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PubMed1995

Mitotic disturbances and micronucleus induction in Syrian hamster embryo fibroblast cells caused by asbestos fibers.

Asbestos and other mineral fibers have long been known to induce lung cancer and mesothelioma. However, the primary mechanisms of fiber-induced carcinogenesis still remain unclear. We investigated the occurrence of mitotic disturbances induced by asbestos (amosite, crocidolite, chrysotile) in an in vitro approach using Syrian hamster embryo (SHE) fibroblast cells. The following endpoints were investigated: micronucleus formation as a result of mitotic disturbances and characterization of the induced micronucleus population by kinetochore staining and visualization of the spindle apparatus. Supravital UV-microscopy was used to analyze changes in interphase chromatin structure, impaired chromatid separation, and blocked cytokinesis. All three asbestos fiber types induced a high frequency of micronucleus formation in SHE cells (> 200/2000 cells) in a dose-dependent manner (0.1-5.0 micrograms/cm2), with a maximum between 48 hr and 66 hr exposure time. At higher concentrations (more than 5.0 micrograms/cm2) the micronucleus formation decreased again as a result of increased toxicity. Kinetochore staining of micronuclei revealed that 48 +/- 2% of asbestos-induced micronuclei reacted positively with CREST (antikinetochore) serum. Furthermore, spindle apparatus deformations occurred in cells with disturbed metaphases and anaphases, while the spindle fiber morphology appeared unchanged. Our results show that asbestos fibers may cause both loss and breakage of chromosomes in the absence of direct interaction with spindle fibers.

Animals↗

PubMed1997

Possible role of lipid peroxidation in the induction of NF-kappa B and AP-1 in RFL-6 cells by crocidolite asbestos: evidence following protection by vitamin E.

Asbestos fibers cause persistent induction of the oxidative stress sensitive transcription factors nuclear factor kappa-B (NF-kappa B) and activator protein-1 (AP-1) in mammalian cells. These transcription factors play an important role in the regulation of cellular activity. Lipid peroxidation, mediated by reactive oxygen species, is thought to be a possible mechanism in the pathogenicity of asbestos fibers. These studies were designed to determine if crocidolite asbestos-induced lipid peroxidation plays a role in the mechanism of formation of NF-kappa B and AP-1. Treatment of a rat lung fibroblast cell line (RFL-6) with crocidolite asbestos in the presence and absence of the membrane antioxidant vitamin E decreased the levels of crocidolite-induced AP-1 and NF-kappa B to background levels. Preincubation of RFL-6 cells with 5,8,11,14-eicosatetraynoic acid, an inhibitor of arachidonic acid metabolism, prior to exposure to crocidolite, abrogated crocidolite-induced NF-kappa B DNA-binding activity to background levels. Coincubation with indomethacin, a cyclooxygenase inhibitor, had no effect on NF-kappa B DNA-binding activity induced by crocidolite. However, nordihydroguaiaretic acid, a lipoxygenase inhibitor, decreased levels of NF-kappa B to background levels. This would suggest that lipoxygenase metabolites of arachidonic acid, produced following lipid peroxidation, are involved in the cellular signalling events to NF-kappa B transcription factor induction by asbestos.

Animals↗

PubMed1999

Comparative hazards of chrysotile asbestos and its substitutes: A European perspective.

Although the use of amphibole asbestos (crocidolite and amosite) has been banned in most European countries because of its known effects on the lung and pleura, chrysotile asbestos remains in use in a number of widely used products, notably asbestos cement and friction linings in vehicle brakes and clutches. A ban on chrysotile throughout the European Union for these remaining applications is currently under consideration, but this requires confidence in the safety of substitute materials. The main substitutes for the residual uses of chrysotile are p-aramid, polyvinyl alcohol (PVA), and cellulose fibers, and it is these materials that are evaluated here. Because it critically affects both exposure concentrations and deposition in the lung, diameter is a key determinant of the intrinsic hazard of a fiber; the propensity of a material to release fibers into the air is also important. It is generally accepted that to be pathogenic to the lung or pleura, fibers must be long, thin, and durable; fiber chemistry may also be significant. These basic principles are used in a pragmatic way to form a judgement on the relative safety of the substitute materials, taking into account what is known about their hazardous properties and also the potential for uncontrolled exposures during a lifetime of use (including disposal). We conclude that chrysotile asbestos is intrinsically more hazardous than p-aramid, PVA, or cellulose fibers and that its continued use in asbestos-cement products and friction materials is not justifiable in the face of available technically adequate substitutes.

