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PubMed2004

Asbestos-induced peritoneal mesothelioma in a construction worker.

Occupational and environmental asbestos exposure continues to represent a public health problem, despite increasingly restrictive laws adopted by most industrialized countries. Peritoneal mesothelioma is a rare and aggressive asbestos-related malignancy. We present the case of a 65-year-old man who developed recurrent ascites after having been exposed to asbestos in the building industry for > 40 years. Liver function and histology were normal. Abdominal computed tomography initially excluded the presence of expansive processes, and no abnormal cells were found in the ascitic fluid. Laparoscopy showed diffuse neoplastic infiltration of the peritoneum. Histopathology of bioptic samples revealed epithelioid neoplastic proliferation with a tubulopapillary pattern, falsely suggesting metastatic adenocarcinomatosis. In consideration of the occupational history, and after further diagnostic procedures had failed to identify the hypothetical primitive tumor, immunostaining of the neoplastic tissue was performed. Results were negative for carcinoembrionary antigen and the epithelial glycoprotein Ber-EP4, whereas results were positive for the mesothelial markers cytokeratins, calretinin, epithelial membrane antigen, and HBME-1, thus leading to the correct diagnosis of peritoneal epithelial mesothelioma. The Italian Workers' Compensation Authority recognized the occupational origin of the disease. Cytoreductive surgery associated with continuous hyperthermic peritoneal perfusion (cisplatin at 42 degrees C, for 1 hr) was performed. The disease relapsed after 4 months and was later complicated by a bowel obstruction requiring palliative ileostomy. The patient died 23 months after diagnosis. This case illustrates the insidious diagnostic problems posed by peritoneal mesothelioma, a tumor which often simulates other malignancies (e.g., metastatic carcinomas) at routine histopathological examination. Occupational history and immunohistochemistry are helpful for the correct diagnosis, which, in turn, is important in relation to prognosis and treatment (adoption of new integrated procedures that seem to promise prolonged survival and increased quality of life), and in relation to medicolegal issues and occupation-related compensation claims following asbestos exposure.

Aged↗

PubMed1974

Penetration of cells by asbestos fibers.

Studies on the behavior of asbestos fibers within tissues have shown that the only cells that regularly contain asbestos are macrophages and their derivatives. However, these cells actively incorporate the asbestos fibers by the process of phagocytosis, and there is little evidence of direct penetration. Examination of the gut lining after prolonged asbestos ingestion has shown no evidence of dust penetration either through or between the epithelial cells. The structure and arrangement of these cells is discussed, and it is suggested that they are exceptionally well adapted to prevent penetration by any solid material.

Animals↗

PubMed1974

Electron microscopical investigation of asbestos fibers.

Examination of asbestos fibers by electron microscopical techniques enables the observer to distinguish among the fiber types by morphological and structural characteristics. Chrysotile asbestos fibers are composed of bundles of fibrils. Fibers are often curvilinear with splayed ends. Individual fibrils consist of a central capillary defined by an electron dense crystalline wall. With increasing time of electron bombardment, the capillary wall decreases in thickness, deforms, and is encapsulated in an electron translucent material. The change in electron opacity is considered to be a product of structural disruption brought about by dehydroxylation due to electron radiation. A well recognized sequential deformation pattern may be used for identification purposes.Amphibole fibers tend to be straight, splintery, and electron-opaque, although curved fibers are occasionally observed. Diffraction contrast figures are visible as dark bands moving parallel and at right angles to the fiber axis. Crocidolite forms the shortest and thinnest fibers, followed in size by amosite and anthophyllite. Size distribution characteristics of the amphibole fiber types are different. The selected area electron diffraction pattern for chrysotile is unique. Reflections range in forms from streaked to arcuate. Reflection intensity and shape are related to the degree of openness of the fiber bundle and the extent of physical degradation of the fiber. The amphibole asbestos fibers possess diffraction patterns having similar characteristics prohibiting individual identification. Microchemical analysis is required for identification in such cases.A discussion of the industrial hygiene threshold limit values for ampliphibole asbestos fibers is presented. The discussion is based on their differing size distribution characteristics.

Air Pollutants, Occupational↗

PubMed1974

Identification and quantitation of asbestos in talc.

