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PubMed1995

Induction of c-fos and c-jun proto-oncogene expression by asbestos is ameliorated by N-acetyl-L-cysteine in mesothelial cells.

Asbestos fibers cause dose-dependent, persistent increases in mRNA levels of c-jun and c-fos proto-oncogenes in rat pleural mesothelial (RPM) cells, the progenitor cells of asbestos-induced mesothelioma (N. Heintz, Y. M. W. Janssen, and B. T. Mossman. Proc. Natl. Acad. Sci. USA, 90: 3299-3303, 1993). Here we report that addition of N-acetyl-L-cysteine decreases asbestos-mediated induction of c-fos and c-jun mRNA levels in a dose-dependent fashion. Exposure of RPM cells to asbestos causes depletion of total cellular glutathione, a response that can be abolished by pretreatment with N-acetyl-L-cysteine. Pretreatment of cells with buthionine sulfoximine, an agent which diminishes glutathione pools, increases the magnitude of induction of c-fos and c-jun mRNA by asbestos. To determine whether asbestos-induced effects on proto-oncogene expression could be attributed to extracellular generation of active oxygen species (AOS), RPM cells were exposed to H2O2 or xanthine and xanthine oxidase, a generating system of AOS. These oxidant stresses did not decrease cellular glutathione levels nor alter mRNA levels of c-fos or c-jun. However, increased mRNA levels of manganese-containing superoxide dismutase and heme oxygenase were observed, indicating that RPM cells respond to AOS by increased expression of genes encoding antioxidant enzymes. These data indicate that the signaling pathways leading to c-fos/c-jun proto-oncogene induction by asbestos are not triggered directly by formation of extracellular AOS. However, intracellular thiol levels appear to influence the expression of c-fos and c-jun, suggesting a redox-sensitive component in the signaling cascade which modulates gene expression of c-fos and c-jun by asbestos.

Acetylcysteine↗

PubMed1995

Mesothelioma: is asbestos exposure the only cause?

BACKGROUND: Although a causal association between mesothelioma and occupational exposure to asbestos is beyond dispute, nearly all population-based studies of mesothelioma have found some proportion of cases with no history of asbestos exposure. DATA: Incidences of mesothelioma in men and women not occupationally exposed to asbestos for the period 1980-1985 were generated from: (i) estimates of occupational exposure to asbestos in the general male population, obtained from population-based controls in a case-control study of incident cancer in South Australia; and (ii) National Mesothelioma Surveillance Program data. The incidence in men not occupationally exposed was 8.5 per 1,000,000 person-years, compared with 2.6 per 1,000,000 person-years in women, a difference of 5.9 per 1,000,000 person-years (90% confidence interval, 4.8-7.2). CONCLUSION: Mesothelioma without a history of asbestos exposure may be caused by asbestos in the general environment, but this fails to explain why such cases occur more commonly in men. Alternative explanations include the existence of another independent cause of mesothelioma, or of a co-factor which, combined with "environmental" levels of asbestos exposure, constitutes a sufficient cause. Such a risk factor is likely to be occupational, in which case mesothelioma may be expected to occur even after occupational asbestos exposures have been eliminated.

Asbestos↗

PubMed1994

[Malignant mesothelioma in families of asbestos workers].

Malignant mesothelioma is primarily an occupational disease of asbestos workers. While there is usually a latent period of 20-40 years between exposure and appearance of the tumor, the duration of exposure may be as short as a single month. Rarely, it may appear in family members and others living with asbestos workers who might be exposed to asbestos from work clothes during laundering, or from fibers on the skin or hair of the asbestos worker. Attention should therefore be paid to those with nonoccupational contact with asbestos. We report 2 cases of pleural mesothelioma in families of asbestos workers. In both cases the laundering of work clothes was done at home. The first was a 33-year-old man; during his childhood his father worked with asbestos boards for 5 years. The second was a 76-year-old woman whose husband worked in an asbestos factory for 32 years, up to 18 years before diagnosis.

