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PubMed1985

Asbestos and gastrointestinal cancer. A review of the literature.

Exposure to asbestos is among several factors cited as possible causes of esophageal, gastric and colorectal cancer. More than 45 published studies have presented mortality data on asbestos-exposed workers. For each cohort, we listed the observed and expected rates of deaths from types of gastrointestinal cancer based on the latest published follow-up. Summary standardized mortality ratios (SMRs) were then derived. Finally, we calculated summary SMRs for total gastrointestinal tract cancer for three occupational groups: asbestos factory workers, insulators/shipyard workers and asbestos miners. Statistically significant elevations in summary SMRs were found for esophageal, stomach and total gastrointestinal tract cancer in all asbestos-exposed workers. Esophageal cancer summary SMRs remained significantly elevated when data were reanalyzed to include only those cohorts with death certificate diagnoses for cause of observed deaths. However, summary SMRs were not statistically significant for stomach and total gastrointestinal tract cancer after reanalysis. Summary SMRs by occupational group showed a significant elevation for total gastrointestinal cancer in insulators/shipyard workers. The elevation was not significant after reanalysis. Based on the results after reanalysis, the elevations in summary SMRs for stomach and total gastrointestinal tract cancer are of a magnitude that could result from diagnostic and investigator error. We conclude that more studies are required before stomach and colorectal cancers are documented as asbestos-related diseases.

Asbestos↗

PubMed1983

First report of asbestos-related diseases in Hong Kong.

There has been no report of malignant mesothelioma or asbestosis in Hong Kong despite the rapid growth of industry in the past few decades. Three patients with malignant pleural mesothelioma and one patient with asbestosis and small cell carcinoma of the lung are reported. All four patients were Chinese in Hong Kong and had a history of occupational exposure to asbestos. Although there is no mining of asbestos in Hong Kong, her rapid industrialization in the past few decades has led to a large population of asbestos-exposed workers in industry. The average annual consumption of crude asbestos (import minus re-export) has grown ten-fold in the past decade to 1.090 tonnes in 1978-79, and the number of workers handling asbestos products was estimated to be 20.000 in 1979. The problem of asbestos related diseases has however been little considered and further epidemiologic studies are warranted.

Adult↗

PubMed1978

[Asbestos fibre dust, an actual hazard (author's transl)].

Late results concerning the effects of fibre dust in the human lungs have enormously raised the actuality of fibronous and cancerous reactions of airborne asbestos fibres. The hithero experiences with diseases, resultant from airborne asbestos fibres (asbestoses, cancer, and mesothelioma) are looked on and discussed with respect to 2 asbestos diseases out of the office of the author. Special attention is given to the asbestos-caused mesothelioma which has also been affiliated in the 7th decree of diseases resulting from the work (Berufskrankheitenverordnung) on the 1.1. 1977. Own experiences resulting as well from preventive control examinations as from special collectives of patients (workers in asbestos contaminated surroudnings and smokers) are discussed with respect to restrictive or obstructive ventilation problems. Finally some examples of asbestos free materials wich could be used substiutionarily are quoted.

Air Pollution↗

PubMed1984

The combined effects of asbestos ingestion and localized X-irradiation of the colon in rats.

We hypothesized that the normal bowel may afford some protection to tissue penetration of ingested asbestos, due to the mucus produced by goblet cells which normally coats the gut surface. To study this, we exposed localized segments of the colons of laboratory rats to X-irradiation. These animals were then divided into 3 groups which were fed either a diet containing 10% chrysotile asbestos, a diet containing 10% non-nutritive cellulose fiber, or a standard laboratory diet. Autopsies and histopathology were performed on all animals that died spontaneously and those that were killed at 350 days. Various types of inflammatory and degenerative lesions were commonly seen, but there was little difference in frequency between the diet groups. Five adenocarcinomas and two sarcomas were seen in the fiber groups (three tumors in the asbestos group and four tumors in the cellulose group) but no tumors were seen in animals on the standard diet. There was not a significant difference in tumor rates between the asbestos and cellulose groups, nor was there a significant difference between the combined fiber groups and the standard diet group. It was concluded that the x-ray treatment resulted in localized damage to the colonic mucosa and, therefore, theoretically disrupted the normal mucus coating allowing the potential for increased tissue penetration by the asbestos. Ingested asbestos did not increase the risk for tumor development and, therefore, does not seem to be co-carcinogenic or a tumor promoter in combination with disruption of mucus coating and localized X-irradiation.

Animals↗

PubMed1984

Enhanced interleukin activity following asbestos inhalation.

