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PubMed1983

Fibre type and concentration in the lungs of workers in an asbestos cement factory.

The predominant asbestos fibre type used in the production of asbestos cement is chrysotile. The use of asbestos in relation to fibre type in a Norwegian asbestos cement plant during 1942-80 was 91.7% chrysotile, 3.1% amosite, 4.1% crocidolite, and 1.1% anthophyllite respectively. Electron microscopy and x ray microanalysis of lung tissue samples of asbestos cement workers who had died of malignant pleural mesothelioma or bronchogenic carcinoma showed a completely inverse ratio with regard to fibre type. The percentage of chrysotile asbestos in lung tissue varied between 0% and 9% whereas the corresponding numbers for the amphiboles were 76% and 99%. These differences are discussed with respect to the behaviour of different fibre types in the human body and to the occurrence of malignant mesothelioma in this asbestos cement factory.

Aged↗

PubMedDate not supplied

Asbestos and cancer in Finland.

Primary prevention carried out today can reduce the disease incidence in the future decades. The present disease panorama is the consequence of past asbestos exposure mainly before the 1970s. The peak incidence of asbestos-induced diseases will be reached around 2010 in Finland. The number of asbestos-related premature deaths is at present annually about 150 which exceeds the figure of fatal work accidents. Asbestos-related cancer will increase still for 15-20 years and reach its maximum, about 300 cases, in 2010, and will start to decrease after that. More than 20,000 asbestos-exposed workers have participated in the medical screening and follow-up. The termination of exposure, antismoking campaigns, improved diagnostics and careful attention to compensation issues, as well as other potentials for prevention, were the central issue of the Asbestos Program of the Finnish Institute of Occupational Health. An important objective of research work is to improve early diagnostics, and thereby treatment prospects, in case of asbestos-induced cancers.

Age Factors↗

PubMed1996

Comparative proliferative and histopathologic changes in rat lungs after inhalation of chrysotile or crocidolite asbestos.

Patterns of cell proliferation in lung and pleura and development of histopathologic lesions were studied in lungs from Fischer 344 rats after inhalation exposure to chrysotile or crocidolite asbestos at average airborne concentrations of approximately 8 mg/m3 air for 5 and 20 days and after 20 days of exposure followed by an additional 20 days in room air (20 + 20 days). To assess cell proliferation rats were injected with 5-bromo-2'-deoxyuridine (BrdU) at various time points after initiation of exposure to asbestos. Image analysis was used to quantitate the effects of chrysotile and crocidolite on BrdU labeling indices in the following lung compartments: (1) interstitium, (2) alveolar duct region, (3) bronchial epithelium, and (4) visceral mesothelium. With the exception of mesothelium, which exhibited significant increases in BrdU incorporation in rats exposed to crocidolite at 20 + 20 days, asbestos-induced elevations in BrdU uptake in other compartments were transient with labeling comparable to sham controls at later time points. Histopathology of rat lungs revealed fibrotic lesions of a greater extent and severity at 20 days in rats exposed to crocidolite, but fibrosis occurred in both asbestos-exposed groups after an additional 20 days in clean air (20 + 20). Quantification of fiber burden in rat lung after inhalation of comparable airborne concentrations of either fiber type demonstrated that inhalation of crocidolite asbestos led to a higher fiber retention when compared to chrysotile asbestos. Our results indicate that chrysotile and crocidolite asbestos induce different patterns of cell proliferation in lung and pleural cells. The protracted increases in BrdU labeling of mesothelial cells by crocidolite may reflect increased retention of fibers and/or inherent differences between types of asbestos.

Administration, Inhalation↗

PubMed1994

Oxidant stress responses in human pleural mesothelial cells exposed to asbestos.

