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PubMedDate not supplied

[Content of asbestos fibers in water sources of the Bazhenovo deposit].

The paper provides preliminary measurements of asbestos levels in water sources from an area of the Bazhenovo chrysotile-asbestos deposit. All study water samples have been found to contain chrysotile-asbestos fibers at concentrations one-three orders less that the values standardized in the USA (7 x 10(6) vol/l). The authors consider it advisable to continue studies to measure asbestos levels in the water sources in the areas in vicinity of other Russian deposits.

Asbestos↗

PubMed2004

Mitochondrial changes induced by natural and synthetic asbestos fibers: studies on isolated mitochondria.

Asbestos fibers, such as chrysotile and crocidolite, are known to have cytotoxic effects on different cell types. in vivo exposure to asbestos fibers can induce both fibrotic and malignant lung diseases , however, the mechanisms linking exposure to the subsequent development of the diseases are unknown. Numerous investigations suggest the involvement of reactive oxygen species (ROS). ROS are known to damage biological macromolecules including proteins, cell membrane lipids and nucleic acids; alterations of these essential cellular components can alter cell function and can drive the cell to neoplastic transformation or to cell death. Because the mitochondrial respiratory chain is an important source of ROS and RNS (reactive nitogen species) in the cells, we have investigated the effects of aqueous extracts of asbestos (natural and synthetic) fibers on some mitochondrial activities. Our data show that crocidolite fibers release substances in solution that may interfere directly with the mitochondrial cytochrome oxidase complex. Moreover, the calcium ions released from these fibers induce opening of the permeability transition pore of the inner membrane leading to a possible cytotoxic effect due to the release of apoptotic factors normally localized in the mitochondrial intermembrane space. In addition, crocidolite extracts enhance the mitochondrial production of ROS. No significant biochemical effects are exerted by chrysotile, either natural or synthetic, on isolated mitochondria. Nevertheless, all asbestos fibers tested induce morphological alterations visualized by transmission electron microscopy and morphometric analysis.

Animals↗

PubMed1989

Mortality rates among employees potentially exposed to chrysotile asbestos at two automotive parts factories.

A study of the mortality rates among 1657 employees at two Ontario automotive parts factories that manufactured friction materials containing chrysotile asbestos was initiated in response to the workers' concerns about the effects of asbestos on their health. A total of 1194 men and 258 women had had their first potential exposure at least 10 years before the end of the study period; 563 of the men and 138 of the women had had such an exposure at least 20 years before the end of the study period. A significantly increased rate of death from laryngeal cancer and an elevated rate of death from lung cancer were observed in a cohort analysis. One or two deaths might have been due to pleural mesothelioma. There was no increase in the rate of death from gastrointestinal cancer or from nonmalignant respiratory disease. Case-control analysis showed no association between the risk of laryngeal or lung cancer and the total duration of employment (a surrogate for the extent of ambient exposure to asbestos or other workplace toxic substances) or employment in departments where asbestos had been used. An association between risk of death and occupational exposure is uncertain.

Adult↗

PubMed1985

Pathologic changes in the small airways of the guinea pig after amosite asbestos exposure.

To determine whether asbestos dust produces pathologic changes in the small airways, and to determine where the anatomic lesions of asbestosis commence, the authors examined lungs from guinea pigs exposed to 10 or 30 mg of amosite asbestos by intratracheal instillation and sacrificed 6 months later. Measurement of airway wall thickness revealed that membranous and respiratory bronchioles of all sizes in exposed animals were significantly thicker than those of controls. Amosite fibers were found embedded in the walls of bronchi and in membranous and respiratory bronchioles; where these fibers penetrated the airway walls, an interstitial inflammatory and fibrotic reaction (asbestosis) occurred. It is concluded that 1) amosite asbestos produces diffuse abnormalities throughout the noncartilagenous airways and possibly the cartilagenous airways as well; 2) this effect is independent of interstitial fibrosis of the parenchyma (classical asbestosis); 3) asbestosis, at least that induced by amosite, commences at any site in the parenchyma to which the asbestos fibers can gain access, either by deposition in alveoli and alveolar ducts or by direct passage of fibers through the walls of all types and sizes of small airways.

Animals↗

PubMed1985

Chronic inhalation of short asbestos fibers.

