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PubMed2003

Trends in asbestos body counts in bronchoalveolar lavage fluid over two decades.

As in most western countries, the use of asbestos has decreased in Belgium since the mid 1970's. Successive regulations have lowered the permissible levels of exposure and prohibited the use of various asbestos products. In order to assess the impact of these prevention measures on the pulmonary fibre burden of asbestos-exposed patients, the bronchoalveolar lavage fluid (BALF) asbestos body (AB) analysis database of the authors' laboratory was reviewed for the period 1983-2000. A total of 4,772 cases were considered, of which 95% were males. AB concentration exceeded 1 AB x mL BALF(-1) in 36.1%. There was essentially no change in the mean concentration of AB over the period evaluated. However, the concentrations in individuals with very high levels decreased over time. This was associated with a shift in exposure categories from primary asbestos workers to those exposed during handling of asbestos-containing materials or to asbestos in place in buildings or industrial sites. This is consistent with epidemiological data indicating that the number of severe cases of asbestosis caused by very high cumulated doses decreases but that benign pleural diseases and mesothelioma remain the most frequent asbestos-related diseases. Past prevention measures are not expected to have a measurable influence on the incidence of mesothelioma in the near future.

Asbestos↗

PubMed2005

Nonmalignant pleural lesions due to environmental exposure to asbestos: a field-based, cross-sectional study.

The aim of the present study was to investigate the frequencies of asbestos-related benign pleural diseases in villagers environmentally exposed to asbestos and the factors affecting these frequencies. A field-based, cross-sectional study was designed. In total, 991 villagers from 10 villages, randomly chosen from 67 villages with known use of asbestos-containing white soil in central Anatolia (Turkey), were investigated. The type of asbestos in the white soil was determined for each village, as well as air-borne fibre concentrations. The villagers were investigated with small-size chest roentgenograms and epidemiological features were recorded. The air-borne fibre levels were generally low. Despite this, pleural plaques were found in 14.4% of the villagers, 10.4% had diffuse pleural fibrosis and 0.4% asbestosis. The significant variables for plaques were age, sex, type of asbestos fibre, e.g. actinolite and tremolite, and exposure duration, while there was a negative relationship with cumulative exposure. The variables affecting diffuse pleural fibrosis were age, exposure duration and cumulative exposure. In conclusion, villagers exposed to environmental asbestos have high frequencies of pleural plaques and diffuse pleural fibrosis, similar to occupationally exposed asbestos cohorts. Different types of asbestos appear to result in different frequencies of pleural lesions.

Adult↗

PubMed1993

Asbestos-induced lung disease.

This review attempts to deal with two major questions concerning asbestos-induced lung disease: How does inhaled asbestos cause cell proliferation and fibrosis? and Will there continue to be risk from exposure to asbestos in schools and public buildings? The first is a scientific question that has spawned many interesting new experiments over the past 10 years, and there appear to be two hypothetical schemes which could explain, at least in part, the fibroproliferative effects of asbestos fibers. One supports the view that toxic oxygen radicals generated on fiber surfaces and/or intracellularly are the central mediators of disease. The second hypothesis is not mutually exclusive of the first, but, in my opinion, may be integral to it, i.e., the cellular injury induced by oxygen radicals stimulates the elaboration of multiple varieties of growth factors and cytokines that mediate the pathogenesis of asbestosis. There is increasing evidence that molecules such as platelet-derived growth factor and transforming growth factor beta, both synthesized and secreted by activated lung macrophages, are responsible, respectively, for the increased interstitial cell populations and extracellular matrix proteins that are the hallmarks of asbestos-induced fibrosis. The challenge today is to establish which combinations of the many factors released actually are playing a role in disease pathogenesis. The issue of continued risk currently is more a question of policy and perception than science because a sufficient database has not yet been established to allow full knowledge of the circumstances under which asbestos in buildings constitutes an ongoing health hazard. The litigious nature of this question does not help its resolution. In as much as public policy statements and risk assessment are not within my purview, I have focused on the state-of-the-art of asbestos as a complete carcinogen. It appears to be generally nongenotoxic, but all asbestos fiber types can induce chromosomal mutations and aneuploidy, perhaps through their ability to disrupt normal chromosome segregation.