The generation of oxidants is a proposed mechanism of cell injury by asbestos fibers. To determine whether human pleural mesothelial cells (HMC) respond to asbestos and active oxygen species (AOS) by induction of antioxidant enzymes, cells obtained from pleural effusion were exposed to crocidolite or chrysotile asbestos or xanthine/xanthine oxidase (X/XO), a chemical-generating system of AOS. Gene expression of manganese-containing superoxide dismutase (MnSOD) and heme oxygenase (HO), endogenous enzymes involved in cell defense against oxidant stresses, was then determined. Dosage-dependent increases in steady-state mRNA levels of MnSOD and HO were observed in HMC exposed to asbestos or X/XO. However, increases in gene expression of MnSOD or HO did not occur in HMC after exposure to particulates such as polystyrene beads or riebeckite, the nonfibrous analog of crocidolite asbestos. Comparative experiments with human adult lung fibroblasts (HAL) showed less striking increases in mRNA levels of MnSOD and HO in response to asbestos, but steady-state mRNA levels for HO were increased more than fivefold in response to X/XO. To determine whether increases in mRNA levels of MnSOD were translated into protein, Western blot analyses were performed on HMC and HAL cells exposed to asbestos or X/XO. Slight increases in MnSOD immunoreactive protein were observed in HMC in response to both agents. In contrast, X/XO caused striking elevations in MnSOD protein levels in HAL cells. These results suggest that certain antioxidant enzymes are inducible in HMC after exposure to asbestos and other oxidants.

Asbestos, Crocidolite↗

PubMed1986

Smoking inhibits asbestos clearance.

To determine whether smoking affects the clearance of asbestos fibers, guinea pigs were given amosite asbestos by intratracheal instillation and divided into 3 groups: (1) nonsmokers, (2) animals exposed to smoke only after asbestos instillation, and (3) animals exposed to smoke both before and after asbestos instillation. Asbestos fiber concentrations and sizes were measured at 1 wk and 1 month after exposure. Between 1 wk and 1 month the asbestos burden in nonsmokers decreased on average 6-fold, whereas both smoking groups failed to show a significant decrease. Over this time period, the mean length of retained fibers increased in the nonsmokers but decreased in both smoking groups. This phenomenon was seen in tissue samples and lavage samples, although lavaged fibers were consistently shorter than tissue fibers. We conclude that in this model, cigarette smoking impedes asbestos clearance, largely by increasing retention of short fibers. This increased pulmonary fiber burden may be important in the increased disease rate seen in asbestos workers who smoke.

Animals↗

PubMedDate not supplied

[Asbestos and disease: review of the scientific knowledge and a rationale for urgent change in the current Brazilian policy about this question].

This paper is a state-of-the-art review of scientific knowledge on both the health effects of asbestos fiber inhalation and possibilities for safe and sustainable prevention, from an ethical, political, and technological point of view. The author provides scientific background and arguments from the ongoing discussion in Brazil concerning the need to redefine current asbestos policy, in order to establish a more advanced and appropriate policy whose priority is the protection of life, human health, and the environment. The first part deals with several technological and economic aspects of asbestos-chrysotile. In the second part, the author presents and discusses a bibliographic review of the construction of scientific knowledge on the health effects of asbestos fibers, first within an international perspective, and then (in the third part), from a Brazilian view. The fourth part analyzes the current debate on the fibrogenicity and carcinogenicity of asbestos-chrysotile. Some current responses from the international community towards the asbestos-chrysotile ban are also discussed. Finally, the author discusses the historical inadequacy of Brazilian asbestos policy and the urgent need to revise it to include a ban on asbestos-chrysotile in this country.

Asbestos↗

PubMed2000

[Chrysotile asbestos: biological effects, the work environment highest allowable concentration and neoplasm risk].