Air Pollution↗

PubMed2004

Clinical correlation of asbestos bodies in BAL fluid.

BACKGROUND: Asbestos bodies (AB) in BAL cells are specific markers of asbestos exposure. METHODS: We retrospectively reviewed BAL cytocentrifuge slides of 30 utility workers with a history of asbestos exposure and 30 normal volunteers. BAL cytocentrifuge slides were blinded and scanned under 40 x light microscope. RESULTS: AB were found more frequently in subjects with a history of asbestos exposure compared to normal volunteers (10 of 30 subjects, 33%, vs 0 of 30 subjects). The mean number of AB seen in the AB-positive group was 2.7 per slide. Demographic data were comparable including age, gender, and smoking. Exposure histories were also similar: duration > 20 years, onset > 30 years ago, and time since last exposure > 7 years. More AB-positive patients reported respiratory symptoms (70% vs 26%, p < 0.05). High-resolution CT scans of AB-positive patients revealed a higher prevalence of parenchymal disease (70% vs 26%, p < 0.05). AB-positive subjects had reduced pulmonary function compared to AB-negative subjects: FVC (86% vs 97% predicted), FEV(1) (77% vs 92% predicted, p < 0.05), and diffusion capacity of the lung for carbon monoxide (76% vs 104% predicted, p < 0.01). CONCLUSION: In individuals with a history of asbestos exposure, the presence of AB in BAL cells is associated with higher prevalence of parenchymal abnormalities, respiratory symptoms, and reduced pulmonary function.

Asbestos↗

PubMed1986

Asbestos burden and the pathology of lung cancer.

To determine whether we could distinguish asbestos-related lung cancers from unrelated ones, we typed and quantified by electron-optical methods the asbestos fibers in the lungs of 75 men with lung cancer. All but eight men had some history of asbestos exposure. On the basis of combined amosite and crocidolite (AC) concentrations, we divided the subjects into three groups (AC fibers per gram of dry lung): low (less than 10(5)); intermediate (10(5) to 10(6)); and high (greater than 10(6)). Age, smoking history, latent period, and type and location of tumors were similar in all three groups. Of 62 evaluated subjects, zero of 14 in the low group, seven of 29 in the intermediate group, and five of 19 in the high group had asbestosis. Epidemiologic studies suggest that persons exposed to concentrations of asbestos that can cause asbestosis are at increased risk for lung cancer. Thus, the subjects in our intermediate and high concentration groups may have been at increased risk for cancer, even when they did not have asbestosis. Because large burdens of asbestos do not always cause pulmonary fibrosis, asbestosis may be a poor marker of fiber-related lung cancer.

Adult↗

PubMed1988

Comparison of light and electron microscopy for defining occupational asbestos exposure in transbronchial lung biopsies.

Since asbestos burden in the lung can very among areas, the usefulness of small tissue samples for identifying past occupational exposure is examined. Simulated transbronchial biopsy samples and open lung biopsy samples were collected from autopsy material from 12 former amosite asbestos workers and ten persons from the general population. Tissue evaluation included (1) paraffin embedment and light microscopy screening for fibrosis and ferruginous bodies, and (2) tissue digestion, which was analyzed by the combination of (A) light microscopy screening for ferruginous bodies and (B) electron microscopy (EM) screening for uncoated fibers. Using standard pathology techniques to classify the small samples was generally unsuccessful, the samples being too small or their size compounding other random sampling problems. The most reliable method of establishing which transbronchial biopsy tissue samples were from the occupationally exposed group occurred when light and EM analyses were used to evaluate digested tissue. The combined data from the EM analysis of two samples per subject indicated controls had two or fewer observed asbestos fibers, while the amosite asbestos workers had six or more fibers. This distinction was valid even in those who, 21 years before sampling, had worked for only a few weeks in the asbestos plant.

Adult↗

PubMed2006

Asbestos-related disease in South Africa: the social production of an invisible epidemic.

South Africa was the third largest exporter of asbestos in the world for more than a century. As a consequence of particularly exploitative social conditions, former workers and residents of mining regions suffered--and continue to suffer--from a serious yet still largely undocumented burden of asbestos-related disease. This epidemic has been invisible both internationally and inside South Africa. We examined the work environment, labor policies, and occupational-health framework of the asbestos industry in South Africa during the 20th century. In a changing local context where the majority of workers were increasingly disenfranchised, unorganized, excluded from skilled work, and predominantly rural, mining operations of the asbestos industry not only exposed workers to high levels of asbestos but also contaminated the environment extensively.