Asbestos↗

PubMed1993

Global problems from exposure to asbestos.

Considerable human-derived data the health consequences of asbestos exposure are available. Usually, less information is available from laboratory models of asbestos-related health effects. Animal data mirror the experience in man, and cellular studies help in to understand the mechanistic changes related to asbestos. Although it is clearly carcinogenic, asbestos has shown much variability when examined for its mutagenic activity. Asbestos, a commercial term referring to a family of six naturally occurring mineral fibers, has been widely used around the world. Disease has been recognized into the last century, and at this time every occupational group that has been examined for possible asbestos-related disease has demonstrated it. Disease associated with asbestos makes no distinction based on race or geography, and wherever asbestos is handled it produces disease. With shifting global commercial patterns, disease patterns can be expected to shift also.

Animals↗

PubMed2000

Asbestos in extrapulmonary sites: omentum and mesentery.

STUDY OBJECTIVES: Asbestos fibers have not been reported in tissues from the peritoneal cavity. Therefore, omentum, mesentery, and lung tissues from 20 individuals in whom mesothelioma was diagnosed were analyzed for asbestos bodies and asbestos fibers. DESIGN: Tissue was digested and prepared filters were analyzed by light microscopy and analytical transmission electron microscopy. RESULTS: Asbestos bodies were found in the lungs of 18 individuals, mesentery samples from 5, and omentum samples from 2. Uncoated asbestos fibers were found in lungs of 19 patients, 17 of whom had fibers in at least one extrapulmonary site. The most common asbestos in the omentum and mesentery was amosite. Several features of asbestos found in lung influenced the likelihood of amphibole fibers being found in the omentum or mesentery. Lung features included total amphibole fiber burden, length, aspect ratio, and ferruginous body burden. An increased total ferruginous body burden was strongly associated with increased likelihood of detecting amphiboles in the omentum (p < 0. 05). CONCLUSION: Asbestos fibers reach areas in the peritoneal cavity where some mesotheliomas develop. This study suggests their presence can be predicted based on concentrations and characteristics of fiber burdens in lung tissue.

Aged↗

PubMed1992

[Health effects of non-occupational exposure to asbestos].

Mesothelioma has occurred in a relative large number not only among miners but also among non-occupationally exposed persons living in the northwestern region of Cape State of South Africa, where crocidolite is mined and transported. The long-term residents of Thetford Mines in Quebec Province, Canada, who have never engaged in mining and milling of chrysolite have not shown an excess mortality of respiratory diseases. Tremolite in soil is responsible for mesothelioma among residents of certain geologic regions such as Cyprus, Corcica, northwestern Greece and Turkey. An increased prevalence of malignant mesothelioma has been reported among residents of three Turkish villages due to exposure to erionite fibers having a high carcinogenic potency. Mesothelioma has infrequently developed in wives who were exposed while washing the work clothes of their husbands contaminated with asbestos, especially amphiboles. The levels of airborne asbestos in public buildings and schools in the U.S.A. and England having walls and ceilings constructed with asbestos containing materials are approximately 1/100 of the permissible concentration of 0.2 f/cm3. The estimated risk from asbestos exposure in schools and buildings is lower than the level of other risks in other society. During the work of removing asbestos from buildings the asbestos concentration is remarkably increased and this persists for many weeks thereafter. The level of asbestos fibers released from brake linings of motor vehicles is higher along roads with heavy traffic, at intersections, and near toll booths than elsewhere. The concentration of asbestos fibers released from motor vehicles is generally low and not of the level to induce mesothelioma.