The authors present the most essential data on physical and chemical properties of chrysotile, sources of its emission, the extent of occupational exposure, and biological effect, used in setting MAC values for chrysotile-containing dusts. Exploitable asbestos deposits do not exist in Poland, but admixtures of asbestos minerals have been found in some deposits of mineral raw materials located in the area of Lower Silesia (melafir, gabbro, dolomite. ore, nickel, magnesite, serpentinite). In the 1970s, about 100,000 tonnes of asbestos, containing 90% of chrysotile, were used annually in Poland. This figure decreased to 30,000 tonnes in 1991. In 1985 the use of crocidolite asbestos was stopped, and in 1999, the use of asbestos-containing products was banned by the virtue of the legal act. At present, the Minister of Economy in agreement with the Minister of Environmental Protection sets regularly the list of asbestos-containing products permitted for the production or in the customs area. Nowadays, the range of dust concentrations in plants which use asbestos products amounts to 0.1-0.6 mg/m3 for total dust and 0.002-0.07 f/cm3 for respirable mineral fibres; and during exploitation of rock raw material deposits 0.7-280 mg/m3, and 0.01-3.3 f/cm3, respectively. During the years 1976-96, 1520 cases of asbestos-related occupational diseases were diagnosed. This figure included 1314 cases of asbestosis, 154 cases of lung cancer and 52 cases of pleura mesothelioma. MAC values for chrysotile and chrysotile-containing dusts are: 0.2 f/cm3 and 1 mg/m3.

Asbestos↗

PubMed1982

Alteration of in vitro immunoglobulin secretion by amosite asbestos.

We investigated the in vitro effects of amosite asbestos on immunoglobulin (Ig) secretion by human peripheral blood mononuclear leukocytes (MNL). Concentrations of 100 to 300 micrograms/ml of amosite asbestos reduced the number of Ig-secreting cells recovered from 6-day cultures of unstimulated MNL or MNL stimulated with Epstein Barr virus. By contrast, the Ig secretory response to pokeweed mitogen was enhanced by 10 to 100 micrograms/ml concentrations of amosite asbestos; however, amosite asbestos no longer enhanced the response to pokeweed mitogen when MNL were first partially depleted of monocytes (to less than 2%) esterase-positive cells remaining). These results indicate that amosite asbestos has multiple effects on the cells involved in Ig secretion: 1) amosite asbestos inhibits unstimulated B cell function; 2) amosite asbestos inhibits the function of B cells stimulated with the direct B cell activator Epstein Barr virus; and 3) amosite asbestos may alter regulator monocyte function allowing enhanced Ig secretion in the presence of monocyte-dependent B cell triggers such as pokeweed mitogen.

Antibody Formation↗

PubMed2004

Chrysophiles versus chrysophobes: the white asbestos controversy, 1950s-2004.

In the first half of the twentieth century, asbestos was a controversial mineral because of its association with asbestosis and asbestos-related lung cancer. It has proved no less so since the 1960s, when another asbestos cancer, mesothelioma, was identified. Mesothelioma appeared to be more strongly linked with blue asbestos (crocidolite) than with the other asbestos varieties, brown (amosite) and white (chrysotile). This finding triggered a fierce debate between "chrysophiles" (those who declared chrysotile innocuous) and "chrysophobes" (those who believed it was a mortal hazard). This essay attempts the first history of the chrysotile controversy, which shows that a scientific consensus on the safety of white asbestos was very slow to emerge. This was only partly due to the complexities of scientific research. Political, economic, and social factors have militated against a speedy resolution of the debate, facilitating the continued production and use of asbestos in the developing world.

Asbestos↗

PubMed1994

Interleukin-1-mediated release of interleukin-8 by asbestos-stimulated human pleural mesothelial cells.

The pleuropulmonary response to inhaled asbestos frequently involves inflammation and release of various cytokines from lung cells. Among these, interleukin-8 (IL-8) released from the mesothelium could augment inflammation of the pleura by attracting neutrophils to the pleural space. We used cultures of human pleural mesothelial cells (HPMC) to examine the mechanism of IL-8 production by asbestos and cytokines. Suspensions of amosite, chrysotile, or crocidolite asbestos in concentrations as low as 5 micrograms/ml enhanced release of IL-8 from HPMC during 6 h of incubation at 37 degrees C. Electron microscopy of asbestos-treated HPMC showed that the cells avidly engulfed each of the different types of asbestos fibers. Two proinflammatory cytokines, interleukin-1 alpha (IL-1 alpha) and tumor necrosis factor-alpha, enhanced IL-8 release within 2 h and had an even greater effect after 6 h. Release of IL-8 was measured by an enzyme-linked immunosorbent assay, and functional activity of the cytokine was assessed by chemotaxis of human neutrophils. Identity of IL-8 in HPMC supernatants was established by absorption with an antibody to IL-8. Preincubation of HPMC with IL-1 receptor antagonist (IL-1ra) significantly decreased release of IL-8 after stimulation with amosite or crocidolite asbestos. We conclude that HPMC release IL-8 in response to asbestos stimulation and that the response is, in part, mediated by IL-1, mainly in the form of IL-1 alpha.

