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PubMed1992

Does asbestos exposure increase the risk of urogenital cancer?

The risk of urogenital cancer to workers exposed to asbestos was evaluated using the results of published studies. The pooled standardized mortality ratios (SMRs), based on the results of cohort studies, were significantly increased (P less than or equal to 0.05) for ovarian and kidney cancer in North American studies but not in other studies. Part of these increases probably is due to the use of inappropriate comparison populations and the failure to take into account risk factors associated with urogenital cancer. Other types of studies generally did not indicate that exposure to asbestos increases the risk of urogenital cancer. Generally, there is insufficient information to show that urogenital cancers are caused by occupational exposure to asbestos.

Asbestos↗

PubMed1985

Increased release of hydrogen peroxide and superoxide anion from asbestos-primed macrophages. Effect of hydrogen peroxide on the functional activity of alpha 1-protease inhibitor.

The ability of asbestos-elicited murine peritoneal macrophages to release superoxide anion and hydrogen peroxide, following in vitro triggering, has been investigated. The asbestos-elicited macrophages produced increased levels of superoxide and hydrogen peroxide compared to control macrophages and similar levels to those produced by Corynebacterium parvum elicited macrophages. The supernatants from asbestos-elicited macrophages which had been triggered in vitro were capable of impairing the ability of alpha 1-protease inhibitor to inhibit elastase function. The catalase sensitivity of this effect showed it to be due to hydrogen peroxide.

Animals↗

PubMed1981

Asbestos fibers in normal and cancerous human kidneys.

Exposure of general population of ubiquitously present asbestos has led investigators to monitor its health effects. This pilot study was undertaken to see if there was an association between kidney cancer and fiber concentration in the kidney. Results of transmission electron microscopic (TEM) analysis for asbestos fibers in normal and cancerous human kidney tissues collected from three Chicago hospitals are presented. Chrysotile fibers were recovered from autopsy or surgery tissues of normal and cancerous kidneys. The study did not indicate a definite association between carcinoma and fiber load of kidney of humans exposed to nonoccupational asbestos.

Adult↗

PubMed1982

[Mesothelioma following occupational contact with asbestos].

From 1975 onwards, mesothelioma is by far the most often seen occupational tumour in Switzerland (about 70%). Between 1969 and 1982, there have been 49 cases registered by the SUVA (Schweizerische Unfallversicherungsanstalt, i.e. Swiss National Accident Insurance Fund). 10 together with asbestosis. Of the first 30 cases, the primary tumour only once was in the peritoneum, in all other cases the tumour always could be located in the pleura. The causative asbestos exposure was found in the production of asbestos cement (9), in the construction and reparation of waggons (6), in the insulation work at chemical plants (5) and in several other industrial work conditions (10). The average exposure time was 21 years. The average interval from exposure to diagnosis 35 years. The survival time after diagnosis about 1 year. Technical prevention consists in substitution of asbestos or elimination of respirable dust (or at least reduction below the TLV). Medical prevention: periodic fitness tests and follow up examinations. New cases should be communicated to the mesothelioma-register in Zurich and to the SUVA, for clarification of the industrial origin.

Asbestos↗

PubMed1986

Asbestos exposure and Alzheimer disease.

10 cases in which an asbestos-related disease (malignant pleural mesothelioma or asbestosis) was associated with severe Alzheimer type lesions in the brain are reported. The patients, all males aged between 67 and 78 years, had been occupationally exposed to asbestos in the shipbuilding industry. The hypothesis that asbestos is a favoring factor in the genesis of Alzheimer disease is discussed.

Aged↗

PubMed2007

Apoptosis induced by crocidolite asbestos in human lung epithelial cells involves inactivation of Akt and MAPK pathways.

Exposure of human lung epithelial (A549) cells to asbestos fibers causes apoptosis, which is largely attributed to release of iron and generation of reactive oxygen species (ROS) within the cells. To mimic the highly oxidative environment generated by asbestos exposure in the absence of the actual fibers, we used two chemicals; buthione sulfoximine (BSO), an inhibitor of glutathione (GSH) synthesis and ferric ammonium citrate (FAC), a source of iron. Here, we report that exposure of A549 cells to crocidolite asbestos led to a significant time-dependent inactivation of signaling proteins, i.e. Akt and all mitogen-activated protein kinases (MAPKs) (p38, ERK1/2 and SAPK/JNK), and subsequently to apoptosis. Unlike crocidolite treatment, the use of BSO and FAC, independently or combined, did not change the phosphorylation status of proteins, nor did it induce apoptosis. Taken together, our results presented herein point to the possibility that crocidolite-induced apoptosis of human lung epithelial cells is not a mere consequence of generation of oxidants but also requires inactivation of major cell growth and differentiation pathways.