The currently used analytical methods for identification, characterization and quantitation of asbestos fiber in consumer talcum products include polarized light microscopy, x-ray diffraction analysis, transmission electron microscopy with selected area electron diffraction and electron microprobe techniques. Light microscope methods have severe limitations imposed by the ultimate size resolution of the light-optical system. Small particles go unresolved; those marginally resolved may possess optical properties different from those properties cited in the literature; most optical properties, e.g., indices of refraction, are difficult to measure on small particles. In addition to these difficulties, talc fibers often possess optical properties different from those of talc plates, which further confound analysis. Light microscopy is recommended for use only as a preliminary tool on limited, large-sized, samples. Transmission electron microscopy is a good standard technique for visualization of contaminant asbestos fibers. Together with selected area electron diffraction, talc fibers may be easily differentiated from amphibole asbestos fibers on the basis of both morphological and structural characterization. Chrysotile fibers are easily distinguished on this basis as well. The amphibole asbestos minerals require chemical characterization to differentiate among the different fiber types. Probe analysis is mandatory for such fibers. The major drawbacks to electron beam instrumentation for the mineralogical characterization of talcum products are the time and effort required for data acquisition. These techniques do not lend themselves to routine study.X-ray diffraction analysis, utilizing the step-scan method, offers a relatively rapid, quantitative technique for gross fiber analysis. Based on comparison with standard specimens the fiber content of talcs may be quantitatively determined. It is essential to employ a specimen preparation technique which yields homogeneously dispersed particles. Tremolite may be determined at levels as low as 0.10% by weight, chrysotile 0.25%, and anthophyllite at 2.0% by weight occurrence in talc. The variance of these values depends upon many factors, including the mass absorption coefficient of the fiber types as compared to talc and selected diagnostic reflections and their relative intensities. Each of the above techniques is described in detail. A method for routine analysis of consumer talcum products is suggested.

Asbestos↗

PubMed1983

Presentation of benzo(a)pyrene to microsomal enzymes by asbestos fibers in the Salmonella/mammalian microsome mutagenicity test.

The potential effect of asbestos fibers on mutagenicity of benzo(a)pyrene was investigated by using the Ames test. Asbestos fibers without a coating of benzo(a)pyrene or benzo(a)pyrene when not dissolved in DMSO lacked any mutagenic effect in the Salmonella/mammalian microsome mutagenicity test. However, when benzo(a)pyrene was adsorbed onto asbestos, significant numbers of mutated bacteria were observed. This shows that asbestos fibers can serve a carrier role presenting benzo(a)pyrene to the enzymatic microsomal system, thus enhancing mutagenicity of this compound.

Adsorption↗

PubMed1983

Accumulation of ingested asbestos fibers in rat tissues over time.

With the use of the transmission electron microscope, asbestos fibers have been assessed in kidney cortex of four groups of rats previously exposed to intermediate-range feeding grade chrysotile asbestos. Newborn rats, from mothers gavaged with asbestos during pregnancy, were gavaged twice a week at the dose level of 50 mg/kg beginning at age day 7 until their natural death or sacrifice. The rats were divided into four groups by age: 0-200, 200-400, 400-600 and 600-800 days. Of the 20 rats comprising the four test groups, 17 were positive, average fiber recovery being 5.34 X 10(3)/mg dry weight. Average fiber level in control tissues was 0.23 X 10(3)/mg dry weight. Fiber recovery in tissues from control animals was shown to be significantly lower (p less than 0.005) than that from test tissues. Test groups showed highly significant differences (p less than 0.005) from each other in the fiber levels. Dose-response relationship was not significant (0.05 less than p less than 0.1). The length distribution and the alterations in morphology of the recovered fibers are described. This study is consistent with the passage of chrysotile asbestos across the gastrointestinal wall.

Animals↗

PubMed1983

Asbestos in water supplies of the United States.

The review of available data on the concentrations of asbestos in U.S. water supplies suggests that the majority of water consumers are not exposed to asbestos concentrations over 1 million fibers/Liter. A few populations, however, may be exposed to concentrations over 1 billion fibers/L. Of the 538 water supplies for which waterborne asbestos data are available, 8% have concentrations of fibers over 10 million fibers/L. The vast majority of asbestos fibers found in U.S. water supplies are under 5 micron in length.