Asbestos inhalation can cause pulmonary fibrosis and is associated with a variety of immunological abnormalities. The purpose of this study was to evaluate the effects of asbestos inhalation on interleukin-1 (IL-1) and interleukin-2 (IL-2) production in a rodent model. Two groups of rats were exposed, by intermittent inhalation, to either amphibole (crocidolite) or serpentine (chrysotile) asbestos. A third (control) group of rats was sham exposed to clean air. Animals from the three exposure groups were thereafter immunized (or not immunized) with fetal calf serum antigens. In order to assay interleukin activity, supernatants were generated from cultures containing alveolar macrophages and autologous splenic lymphocytes, and from cultures containing alveolar macrophages alone. Using assay systems designed to detect IL-1 and IL-2 functional activity, the supernatants were evaluated for their capacity to stimulate lymphoproliferation and fibroblast DNA synthesis. Macrophage-lymphocyte co-culture supernatants, when obtained from immunized, asbestos exposed rats, contained greater IL-1 and IL-2 activity than identical supernatants from immunized, sham exposed animals. These between group differences were not, however, observed in supernatants from unimmunized rats, or when supernatants were generated in the absence of immune lymphocytes. These observations suggest that asbestos exposure is associated with enhanced activation of lymphocytes by antigens. The possible relevance of these findings to asbestos related fibrogenesis and immunological stimulation is discussed.

Animals↗

PubMed1982

Numbers and types of asbestos fibers in subjects with pleural plaques.

The authors analyzed asbestos fibers in lung samples from 20 subjects with pleural plaques discovered on autopsy and compared the findings to their previous analyses of lungs from subjects with little or no asbestos exposure and no plaques. Sixteen of the subjects with plaques had a history of exposure to asbestos. The authors used electron-optical methods and energy-dispersive x-ray spectroscopy to investigate the structure, diffraction patterns, and chemical composition of the asbestos fibers. The subjects with plaques had significantly higher median concentrations than the control subjects for amosite and crocidolite fibers (P less than 0.01) but not for the other fiber types. Minimal microscopic asbestosis was present in the 3 subjects who had the highest amosite concentrations. In the subjects with typical plaques, a history of asbestos exposure, and more fibers than in the control population, the relation of the plaques to asbestos was confirmed; for others, it was uncertain.

Adult↗

PubMed1982

Asbestos related changes in pulmonary and systemic immune responses--early enhancement followed by inhibition.

We recently developed an animal model in order to study the pulmonary and systemic reactions following exposure to environmental pollutants. In this model, conscious sheep received repeated intratracheal instillations of a suspension of 0 (controls), 2mg (low dose) or 128 mg (high dose) of chrysotile asbestos fibres over a 12 month period. A significant dose-dependent enhancement in proliferative responses of pulmonary free airway cells (FAC) to four mitogens was observed after a first instillation. A somewhat weaker stimulation was also observed in peripheral blood mononuclear leucocytes (PBML). At 6 months, the high dose animals no longer displayed the dose-dependent enhancement of FAC responses and manifested actual depression of PBML responses. At 12 months, all asbestos exposed animals showed impaired responses of FAC, whereas only the PBML of high dose animals were showing such an impairment. These data suggest that asbestos exposure has a dose-dependent initial enhancement of local pulmonary as well as systemic responses to mitogens while prolonged exposure and higher doses can subsequently lead to a relative depression of local and systemic cellular immune activity. Although responsive early after asbestos exposure, systemic immunity appears to lag behind local immunity in the late depressive effect of asbestos fibres on mitogen responsiveness. In addition to these cell-directed effects serum factors seem to play an inhibitory role in lymphocyte responses to mitogens in animals repeatedly exposed to asbestos.

Animals↗

PubMed1980

Asbestos retention in human respiratory tissues: comparative measurements in lung parenchyma and in parietal pleura.

Asbestos fibres in respiratory tissues from 29 cases diversely exposed to asbestos dusts have been characterized, sized and counted using a transmission electron microscope. Comparison of data obtained by measurement of fibres in lung parenchyma and in parietal pleura samples showed the following: -- In each case, the proportion of chrysotile fibres (as opposed to amphiboles) was higher in parietal pleura than in lung parenchyma. (The proportion of chrysotile in pleura was greater than 90% in 30 of the 40 samples.) -- Fibres encountered in parietal pleura were shorter than those in the parenchyma. -- There was no evident correlation between numerical concentrations of fibres in lung parenchyma and those in parietal pleura. This study has shown that characteristics of asbestos retention in parietal pleura cannot be derived from measurements in lung parenchyma. On the basis of the cases analysed here, who were exposed to mixed types of asbestos dust, chrysotile seems to be the asbestos type retained almost exclusively in parietal pleural tissues. These findings might be taken into account when assessing the risk of pleural diseases (especially mesothelioma) attributable to each type of asbestos fibre.