Apoptosis↗

PubMed1978

Asbestos exposure and related neoplasia. The 28 year experience of a major urban hospital.

In a retrospective study of 49 cases of asbestosis, a steady increase in the frequency of diagnosis of asbestosis and asbestos-related neoplasia is documented from a major urban hospital since 1960. Although in the majority of cases the subjects were exposed to asbestos in a neighboring shipyard, in 20 per cent of the cases, asbestos exposure was in industries not related to shipbuilding, reflecting its widespread use. This selective population of patients with asbestosis more often than not had an associated neoplasm. The most likely accompanying tumor was pleural mesothelioma, and among cell types of lung cancer, adenocarcinoma was notably frequent.

Adenocarcinoma↗

PubMed1990

Iron mobilization from asbestos by chelators and ascorbic acid.

The ability of chelators and ascorbic acid to mobilize iron from crocidolite, amosite, medium- and short-fiber chrysotile, and tremolite was investigated. Ferrozine, a strong Fe(II) chelator, mobilized Fe(II) from crocidolite (6.6 nmol/mg asbestos/h) and amosite (0.4 nmol/mg/h) in 50 mM NaCl, pH 7.5. Inclusion of ascorbate increased these rates to 11.4 and 4.9 nmol/mg/h, respectively. Ferrozine mobilized Fe(II) from medium-fiber chrysotile (0.6 nmol/mg/h) only in the presence of ascorbate. Citrate and ADP mobilized iron (ferrous and/or ferric) from crocidolite at rates of 4.2 and 0.3 nmol/mg/h, respectively, which increased to 4.8 and 1.0 nmol/mg/h in the presence of ascorbate. Since ascorbate alone mobilized iron from crocidolite (0.5 nmol/mg/h), the increase appeared to result from additional chelation by ascorbate. Citrate also mobilized iron from amosite (1.4 nmol/mg/h) and medium-fiber chrysotile (1.6 nmol/mg/h). Mobilization of iron from asbestos appeared to be a function not only of the chelator, but also of the surface area, crystalline structure, and iron content of the asbestos. These results suggest that iron can be mobilized from asbestos in the cell by low-molecular-weight chelators. If this occurs, it may have deleterious effects since this could result in deregulation of normal iron metabolism by proteins within the cell resulting in iron-catalyzed oxidation of biomolecules.

Asbestos↗

PubMed1978

Asbestos cement dust inhalation by hamsters.

Two groups of 96 male Syrian golden hamsters were exposed to respirable asbestos cement aerosol at concentrations of approximately 1 and approximately 10 micrograms/liter, respectively, 3 hours/day, 5 days/week. Average fiber counts ranged from 5 to about 120 fibers/cm3. Each group was randomly divided into six subgroups of 16 animals. The first subgroup was sacrificed after 3 months of exposure, the second after 6 months, and the third after 15 months. The fourth subgroup was withdrawn from exposure after 3 months, observed for an additional 3 months, and then sacrificed. The fifth and sixth subgroups were withdrawn after 3 and 6 months of exposure, respectively, and maintained for observation up to the 15-month exposure point of the third subgroup at which time all surviving animals were sacrificed. All other experimental procedures were similar to those delineated in a previous publication describing the development of an animal model, techniques, and an exposure system for asbestos cement dust inhalation (A. P. Wehner, G. E. Dagle, and W. C. Cannon, 1978, Environ. Res. 16, 393-407). The asbestos cement exposures had no significant effect on body weight and mortality of the animals. Higher aerosol concentration and longer exposure times increased the number of macrophages and ferruginous bodies found in the lungs of the exposed animals. Recovery periods had no effect on the incidence of macrophages and ferruginous bodies. The incidence of very slight to slight fibrosis in the animals sacrificed after 15 months of exposure shows a significant (P less than 0.01) trend when the untreated control group and the 1 and 10 microgram/liter dose level groups are compared, indicating a dose-response relationship. Development of minimal fibrosis continued in animals withdrawn from exposure. No primary carcinomas of the lung and respiratory tract and no mesotheliomas were found.

Aerosols↗

PubMed1985

Calculated solubility of chrysotile asbestos in physiological systems.