An animal inhalation study was initiated to study the chronic biological effects of inhalation of short chrysotile asbestos fibers. Rats and monkeys were exposed for 18 months, 7 hr/day, 5 days/week to a specially prepared, chrysotile asbestos aerosol. Based upon daily chamber measurements, the mean concentration of fibers in the chamber air was 1.0 mg/m3. By phase contrast microscopy, the number of fibers greater than 5 micron in length was determined to be 0.79 fiber per cubic centimeter. Rats were autopsied for pathological and histochemical examination at 1, 3, 6, 12, 18, and 24 months after initiating exposures. No significant differences in the histochemical data were seen between the exposed and control groups. Gross and histopathologic examination of exposed and control groups of rats indicated no compound-related lesions, including fibrosis. Open lung biopsies were performed on the chrysotile-exposed and the control monkeys 28 months after initiating exposures. Histopathologic evaluation of the lung biopsy tissue showed the presence of asbestos bodies adjacent to the terminal bronchioles of the asbestos-exposed monkeys. There was no observed fibrosis in pulmonary tissue. All monkeys are being maintained for an indefinite period and observed for signs of latent pulmonary disease.

Aerosols↗

PubMed1986

[The risk of death from malignant tumors is dependent on the amount of exposure to asbestos dust].

The investigation was carried out in an asbestos plant producing yarn, cords, gaskets and frictional products. Only chrysotile asbestos was used in the production process. The follow-up covered a cohort composed of 2403 men and 1190 women employed in the plant of various asbestos products for at least 3 months during 1945-1973. The availability was 91.3% for men and 89.6% for women. Due to considerably changed working conditions in the plant, resulting from modernization carried out in 1956, the results were analysed for a subcohort employed during 1945-1955, composed of 670 men and 349 women. Men demonstrated increased standardized mortality rates (SMR) from malignant tumours of respiratory organs and thorax under increased dust concentrations. SMR = 243,2 was statistically significant only in the subcohort of men employed during 1945-1955 in a group with a mean asbestos dust concentration considerably exceeding TLVs. The risk analysis, depending on the dose, exhibited in the subcohort of men working during 1945-1955 who were affected by the highest dose of dust, increased, over 3-fold, the risk of death from lung cancer (SMR = 327.9). In the subcohort of women the risk of death from malignant tumours was higher only in the group of high dust concentration, as compared to the reference population (SMR = 210.2). A significant increase in the risk of death from cancer of the digestive organs and peritoneum as well as malignant tumours of the liver and pancrease was found in the group of high and low dust concentrations alike.(ABSTRACT TRUNCATED AT 250 WORDS)

Asbestos↗

PubMedDate not supplied

[Atmospheric asbestos pollution in the urban environment: Rome, Orbassano and a control locality (II)].

To complete our previous study which evaluated by TEM the atmospheric concentrations of asbestos in the urban areas of Milan, Casale Monferrato, Brescia, Ancona, Bologna and Florence, the concentrations measured in Rome, Orbassano and in two mountain test locations, one with serpentine rock (Valle di Susa) and the other with granitic rock (Adamello), are now reported. Compared with the towns in northern Italy, which had already shown decreasing pollution levels from Casale Monferrato to Milan, Brescia, Ancona, Bologna and Florence, the levels measured in Rome were extremely low, about ten times lower than those measured in Florence, which were in turn ten times lower than those measured in Milan. In Orbassano the levels near serpentine quarries were slightly higher than the geologic background values. The geologic background level in Valle di Susa was approximately 1 fibre/litre (> 5 microns) and 2.5 fibres/litre (total fibres); asbestos fibres were totally absent in the mountain area with granitic rock. The clearly decreasing values of pollution starting from the northern cities down to Rome lead to the exclusion of motor vehicle traffic as one of the "primary" sources of fibre dispersion. In fact, traffic becomes significant in producing pollution only in the presence of other dispersion sources since it gives rise to "secondary" pollution consisting of ultra-thin fibres through grinding of coarse fibres dispersed from other sources and sedimented on the ground. The authors attribute the main responsibility in maintaining comparatively high concentrations of asbestos fibres in the urban areas of northern Italy to weathered asbestos-cement coverings which act as "primary" sources.

Air Pollutants↗

PubMed1998

Participation of iron and nitric oxide in the mutagenicity of asbestos in hgprt-, gpt+ Chinese hamster V79 cells.

