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PubMed1983

NTP Lifetime Carcinogenesis Studies of Amosite Asbestos (CAS No. 12172-73-5) in Syrian Golden Hamsters (Feed Studies).

Carcinogenesis studies of amosite asbestos were conducted by administering diets containing 1% of the asbestos in pellets from the conception of the mothers through the lifetime of male and female Syrian golden hamsters. Control groups consisted of 127 male and 126 female hamsters and the amosite asbestos groups consisted of 252 male and 254 female hamsters. No adverse effect on body weight gain or survival was observed from treatment with amosite asbestos. Neither of the amosite asbestos groups showed increased neoplasia in any organ or tissue compared to the control groups. Under the conditions of these studies, the ingestion of amosite asbestos at a level of 1% in the diet for their lifetime was not toxic and did not cause a carcinogenic response in male and female Syrian golden hamsters. Levels of Evidence of Carcinogenicity: Male Hamsters: Negative Female Hamsters: Negative

Journal Article↗

PubMedDate not supplied

[A follow-up study of lung function among ex-asbestos workers with and without pleural plaques].

BACKGROUND: Pulmonary function testing is widely accepted as an integral part of medical surveillance of occupational lung diseases. There are several cross-sectional studies evaluating lung function among asbestos-exposed workers, but only few longitudinal surveys have been performed. OBJECTIVES: To evaluate, over a mean follow-up period of 3.7 (SD 1.8) years, the loss of lung function in a group of 103 workers with previous exposure to asbestos (mainly ship building/repairing), according to the presence or absence of pleural plaques at radiological examination. METHODS: Chest radiographic examination was used to ascertain the presence/absence of pleural plaques. If chest X-ray films were positive for pleural plaques, HRCT (High Resolution Computed Tomography) was used to exclude any parenchymal disease. The assessment of lung function over time included repeated measurement of vital capacity (VC), forced expiratory volume in one second (FEV1) and total lung capacity (TLC). Smoking was assessed in terms of pack-years. A Generalized Estimating Equations (GEE) approach to repeated spirometric measurement was used to investigate the relationship between the loss of pulmonary function and (i) presence/absence of pleural plaques, (ii) smoking status, and (iii) work seniority in workplaces with exposure to asbestos. RESULTS: In the ex-asbestos workers, mean age at the first examination was 49 (SD 6) years and work seniority averaged 25 (SD 7) years; 36% were non-smokers, 27% smoked < 15 pack-years, and 37% smoked > or = 15 pack-years. Thirty-six workers showed pleural plaques at radiological examination. Overall, 236 measurements of VC and FEV1, and 234 determinations of TLC were available. Multivariate GEE approach to age- and height-adjusted spirometric data showed that pleural plaques were not associated with a significant loss of pulmonary function during the follow-up. When compared with non-smokers, heavy smokers (> or = 15 pack-years) showed on average a significant loss of VC (-5.3%, IC 95%: -9.4 - -1.2%), FEV1 (-8.4%, IC 95%: -13.2 - -3.5%), and TLC (-4.0%, IC 95%: -7.4 - -0.5%). An occupational history of previous exposure to asbestos was significantly associated with an 10-year decrease in VC (-3.1%, IC 95%: -5.9 - -0.3%) and FEV1 (-4.9%, IC 95%: -8.3 - -1.5%). CONCLUSIONS: The results of this follow-up study showed that smoking and previous asbestos exposure were associated with a mild, but statistically significant, loss of lung function. Radiological findings of pleural plaques were not related to deterioration of lung function over the follow-up period.

Asbestosis↗

PubMed1990

[Asbestos-induced lung diseases].

Asbestos fibres have potent cancerogenic and fibrogenic properties and may lead to development of cancer and fibrosis in the lung parenchyma and pleura. The Danish Ministry of Employment has established rules which should prevent development of disease when working with asbestos in future but, on account of the very long latent period between exposure and development of asbestos-related disease, these conditions will still occur during the next 30-40 years. Primarily, the more benign pleural plaques will be concerned but serious disease such as bronchial carcinoma and pleural mesothelioma will occur in the future. When patients are encountered who present symptoms or objective/paraclinical findings which are compatible with disease produced by asbestos, it is important to remember that exposure to asbestos may be many decades ago and, particularly where the malignant conditions are concerned, exposure need not have been particularly massive or prolonged. All cases where asbestos-related disease is suspected should be notified to the insurance administration.