Adult↗

PubMedDate not supplied

[A comparison between phase-contrast optical microscopy and scanning electron microscopy for the analysis of air-borne asbestos fibers in an office environment].

There is no general agreement on the relationship between results obtained by optical microscopy (PCOM) and electron scanning microscopy (SEM) or electron transmission microscopy (TEM) for airborne asbestos fibres. However, a considerable amount of data has been produced in latter years indicating that a general correlation factor, not differing greatly from unity, can be established between the two analytical techniques if counts are limited to fibres longer than 5 microns. A study was made of the relationship between SEM and PCOM when used simultaneously for determination of background concentrations of asbestos in office buildings. Twenty-four couples of samples were collected in parallel for PCOM and SEM in different locations distributed over the various floors of two buildings containing amosite sprayed on structural parts. Asbestos and total fibre counts by SEM were performed following the Verein Deutscher Ingenieure (VDI) method 3492. For total fibre counts the European PCOM method was mainly used. Discrimination of asbestos from non-asbestos fibres was performed using criteria based on birefringence and morphological characteristics of fibres. Counts included only those fibres longer than 5 microns, diameter less than 3 microns and aspect ratio greater than 3. Both total fibres and asbestos fibres were recorded separately by PCOM and SEM. the arithmetic and geometric means of the ratio between PCOM and SEM were 1.3 and 1.1 respectively for total fibres and 1.2 and 1.1 for asbestos fibres (excluding one outlying value). The regression study showed a significant linear correlation (P = 0.01) with correlation coefficients of 0.84 for asbestos fibres and 0.52 for total fibres.

Air Pollution, Indoor↗

PubMed1995

Malignant mesothelioma associated with low pulmonary tissue asbestos burdens: a light and scanning electron microscopic analysis of 18 cases.

Most malignant mesothelioma cases are associated with pulmonary asbestos body (AB) counts significantly greater than those of the general population. However, the question remains whether malignant mesothelioma cases associated with "normal" AB counts (i.e., indistinguishable from the general population) represent background incidence levels or are, actually, asbestos related. We performed AB counts (by light microscopy) and mineral fiber analysis (by scanning electron microscopy) in 18 mesothelioma cases with AB counts within our normal range (0 to 20 AB/G wet lung) and in 19 "control" cases. Our study demonstrated that approximately one-third (6 of 18) of the mesothelioma cases have asbestos fiber burdens greater than 95% of the control levels. These results suggest that these six mesothelioma cases may be asbestos related despite AB counts similar to those of the general population. An asbestos etiology was suggested in three additional cases, but too few amphibole fibers were identified in these cases to be certain of a value above background. The remaining nine cases showed no evidence of an asbestos etiology. Electron microscopic analysis of pulmonary mineral fibers may be required to differentiate asbestos-related mesotheliomas from non-asbestos-related cases when AB counts are within the range of background values.

Adult↗

PubMed1996

[Exposure to asbestos and levels of selected tumor biomarkers].

Occupational exposure to asbestos, a recognised carcinogen, poses a risk for such diseases as asbestosis, lung cancer and mesothelioma. It is thought that asbestos fibres may damage microphages which undergo neoplastic transformation as well as fibroblast, while partial phagocytosis may generate free oxygenic radicals which induce cellular peroxidase and damage macromolecules. A search for cellular changes or changes in cellular metabolism products, present in biological fluids, in order to detect early stages of a neoplastic process is an important factor in the prophylaxis of workers exposed to asbestos. Neoplastic biomarkers such as tissue polypeptide antigen (TPA) or carcinoembryonic antigen (CEA) are now used for this purpose. The aim of the work was to identify workers exposed to asbestos in the population, especially high risk groups neoplastic diseases and to evaluate the usefulness of TPA and CEA determinations. The study covered a group of asbestos exposed workers (n = 4000 and the control group of workers (n = 135) nonexposed to any toxic factor at work. Age, exposure time, smoking habits and workpost characteristics were taken into consideration in the analysis of the results. It was revealed that in 38 persons exposed to asbestos, TPA values were above the concentration limit set on the basis of studies carried out in the control group, and elevated CEA values applied to 13 persons. Significant differences between groups under study were found in the proportion of pathological TPA values. Such a relationship was not observed in regard to CEA values. In the exposed group the results also indicated an evident effect of age and exposure time on the number of persons with TPA values above concentration limit. There is a growing tendency in those changes but only in regard to TPA values. The effect of smoking on the frequency of pathological TPA values was also clear-cut in workers exposed to asbestos. Taking into account three types of employment: blue collar workers, white collar workers and other personnel, the analysis indicated significant differences in TPA values between blue collar workers and other personnel; and between white collar workers and other personnel. This means a similar percentage of pathological TPA values in the group of blue collar and white collar workers. The study carried out allowed to identify persons exposed to asbestos who should be covered with targeted medical care. They also proved that TPA biomarker is better than CEA one for this kind of studies.

