to environmental exposure of the general population to asbestos dust has been estimated to be 22 cases p.a. This seems to be very low, considering that the total number of deaths from lung cancer in Poland in 1992 was about 17.5 thousand. The environmental asbestos exposures and their health effects are limited mainly to the areas located in the vicinity of asbestos plants and are attributable primarily to improper utilization of the plant wastes (for example as the surface of local roads and sports grounds at schools) and their unathorized disposal. The incidence of pleural mesothelioma among the inhabitants of those areas seems to be endemic. The endemic character of pleural mesothelioma occurrence has been recently revealed in the vicinity of one of major Polish asbestos and cement plant.

Air Pollutants↗

PubMed1977

Analysis of the cores of ferruginous (asbestos) bodies from the general population. I. Patients with and without lung cancer.

Ferruginous (asbestos) bodies may be found in the lungs of almost everyone in the population, but little information is available as to whether such bodies are nucleated on asbestos or on some other fibrous dust. In this study morphologically "typical" ferruginous bodies were isolated from the lungs of 23 autopsy and surgical patients, none of whom had primary asbestos exposure. Eleven patients had carcinoma of the lung. To determine the nature of the core, 328 bodies were examined by electron diffraction. Of these, 264 (80%) showed the diffraction patterns of amphibole asbestos, whereas six showed the pattern of chrysotile asbestos. No amorphous cores or crystalline nonasbestos cores were identified. Fifty-eight (18%) bodies could not be diffracted because of the thickness of the iron-protein coat. No differences were seen between patients with and without lung cancer. We conclude that typical ferruginous bodies have asbestos cores, which are usually amphibole type. The findings suggest widespread exposure to asbestos dust; occupational histories appeared to indicate the source of exposure in some but not all patients.

Aged↗

PubMed1997

In vitro assessment of asbestos fibers genotoxicity.

This study was carried out in order to assess the genotoxic effect of in vitro exposure to commercial chrysotile asbestos. V 79 cell line, known as a well-established cellular model, was used for detection of asbestos genotoxic potency. Conventional structural chromosomal aberration analysis and sister chromatid exchange (SCE) method were both used for asbestos genotoxicity assessment. Within the experimental protocol applied, V 79 cells were treated with asbestos in concentrations of 100 and 200 micrograms/ml F-10 (HAM) media during 90 days, respectively. Analysis of changes in chromosome structure as well as of cell ploidy was performed each tenth day of the experimental course, consecutively. Two hundred well spread metaphases were taken into account for chromosomal aberration analysis. Frequency of sister chromatid exchanges was observed in 50 cells per sample. The results of cytogenetic tests revealed structural chromosomal damages, SCE-elevation and changes in cell ploidy. Cytogenetic effect of asbestos obviously depended on the dose applied and on the period of incubation. The results of this study suggest that significant cytogenetic changes occurring after asbestos treatment might directly or indirectly be the part of the biological events responsible for eliciting asbestos-induced carcinogenesis.

Animals↗

PubMed1998

[Chrysotile asbestos in Russia: certain results and promising research directions].

The article summarizes studies carried in RAMSc Research Institute for Occupational Medicine on chrysotile asbestos. Not denying potential carcinogenicity characteristic for all kinds of asbestos, those studies stress low biologic aggression of chrysotile asbestos during occupational exposure, even if the excessive MAC is demonstrated formerly in asbestos industry enterprises. Work with chrysotile asbestos, as every one in mining industry, requires not ban, but accomplishment of proper measures aimed to prevent pneumoconiosis and dust bronchitis. The article demonstrates unique experience of Russian scientists--evaluation of exposure to chrysotile without admixtures and amphibole additives. The authors define prospective research trends that, if being international, could correctly solve problems associated with further use of chrysotile asbestos, rising no "anti-asbestos" boom.

Asbestos, Serpentine↗

PubMed1998

Lack of asbestos contamination of paraffin.