Adult↗

PubMed1978

[Asbestos fibers in alcoholic beverages. Contaminating role of filtration material].

The presence of asbestos fibres was searched for in samples of wines, brandies and spirits which had or had not been filtered through asbestos filters. The materials examined were filtered on a micropore membrane that was then handled for electron microscope examination. Asbestos fibres were identified by their morphology and X-ray diffraction pattern and in certain cases additionally by punctual ultimate analysis (Edax). The presence of chrysotile fibres, generally separate but sometimes in clumps, was found in all the drinks which had been filtered through asbestos filters, while the non filtered drinks contained only a small concentration that was approximately equal to the one found in water analysed elsewhere. Only two samples of liquor, raw or filtered through a filter not containing asbestos, were absolutely free from fibres. On the other hand, the use of mixed filters of asbestos and cellulose resulted in only contamination by such mineral fibres.

Alcoholic Beverages↗

PubMed1993

[Hygienic evaluation of contact with asbestos-containing dusts at thermoelectric power plants].

Hygienic evaluation of air in heating power stations revealed the contamination caused by putting and removing heat-proof covers and showed that insulating workers are exposed to asbestos in concentrations sufficient to cause asbestos-related diseases including malignancies. All this is supported by roetgenologic signs of exposure to asbestos, which were seen during the primary medical examination of the workers having long length of service. The study showed that the staffers out of deal with asbestos are also exposed to the asbestos-containing dust in concentrations exceeding the MAC. So all personnel of heating power stations could be assigned to the group for asbestos-related diseases development.

Asbestos↗

PubMed1993

The production of TNF-alpha and IL-1-like activity by bronchoalveolar leucocytes after intratracheal instillation of crocidolite asbestos.

We have used a rat intratracheal instillation model to study the effect of crocidolite asbestos exposure on cytokine production by bronchoalveolar lavage (BAL) leucocytes. In unexposed controls, the normal BAL leucocytes were mostly macrophages which spontaneously produced interleukin 1 (IL-1)-like activity and tumour necrosis factor (TNF-alpha) in culture; these levels were enhanced by stimulation with LPS. In animals exposed to crocidolite asbestos, two new types of cell, neutrophils and eosinophils, were recruited into the bronchoalveolar space by 1-3 days after instillation. However, the BAL profile had returned to normal by 14 days. The production of IL-1-like activity was decreased considerably compared to control from 1 to 14 days after asbestos instillation, but was increased at 30 days. However, the leucocytes produced increased TNF-alpha as early as 3 days after asbestos instillation and maintained this elevated level throughout the experimental period. Crocidolite asbestos in vitro also stimulated normal BAL leucocytes to release significantly increased amounts of IL-1-like activity and TNF-alpha. We conclude that the deposition of crocidolite asbestos fibre in the lung by instillation causes reduced production of IL-1-like activity in the acute phase, but elevated production of both IL-1-like activity and TNF in the chronic phase, suggesting that enhanced activities of these cytokines may contribute to the development of lung pathological changes in the long term.

Animals↗

PubMedDate not supplied

Mesotheliomas following exposure to asbestos used in railroads: 130 Italian cases.

The available knowledge on the oncogenic risks of asbestos, the data on the uses of asbestos in railroads, with particular regard to the Italian State Railroads (Ferrovie dello Stato = FS), and the groups at risk due to the exposure to asbestos used in railroads were briefly reviewed. The available data on the pathological effects of such exposure, and particularly on the onset of mesotheliomas among machinists and other railroad workers, were also summarized. One hundred and thirty cases of mesothelioma (122 pleural, 1 pericardial, 6 peritoneal and 1 pleuro-peritoneal), related to the exposure to asbestos used in railroads, observed in various Italian regions, were reported. Fifty-three of these cases (among which 49 reported in the Emilia Romagna Region) were submitted to a detailed study at the Bologna Institute of Oncology. Seventy-seven cases of mesothelioma occurred among occupationally exposed FS workers, in particular machinists; 45 cases occurred among rolling-stock machinists and workers engaged in the repair and demolition of the rails of workshops not belonging to the FS; 3 cases occurred among travelling workers of rolling-stock, not belonging to the FS; and 5 cases were found in family members (1 daughter, 3 wives and 1 sister) of railroad workers. This series of cases, together with similar data from the literature, proves the existence of an actual health risk due to asbestos used in railroads, and indicates its gravity. On the basis of the available data, the following steps are considered necessary: the promotion of systematic epidemiological investigations, the adoption of preventive measures, the performance of medical oncological surveillance, and the automatic compensation for tumours following the exposure to the asbestos used in railroads.