Air Pollution, Indoor↗

PubMed2004

Effect of platelet-derived growth factor on the development and persistence of asbestos-induced fibroproliferative lung disease.

Platelet-derived growth factor (PDGF) isoforms and PDGF receptor-alpha are upregulated in fibroproliferative lesions in response to asbestos exposure. To examine the functional role of PDGF in asbestos-induced lung disease, we have evaluated the impact of PDGF-B overexpression in the lung on the development of pulmonary fibrosis induced by asbestos inhalation. Transgenic mice expressing PDGF-B from the surfactant protein C promoter and wild-type C57BL/6 mice were exposed to aerosolized chrysotile asbestos fibers via three different exposure regimens: 3 consecutive days to 9 mg/m(3), once a week for 5 weeks to 12 mg/m(3), or once a week for 8 weeks to 11 mg/m(3). The 3-day exposure did not produce fibroproliferative lesions in SPC-PDGFB or wild-type mice, indicating that PDGF expression did not increase susceptibility to a subthreshold dose of asbestos. Transgenic and wild-type mice subjected to the 5-week exposure protocol exhibited similar fibrogenic lesions histologically 48 hours and 8 weeks postexposure, but lungs from transgenic mice had elevated lung hydroxyproline content 8 weeks postexposure relative to wild-type mice. In addition, SPC-PDGFB transgenic mice developed pronounced thickening of arterioles following the 5-week exposure regimen. Mice exposed to asbestos for 8 weeks and examined 10 months later showed pronounced, diffuse fibrotic lesions of terminal bronchioles and alveolar ducts, but no histological differences between transgenic and nontransgenic mice were observed. These results indicated that PDGF-B overexpression can stimulate increased collagen deposition and vascular smooth muscle hyperplasia following asbestos inhalation and that a limited exposure (8 times) to chrysotile aerosol can produce long-lasting fibrotic lesions. The 8-week exposure regimen provides an animal model that encompasses an important aspect of human asbestosis-i.e., persistence of fibrosis for long periods after cessation of asbestos exposure.

Animals↗

PubMed2004

Physical and biochemical interactions of soil fungi with asbestos fibers.

Iron, a structural component of most asbestos, is thought to play a crucial role in asbestos toxicity. Surface iron favors fiber uptake by mammalian cells and promotes the generation of free radicals with consequent DNA and lipid damage. In some cases, chemical removal of iron from asbestos fibers has reduced several cellular responses to asbestos. Since iron represents an essential element for soil microorganisms, many of them have developed mechanisms to scavenge this element from poorly soluble forms. We have investigated the ability of some soil fungi to produce iron chelators capable of extracting iron from crocidolite (blue asbestos). Many of the species/isolates investigated could remove significant amounts of iron from crocidolite fibers, Fusarium oxysporum being the most effective. The fungal responses following exposure to asbestos fibers also have been investigated with morphological and biochemical approaches. In liquid cultures, the fibers were visibly cleared from the suspension because they were tightly bound to the fungal hyphae. Modifications in the fungal protein profiles were observed following exposure to asbestos fibers. By binding the fibers and depriving them of iron, selected species/strains of soil fungi might represent interesting tools for the bioremediation of asbestos-contaminated soils.

Asbestos, Crocidolite↗

PubMed1980

Impending proliferation of asbestos.

The international asbestos industry is under considerable pressure in some countries to control dust exposures in the workplace and restrict pollution. In addition, major firms in the United States face mounting compensation costs for past failures to protect asbestos workers. At the same time, however, the asbestos industry is expanding in developing nations, largely on the strength of sales of asbestos-cement construction materials. This report describes problems encountered with the use of asbestos-cement in schools and low-income housing in Puerto Rico, resulting in the condemnation of these buildings and the relocation of over 1,000 families at public expense. The manufacturer of the asbestos-cement panels, a Colombian affiliate of the European-based multinational Eternit, escaped all liability. The issue is presented as a needless, expanding threat to public health worldwide. Safe, economic alternatives exist, such as the use in some cases of crop waste fibers in place of asbestos as a cement binder. There have also been major advances in the commercialization of asbestos-free brake and clutch friction products.