Adult↗

PubMed1997

Asbestos causes translocation of p65 protein and increases NF-kappa B DNA binding activity in rat lung epithelial and pleural mesothelial cells.

The mechanisms of cell signaling and altered gene expression by asbestos, a potent inflammatory, fibrogenic, and carcinogenic agent, are unclear. Activation of the transcription factor, nuclear factor (NF)-kappa B, is critical in up-regulating the expression of many genes linked to inflammation and proliferation. Inhalation models of crocidolite- and chrysotile-induced inflammation and asbestosis were used to study the localization of p65, a protein subunit of the NF-kappa B transcription factor, in sham control rats and those exposed to asbestos. In addition, we investigated, using electrophoretic mobility shift analysis, whether in vitro exposure of rat lung epithelial cells and rat pleural mesothelial cells to asbestos increased binding of nuclear proteins, including p65, to the NF-kappa B DNA response element. Furthermore, translocation of p65 into the nucleus was determined by confocal microscopy. In comparison with sham animals, striking increases in p65 immunofluorescence were observed in airway epithelial cells of rats at 5 days after inhalation of asbestos. These increases were diminished by 20 days, the time period necessary for development of fibrotic lesions. In contrast, although inter-animal variability was observed, immunoreactivity for p65 was more dramatic in the interstitial compartment of asbestos-exposed rat lungs at both 5 and 20 days. Changes in p65 expression in pleural mesothelial cells exposed to asbestos in inhalation experiments were unremarkable. Exposure to asbestos also caused significant increases in nuclear protein complexes that bind the NF-kappa B consensus DNA sequence in both rat lung epithelial and rat pleural mesothelial cells. Using confocal microscopy, we observed partial nuclear translocation of p65 in rat pleural mesothelial cells exposed to asbestos. This partial response contrasted with the effects of lipopolysaccharide, which caused rapid and complete translocation of p65 from cytoplasm to nucleus. Our studies are the first to show the presence of the NF-kappa B system in lung tissue and evidence of activation in vitro and in vivo after exposure to a potent inflammatory, fibrinogenic, and carcinogenic environmental agent.

Animals↗

PubMed1997

[The clinical utility of asbestos body counts in bronchoalveolar lavage fluid].

To assess the clinical utility of measuring the number of asbestos bodies (AB) present in bronchoalveolar lavage fluid (BALF), we counted the number of AB in BALF from 119 subjects using light microscopy. The results were analyzed according to occupational histories, radiological findings of asbestos-induced lung and pleural changes, and asbestos-related diseases. The 94 subjects in group 1 had a history of dust exposure, whereas group 2 subjects (n = 25) had no dust exposure. Group 1 was subdivided into subjects with obvious exposure to asbestos (group 1A, n = 61), and subjects with no known exposure to asbestos (group 1B, n = 33). The distribution of AB counts per ml of BALF (means +/- SEM) differed significantly between groups 1 and 2 (38.8 +/- 17.4 vs 0.06 +/- 0.04, p < 0.0001). The AB counts were significantly different between groups 1A and 1B (57.9 +/- 26.6 vs 3.4 +/- 1.2, p = 0.01). Subject, exposed to dust who had radiological evidence of pleural thickening had significantly higher AB counts than subjects in whom pleural thickening was absent (66.0 +/- 31.1 vs 5.1 +/- 4.2, p = 0.03). In group 1, the BALF was positive for AB in 7 of 14 patients with pulmonary fibrosis, 4 of 5 patients with lung cancer, all 6 patients with malignant mesothelioma, and all 4 patients with benign asbestos pleural effusion. We conclude that AB counts in BALF are useful for evaluating both the history of asbestos exposure in a population exposed to dust, as well as patients having asbestos-related diseases.