Asbestos↗

PubMed1983

Cancer risk from asbestos in drinking water: summary of a case-control study in western Washington.

We conducted a case-control, interview-based study of the risk of developing cancer from asbestos in drinking water. An area that included Everett, Washington, was selected for the study because of the unusually high concentration of chrysotile asbestos in drinking water from the Sultan River. Through a population-based tumor registry, 382 individuals with cancer of the buccal cavity, pharynx, respiratory system, digestive system, bladder, or kidneys, diagnosed between 1977 and 1980, were identified, and they or their next of kin were interviewed. We conducted validation checks of our interviews, including a comparison with secondary sources. Data on asbestos exposure were collected based on residence and workplace history, and on individual water consumption. Logistic regression was used to estimate cancer risk. We found no convincing evidence for increased cancer risk from imbibed asbestos. Confidence intervals for relative risks for almost all sites included unity. There were significantly elevated risks only for male stomach and male pharyngeal cancer, but these sex-inconsistent results, based on small numbers of cases, are probably due to other factors.

Adult↗

PubMed1983

Comparing epidemiologic studies of ingested asbestos for use in risk assessment.

Epidemiologic data can be used in risk assessment in various ways: to calculate the dose-response relationship between exposure levels and adverse effects; to establish ranges of exposure known to be safe or unsafe; to verify an endpoint in humans derived from a route or species extrapolation; to support assumptions necessary for performing extrapolation procedures. These points are illustrated in the risk assessment for exposure to asbestos in drinking water. A previous risk assessment for asbestos, the EPA's Ambient Water Quality Criteria (AWQC) for Asbestos, was derived from cohort studies of inhalation exposure. Epidemiologic studies of ingested asbestos, all of geographical correlation design, were compared on the basis of their ability to add information in support of both the route extrapolation and low-dose extrapolation used in this risk assessment. Results of these ingestion studies were inconsistent due to variable ability to detect a risk from chronic low-level exposure. After preliminary comparisons of factors that determine scientific validity and statistical power, two ingestion studies were selected to determine if they had the potential to detect the risk predicted by the AWQC. This evaluation has shown that these studies do not offer quantitative data for estimating levels associated with a defined risk. Due to short exposure duration and limited power, clearly safe and clearly unsafe ranges could not be definitely identified. The most appropriate ingestion studies suggest, but do not prove, the endpoint derived from the route extrapolation in the AWQC.

Asbestos↗

PubMed1985

Health implications of environmental exposure to asbestos.

The health impact of environmental pollution resulting from the industrial use of asbestos can be assessed in three ways. First, there are the direct epidemiological surveys. These indicate that domestic exposure has been responsible for cases of mesothelioma and possibly lung cancer and radiological changes in family contacts of asbestos workers. Exposure in the neighborhood of crocidolite mines and factories has also resulted in cases of mesothelioma but no similar evidence exists for chrysotile or amosite. Neither air nor water pollution has been directly incriminated as a cause of either respiratory or digestive malignancies. Second, a few attempts have been made to extrapolate from exposure response findings in industrial cohorts. For several reasons, even for lung cancer, this approach is dubious: the observed gradients have a 100-fold range in slope; the equivalences of dust, fiber and gravimetric measures are largely guesswork; and the carcinogenic potential of mineral fibers, particularly for the pleura, varies enormously with fiber type and/or dimensions. No adequate exposure-response observations have been made for mesothelioma. A third approach makes use of the differing incidence of mesothelioma in men and women. Data from several countries indicate that, until the 1950s (i.e., 30-40 years after significant industrial use of asbestos began), the rates were similar in both sexes. Since then, the incidence in males has risen steeply--in the U.S. and U.K. at about 10% per annum. In females, on the other hand, there has been little or no convincing increase. These data suggest that the "background" level of mesothelioma in both sexes is and has been about 2 per million per annum and that--as at least some mesothelioma cases in females are directly or indirectly attributable to occupational exposure--there is little room left for any contribution from the general environment. It is recommended that mesothelioma surveillance, backed by appropriate epidemiological inquiries, offers an effective method of monitoring the health impact of asbestos air pollution.