Asbestos↗

PubMed1991

Cell toxicity, hemolytic action and clastogenic activity of asbestos and its substitutes.

The cell toxicity, hemolytic and clastogenic activity were examined in various kinds of asbestos and some asbestos substitutes with reference to the their mineralogical and physicochemical characteristics. There were thirty-five fibrous and non-fibrous samples including UICC chrysotile, size-selected samples of UICC chrysotile, chrysotile altered by heating and grinding, Yamabe (Japan) chrysotile with long and short fibers, Coalinga (U.S. A.) chrysotile with short fibers, UICC crocidolite, amosite, and 19 non-asbestos samples such as, glass fibers, calcium silicates, sepiolites and some clay minerals. The cell toxicity and the hemolytic and clastogenic activity of asbestos were the strongest for chrysotile among all of the asbestos samples tested, and their strengths varied with fiber length and with the conditions of grinding and heating. These cellular effects of Yamabe chrysotile with long fibers and size-selected UICC chrysotile with long fibers were stronger than those of chrysotile of the same origin but with short fibers. These effects were weaker in chrysotile altered by heating and grinding. Among the asbestos substitutes, the cell toxicity, hemolytic and clastogenic activities of thin glass fibers were more marked than those of thick glass fibers. The four types of sepiolite were strongly hemolytic, but their cell toxicity and clastogenicity varied according to their grade of crystallinity and/or fiber size. These effects of calcium silicates and some clay minerals were generally low but varied with mineral species. In general, the cell toxicity, hemolytic and clastogenic activities of the asbestos substitutes tested here were mild compared with those of asbestos.

Animals↗

PubMed2001

Urinary 8-oxo-7, 8-dihydro-2'-deoxyguanosine and biopyrrins levels among construction workers with asbestos exposure history.

It has been suggested that oxidative stress is associated with the cancers caused by asbestos. Since construction workers are sometimes exposed to low levels of asbestos, we investigated whether oxidative stress was elevated in construction workers who had been exposed to low levels of asbestos. The subjects were 48 Japanese construction workers. The defined asbestos-exposed group consisted of subjects who had the history of suspected exposure to asbestos and were diagnosed to have irregular opacities or pleural plaques. We measured the amount of 8-oxo-7, 8-dihydro-2'-deoxyguanosine (8-oxodG) and biopyyrins in the urine of the subjects. The results showed that 8-oxodG and biopyyrins levels in the defined asbestos-exposed group were higher, although they were not statistically significant, than those in the control group. In addition, the urinary 8-oxodG levels tended to correlate positively with the duration of suspected exposure to asbestos. These results suggest that even low-level asbestos exposure may induce oxidative stress and that the resulting's the oxidative stress might be related to lung cancer in construction workers.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2001

Epidemiology of occupational asbestos-related diseases in China.

In 1950s and 60s, asbestosis had been a major health hazard for asbestos exposed workers. In the late 1970s, lung cancers with or without asbestosis were found among asbestos workers. All cohort studies on asbestos workers and on chrysotile miners in China showed excess deaths from lung cancer. In a large scale of cohort study on asbestos workers, a synergistic effect was found between cigarette smoking and asbestos exposure in the production of lung cancer. There have been not so many cases of malignant mesotheliomas reported, so far. In the cohort of chrysotile miners, 4 cases of pleural mesothelioma were observed. In the large scale of cohort study on asbestos workers in 9 factories using only chrysotile only one case of pleural mesothelioma was detected for 10 years' observation. In another 2 cohort studies, 2 cases of peritoneal mesotheliomas were found, one in Shanghai asbestos factory where a small amount of crocidolite had been used in 1960s, and one in Anqing asbestos factory that was located near tremolite mine. Further study is needed especially for the relationship between exposure to Chinese chrysotile and malignant mesotheliomas.