OBJECTIVE: To investigate possible asbestos contamination of paraffin and migration by asbestos fibers during the tissue-embedding process. DESIGN: Three sample categories were included in the study: (1) commercially available paraffin samples; (2) procedural control samples, which were prepared by processing the paraffin through the use of standard solvents and instruments; and (3) samples taken from areas adjacent to embedded tissue and evaluated for migration of asbestos from the tissue into the surrounding paraffin. The analysis of collected material from all samples was performed with analytical transmission electron microscopy. RESULTS: Only one extremely small tremolite fiber was found in any of the commercially available samples of paraffin. No asbestos fibers were found either in the procedural control samples or in the samples taken adjacent to the embedded lung tissue. CONCLUSIONS: First, it was extremely unlikely that any of the commercial paraffin samples would have skewed data due to embedded tissue. Second, the processing and instrumentation was not found to contribute asbestos material to the paraffin during the preparations. Finally, embedded tissue that contained high numbers of fibers, both uncoated fibers and asbestos bodies, did not contribute asbestos to the adjacent paraffin.

Asbestos↗

PubMed1985

Correlation of in vitro genotoxicity and oncogenicity induced by radiation and asbestos fibres.

The in vitro cytotoxicity and oncogenic potential of both native and acid leached asbestos fibres were studied using the C3H 10T1/2 cell model. Both native and leached fibres induced a dose-dependent toxicity. At high fibre concentrations, acid leached fibres were significantly less toxic than their untreated counterparts. While asbestos fibres alone do not induce oncogenic transformation at the concentration examined, it was found that both leached and native fibres substantially enhanced the oncogenicity of gamma-irradiation in a more than additive fashion. Although no significant chromosomal aberrations or sister chromatid exchanges (SCE) were found in asbestos treated cultures, a significantly higher number of SCEs was observed in cells treated with both asbestos and radiation compared to cells receiving radiation alone. The results suggest that the enhancement in radiation induced oncogenicity by asbestos fibres may be attributed to the mere physical presence of the fibres rather than any chemical contaminants the fibres may contain. Furthermore, the carcinogenicity of asbestos may be unrelated to genotoxicity.

Animals↗

PubMed2000

In vitro cleavage by asbestos fibers of the fifth component of human complement through free-radical generation and kallikrein activation.

Chrysotile and crocidolite fibers incubated in normal human plasma (NHP) generated from the C5 component of complement C5a-type fragments that stimulated polymorphonuclear leukocyte (PMN) chemotaxis. Absorption of NHP with antiserum against C5a totally abolished neutrophil chemotactic activity. Asbestos fibers also produced C5a small peptides in the presence of ethylene glycol bis(beta-aminoethyl ether) N,N,N'N'-tetraacetic acid (EGTA) but not ethylene diamine tetraacetic acid (EDTA). Activation of C5 was significantly inhibited when asbestos fibers were pretreated with iron chelators such as sodium dithionite (DTN), deferoxamine (DFX), or ascorbate (AA). Concentration-related inhibition of C5 activation was also observed when asbestos fibers were added concurrently to plasma in the presence of DFX, 1,3-dimethyl-2-thiourea (DMTU), a strong hydroxyl scavenger, or aprotinin (APR), a specific protease inhibitor. Further, chrysotile and crocidolite significantly increased plasma kallikrein activity. Data demonstrate that asbestos-induced C5 activation plays a role in inflammatory reactions characteristic of asbestosis through mechanisms involving iron ions, hydroxyl radicals, and oxidized C5-ike fragments. The ferrous ions present at the asbestos fiber surface trigger this activation and catalyze, via Fenton reaction, the production of hydroxyl radicals, which in turn convert native C5 to an oxidized C5-like form. This product is then cleaved by kallikrein, activated by the same asbestos fibers, yielding an oxidized C5a with the same functional properties as C5a.

Adult↗

PubMed2001

Community health risk assessment after a fire with asbestos containing fallout.

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.

Asbestos↗