Antibodies, Monoclonal↗

PubMed1998

Asbestos exposure: a potential cause of retroperitoneal fibrosis.

The etiology of retroperitoneal fibrosis is unknown in 70% of the cases. The aim of our study was to examine the possible association between occupational asbestos exposure and retroperitoneal fibrosis; only two cases have been reported in the literature. We gathered all the cases of retroperitoneal fibrosis diagnosed in the Tampere University Hospital between 1987 and 1995. We examined their hospital records to evaluate the possible etiology of the disease. We also sent a structured questionnaire to all living patients (10/13) to obtain information on their asbestos exposure. The chest radiographs of the patients were re-read to evaluate possible changes resulting from asbestos exposure. We found 13 cases of idiopathic retroperitoneal fibrosis. Seven patients (all male) had been exposed to asbestos in the past. The chest radiographs of the four most-exposed patients showed characteristic asbestos-related abnormalities, including bilateral pleural plaques, round atelectasis and small irregular lung opacities. In our study, we found that asbestos exposure and asbestos-induced changes in the lung and pleura were common among male retroperitoneal fibrosis patients. We suggest that occupational exposure to asbestos may be an important etiological factor for retroperitoneal fibrosis.

Adult↗

PubMed2002

Association between asbestos exposure, cigarette smoking, myeloperoxidase (MPO) genotypes, and lung cancer risk.

BACKGROUND: As observed in tobacco-associated carcinogenesis, genetic factors such as the polymorphic metabolic/oxidative enzyme myeloperoxidase (MPO) could modulate individual susceptibility to asbestos-associated carcinogenesis. METHODS: RFLP-PCR analysis identified the MPO genotypes in 375 Caucasian lung cancer cases and 378 matched controls. An epidemiological interview elicited detailed information regarding smoking history and occupational history and exposures. RESULTS: Asbestos exposure was associated with a significantly elevated risk estimate (OR = 1.45; 95% CI 1.04-2.02). On stratified analysis, we found the MPO genotypes modified the effect of asbestos exposure on lung cancer risk. Specifically, G/G carriers who were exposed to asbestos had an odds ratio (OR) of 1.72 (95% CI; 1.09-2.66), while A-allele carriers (G/A + A/A) exposed to asbestos exhibited a reduced OR of 0.89 (95% CI; 0.56-1.44). The OR was further reduced to 0.73 (0.49-1.06) for A-allele carriers not exposed to asbestos. A similar trend was observed for the joint effects between the MPO genotypes and pack-years smoking. Next, all three risk factors (MPO genotypes, asbestos exposure, and smoking) were analyzed simultaneously for joint effects. Heavy smokers with the G/G genotype and a history of asbestos exposure demonstrated a statistically significant elevated risk estimate (OR = 2.19; 95% CI 1.16-4.11), while the A-allele carriers with the same exposure profile were at a lower risk for lung cancer (OR = 1.18; 95% CI 0.58-2.38). The A-allele genotypes demonstrated similar protective effects for the other three exposure profiles. CONCLUSIONS: For a similar level of exposure to established carcinogens, individuals with the MPO A-allele genotypes appear to have a reduced risk of lung cancer.

Aged↗

PubMed1989

Asbestos and kidney cancer: the evidence supports a causal association.