Asbestos↗

PubMed1993

Interaction between smoking and asbestos in human lung adenocarcinoma: role of K-ras mutations.

To investigate the role of tobacco smoking and asbestos fibers in the etiology of human lung cancer, we examined the activating point mutations in the K-ras oncogene in DNA samples from 49 patients. Mutations were found more often in tissue from adenocarcinomas (12/21) than in tissue from tumors other than nonadenocarcinomas of the lung (3/28). Among the adenocarcinoma patients, asbestos exposure was predictive of K-ras mutation (odds ratio, 4.9; 95% confidence interval, 0.7-34.3); in patients with other types of lung cancer, the relation appeared to be an inverse one, but the numbers were small. The proportion of heavy smokers (over 50 pack-years) was 60% among people with K-ras mutations and 35% among the K-ras-negative subjects, suggesting that smoking causes K-ras mutations. If mutations in K-ras genes are caused by smoking, asbestos would act as a promoting agent by conferring selective growth conditions for clonal expansion on these mutated cells. Asbestos may favor recruitment of (initiated) K-ras mutation-positive cells in the multistage process of carcinogenesis by stimulating cellular growth.

Adenocarcinoma↗

PubMed1991

A case-control study of lung cancer with special reference to asbestos exposure.

A case-control study of lung cancer was carried out in Yokosuka City, Kanagawa Prefecture, the location of a pre-war Japanese Imperial naval factory and present site of a U.S. naval base. Cytologically or pathologically confirmed male fatal cases of lung cancer during the period of 1978 to 1982 in Yokosuka Kyosai Hospital were compared with a control group in the same hospital. Controls who died from causes other than cancer, pneumoconiosis, accident, or suicide were matched by age to the cases. Information that included occupational and smoking history was obtained by interviews with the families of the 96 cases and 86 controls. Major results were as follows: a) The relative risks of lung cancer associated with asbestos exposure and suspected exposure were 2.41 (p less than 0.05) and 1.56, respectively, after controlling for age and smoking history, and the relative risk associated with smoking was 6.01 (p less than 0.05) after adjusting for age and asbestos exposure. b) The age- and smoking-adjusted relative risks of lung cancer associated with asbestos exposure were 3.40 (p less than 0.01) and 1.72 for Kreyberg groups I and II, respectively. Significantly elevated relative risk associated with smoking history was demonstrated for Kreyberg group I, but not for group II, after controlling for age and asbestos exposure.

Asbestos↗

PubMed1997

Chemical characterization and reactivity of iron chelator-treated amphibole asbestos.

Iron in amphibole asbestos is implicated in the pathogenicity of inhaled fibers. Evidence includes the observation that iron chelators can suppress fiber-induced tissue damage. This is believed to occur via the diminished production of fiber-associated reactive oxygen species. The purpose of this study was to explore possible mechanisms for the reduction of fiber toxicity by iron chelator treatments. We studied changes in the amount and the oxidation states of bulk and surface iron in crocidolite and amosite asbestos that were treated with iron-chelating desferrioxamine, ferrozine, sodium ascorbate, and phosphate buffer solutions. The results have been compared with the ability of the fibers to produce free radicals and decompose hydrogen peroxide in a cell-free system in vitro. We found that chelators can affect the amount of iron at the surface of the asbestos fibers and its valence, and that they can modify the chemical reactivity of these surfaces. However, we found no obvious or direct correlations between fiber reactivity and the amount of iron removed, the amount of iron at the fiber surface, or the oxidation state of surface iron. Our results suggest that surface Fe3+ ions may play a role in fiber-related carboxylate radical formation, and that desferrioxamine and phosphate groups detected at treated fiber surfaces may play a role in diminishing and enhancing, respectively, fiber redox activity. It is proposed that iron mobility in the silicate structure may play a larger role in the chemical reactivity of asbestos than previously assumed.

Asbestos, Amphibole↗

PubMed1997

Early mesothelial cell proliferation after asbestos exposure: in vivo and in vitro studies.