Asbestosis↗

PubMed1988

Asbestos bodies in children's lungs. An association with sudden infant death syndrome and bronchopulmonary dysplasia.

Lungs from 46 autopsied children (age range, 1 to 27 months) were examined for asbestos bodies using a bleach-digestion extraction technique. Ten (21.7%) of 46 children had asbestos bodies in their lungs. Of these ten children, seven were diagnosed with sudden infant death syndrome, and three were diagnosed with bronchopulmonary dysplasia. Thus, 46.6% of children with sudden infant death syndrome and 42.8% of children with bronchopulmonary dysplasia had asbestos bodies. Impaired lung-clearing mechanisms due to either abnormal lung physiology or reorganization of pulmonary architecture may be significant in the formation of asbestos bodies. Additionally, children with asbestos bodies may have been exposed to higher ambient levels of asbestos and other pollutants.

Asbestosis↗

PubMed1995

[Fatal pleural mesothelioma diseases caused by familial household contacts with asbestos fiber dust].

The case histories of a family are described where 3 out of 4 developed asbestos-related diseases. Only the husband had direct occupational exposure handling blue-asbestos materials while working in a producing insulating factory in 1950-59. He died of pulmonary asbestosis as an occupational disease. His wife and his son died of asbestos related mesothelioma. Detailed exposure history revealed exposure to asbestos by laundering her husband's contaminated working clothes. His son was exposed to asbestos during childhood by helping his mother laundering the father's working clothes and in addition by visiting his father's working place regularly. The significance of nonoccupational exposure to asbestos is emphasized as a causative factor in the development of malignant mesothelioma.

Adult↗

PubMed1993

The changes of some immunological parameters in subjects exposed to asbestos in dependence on age, duration of exposure, radiological findings and smoking habits.

We followed the changes in some parameters in men exposed to asbestos (to chrysotile and in part to crocidolite). The studied group consisted of exposed workers and retired workers who had been exposed to asbestos in the past. The results were compared with those in the control group of unexposed adults and analysed according to age, duration of exposure, smoking habits and radiological findings. Investigated were: the levels of immunoglobulins IgA, IgG, IgM, complement components C3, C4, alpha-1-antitrypsin and transferrin (humoral immunity) as well as the phagocytic activity of the leukocytes in peripheral blood (natural immunity). The comparison of the results with those in the control group showed that asbestos exposure stimulated markedly IgG and C4 production and to a lesser extent also IgA, IgM, C3 and transferrin production and it suppressed natural immunity. Comparison of the results of the same age categories--control (40.8), with the subgroup of active workers (44.4), showed significantly increased levels of IgA, IgG, IgM, C4 and decreased values of natural immunity in asbestos exposed group. Comparison of different age categories (pensioners--63.2: workers--44.4) showed, that from five parameters in which statistically significant differences were found, four had decreased values in pensioners. Radiological findings suggested, that changes in immunological parameters probably preceded pathologic processes. There were statistically significant differences in the levels of IgM in smokers compared with nonsmokers in the subgroup of workers exposed to asbestos and in the levels of IgG and C4 in the group of workers + pensioners together. It follows from the present study that asbestos exposure modulates the immune response and leads to significant changes of humoral and natural immunity.

Adult↗

PubMed1996

[Benign asbestos pleural effusion. Report of a first series in Spain].