Crocidolite asbestos is known to cause cellular damage, leading to asbestosis, bronchogenic carcinoma, and mesothelioma in humans. The mechanism responsible for the carcinogenicity of asbestos is not known. Iron associated with asbestos is thought to play a role by catalyzing the formation of reactive oxygen species, which may cause DNA damage, leading to mutations and cancer. Here, we examined whether asbestos can induce mutations in Chinese hamster hgprt+ V79 cells or transgenic hgprt-, gpt+ V79 cells (G12). Treatment with 6 microg/cm2 crocidolite for 24 h caused a 2-fold increase in the mutation frequency at the gpt locus of G12 cells, but no increase at the hgprt locus of V79 cells. The mutation frequency at the gpt locus of G12 cells increased with increasing treatment dose of crocidolite. The mutations induced by crocidolite appeared to be due to the generation of reactive oxygen species catalyzed by iron associated with the fibers, because treatment of G12 cells in iron-free medium with fibers from which redox active iron had been removed with desferrioxamine B prevented all of the gpt- mutations above untreated control levels. In addition, treatment of cells with a soluble form of iron, 1.5 mM ferric ammonium citrate, resulted in an increase in mutation frequency at the gpt locus of approximately 1.5 fold above that of untreated G12 cells with no increase in mutations at the hgprt locus of V79 cells with ferric ammonium citrate. We also investigated the effect of nitric oxide on the mutagenicity of crocidolite in G12 cells. When G12 cells were treated with 3 microg/cm2 of crocidolite in the presence of nitric oxide-generating compound, 200 microM diethyltriamine/NO, the mutation frequency increased to a level that was more than additive for crocidolite or diethyltriamine/NO treatment alone. These results strongly suggest that the presence of iron and nitric oxide may either lead to the generation of another reactive, mutagenic species, such as peroxynitrite, or that nitric oxide inhibits a DNA repair enzyme(s), leading to an increase in mutations.

Animals↗

PubMed1998

Fibroblast mitogens in bronchoalveolar lavage (BAL) fluid from asbestos-exposed subjects with and without clinical evidence of asbestosis: no evidence for the role of PDGF, TNF-alpha, IGF-1, or IL-1 beta.

Asbestosis is a fibrotic lung disease resulting from inhalation of asbestos fibres. Its pathogenesis is poorly understood but probably involves stimulation of fibroblast proliferation and collagen production by mediators released from inflammatory and resident lung cells. In vitro studies have implicate PDGF, TNF-alpha, IGF-1, TGF-beta, and IL-1 in asbestosis, but the role of these mediators in vivo is not known. This study aimed to characterize mediators in bronchoalveolar lavage (BAL) fluid from patients exposed to asbestos with (n = 24) or without (n = 34) asbestosis, compared with ten normal subjects. Human lung fibroblasts were exposed to serial dilutions of BAL fluids and the effects on fibroblast proliferation were assessed. The median mitogenic activity of BAL fluid from asbestos-exposed (17 per cent above medium control, range 3-44 per cent) and asbestosis (14 per cent, range 2-60 per cent) groups was higher than that of BAL fluid from controls (10 per cent, range 2-20 per cent; P < 0.01 and P < 0.05, respectively), but there was no significant difference between the patient groups. The mitogenic activity of BAL fluids was not reduced by incubation with neutralizing antibodies to PDGF-AA, PDGF-AB, PDGF-BB, TNF-alpha, IGF-1, and IL-1 beta. We conclude that BAL fluids from patients exposed to asbestos contain mitogens for human lung fibroblasts, but that PDGF, TNF-alpha, IGF-1, or IL-1 beta do not contribute to this activity.

Adult↗

PubMed1996

Lung cancer and asbestos exposure: asbestosis is not necessary.

Recent commentaries on the issue of asbestos-related lung cancer have raised important points. One major question is whether lung cancer can be attributed to asbestos exposure in the absence of asbestosis. This review attempts to place the debate in the proper context for establishing causation. Relevant epidemiologic and pathologic studies are analyzed, as well as the scientific basis for each position in the debate. The assertion that asbestosis must be present in order to attribute a lung cancer to asbestos exposure does not meet accepted standards for establishing causation. In addition, some evidence has been incorrectly cited in support of this position. This discussion can benefit from clearer definitions of asbestosis, a more thorough evaluation of the available scientific information, and a proper context for determining causation. This review of the available evidence indicates that lung cancers can occur as a result of asbestos exposure, in the absence of clinical or histologic asbestosis. Causation in an individual should be assessed by considering duration of exposure, intensity of exposure, and appropriate latency.

Asbestos↗

PubMed1997

Gastrointestinal cancer mortality of workers in occupations with high asbestos exposures.