Adult↗

PubMedDate not supplied

[Malignant mesothelioma of the pleura with etiological association to asbestos: report of 3 clinical cases].

UNLABELLED: Diffuse Malign Mesotheliomas (DMM) has a low background prevalence. High incidences of this tumor have been related to asbestos exposure in the past. PURPOSE: To describe and discuss three clinical cases treated in our hospital, in which precise histopathologic diagnosis was made, and detailed occupational and environmental histories were taken, trying to identify in their past some kind of asbestos exposure. METHODS: Three cases of DMM are described. Diagnosis was confirmed by histochemical analysis and electronmicroscopy. Detailed occupational and environmental histories were taken from subjects and their families, searching for past contact with asbestos. RESULTS: The cases were diagnosed in a short period of time (two years), in a region of the country where many asbestos cement plants are located since the mid sixties. Skillful histological procedures were used. From these cases we found out that one had a twelve months period of exposure, 24 years before, in one of those plants. Another patient had an exposure for three years, as a bystander, in the same plant (also 24 years before) and a third patient was contaminated by asbestos brought home by his father in the 1950s (latency period of 30 years). All cases were histochemically studied and diagnosis confirmed by the presence of microvilli at electronmicroscopic examination. CONCLUSIONS: These three cases seem to confirm the existence of the epidemiologic association with asbestos exposure in our country. Definition of diagnosis criteria, centralization of cases registry and the necessity of more attention to this kind of asbestos related disease are discussed and stressed, as many new cases like those described are thought to occur in the near future, as the latency period of the disease seems to match with that of industrial asbestos manipulation in Brazil.

Adult↗

PubMed1984

Malignant mesothelioma induced by asbestos and zeolite in the mouse peritoneal cavity.

The carcinogenicity of asbestos (amosite and chrysotile) and zeolite (fibrous erionite, mordenite, and synthetic zeolite 4A) were studied in the peritoneum of 586 BALB/C male mice after a single intraperitoneal or intraabdominal wall injection. As controls, 182 mice treated with and without saline solution were used. Both asbestos types and fibrous erionite frequently produced malignant peritoneal tumors after long latency; tumors developed in 93 of 394 animals (23.6%) treated with asbestos or fibrous erionite 7 months or more after administration. All of the induced peritoneal tumors were intimately associated with marked peritoneal fibrosis, in which asbestos or erionite fibers were regularly detected. Histopathologically, 83 (73 fibrous, 9 biphasic, and 1 epithelial) of 93 were consistent with malignant mesotheliomas. Other tumors consisted of 6 plasmacytomas, 1 histiocytoma, 1 liposarcoma, 1 osteosarcoma, and 1 adenocarcinoma of the pancreas. Two of the cases of mesotheliomas were associated with plasmacytoma. In many instances, the primary site of the mesotheliomas seemed to be multiple, the favorite sites being the omentum, mesentery, serosae of the gastrointestinal and genital organs, the diaphragm, the capsule of the liver and spleen, and the abdominal wall peritoneum. In these cases, asbestos or erionite-tissue burden followed by fibrosis was frequently observed. In addition to the 93 peritoneal tumors, 3 extraperitoneal tumors (1 fibrosarcoma and 2 rhabdomyosarcomas) were induced by amosite which was probably accidentally injected into the extraperitoneal connective tissue and the striated muscle tissue of the abdominal wall, respectively. These three tumors were also intimately associated with focal fibrosis in which amosite fibers were detected. Among the three different types of zeolite, only fibrous erionite showed striking carcinogenicity and marked fibrogenicity. The erionite-induced mesotheliomas were similar to those induced by asbestos in exhibiting long latency, in gross appearance, in histology, and in close association with fibrosis. Long-term persistence of asbestos or fibrous erionite around progenitor cells of the induced tumors and the consequent fibrosis seemed to be an important precondition of the malignant transformation of the progenitor cells.