Up to now, only 2 cases of benign asbestos pleural effusion have been described in Spain. We report our experience of 15 patients diagnosed of benign asbestos pleural effusion (BAPE). Between 1980 and January 1995, 15 patients were diagnosed of BAPE according to the following criteria: a) evidence of pleural effusion; b) previous asbestos exposure, and c) exclusion of other etiologies of last during 3 years of follow-up. Retrospective review of diagnostic and evolutive data from the patients' clinical records. Asbestos exposure was intense in 8 patients and slight in 7. There were 11 effusions on the left side and 4 on the right side. All effusions were exudative, with a pleural adenosine deaminase level lower than 43 U/l. Eleven patients had a lymphocytic pleural fluid. All patients had nonspecific pleural histology, and asbestos bodies were detected in one case. Eleven patients achieved a radiographic resolution in less than 3 months, and 3 patients presented relapses. Fourteen patients had a good outcome, and one patient presented a lung adenocarcinoma after 5 years of follow-up. Benign asbestos pleural effusions are predominant on the left side, have a tendency to relapse and the exposition can be occasional. The outcome is good in most of the cases.

Adult↗

PubMed1999

Inferences on the kinetics of asbestos deposition and clearance among chrysotile miners and millers.

BACKGROUND: The health effects of asbestos are intimately related to the fate of inhaled fibers in the lungs. The kinetics of asbestos fibers have been studied primarily in rodents. The objective of this study was to explore the application of these kinetic models to human autopsy data. METHODS: We analyzed the asbestos fiber content of the lungs of 72 Quebec chrysotile miners and millers and 49 control subjects using analytical transmission electron microscopy. Statistical methods included standard multivariate linear regression and locally weighted regression methods. RESULTS: The lung burdens of asbestos bodies and chrysotile and tremolite fibers were correlated, as were the concentrations of short, medium, and long fibers of each asbestos variety. There were significant associations between the duration of occupational exposure and the burdens of chrysotile and tremolite. The concentration of chrysotile decreased with the time since last exposure but the concentration of tremolite did not. The clearance rate varied inversely with the length of chrysotile fibers. For fibers greater than 10 mu in length the clearance half-time was estimated to be 8 years. CONCLUSIONS: The patterns in our data are compatible with both of the hypotheses suggested from rodent experiments; the existence of a long-term sequestration compartment and overload of clearance mechanisms in this compartment.

Aged↗

PubMed1994

Asbestos-related disease associated with exposure to asbestiform tremolite.

Tremolite is nearly ubiquitous and represents the most common amphibole fiber in the lungs of urbanites. Tremolite asbestos is not mined or used commercially but is a frequent contaminant of chrysotile asbestos, vermiculite, and talc. Therefore, individuals exposed to these materials or to end-products containing these materials may be exposed to tremolite. We have had the opportunity to do asbestos body counts and mineral fiber analysis on pulmonary tissue from five mesothelioma cases and two asbestosis cases with pulmonary tremolite burdens greater than background levels. There were no uncoated amosite or crocidolite fibers detected in any of these cases. Three patients were occupationally exposed to chrysotile asbestos; two patients had environmental exposures (one to vermiculite and one to chrysotile and talc) and one was a household contact of a shipyard worker. The tremolite burdens for the asbestosis cases were one to two orders of magnitude greater than those for the mesothelioma cases. Our study confirms the relationship between tremolite exposure and the development of asbestos-associated diseases. Furthermore, the finding of relatively modest elevations of tremolite content in some of our mesothelioma cases suggests that, at least for some susceptible individuals, moderate exposures to tremolite-contaminated dust can produce malignant pleural mesothelioma.

Adult↗

PubMed1991

Carcinogenicity of chrysotile asbestos: a case control study of textile workers.

Chrysotile is the predominant type of asbestos used in the United States and thus represents the most important source of exposure to asbestos already in place. While the steepest exposure-response observed for lung cancer has been in workers exposed to chrysotile in textile operations, some argue that chrysotile is less carcinogenic than amphibole asbestos types. Mineral oil exposures have been hypothesized to be responsible for the highly elevated lung cancer risk seen in textile workers. A lung cancer case-control analysis among a cohort of South Carolina chrysotile asbestos textile workers was conducted. Only a modest reduction in the slope of the lung cancer exposure-response relationship was observed after controlling for mineral oil exposures. These data do not support mineral oil exposure as a plausible explanation for the elevated lung cancer risk seen in chrysotile asbestos textile workers. The possible role of longer, thinner, more carcinogenic fibers in textiles is one plausible hypothesis needing further investigation.