Adult↗

PubMed1995

[Assessment of cancer risk in the general population of Poland due to asbestos exposure. I. Basis of methodology].

Two mathematical models facilitating calculation of cancer risk in people exposed to asbestos dust in the communal environment are discussed. The first helps determine a dose-response relationships when lung cancer is the exposure effect whereas the second permits calculating the probability of pleural or peritoneal mesotheliomas induction based on the level of asbestos exposure. In the case of lung cancer, the exposure is measured as a cummulated dose which equals to a product of an average concentration of asbestos fibres in 1 ml of the air multiplied by duration of exposure (in years). Thus determined relationship between asbestos exposure and the risk involved is a linear function. The effect of smoking, which undoubtedly accounts for lung cancer induction, is an element of the assessment in this model. The relationship between the risk of mesothelioma and exposure level, which is a non-linear function, is associated with the duration of exposure (in years) and the number of years since first asbestos exposure, however, it is not related to the age of person when first exposure occured or smoking habit. It may assumed that, in the case of environmental exposures, the level of exposure could be measured by the duration of exposure to a determined concentration (the exposure starts at birth to be continued throughout the whole lifetime until death). The models presented allow forecasting cancer risk based on the adopted level and duration of exposure to asbestos dust.

Aged↗

PubMed1997

Molecular regulation of IL-6 activation by asbestos in lung epithelial cells: role of reactive oxygen species.

IL-6 has been characterized as a pleiotropic cytokine with multiple biologic activities, but its induction and role in asbestos diseases have not been studied. Asbestos fibers were found to stimulate IL-6 expression and secretion in pulmonary type II-like epithelial A549 cells as well as in normal human bronchial epithelial cells. IL-6 induction was dependent on the intracellular redox-oxidative state, since intracellular hydroxyl scavengers and N-acetylcysteine, a precursor of glutathione, abrogated IL-6 secretion by asbestos or H2O2. IL-6 induction paralleled increased DNA binding activity to the nuclear factor-kappa B (NF-kappa B)- and NF-IL-6-recognized sites in the IL-6 promoter. The NF-kappa B and NF-IL-6 DNA binding proteins were immunochemically characterized as a heterodimer p65/p50 and a homodimer C/EBP beta, respectively. Stimulation of DNA binding activity to the NF-kappa B and NF-IL-6 binding sites of the IL-6 promoter by asbestos or H2O2 were inhibited by tetramethylthiourea, a hydroxyl radical scavenger. The role of local IL-6 production in the pathophysiologic processes of fiber-induced lung disorders was examined. Although less active than fibroblast growth factor, human rIL-6 also stimulated lung fibroblast growth, as evidenced by increased [3H]thymidine incorporation. Furthermore, elevated IL-6 levels were found in bronchoalveolar lavage fluids from patients diagnosed with lung fibrosis and work-related histories of long term asbestos exposure. Taken together, the results suggest that asbestos-induced oxidative stress is involved in the activation of NF-kappa B and NF-IL-6 transcription factors, which recognize the IL-6 promoter. The resulting increase in IL-6 expression may be involved in both inflammatory and fibrotic processes in the lung.

Adenocarcinoma, Bronchiolo-Alveolar↗

PubMed1998

Increased epidermal growth factor-receptor protein in a human mesothelial cell line in response to long asbestos fibers.

Epidermal growth factor (EGF) is a potent mitogen for human mesothelial cells, and autophosphorylation of the EGF receptor (EGF-R) occurs in these cell types after exposure to asbestos, a carcinogen associated with the development of mesothelioma. Here, the intensity and distribution of EGF-R protein was documented by immunocytochemistry in a human mesothelial cell line (MET5A) exposed to various concentrations of crocidolite asbestos and man-made vitreous fibers (MMVF-10). Whereas cells in contact with or phagocytizing shorter asbestos fibers (<60 microm length) or MMVF-10 at a range of concentrations showed no increase in EGF-R protein as determined by immunofluorescence, elongated cells phagocytizing and surrounding longer fibers (> or =60 microm) showed intense staining for EGF-R. In contrast, human A549 lung carcinoma cells showed neither elongation nor increased accumulation of EGF-R protein in response to long fibers. Patterns of aggregation and increases in EGF-R protein in mesothelial cells phagocytizing long asbestos fibers were distinct from diffuse staining of phosphotyrosine residues observed in asbestos-exposed cultures. These studies indicate that aggregation of EGF-R by long fibers may initiate cell signaling cascades important in asbestos-induced mitogenesis and carcinogenesis.