The role of asbestos in the etiology of lung cancer and of mesothelioma of the pleura and peritoneum has been well documented. The evidence for a causal association between asbestos and other human cancers is not as extensive but suggests that asbestos may be carcinogenic at several different sites. This paper is concerned specifically with a possible causal association between asbestos and human kidney cancer. A review of the evidence to date indicates that only three human studies have sufficient statistical power to detect an excess mortality from kidney cancer among workers exposed to asbestos. All three were occupational cohort studies, and two of these gave strong direct evidence for such an excess; a study of U.S. insulators (kidney cancer SMR = 2.22, 90% CI 1.44-3.30), and a study of U.S. asbestos products company workers (kidney cancer SMR = 2.76, 90% CI 1.29-5.18). The third study, of Italian shipyard workers, reported excess mortality from "cancers of the kidney, urinary bladder, and other urinary organs" (SMR = 1.98, 90% CI 1.42-2.70). Further support for a causal association includes studies finding asbestos fibers in human kidneys and urine, as well as reports of kidney tumors in two animal bioassays. It is concluded that asbestos should be regarded as a probable cause of human kidney cancer.

Animals↗

PubMed2004

Environmental contamination of chrysotile asbestos and its toxic effects on growth and physiological and biochemical parameters of Lemna gibba.

Asbestos was monitored in water, sediment, and aquatic plant samples around an asbestos cement factory. Based on asbestos concentration found in aquatic plants during monitoring, and the propensity of asbestos to cause oxidative stress in animal models, laboratory experiments were conducted to assess toxicity of chrysotile asbestos on an aquatic macrophyte, duckweed (Lemna gibba). L. gibba plants were exposed to two concentrations of chrysotile asbestos (0.5 microg and 5.0 microg chrysotile in 5.0 microl double distilled water) twice per week during a period of 28 days and cultured in medium containing 0.1 g chrysotile/L. Control plants were cultured in medium without chrysotile asbestos. Effect of chrysotile exposure on certain growth and physiological and biochemical parameters was evaluated. An inhibition effect of chrysotile exposure was found on the number of fronds, root length, and biomass. Similar alterations in contents of chlorophyll, carotenoid, total free sugar, starch, and protein were also found. Contrary to effect on these parameters, a dose- and time-dependent increase in efflux of electrolytes, lipid peroxidation, cellular hydrogen peroxide, catalase, and superoxide dismutase activity was found. The results indicate oxidative stress and phytotoxicity of chrysotile asbestos on duckweed.

Araceae↗

PubMed1983

Asbestos-related increase in pulmonary levels of vasoactive intestinal peptide (VIP).

Vasoactive intestinal peptide (VIP), leucine-enkephalin (Leu-Enk), dynorphin (Dyn), neurotensin (NT) and substance P (SP) were measured by radioimmunoassay in lung and bronchoalveolar lavage (BAL) fluids of sham operated control rats and rats exposed to asbestos (5 and 10 mg, single intratracheal injections) for 3 and 6 months. Among these peptides, VIP, Leu-Enk and Dyn were the most abundant with 6 to 25 pmoles per g of lung tissue as compared with 0.95 to 1.2 pmoles per g for the other neuropeptides. In the presence of asbestos, VIP levels were selectively increased up to 2.7 times in lung tissue and 4.3 times in BAL fluids. On high pressure liquid chromatography (HPLC), the immunoreactive VIP coeluted with synthetic VIP. It is concluded that this selective increase may be involved in the pathogenesis of asbestos-related diseases. Exposure to asbestos causes chronic inflammatory reactions in the lung which may lead to fibrosis (1) and increase the incidence of pleuropulmonary cancers (2). Little is known concerning the biochemical changes responsible for the deleterious effects of asbestos on pulmonary functions. Previous studies have documented the vast complexity and diversity of lung biochemistry including its ability to metabolize lipids, inactivate certain enzymes and produce physiologically active amines (3-6). Recently, the lung has been recognized as an important source of peptidergic substances. VIP and SP were reported to be localized in nerve terminals of the main airways and in axons of the parasympathetic conducts (7-11). Other neuropeptides including bombesin (12, 13), calcitonin (13, 14) and Leu-Enk (13) were also detected in the lung. However, these latter peptides were mainly confined to diffuse granule-containing cells also known as APUD cells (amine precursor uptake and decarboxylation cells) (15). The role of these neuropeptides in normal lung function and in pulmonary diseases is unknown. However, it has recently been demonstrated that APUD cells proliferate in the rat lung following asbestos inhalation (16) and lung exposure to carcinogens (17, 18). In addition, Moody et al. (19) and Sorenson et al. (20) have observed high levels of bombesin in human cell lines derived from small-cell lung carcinoma. It was then of particular interest to verify if lung exposure to asbestos can induce some changes in the levels of various neuropeptides. In the present study, we report that VIP is significantly increased in the lungs and BAL fluids of rats exposed to asbestos while no significant change in the levels of Leu-Enk, Dyn, NT and SP is observed.