Asbestos↗

PubMed1992

Activation of human CD4+CD45RA+ T cells by chrysotile asbestos in vitro.

Chrysotile asbestos stimulates T lymphocyte subsets. Cell surface CD4 or CD45RA expression in peripheral blood mononuclear cells (PBMC) was downregulated after incubation with chrysotile asbestos in vitro temporarily. The percentage of CD4+CD45RA+ cells and mean fluorescence intensity in CD4 or CD45RA decreased after incubation with asbestos and returned to the original level after 24 h of incubation, which suggests that chrysotile asbestos activates CD4+CD45RA+ cells. No change was observed in CD29 expression. An increased percentage of IL-2R positive cells and an elevated intracellular Ca++ level were also indicative of the activation of PBMC by chrysotile asbestos.

Antigens, CD↗

PubMed1993

Asbestos induces aberrant crypt foci in the colon of rats.

The carcinogenicity of asbestos to the gut is controversial. The aberrant crypt focus (ACF) assay is proposed as a test for colon carcinogens. We have scored ACF in the colon of rats and mice, one month after per os gavages with suspensions of asbestos fibers. Crocidolite asbestos induced ACF in the colon of rats in two independent experiments (P = 0.02 and P < 0.01 compared to controls given water), and was ten times less effective than the carcinogen azoxymethane. Chrysotile asbestos also induced ACF in rats. Neither crocidolite nor chrysotile induced ACF in mice. The data suggest that ingested asbestos may be carcinogenic to the colon.

Animals↗

PubMed1991

Increased production of plasminogen activator inhibitor in vitro by pleural leukocytes from rats intratracheally instilled with crocidolite asbestos.

We have previously reported that normal pleural leukocytes secrete a urokinase-type plasminogen activator inhibitor (PAI) in culture. In view of the pathogenic effects of asbestos on the pleura, in particular pleural fibrosis, we have extended these observations to crocidolite asbestos-exposed rats. Pleural leukocytes from rats exposed to crocidolite asbestos were found to secrete more PAI in culture than controls. The activity of PAI in pleural leukocyte-conditioned medium increased in a dose-dependent manner in relation to the quantity of asbestos injected into the lung. However, with increasing time post asbestos instillation, there was no significant change in the secretion of PAI by pleural leukocytes in culture compared with earlier time points of crocidolite-exposed rats. Plasminogen activator was not detectable in the conditioned medium at any time point. The data derived from this study may help to elucidate the pathogenesis of some pleural disorders caused by exposure to fibrous dusts in the lungs.

Animals↗

PubMed1986

Effects of asbestos fibers on cell division, cell survival, and formation of thioguanine-resistant mutants in Chinese hamster ovary cells.

The ability of crocidolite fibers to induce point mutations and mitotic abnormalities in Chinese hamster ovary (CHO) cells was examined in cell cultures. The purpose has been to study the possibilities for establishing in vitro test methods to quantify genetic damage induced by asbestos and other mineral fibers. Results obtained with the CHO/hypoxanthine guanine phosphoribosyl transferase system indicated that crocidolite fibers per se do not significantly increase the number of thioguanine-resistant mutants. Crocidolite fibers also failed to potentiate the mutagenicity of benzo[a]pyrene. Time-lapse cinematography and microscopy showed that asbestos (crocidolite) fibers were markedly cytotoxic. Among surviving cells some underwent abnormal cell divisions which resulted in multi- and micronucleate cells. Many cells that contained a few asbestos fibers, however, underwent mitosis and successfully formed two mononucleate daughter cells capable of further divisions. Individual, fiber-containing cells were examined by time-lapse television recordings for 4-5 days. During this time period some cells underwent six divisions and generated an almost normal number of daughter cells. Cells which contained fibers that were longer or equivalent to the diameter of the mitotic cell (20 microns), showed different forms of mitotic abnormalities. The frequency of multinucleate cells was drastically increased following exposure to asbestos fibers. Only rarely, however, did these cells divide to produce viable daughter cells capable of continued cell multiplication. The frequency of multinucleate cells was dependent on the dose of exposure to asbestos fibers and could possibly be used as an index of the degree of mitotic disturbances induced by mineral fibers.