Chrysotile asbestos fibers which are ingested into a physiological system will dissolve in fluids to which they are exposed. The rate of dissolution can be estimated by formulating an appropriate rate law and retrieving rate constants from published experiments. The rate of dissolution calculated for asbestos fibers is dependent on the surface area of dissolving mineral, mass of solution to which the fibers are exposed within cells, the rate of transport of H+ into the cells, and the rate of transport of Mg2+ and SiO2 out of the cells. The maximum rate of dissolution of a single 10-micron X 1-micron fiber within a cell is 2.13 X 10(-7) moles hr-1 kg-1 consistent with dissolution rates measured in vivo by Morgan et al. (A. Morgan, A. Holmes, and C. Gold. Studies of the solubility of constituents of chrysotile asbestos in vivo using radioactive tracer techniques. Environ. Res. 4, 558-570, 1971).

Animals↗

PubMed1990

Guadalupe corridor transportation project asbestos health risk assessment, San Jose, California.

A study was conducted to assess health risks and identify a set of appropriate mitigation measures to control airborne emissions of natural asbestos from construction of the Guadalupe Corridor Transportation Project, a highway and light-rail construction project in San Jose, California. This study supported a state-mandated Environmental Impact Report. Communication Hill, along the project route, is known to contain natural chrysotile asbestos-bearing rock. The study described in this paper estimated potential asbestos emissions, identified and evaluated mitigation measures, and evaluated air pathway exposure and health risks. With mitigation, estimated risks were found to be acceptable by the regulatory agency, and construction proceeded.

Asbestos↗

PubMed1984

Asbestos-exposed populations: prevention, care, and compensation.

In Israel, the prevention and care of asbestos-associated diseases with latency periods of one to four decades (asbestosis, mesothelioma, increased frequency of cancer of the lung and other sites) are not satisfactory, and new national policies are required. Such policies have three major goals: (a) elimination or reduction of exposure to asbestos dust; (b) measures to promote cessation or drastic reduction of cigarette smoking among those currently or formerly exposed; and (c) equitable compensation for the consequences of past exposures. The practical elements of a program to achieve these three goals include (a) exposure standards and control technology; (b) identification of sources, routes, and levels of exposure and groups at risk; (c) compensation and job security; (d) medical monitoring and follow-up; (e) smoking cessation; (f) selective substitution of other substances for asbestos; and (g) establishment of a panel for policy supervision and the overseeing of compensation programs. Delay in implementation risks higher death rates for asbestosis and cancer among previously exposed workers, greater exposure among current workers, loss of experienced workers from the work force, and unnecessary hardship for families not adequately compensated.

Adult↗

PubMed1980

Phospholipase A activity and prostaglandin release from alveolar macrophages exposed to asbestos.

The effect of asbestos (canadian chrysotile B) was studied on macrophages harvested by guinea-pig bronchoalveolar lavage. In short term incubation (3 hrs), asbestos (1 mg) induced a highly significant increase in macrophage phospholipase A activity and prostaglandin synthesis. At lower concentrations of the fibers (10 micrograms and 100 micrograms), no significant change of macrophage activity was noted following our incubation period. The modification by asbestos of membrane integrity and functions is suggested.

Animals↗

PubMed1993

Peculiarities of the clastogenic properties of chrysotile-asbestos fibers and zeolite particles.

It has been established that chrysotile-asbestos fibers and zeolite particles induce chromosome aberrations in human lymphocytes from whole blood cultures, peritoneal fluid cells and bone marrow cells of mice. It is shown that the level of cytogenetic response from the intraperitoneal administration of chrysotile-asbestos fibers and zeolite particles depends on the time of their exposure. Further, it is shown that SOD eliminates the cytogenetic effect of chrysotile-asbestos fibers, while catalase inhibits that of zeolite particles. Recommendations concerning testing for the mutagenic properties of mineral fibers and particles are given, and possible mechanisms of their damaging effects are discussed.

Animals↗

PubMed1994

In vitro genotoxicity studies of chrysotile asbestos fibers dispersed in simulated pulmonary surfactant.