Aluminum Silicates↗

PubMed2002

Smoking enhances asbestos-induced genotoxicity, relative involvement of chromosome 1: a study using multicolor FISH with tandem labeling.

Several experimental and epidermological studies have indicated augmentation of asbestos induced diseases by cigarette smoke by the mechanisms, which are still unknown. To determine whether smoking affects genetic system of the cells and further modifies asbestos induced genotoxicity, whole blood from non-smokers and smokers was exposed to asbestos fibres separately in vitro and micronucleus test was performed. The number of micronuclei was found to be significantly higher (P<0 05) in cases of smoker's lymphocytes, asbestos exposed non-smokers lymphocytes as well as asbestos exposed smokers lymphocytes, as compared with unexposed non-smokers lymphocytes. Further we investigated involvement of chromosome 1 in the damaging process using multicolor FISH technique. FISH is fast and reliable method, distinguishing both structural and numerical alterations. The centric/pericentric regions of chromosome 1 (cen-q12) were labeled, as the pericentric heterochromatin region 1 (q12) is quite large, highly repetitive and prone to breakage. Multicolor FISH assay suggested that the genetic damage by asbestos fibres mainly involve chromosome 1 but in case of cigarette smoking the damage is not strictly connected to chromosome 1 only, but also involves damage to other chromosomes. Further the study suggested that smoking makes genetic system of the cells more vulnerable to the deleterious effects of asbestos.

Adult↗

PubMed2000

Asbestos exposure induces MCP-1 secretion by pleural mesothelial cells.

We showed previously that both crocidolite and chrysotile asbestos inhalation induced a persistent macrophage inflammatory response within the pleural space of the rat. We postulated that the stimulus for pleural macrophage recruitment after asbestos exposure was the induction of monocyte chemoattractant protein-1 (MCP-1) synthesis by pleural mesothelial cells. To test this hypothesis, rat pleural mesothelial cells (RPMC) were cultured with or without chrysotile or crocidolite asbestos fibers (8 micrograms/cm2) in the presence (50 ng/mL) or absence of either tumor necrosis factor-alpha (TNF-alpha) or interleukin-1 beta (IL-1 beta). MCP-1 mRNA expression was assessed by RT-PCR in RPMC cultured for 2 to 24 hours, and MCP-1 protein secretion was measured by ELISA in conditioned medium from 24-hour and 48-hour cultures. Crocidolite and chrysotile fibers induced MCP-1 mRNA expression in RPMC which was maximal after 12 hours in the absence of cytokines, but which peaked after 2 hours when RPMC were challenged with asbestos + TNF-alpha or IL-1 beta. Both types of asbestos also significantly increased MCP-1 protein secretion after 24 and 48 hours (P < .0001), an effect that was potentiated by cytokine stimulation. Rats exposed by inhalation to either chrysotile or crocidolite asbestos fibers also had greater amounts of MCP-1 protein in their pleural lavage fluid than did sham-exposed rats. These findings suggest that MCP-1 secretion by RPMC may have a role in the initiation and/or potentiation of asbestos-induced pleural injury.

Animals↗

PubMed1990

Modification of asbestos bioactivity for the alveolar macrophage by selective protein adsorption.