Animals↗

PubMed1994

Infrared and nuclear magnetic resonance studies of some surface properties of asbestos-albumin interactions.

The interaction capacity of asbestos with albumin was studied. Asbestos fibres were treated with bovine serum albumin and were investigated by Fourier transform infrared (IR) spectrometry, conventional IR spectrometry and wide-line nuclear magnetic resonance spectrometry. In asbestos, the presence of active sites on the surface of the fibres was evidenced through external and internal OH stretching vibrations. It was also demonstrated that in asbestos fibres treated with albumin mixed hydrogen bonds of the type O-H...Nalbumin or O...H-Nalbumin occur. A physical interaction between asbestos fibres and albumin was demonstrated.

Asbestos, Crocidolite↗

PubMed1988

Asbestos fibers mediate transformation of monkey cells by exogenous plasmid DNA.

We have tested the ability of chrysotile asbestos fibers to introduce plasmid DNA into monkey COS-7 cells and the ability of this DNA to function in both replication and gene expression. Chrysotile fibers are at least as effective as calcium phosphate in standard transfection assays at optimal ratios of asbestos to DNA. After transfection with chrysotile, a minor percentage of introduced plasmid DNA bearing a simian virus 40 origin of replication replicates after 24 hr. Fragmentation of entering DNA is more prominent with asbestos than with calcium phosphate, and after 72 hr most DNA introduced by asbestos is associated with chromosomal DNA. Cells transfected with plasmid p11-4, bearing the p53 protooncogene, express this gene. Cells transfected with pSV2-neo express a gene conferring resistance of antibiotic G418, allowing isolation of colonies of transformed cells after 18 days. The introduction of exogenous DNA into eukaryotic cells could cause mutations in several ways and thus contribute to asbestos-induced oncogenesis.

Animals↗

PubMed2003

Soluble ICAM-1, MCP-1, and MIP-2 protein secretion by rat pleural mesothelial cells following exposure to amosite asbestos.

Pleural inflammation is a sequela of exposure to toxic mineral fibers such as amosite asbestos. This inflammatory response involves the influx of leukocytes from the vasculature into the pleural space. Adhesion molecules such as intercellular adhesion molecule-1 (ICAM)-1 and chemokines such as monocyte chemoattractant protein-1 (MCP)-1 and macrophage inhibitory protein-2 (MIP)-2 are known to be important in pulmonary inflammation following inhalation of particulate matter. However, little is known about their role in pleural inflammation secondary to amosite asbestos exposure. Because the pleural mesothelial cell is believed to be a key target cell of asbestos exposure, the purpose of this study was to determine if ICAM-1, MCP-1, and MIP-2 proteins were secreted by these mesothelial cells following in vitro and in vivo exposure to amosite asbestos. Increased levels of ICAM-1 and MCP-1 protein were measured following 24 or 48 hours exposure of cultured rat pleural mesothelial cells to amosite fibers (1.5 to 5.0 micro g/cm(2)). Increased levels of ICAM-1, MCP-1, and MIP-2 protein were found in pleural lavage fluid from Fischer-344 rats exposed to amosite asbestos for 4 and 12 weeks and after a 12-week recovery period (following the 12-week exposure period). These findings suggest that the secretion of ICAM-1, MCP-1, and MIP-2 by rat pleural mesothelial cells may contribute to amosite-induced pleural inflammation.

Administration, Inhalation↗

PubMed1990

Brake mechanics, asbestos, and disease risk.

Health risks posed by inhalable asbestos fibers are known to exist in a variety of industrial and nonindustrial settings. Although early studies described an increased risk of asbestosis, lung cancer, and mesothelioma in asbestos-industry workers, subsequent research revealed the existence of a potential asbestos-related health hazard in nonasbestos industries such as the textile and railroad industries. Brake mechanics and garage workers constitute a large work force with potential exposures to levels of asbestos capable of producing disease. Unfortunately, the health risk faced by these workers has received little attention. This article briefly discusses currently available information on the asbestos health risks of workers in this setting, and highlights the need for further investigations of this occupational group.

Asbestos↗