Asbestos, which is a well-known risk factor for lung cancer and malignant mesothelioma, has also been suggested as a gastrointestinal (GI) carcinogen. This study was conducted to assess the relationship between high asbestos exposure occupations and the occurrence of G1 cancer. Death certificate data were analyzed from 4,943,566 decedents with information on occupation and industry from 28 states from 1979 through 1990. Elevated proportionate mortality ratios (PMRs) for mesothelioma were used to identify occupations potentially having many workers exposed to asbestos. All PMRs were age-adjusted and sex- and race-specific. The PMRs for GI cancers in white males were then calculated for these occupations after excluding mesothelioma, lung cancer, and non-malignant respiratory disease from all deaths. We identified 15,524 cases of GI cancer in the 12 occupations with elevated PMRs for mesothelioma. When these occupations were combined, the PMRs for esophageal, gastric, and colorectal cancer were significantly elevated at 108 (95% confidence interval = 107-110), 110 (106-113), and 109 (107-110), respectively. Esophageal cancer was elevated in sheet metal workers and mechanical workers. Gastric cancer was elevated in supervisors in production and managers. Colorectal cancer was elevated in mechanical and electrical and electronic engineers. However, high exposure occupations like insulation, construction painter supervisors, plumbers, furnace operators, and construction electricians showed no elevations of GI cancers. In conclusion, this death certificate study supports an association between asbestos exposure and some GI cancer, however the magnitude of this effect is very small.

Asbestos↗

PubMed1999

Cellular and molecular mechanisms of asbestos-induced fibrosis.

Pleural and pulmonary fibrosis (asbestosis) are ramifications of occupational exposures to asbestos fibers, a diverse family of ubiquitous, naturally-occurring minerals. The pathogenesis of asbestos-associated fibrosis involves the participation of a number of cell types and is characterized by an early and persistent inflammatory response that involves the generation of oxidants, growth factors, chemokines, and cytokines. These mediators may also contribute directly to cell injury, proliferation, and fibrogenesis. After interaction with cells, asbestos fibers trigger a number of signaling cascades involving mitogen-activated protein kinases (MAPK) and nuclear factor kappa-B (NF-kappaB). Activation of transcription factors such as NF-kappaB and activator protein-1 (AP-1) may be linked to increases in early response genes (e.g., c-jun and c-fos) which govern proliferation, apoptosis, and inflammatory changes in the cells of the lung. The goal of this article is to review the cellular and molecular mechanisms of asbestos-induced fibrosis that may be critical to the development of effective treatment regimens.

Asbestos↗

PubMed1977

Cancer following occupational exposure to asbestos and vinyl chloride.

A review is presented of the various factors important in the identification of carcinogenic disease from occupational and environmental exposure to asbestos and vinyl chloride. The long lapsed period, usually of 20 or more years from first exposure to these materials, is discussed, as well as the requirement for sufficiently long observation periods in prospective epidemiological studies. The multiple-factor etiology of lung cancer involving cigarette smoking and asbestos exposure is illustrated. The risks of asbestos-related cancers to other than those directly working with the material are discussed in a variety of circumstances, and finally the effectiveness of control procedures for vinyl chloride and asbestos are compared.

Asbestos↗

PubMed1979

Asbestos, dental X-rays, tobacco, and alcohol in the epidemiology of laryngeal cancer.

A case-control study of 47 laryngeal cancers in males of three counties of Washington State was conducted. Personal interview was used to obtain information on smoking, alcohol use, exposure to asbestos, and other substances, and x-rays of the head and neck area. Smoking and alcohol consumption were found to increase risk of laryngeal cancer independently, with a clear dose-response relationship. Neither asbestos exposure nor exposure to other substances was found to significantly increase the risk of laryngeal cancer, although the relative risk with asbestos exposure was 1.75. Lifetime history of exposure to dental x-rays on five or more occasions was associated with significantly increased risk of laryngeal cancer among heavy smokers but not among light smokers. The importance of tobacco and alcohol in the epidemiology of laryngeal cancer was re-affirmed, the importance of asbestos exposure was brought into question, and a possible relationship of laryngeal cancer with exposure to dental x-rays among heavy smokers was demonstrated.

Aged↗

PubMed2001

Asbestos and man-made vitreous fibers as risk factors for diffuse malignant mesothelioma: results from a German hospital-based case-control study.