Asbestos↗

PubMed2001

Biological effects of asbestos fibers on human cells in vitro--especially on lymphocytes and neutrophils.

Biological effects of asbestos fibers were reviewed in relation to the polyclonal activation of human lymphocytes and to the release of free radicals from human neutrophils in vitro. Chrysotile, crocidolite, and amosite asbestos activate CD4+ T lymphocytes polyclonally, followed by activation-induced cell death (a type of apoptosis). The activation is HLA class II dependent, and certain Vbeta repertoire, e.g. Vbeta 5.3, are detected among the fractionated T cells with a high Ca++ level that had been stimulated by asbestos fibers. These observations support the possibility that asbestos acts as a superantigen, and that asbestos stimulate lymphocytes repeatedly in vivo. It has been reported that asbestos-induced cytotoxicity can be suppressed by the scavengers of superoxide or hydroxyl radical. Some of these scavengers such as dimethylsulfoxide (DMSO) or retinoic acid are known as inducers of cell differentiation. The biological functions of DMSO for cell differentiation of HL-60 cells to neutrophils are suppressed by co-culturing of crocidolite asbestos, because DMSO reacts with the hydroxyl radical released after the stimulation with crocidolite and spent itself. Superoxide dismutase (SOD) inhibited the effects of crocidolite, reacting rapidly with *O2- before the secondary release of *OH. It seems to be probable that asbestos fibers, especially crocidolite, suppress the tissue cell differentiation by releasing free radicals and by wasting inducers of cell differentiation as radical scavengers.

Apoptosis↗

PubMed1994

Asbestos and cancer: epidemiological and public health controversies.

This paper discusses many of the currently controversial issues surrounding asbestos health effects and their relationship to cancer risk assessment and risk management. The major conclusions reached from this analysis are: (1) All asbestos fiber types are carcinogenic and pose a threat to human health. Therefore, all fiber types should be regulated similarly. (2) The health risks associated with indoor asbestos exposure are uncertain. Available data show that some groups, such as building maintenance personnel (among others), may contract asbestos-related diseases secondary to indoor exposure. Clearly, additional research is needed to accurately determine the extent and nature of disease risk under these conditions. (3) Controlled use has proved an elusive goal. Limited information from underdeveloped countries parallels the experience of Western industrialized nations. Efforts by the Canadian government to establish markets for asbestos in these areas should be opposed. (4) Finally, asbestos-related cancer risk is no longer confined to asbestos industry workers. Asbestos-related mesothelioma has been documented in a wide variety of occupational and nonoccupational settings, highlighting the need for continued surveillance to minimize potential health risks.

Air Pollutants↗

PubMed2003

Asbestos exposure and antineutrophil cytoplasmic Antibody (ANCA) positivity.

The authors used indirect immunofluorescence to examine the association of antineutrophil cytoplasmic antibodies (ANCAs) with exposure to asbestos among 61 asbestos-exposed patients (mean exposure = 24.6 yr) and 39 nonexposed controls. ANCA positivity was detected significantly more frequently (p = 0.034) in the asbestos-exposed group (21.3%) than in the control group (5.1%). ANCA-associated diseases did not occur more frequently among subjects exposed previously to asbestos than among unexposed controls. These findings confirmed that exposure to asbestos is another occupational factor, as is silica exposure, that is associated with ANCA positivity. The influence of asbestos appears stronger than that of silica because ANCA positivity was found among subjects who had histories of exposure to asbestos but who did not exhibit typical radiographic signs of asbestosis on their chest x-rays. Additional stimuli may be necessary to induce systemic vasculitis in asbestos-exposed persons.

Antibodies, Antineutrophil Cytoplasmic↗

PubMed1994

Asbestos exposure and the risk of lung cancer in a general urban population.