Adolescent↗

PubMed2007

Asbestos-induced peribronchiolar cell proliferation and cytokine production are attenuated in lungs of protein kinase C-delta knockout mice.

The signaling pathways leading to the development of asbestos-associated diseases are poorly understood. Here we used normal and protein kinase C (PKC)-delta knockout (PKCdelta-/-) mice to demonstrate multiple roles of PKC-delta in the development of cell proliferation and inflammation after inhalation of chrysotile asbestos. At 3 days, asbestos-induced peribronchiolar cell proliferation in wild-type mice was attenuated in PKCdelta-/- mice. Cytokine profiles in bronchoalveolar lavage fluids showed increases in interleukin (IL)-1beta, IL-4, IL-6, and IL-13 that were decreased in PKCdelta-/- mice. At 9 days, microarray and quantitative reverse transcriptase-polymerase chain reaction analysis of lung tissues revealed increased mRNA levels of the profibrotic cytokine, IL-4, in asbestos-exposed wild-type mice but not PKCdelta-/- mice. PKCdelta-/- mice also exhibited decreased lung infiltration of polymorphonuclear cells, natural killer cells, and macrophages in bronchoalveolar lavage fluid and lung, as well as increased numbers of B lymphocytes and plasma cells. These changes were accompanied by elevated mRNA levels of immunoglobulin chains. These data show that modulation of PKC-delta has multiple effects on peribronchiolar cell proliferation, proinflammatory and profibrotic cytokine expression, and immune cell profiles in lung. These results also implicate targeted interruption of PKC-delta as a potential therapeutic option in asbestos-induced lung diseases.

Animals↗

PubMed1995

Effects of smoking on respiratory function and exercise performance in asbestos workers.

To determine the role of smoking in the development of pulmonary impairment in asbestos workers, 66 nonsmoking asbestos workers and 70 smoking asbestos workers were studied. Occupational and medical questionnaires, lung function and exercise test were conducted in all subjects. The frequencies of dyspnea and cough on questions were significantly higher in the smoking workers than those in nonsmoking workers. Similarly, FEV1, FEV1/FVC and DLco were significantly lower in the smoking workers. Exercise performance showed that the smoking workers had higher index of dyspnea and lower breathing reserve, Vo2 and Vo2 max than nonsmoking workers did. We concluded that cigarette smoking has marked effects on both of respiratory function and exercise performance in asbestos workers. Among them, smokers show more serious obstructive impairment in static lung function testing and more significant limitation during exercise. The history of cigarette smoking deserves close attention in the evaluation of pulmonary impairment from asbestos exposure.

Asbestos↗

PubMed2003

The role of smoking and exposure to asbestos and man-made vitreous fibers in a questionable case of mesothelioma.

A remaining uncertainty in the U.S. cohort study of man-made vitreous fiber (MMVF) workers is whether asbestos exposure contributed to 10 questionable cases of mesothelioma. We report further details on one case from our previous mesothelioma investigation, including results of a recent lung tissue analysis. Case is a 68 year-old white male employed 1951-54 in a rock/slag wool plant where asbestos-containing products were manufactured. Cause of death was recorded as "mesothelioma, malignant, right pleural cavity" (ICD9: 163.9). Analysis for presence of asbestos bodies identified 18,300 asbestos bodies per gram of wet lung tissue (AB/gm), which greatly exceeds the normal range of 0-20 AB/gm. No MMVFs were identified in this sample. We conclude that this patient's tumor was not a mesothelioma, but a carcinoma possibly arising in the lung or mediastinum, and that this case supports the view that the few suspected mesotheliomas found in the U.S. cohort may have been caused by asbestos exposure.

Aged↗

PubMedDate not supplied

Asbestos-induced release of a human alveolar macrophage-derived neutrophil chemotactic factor.