BACKGROUND: This study examines the role of occupational factors in the development of diffuse malignant mesothelioma with special emphasis on the dose-response relationship for asbestos and on the exposure to man-made vitreous fibers (MMVFs). METHODS: One hundred and twenty-five male cases, diagnosed by a panel of pathologists, were personally interviewed concerning their occupational and smoking history. The same number of population controls (matched for sex, age and region of residence) underwent similar interviews by trained interviewers. Odds ratios (OR) were calculated for an expert-based exposure index using conditional logistic regression. RESULTS: Exposure to asbestos shows the expected sharp gradient with an OR of about 45 for a cumulative exposure > 1.5 fiber years (arithmetic mean 16 fiber years). A significant OR was calculated even for the lowest exposure category "> 0 - < or = 0.15 fiber years". Although the mean cumulative exposure to MMVF is roughly 10% of the exposure to asbestos, an increased OR is observed in an ever/never evaluation. This observation is heavily hampered by methodical problems. A corresponding case-control study was performed using a lung tissue fiber analysis in addition to interviews. Both interviews and the lung tissue analysis yielded similar OR levels between the reference and the maximum exposure intervals. CONCLUSIONS: Despite a possible influence as a result of selection and information bias, our results confirm the previously reported observation of a distinct dose-response relationship even at levels of cumulative exposure below 1 fiber year. Moreover, the study confirms that asbestos is a relevant confounder for MMVF. A causal relationship between exposure to MMVF and mesothelioma could neither be detected nor excluded, as in other studies.

Aged↗

PubMed2003

Asbestos fiber length as related to potential pathogenicity: a critical review.

BACKGROUND: Asbestos inhalation is recognized as an exposure that increases the risk for the development of lung disease. It is unique among dusts in that it is both a carcinogen and capable of inducing extrapulmonary responses such as pleural thickening and fibrosis as well as malignancy. One feature of asbestos suggested as crucial in its pathological activity is its fibrous morphology. Long fibers that have been inhaled are cleared less readily and are thus more persistent in the body. Furthermore certain experimental models link fiber length to levels of risks for development of certain diseases. The present review will survey the data on this subject. METHODS: The review considers experimental models that have been used to assess the response to various lengths of fibers in animal models in addition to data obtained from studies of human materials. The review also emphasizes the importance in defining the method by which a sample is categorized. RESULTS: Data are offered which support the potential for longer fibers as well as shorter fibers to contribute to pathological responses. CONCLUSIONS: The data presented argue that asbestos fibers of all lengths induce pathological responses and that caution should be exerted when attempting to exclude any population of inhaled fibers, based on their length, from being contributors to the potential for development of asbestos-related diseases.

Asbestos↗

PubMed2001

Malignant mesothelioma from neighborhood exposure to anthophyllite asbestos.

BACKGROUND: Anthophyllite asbestos has been reported to cause asbestosis, lung cancer, mesothelioma, and pleural plaques in occupationally exposed workers. Anthophyllite has also been associated with pleural plaques in Finland and Japan among those who live near mines and mills and have neighborhood or environmental exposure. METHODS: We evaluated a 38-year-old patient with pleural mesothelioma who lived, attended school, and delivered newspapers near a manufacturing facility that used exclusively anthophyllite asbestos fiber from ages 8-17 years. He had no work exposure to asbestos. RESULTS: The pleural mesothelioma was an epithelial type with tubulopapillary structures and was treated with an extrapleural pneumonectomy followed by radiation therapy. The malignant cells were positive by immunohistochemistry for cytokeratin but negative for carcinoembryonic antigen, S100, B72.3, and leu M1 antigen. Anthophyllite fibers were > 5 microm in length in lung tissue compared to 3 microm from a general population study. CONCLUSIONS: Anthophyllite asbestos has been associated with neighborhood environmental exposure and pleural plaques; we now report a neighborhood exposure and pleural mesothelioma.

Adult↗

PubMed2005

Mesothelioma in household members of asbestos-exposed workers: 32 United States cases since 1990.

BACKGROUND: Mesothelioma is significant as an indicator of asbestos exposure, as a continuing major cause of death in those exposed, and as a risk following lesser exposures. One such exposure is living in the household of an asbestos worker, and coming into contact with fibers brought home on his/her body, clothing, etc. METHODS: Law firms throughout the US known for their pursuit of asbestos claims were polled for mesothelioma claims brought on behalf of family members of identifiable asbestos-exposed workers. Cases with any occupational, environmental, or other possible exposure were not included. RESULTS: This study reports 32 household-exposure mesothelioma cases, diagnosed since 1990. Relationships were wife (15), daughter (11), son (3), sister-in law (1), niece (1), and boarder (1). Occupations of the workers included shipyard (13), insulator (7), and other (12). Of the 27 pleural cases, 13 were epithelial, 5 fibrous, 3 biphasic, and 6 not specified; of the 5 peritoneal cases, 4 were epithelial and 1 fibrous. Latency was greater than 40 years in 27 cases; 6 cases were 40-49 years of age and 17 were 60 or older. CONCLUSIONS: Records from law firms were a useful source of information. Mesothelioma resulting from household exposure is a continuing problem. It is more likely to present in the elderly, after latencies of >40 years.

Adolescent↗