Micronucleus (MN) formation and sister-chromatid exchange (SCE) assays were performed for asbestos in cultured Chinese hamster lung (V79) cells to determine the effect of surfactant treatment on the genotoxicity of two chrysotile asbestos samples of different fiber lengths. The cells were challenged in vitro with NIEHS intermediate- and short-length chrysotile fibers in both their native state and with surfactant pretreatment. For the surfactant pretreatment, the fibers were incubated in a simulated pulmonary surfactant which was prepared by ultrasonically dispersing dipalmitoyl lecithin (DPL), a primary component of pulmonary surfactant, in minimal essential medium (MEM). Chrysotile asbestos was ultrasonically mixed into the prepared surfactant dispersion or into MEM. V79 cells were exposed to DPL-treated intermediate-length chrysotile (TICA), intermediate-length chrysotile (ICA), DPL-treated short-length chrysotile (TSCA) or short-length chrysotile (SCA) fibers for 48 h. For each treatment, 2000 mononucleated cells were scored for MN formation, and 30 M2 metaphase cells were scored for SCE induction. The results showed that all samples, TICA, ICA, TSCA and SCA, caused significant elevation in the frequency of cells with micronuclei and of cells with two or more nuclei. The increase in micronucleus frequency was greatest in cells challenged with untreated intermediate-length fibers, and was greater for untreated than for DPL-treated short-length fibers. For the short-length fiber samples, DPL surfactant treatment decreased activity for multiple nucleus formation, while DPL treatment did not result in consistent changes in that activity for intermediate-length fibers. Results of SCE assays were either negative or inconclusive. Cells were more viable following TICA and TSCA than following ICA and SCA challenge as measured by cell counts after 48 h of incubation.

Animals↗

PubMed1983

An investigation of the penetration of ingested asbestos into the normal and abnormal intestinal mucosa of the rat.

To characterize the tissue response associated with the presence of asbestos fibres in the gastro-intestinal wall, duodenal tissues of Wistar rats were examined by light microscopy following injection of a suspension containing amosite fibres into the wall of the duodenum. Intestinal tissues were also examined by light microscopy following oral administration of amosite for 5 days to healthy animals and for up to 7 days to animals with induced gastro-intestinal ulcers. Injection of amosite into the wall of the gastro-intestinal tract resulted in granulomatous lesions characterized by large numbers of macrophages containing crystals with the polarizing characteristics of amosite fibres. Examination by polarizing light microscopy following ingestion of asbestos revealed no such lesions or other histopathological abnormalities in the gut wall of the healthy animals and no intracellular fibres were observed in the animals with ulcers. Light microscopy, therefore, yielded no pathological evidence of widespread transmigration of asbestos from the gastro-intestinal tract of rats, even under conditions of mucosal loss. Further studies involving analysis by electron microscopy are under way.

Administration, Oral↗

PubMed1986

Effect of asbestos fibers on aryl hydrocarbon hydroxylase and aminopyrine N-demethylase activities of rat liver microsomes.

Chrysotile asbestos fibers impair the activities of rat liver microsomal aryl hydrocarbon hydroxylase (AHH), aminopyrine (AP) N-demethylase and dimethylnitrosamine (DMN) demethylase in vitro. This inhibition is concentration-dependent. Preincubation of 3-methylcholanthrene (3-MC)-pretreated rat liver microsomes with chrysotile depresses the overall metabolism of [G-3H]benzo[a]pyrene (BaP). Various forms of asbestos employed inhibit AHH activity to the same extent. However, other types of asbestos are not as effective as chrysotile in diminishing AP demethylase activity. Chrysotile and crocidolite fibers are not found to significantly change the apparent Km of AHH activity, from 3-MC-pretreated rat liver microsomes, for BaP. Increasing the microsomal protein concentration partially abolishes the inhibition of AHH activity caused by chrysotile fibers. Inhibition of AP demethylase and AHH activities is attenuated by bovine serum albumin (BSA) or ferritin. Depression of AHH activity by crocidolite is significantly reversed by ferritin. Since polymers such as ferritin override enzyme inhibition by chrysotile as well as crocidolite, surface chemical groups of the fibers may be involved in enzyme modification.

Aminopyrine N-Demethylase↗

PubMed1991

Examination of factors that may influence disposition of benzo[a]pyrene in vivo: vehicles and asbestos.

Effects of vehicles and of asbestos on disposition of benzo[a]pyrene (B[a]P) were examined in vivo. [3H]B[a]P dissolved in triethylene glycol, ethyl laurate, or tricaprylin was intratracheally administered to male Sprague-Dawley rats. Excretion was most rapid when triethylene glycol was the vehicle, with 70.5% of the recovered dose appearing in bile in 6 h. Lower amounts were excreted into bile when ethyl laurate (58.4%) or tricaprylin (56.2%) were the vehicles, with comparably higher amounts remaining in lungs. When chrysotile asbestos was intratracheally instilled 24 h prior to instillation of [3H]B[a]P dissolved in triethylene glycol, the rate of excretion of radioactivity was slower than without asbestos pretreatment, with only 61.8% of the dose appearing in bile in 6 h.

Animals↗