Neutrophils accumulate in the alveoli of asbestos-exposed individuals. In determining whether asbestos fibers induce the release of neutrophil chemotactic factor (NCF) from human alveolar macrophages, alveolar macrophages (10(6) cell/mL) obtained by bronchoalveolar lavage from six non-asbestos-exposed control subjects were exposed to crocidolite (0.1 and 1 mg/mL), chrysotile (1 mg/mL), or medium alone for 4 h, and NCF activity was measured in the supernatants in a 48-well microchemotaxis chamber with polycarbonate membrane filters (pore size, 3 microns) and purified human neutrophils. Alveolar macrophages in medium alone released negligible amounts of NCF (4 +/- 1 neutrophils per high-power field [N/HPF]). When macrophages were exposed to crocidolite (0.1 and 1 mg/mL), significant NCF release occurred (43 +/- 9 and 105 +/- 32 N/HPF, respectively; p less than 0.01 for each amount compare to alveolar macrophages cultured in medium alone). Chrysotile (1 mg/mL) induced similar NCF release (96 +/- 14 N/HPF; p less than 0.01 compared to unstimulated alveolar macrophages). Partial characterization of the NCF by Sephadex G-25 fine gel filtration demonstrated a molecular size of less than 1,000 daltons. These results show that human alveolar macrophages release NCF after exposure to asbestos. Release of NCF by alveolar macrophages in asbestos-exposed individuals may play a central role in the pathogenesis of asbestosis.

Asbestos↗

PubMedDate not supplied

Influence of continued asbestos exposure on the outcome of asbestosis in sheep.

Clinical recognition of asbestosis is generally followed by exclusion of the worker from the active workforce and appropriate compensation. Given the better industrial hygiene conditions of the 1990s, and a recent report suggesting that low-level asbestos exposure may not affect progression of asbestosis, the medical rationale to pension asbestos workers with early asbestosis has been questioned in the legal courts. To study the influence of asbestos exposure after established asbestosis, we enrolled 25 sheep. Ten were normal controls (group A) and 15 had asbestosis, after 2 years of repeated 10-day interval, 100-mg chrysotile exposure (Eur Respir J 3:81-90, 1990). The asbestotic sheep were divided into a group of five without further asbestos exposure (group B), a group of five with continued exposure at induction doses (group C), and a group of five with continued exposure of 10% induction doses (group D). All were followed by chest radiography, lung function, and lung lavage at 3-month intervals and histopathology when appropriate. During the 12-month study, mortality occurred only in groups C and D (40% in both, P less than .02). Chest radiograph and lung function were worse in groups C and D. The enhanced macrophagic and neutrophilic alveolitis observed on lung lavage and the pathological findings in the deceased sheep suggested progression of asbestosis and bacterial infections as the major contributors to the higher mortality of sheep in groups C and D. In conclusion, asbestos exposure after disease recognition was associated with increased mortality in our sheep and this was largely associated with progression of asbestosis and added lung infection.

Animals↗

PubMedDate not supplied

Intratracheal injection of crocidolite asbestos depresses the secretion of tumor necrosis factor by pleural leukocytes in vitro.

Tumor necrosis factor (TNF) is a cytokine released predominantly by monocytes/macrophages that has been shown to modulate a variety of different immune and metabolic functions. To understand the regulatory mechanisms of TNF in governing responses in the pleural cavity following deposition of fibrous dust in the airspace of the lung, we studied the capability of leukocytes, lavaged from the pleural cavity, to release TNF in culture. TNF production by lavaged pleural leukocytes was measured using the L-929 TNF-sensitive cell line, after intratracheal instillation of crocidolite asbestos. A high level of TNF activity was found in the supernatants of normal, unstimulated pleural leukocytes; the addition of 100 ng/ml lipopolysaccharide to the culture increased the activity up to threefold. Following intratracheal instillation of 5 mg crocidolite asbestos, the pleural leukocytes secreted less TNF than the control. With increasing mass of intratracheally instilled asbestos, there was a dose-dependent reduction in TNF release. Changes in the population of the pleural leukocytes or their number could not be related to variation in TNF activity. These results suggest that exposure of rat lungs to crocidolite asbestos by intratracheal instillation affects the response of pleural leukocytes without causing changes in the population. Such changes in the bronchoalveolar space may be related to the pleural pathology found in asbestos-exposed individuals.

Animals↗

PubMed1984

Mutagenesis of Escherichia coli (CSH50) by asbestos.

The mutagenic character of richterite asbestos was detected in Escherichia coli strain CSH50, using a modified Ames test. Two sets of experimental plates which contained naturally occurring asbestos were used, to one set of which S-9 rat liver homogenate was added. Control plates contained no asbestos. Mutant colonies appeared in significantly greater frequency in both experimental sets as compared with controls, and experimental plates with rat liver homogenate contained the greatest number of mutant colonies. It is postulated that enzymes contained in rat liver metabolize some unknown mutagen introduced with the natural asbestos sample other than the inert richterite fibers themselves. This finding, together with the unlikelihood that bacterial cell walls could be easily penetrated by asbestos fibers, tends to negate fiber penetration as the mechanism of mutagenesis. The mutagenic mechanism operative in E. coli (CSH50) may be applicable to animal cell systems.