OBJECTIVES: The aim of the study was to investigate the asbestos-associated risk of lung cancer according to histological type of cancer, lobe of origin, pulmonary concentration, and type of amphibole fibers and also to estimate the etiologic fraction of asbestos for lung cancer. METHODS: The pulmonary concentration of asbestos fibers in 113 surgically treated male lung cancer patients and 297 autopsy cases among men serving as referents was determined by scanning electron microscopy. The age- and smoking-adjusted odds ratios of lung cancer were calculated according to pulmonary fiber concentration for all lung cancer types, squamous-cell carcinoma, and adenocarcinoma and for the lower-lobe and the upper- and middle-lobe cancers. RESULTS: The risk of lung cancer was increased according to the pulmonary concentration of asbestos fibers (f) of 1.0 to 4.99 x 10(6) f.g-1 [odds ratio (OR) 1.7] and > or = 5.0 x 10(6) f.g-1 (OR 5.3). The odds ratios associated with fiber concentrations of > or = 1.0 x 10(6) f.g-1 were higher for adenocarcinoma (OR 4.0) than for squamous-cell carcinoma (OR 1.6). The asbestos-associated risk was higher for lower lobe tumors than for upper lobe tumors. The risk estimates for anthophyllite and crocidolite-amosite fibers were similar, except for the risk of squamous-cell carcinoma. An etiologic fraction of 19% was calculated for asbestos among male surgical lung cancer patients in the greater Helsinki area. CONCLUSIONS: Past exposure to asbestos is a significant factor in the etiology of lung cancer in southern Finland. The asbestos-associated risk seems to be higher for pulmonary adenocarcinoma and lower-lobe tumors than for squamous-cell carcinoma and upper-lobe tumors.

Adult↗

PubMed1986

A case-referent study of lung cancer, occupational exposures and smoking. II. Role of asbestos exposure.

In a hospital-based case-referent study of 176 incident lung cancer cases, ascertained during a five-year period from two county hospitals, the role of asbestos exposure and smoking has been studied. Information on asbestos exposure was obtained from personal interviews, and allocated to four exposure categories, according to the intensity and duration of the exposure. Twenty-five percent of the cases and 10% of the referents had been moderately to heavily exposed to asbestos during their working career. A statistically significant trend in risk ratio related to the degree of exposure was observed, with a more than fourfold risk among the heavily exposed. The strongest association was found between asbestos exposure and small cell carcinoma, and the weakest association between asbestos exposure and adenocarcinoma. Very high risk ratios were observed among asbestos-exposed subjects who were heavy smokers, and the interaction observed between asbestos and smoking conformed more closely to a multiplicative model than to an additive one. The results suggest that the observed association between lung cancer and occupational exposures in this study was, to a large extent, due to asbestos exposure. Information on such exposure was missing in 90% of the medical records of these patients.

Adult↗

PubMed1998

[Damage effects of asbestos and cigarette smoke solution on human embryo lung cell DNA].

OBJECTIVE: To study the combined damage effects of asbestos and cigarette solution on human embryo lung cell (HEL) DNA. METHODS: Unscheduled DNA synthesis (UDS) assay was used. Repair and synthesis on DNA in HEL treated with asbestos and/or cigarette smoke was studied. RESULTS: It showed that UDS in HEL could be induced by exposure to asbestos or cigarette smoke only with a significant dose-response relationship, and the amounts of [3H]-TdR incorporation in cells treated with combination of asbestos and cigarette smoke was significantly higher than their sum in cells treated with asbestos or cigarette only. CONCLUSION: There is a synergistic damage effect of asbestos and cigarette on DNA of HEL. In addition, dimethyl sulfoxide (DMSO), a scavenger of .OH, can partly inhibit [3H]-TdR incorporation caused by asbestos. And .OH plays certain role in damage to DNA of cells caused by asbestos.

Asbestos, Serpentine↗