Animals↗

PubMed1992

Exposure to airborne asbestos in buildings.

The concentration of airborne asbestos in buildings and its implication for the health of building occupants is a major public health issue. A total of 2892 air samples from 315 public, commercial, residential, school, and university buildings has been analyzed by transmission electron microscopy. The buildings that were surveyed were the subject of litigation related to suits alleging the general building occupants were exposed to a potential health hazard as a result of exposure to the presence of asbestos containing materials (ACM). The average concentration of all asbestos structures was 0.02 structures/ml (s/ml) and the average concentration of asbestos greater than or equal to 5 microns long was 0.00013 fibers/ml (f/ml). The concentration of asbestos was higher in schools than in other buildings. In 48% of indoor samples and 75% of outdoor samples, no asbestos fibers were detected. The observed airborne concentration in 74% of the indoor samples and 96% of the outdoor samples is below the Asbestos Hazard Emergency Response Act clearance level of 0.01 s/ml. Finally, using those fibers which could be seen optically, all indoor samples and all outdoor samples are below the Occupational Safety and Health Administration permissible exposure level of 0.1 f/ml for fibers greater than or equal to 5 microns in length. These results provide substantive verification of the findings of the U.S. Environmental Protection Agency public building study which found very low ambient concentrations of asbestos fibers in buildings with ACM, irrespective of the condition of the material in the buildings.

Air Pollutants↗

PubMed2005

Asbestos and mesothelioma: worldwide trends.

A correlation between national asbestos consumption and the incidence of asbestos disease, including mesothelioma, has been observed. Towards the end of the 20th century, governments in many developed countries banned or seriously restricted the use of asbestos. As a result, global asbestos producers have engaged in aggressive marketing campaigns to sell asbestos to developing countries; consumption of white asbestos is increasing in Asia, Latin America and the Commonwealth of Independent States. In most of the countries, there is little, if any, control on hazardous asbestos exposures from occupational, environmental and domestic sources. It is likely that the lethal asbestos harvest which is occurring in the U.S., the UK and Australia will be reproduced in the developing world.

Asbestos↗

PubMed1987

Prevention of asbestos-induced cell death in rat lung fibroblasts and alveolar macrophages by scavengers of active oxygen species.

Cell injury and inflammation caused by asbestos are critical to the pathogenesis of pulmonary fibrosis (asbestosis). Our goal in studies here was to investigate the possible modulation of asbestos-related cell death using antioxidants in both target and effector cells of asbestosis. After exposure to crocidolite asbestos at a range of concentrations (2.5-25 micrograms/cm2 dish), the viability of a normal rat lung fibroblast line (RL-82) and freshly isolated alveolar macrophages (AM) was determined by exclusion of trypan blue and nigrosin, respectively. In comparison to fibroblasts, AM were more resistant to the cytotoxic effects of asbestos. Cytotoxic concentrations of asbestos then were added to both cell types in combination with the antioxidants, superoxide dismutase (SOD), a scavenger of superoxide (O2-.), and catalase, an enzyme scavenging H2O2. Dimethylthiourea (DMTU), a scavenger of the hydroxyl radical (OH.) and deferoxamine, an iron chelator, also were evaluated in similar studies. Results showed significant dosage-dependent reduction (P less than 0.001) of asbestos-associated cell death with all agents. In contrast, asbestos-induced toxicity was not ameliorated after addition of chemically inactivated SOD and catalase or bovine serum albumin. Results above suggest asbestos-induced cell damage is mediated by active oxygen species. In this regard, the iron associated with the fiber and/or its interaction with cell membranes might be critical in driving a modified Haber-Weiss (Fenton-type) reaction resulting in production of OH(.).

Animals↗