Animals↗

PubMed1997

Surveillance and intervention studies on respiratory cancers in asbestos-exposed workers.

A systematic review of the literature on the surveillance of workers at presumed increased risk for respiratory cancer because of their exposure to asbestos revealed surveillance programs at the national, population, industrial, and factory (workplace) levels. Furthermore, 3 randomized chemoprevention trials involving workers exposed to asbestos were found. The nationwide programs to survey problems related to occupational exposure to asbestos were conducted in Europe. Some of the countries have policies for the surveillance of workers exposed either currently or formerly to asbestos. The results of the chemoprevention trials suggest that there are, as yet, no practical tools for efficient, safe chemoprevention of asbestos-induced respiratory malignancies.

Anticarcinogenic Agents↗

PubMed1997

Asbestos, asbestosis, pleural plaques and lung cancer.

Inhalation of asbestos fibers increases the risk of bronchial carcinoma. It has been claimed that asbestosis is a necessary prerequisite for the malignancy, but epidemiologic studies usually do not have enough statistical strength to prove that asbestos-exposed patients without asbestosis are without risk. Several recent studies do actually indicate that there is a risk for such patients. In addition, case-referent studies of patients with lung cancer show an attributable risk for asbestos of 6% to 23%, which is much higher than the actual occurrence of asbestosis among these patients. Thus there is an increasing body of evidence that, at low exposure levels, asbestos produces a slight increase in the relative risk of lung cancer even in the absence of asbestosis. Consequently, all exposure to asbestos must be minimized.

Adult↗

PubMed1988

An 11-year longitudinal study of the occupational dust exposure and lung function of polyvinyl chloride, cement and asbestos cement factory workers.

Standardized questionnaires and lung function tests were administered in 1973, 1980, and 1984 to 126 workers occupationally exposed to polyvinyl chloride (PVC) dust, to cement dust, or to asbestos cement dust until 1974-1978 and to PVC thereafter. The workers in the last group were assigned to two asbestos exposure categories (heavy and slight). The decline in forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1.0) was analyzed with regard to the length of time since the data of first employment. After adjustment for age, height, and smoking status at the date of first employment, the decline in FVC and FEV1.0 among the nonsmokers-light smokers was slightly accelerated with length of employment in the PVC and slight asbestos exposure groups and markedly accelerated with time since first employment in the heavy asbestos exposure group. The heavy smokers in all the exposure groups had FVC and FEV1.0 predicted values that were lower than those of the nonsmokers-light smokers; these differences remained constant with length of employment. Cessation of asbestos exposure for about 10 years did not seem to change lung function decline.

Adult↗

PubMed2000

Past occupational exposure to asbestos among men in France.

OBJECTIVES: This study aimed at reconstructing changes in the frequency and levels of occupational asbestos exposure in France over the past century. METHODS: Work histories were collected during 11 population-based case-referent studies recently carried out in France, and an asbestos-specific job-exposure matrix including 10 625 jobs was used to estimate indices of past occupational asbestos exposure. The results were estimated from a sample of 4287 subjects, bootstrapped 200 times. RESULTS: The distribution of socioeconomic categories within the sample was compared with that of the general population in 1954, 1962, 1968, 1975, and 1982. The proportion of blue-collar workers was similar. The highest proportion of exposed subjects was found between 1950 and 1980. Around 10% of each 10-year age class was exposed to asbestos. For those born in 1930-1939, 15.2% was exposed between the ages of 20 and 29 years. For each age class born in 190-1939, the proportion exposed at least once by 60 years of age ranged from 18.2% to 24.5 % and, of those exposed, the cumulative duration of exposure ranged from 11.3 to 15.4 years by the age of 60 years. A population exposure index showed that the heaviest exposure occurred between 1960 and 1970 and that the age classes born between 1920 and 1929 were the most heavily exposed. Time trends showed that the mean value of this index for the men aged 20-59 years reached a peak in the 1960s and then decreased. CONCLUSIONS: This study presents data of reasonable validity about occupational asbestos exposure in France and its trends over the past century; the data are being used to forecast the development of male mortality from mesothelioma in France.

Adolescent↗