The bioactivity of an inhaled particulate is likely to be influenced significantly by the adsorption of proteins and lipids from the fluid lining the respiratory tract. We have shown previously in vitro that the presence of immunoglobulin G, a protein constituent of the lining fluid, significantly and specifically enhances the response of the guinea pig alveolar macrophage to chrysotile, but not crocidolite, asbestos. In order to understand the differential response of the guinea pig alveolar macrophage to chrysotile and crocidolite, as well as to obtain a better understanding of the factors that determine the adsorption of proteins onto asbestos, we have quantitated the adsorption of model proteins, including IgG, onto asbestos. The apparent surface density to which a given protein adsorbed was found to be influenced significantly by the surface charge of the asbestos, by the net protein charge, i.e., its isoelectric point (pI), and most dramatically, by the presence of other proteins. Thus, for example, even when guinea pig IgG (gpIgG; pI approximately 8.5) and bovine serum albumin (BSA; pI = 4.8) were present together at a high molar ratio of BSA to gpIgG, gpIgG was selectively adsorbed on negatively charged crocidolite asbestos. An analogous result was found for the adsorption of gpIgG and cytochrome c (CYT; pI = 10) on positively charged chrysotile asbestos, i.e., even at high molar ratios of CYT to gpIgG, gpIgG was selectively adsorbed. This latter result provides an explanation for the differential bioactivities of chrysotile and crocidolite asbestos previously noted in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Adsorption↗

PubMed1991

In vitro bioactivity of asbestos for the human alveolar macrophage and its modification by IgG.

The alveolar macrophage (AM) is likely to play a central role in the initiation and development of the fibrosis associated with asbestos exposure due to its ability to produce factors that modulate cellular functions of the immune system of the lung. In this study, we examine the effects of IgG, albumin, and dipalmitoylphosphatidylcholine (DPPC), the major protein and lipid constituents of alveolar lining fluid, on the interaction between the human AM and chrysotile and crocidolite asbestos, silica, and aluminum beads. We show that both chrysotile and crocidolite asbestos, but not silica and aluminum beads, stimulate the human AM to produce superoxide anion. Preincubating chrysotile and crocidolite asbestos with IgG resulted in an enhancement of their ability to stimulate superoxide anion production. IgG subclasses were studied to determine the subclass specificity of this enhancing effect; on a molar basis, IgG1 was the most potent. After preincubation with IgG, both silica and aluminum also stimulated superoxide anion production to levels similar to the IgG-preincubated asbestos. When albumin and DPPC were included in the preincubation mixture, the IgG-mediated enhancement of superoxide anion production by asbestos was unaffected, while that of silica and aluminum was abolished. In summary, these results indicate that IgG can significantly enhance the bioactivity of particulates for human AM in vitro, and that chrysotile and crocidolite asbestos are unique in their ability to retain this enhancement in the presence of albumin and DPPC. These results are consistent with the suggestion that superoxide anion production by the AM may play an important role in the development of asbestosis.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed1983

Effects of crocidolite and chrysotile asbestos on cellular uptake and metabolism of benzo(a)pyrene in hamster tracheal epithelial cells.

The incidence of bronchogenic carcinoma is increased substantially in asbestos workers who smoke. We used several approaches to determine possible mechanisms of synergism at the cellular level between asbestos and the polycyclic aromatic hydrocarbon (PAH), benzo(a)pyrene (BaP), a chemical carcinogen in cigarette smoke. Specifically, we hypothesized that cellular uptake and metabolism of BaP might be facilitated when the hydrocarbon was coated on asbestos. In addition, we were interested in whether asbestos, alone or in combination with BaP, caused single strand breakage of DNA in epithelial cells of the airway. UICC reference samples of crocidolite and chrysotile were coated with 3H-BaP before their addition to monolayers of hamster tracheal epithelial cells. In comparative studies, 3H-BaP at identical amounts was added to cells in culture medium. At intervals thereafter, uptake of BaP by cells was documented by scintillation spectrometry and by autoradiography. In addition, cells and media were assayed by use of high pressure liquid chromatography (HPLC) to demonstrate the water-soluble metabolites of BaP. The integrity of DNA was monitored by alkaline elution at intervals after exposure of tracheal cells to various concentrations of asbestos, BaP and BaP-coated asbestos. A rapid transfer of BaP to cells occurred after addition of BaP-coated asbestos to cultures. When BaP was adsorbed to both types of fibers before their addition to cultures, 70% of the total BaP introduced entered the cell within 1 hr; 50% remained intracellular after 8 hr. In contrast, if identical amounts of BaP were added directly to medium, an initial influx of 20% was observed and cells retained only 5% of the initial amount at 8 hr.(ABSTRACT TRUNCATED AT 250 WORDS)

Adsorption↗

PubMed1987

Visceral pleural thickening in asbestos exposure: the occurrence and implications of thickened interlobar fissures.