Asbestos↗

PubMedDate not supplied

The relation of exposure to asbestos and smoking habit with pulmonary function tests and chest radiograph.

Environmental cum medical study was conducted in asbestos cement factory. The environment was evaluated for asbestos fiber by the methods recommended by BIS. Total 355 exposed and 312 suitably matched control workers were investigated by spirometer, Wright's peak flow meter and full sized postero-anterior chest radiograph. The levels of asbestos fiber were 2 to 3 times higher than TLV i.e. 2 f/ml in pipe cutting dept., crude fiber grinding inlet count was more than the ACGIH recommended limit i.e. 5 mpccf of air in pipe cutting dept. and silica mill. In the rest of the department, fiber level as well as dust particle count were below prescribed limit. The comparison of mean values of PFT parameters of workers with 16-20 years exposure history with control one was showing statistically significant decline in mean values of FVC only suggesting restrictive type of PFT impairment in this group of workers. But in workers with more than 20 years exposure, the mean values of all the parameters studied were reduced as compared to control one suggesting combined type of PFT impairment. When the mean values of PFT parameters of exposed smokers were compared with exposed non-smokers there was statistically no significant difference. This can be due to marginal contribution of smoking habit in impairment of PFT parameters of exposed smokers. The percentages of workers with parenchymal and pleural changes due to asbestos exposure were nearly two times more in more than 20 years exposure groups as compared to 11-20 years exposure groups. The parenchymal and pleural changes due to asbestos exposure were more common in exposed smokers as compared exposed non-smokers. However the detailed analysis revealed that if smoking contributes to the development of interstitial fibrosis, the contribution is a marginal one in comparison to the effect of asbestos dust exposure.

Adult↗

PubMed1998

Spontaneous and asbestos-induced transformation of mesothelial cells in vitro.

The processes of spontaneous and asbestos-induced transformation of rat mesothelium were studied using cell cultures obtained in the laboratory. The same changes in cell properties were established in both spontaneous and asbestos-induced transformation: change in epidermal growth factor (EGF) response, in some cases appearance of fibroblast-like cells instead of polygonal ones, appearance of multilayer cell growth foci, and ability to grow in semisolid agar. The response to fibroblast growth factor, insulin-like growth factor 1, and insulin did not change during transformation as well as the P450 system activity measured by benz(a)pyrene (BP) and 7,12-dimethylbenzanthracene (DMBA) cytotoxicity. The asbestos-induced transformation began earlier than the spontaneous one. EGF began to stimulate mesothelium proliferation instead of its inhibition at 6-7 passages in the case of asbestos-induced transformation, whereas during spontaneous transformation this change began at 9-10 passages. Elongated rather than polygonal cells appeared at 10-11 instead of 17-18 passages (this morphological change did not take place at all lines studied). The ability to grow in semisolid agar was found at 14-16 passages with asbestos and at 22-24 passages without it. The results allow us to propose the necessity of a positive EGF response for mesothelial cell transformation and the similarity of mechanisms of spontaneous and asbestos-induced transformation.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1995

Synthesis of poly(ADP-ribose) in asbestos treated rat pleural mesothelial cells in culture.

To investigate the origin of DNA repair in rat pleural mesothelial cells (RPMC) exposed to asbestos fibers, poly(ADP-ribose) polymerase (PARP) activity was measured in the asbestos-treated cells. As bleomycin has been shown to activate poly(ADP-ribose) synthesis in several cell systems, the response to bleomycin with regard to PARP assay was first investigated. Bleomycin produced a dose-dependent increase of poly(ADP-ribose) synthesis in RPMC. Likewise both chrysotile and crocidolite fibers produced a concentration-dependent PARP activation indicating that the formation of DNA strand breaks is one type of damage produced by asbestos in RPMC. Enhancement of DNA repair, assessed by the measurement of [3H] methylthymidine incorporation in growth arrested cells, was not detectable in the presence of 3-methoxybenzamide (3-MBA), a PARP inhibitor, confirming a relation between PARP activation and DNA repair. The participation of DNA breakage in asbestos toxicity on RPMC was determined by the colorimetric 3-4(5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. There was no relationship between DNA breakage and cytotoxicity since the use of PARP inhibitors did not change cell viability. These results indicate that asbestos produce DNA damage that is repaired in RPMC.

Animals↗