We evaluated fissural (ie, visceral pleural) thickening on radiographs in two asbestos-exposed study populations and a control group. Asbestos workers had an incidence of fissural thickening of 54.5% compared with 16.0% in the unexposed control group, with a strong positive statistical effect due to asbestos exposure beyond that attributable to age. Fissural thickening occurred in 85% of workers with parietal plaques and in 36% without pleural plaques. Fissural thickening occurred in 45% without radiographic evidence of pulmonary fibrosis, but it was very common (85%) in those with pulmonary fibrosis. Data analysis showed that fissural thickening responds more strongly to asbestos exposure than does plaque formation, with 21 years of asbestos exposure needed for a 50% chance of developing fissural thickening, while 31 years of exposure were needed for a 50% chance of forming pleural plaques. From a second group of 57 asbestos workers evaluated clinically, 8 were diagnosed as having asbestosis with radiographically clear lungs and fissural thickening. We conclude that visceral pleural thickening is common in asbestos exposure, that it is related to the years since first asbestos exposure, and that its presence may indicate the presence of pulmonary asbestosis, even with radiographically normal lungs.

Asbestosis↗

PubMed1988

NTP Toxicology and Carcinogenesis Studies of Crocidolite Asbestos (CAS No. 12001-28-4) In F344/N Rats (Feed Studies).

Carcinogenesis studies of crocidolite asbestos were conducted with male and female F344/N rats. This form of asbestos was administered at a concentration of 1% in pelleted diet for the lifetime of the rats, starting with the dams of the study animals. The studies were started in January 1978 and ended in December 1980. Group sizes were 118 for male and female controls and 250 for male and female crocidolite asbestos-exposed rats. The offspring from mothers exposed to crocidolite asbestos and the controls were similar in size at birth but were slightly smaller at weaning and remained so throughout their life. Feed consumption and survival were comparable in the exposed and control groups. No overt toxicity was observed in the crocidolite asbestos-exposed animals. There was an elevated (P<0.05) incidence of thyroid gland C-cell adenomas (control, 4/117, 3%, vs. exposed, 23/250, 9%) and of thyroid gland C-cell carcinomas (12/117, 10%, vs. 46/250, 18%) in crocidolite asbestos-exposed female rats relative to concurrent controls. Because these control incidences were low relative to control incidences observed in other contemporary studies at this laboratory (21% for thyroid gland C-cell tumors), this slight increase was not regarded as being biologically important. The data, documents, and pathology materials from the lifetime studies of crocidolite asbestos have been audited. The audit findings show that the conduct of these studies is documented adequately and support the data and results presented in this Technical Report. Conclusions: Under the conditions of these feed studies, crocidolite asbestos was not overtly toxic and did not cause a carcinogenic response when ingested at a concentration of 1% in the diet by male and female F344/N rats for their lifetime. Levels of Evidence of Carcinogenicity: Male Rats: Negative Female Rats: Negative

Journal Article↗

PubMed1996

Chrysotile asbestos is the main cause of pleural mesothelioma.

In contrast to amphibole forms of asbestos, chrysotile asbestos is often claimed to be only a minor cause of malignant pleural mesothelioma, a highly fatal cancer of the lining of the thoracic cavity. In this article we examine the evidence from animal and human studies that relates to this issue. Reported data do not support widely quoted views regarding the relative inertness of chrysotile fibers in mesothelioma causation. In fact, examination of all pertinent studies makes it clear that chrysotile asbestos is similar in potency to amphibole asbestos. Since asbestos is the major cause of mesothelioma, and chrysotile constitutes 95% of all asbestos use world wide, it can be concluded that chrysotile asbestos is the main cause of pleural mesothelioma in humans.

Air Pollutants, Occupational↗