There is some evidence that proliferation of pleural mesothelial cells (MC) occurs soon after deposition of asbestos fibers. To study this effect, we instilled a single dose of 0.1 mg crocidolite into the lungs of mice for 1 and 6 weeks and counted labeled nuclei after 3H-thymidine (3HT) injection. Short fibers (< 1 micron) induced little change in the lung; they were mostly phagocytized and had a minimal effect on MC labeling. Long fibers up to 20 microns damaged the bronchiolar epithelium and were incorporated into connective tissue. Increased 3HT uptake was seen in fibroblasts and epithelial cells and also in MC, which peaked at 2% labeled at 1 week compared to near 0% labeling in controls. No fibers were found in or near labeled MC, which suggested that a cytokine generated in the lung during the early response phase might induce MC proliferation. To look for a cytokine effect in vitro, we instilled asbestos into rat lungs and, after 1 and 6 weeks, bronchoalveolar and pleural lavage fluids as well as macrophages were collected. Alveolar macrophages contained fibers, but pleural macrophages (PM) did not. After short-term culture, macrophage supernatants and the lavage fluids were tested on rat lung MC in culture. At 1 week, PM secreted growth factor(s) for MC, and the mitogenic effect was more pronounced with lavage fluids. No effects on MC were found using material prepared 6 weeks after asbestos. The early MC growth increase was not blocked by antibodies to cytokines, such as platelet-derived growth factor, fibroblast growth factors, or tumor necrosis factor, but was inhibited by anti-keratinocyte growth factor (anti-KGF). The results show that an early growth phase of MC after asbestos exposure appears unrelated to particle translocation to the pleura but is associated with cytokine release, most likely KGF, by lung cells.

Animals↗

PubMed1998

Selected new developments in asbestos immunotoxicity.

Research over the past three decades has shown that the mammalian immune system can be altered by the occupational exposure of asbestos. Early clinical studies generally focused on systemic observations of immune alteration such as the number and function of peripheral lymphocytes and monocytes. More recently as the regulatory influence of local immunity in health and disease becomes more defined, immunologic changes occurring in the lung, the primary target organ of asbestos, have been significant areas of investigation. This review will focus on recent studies that examine the influence of asbestos on pulmonary immunity as well as the role of host immune competence in asbestos-related disease.

Animals↗

PubMed2002

The attribution of lung cancers to asbestos exposure: a pathologic study of 924 unselected cases.

We studied a series of 924 nonselected surgical cases of lung carcinoma (without occupational history in clinical records) by histologic examination and light microscopic determination of asbestos body (AB) concentration to determine cancers attributable to asbestos exposure. Lower lobes showed higher concentrations, but no significant associations were recorded between concentrations and histologic type of the lung carcinomas. Histologic asbestosis was demonstrated in 56 cases considered definitely asbestos-related. In 12 of them, the demonstration of asbestosis was attained only after repeated examination of additional sections, suggested by thefinding of more than 1,000 ABs per gram of dry weight (gdw), an indicator of occupational asbestos exposure. In the 56 cases, the media

Air Pollutants↗

PubMed1988

Neutrophil chemotactic factor release and neutrophil alveolitis in asbestos-exposed individuals.

Alveolar neutrophil accumulation occurs in asbestosis. To evaluate a possible role for release of neutrophil chemotactic factor (NCF) in the pathogenesis of asbestosis, spontaneous NCF release from alveolar macrophages obtained by bronchoalveolar lavage (BAL) in eight individuals with asbestosis, 13 asbestos-exposed individuals without asbestosis, and five control subjects has been studied. Alveolar macrophages were incubated in medium (four hours; 37 degrees C), and neutrophil responses to the supernatants were assayed in a microchemotaxis chamber. Alveolar macrophages from subjects with asbestosis released more NCF (97 +/- 19 neutrophils per high-power field [N/HPF]) than controls (3 +/- 1 N/HPF; p less than 0.01). Alveolar macrophages from individuals with asbestos exposure and increased BAL neutrophil proportions (n = 7) released more NCF (93 +/- 24 N/HPF) than individuals with asbestos exposure and normal BAL neutrophil proportions (n = 6; 11 +/- 6 N/HPF; p less than 0.02). The results show that spontaneous NCF release occurs in asbestosis and that NCF release is associated with neutrophil alveolitis in asbestos-exposed individuals without asbestosis, suggesting a pathogenic role for NCF in mediating this neutrophil alveolitis. The results of the study also suggest that the presence of crackles is a better predictor of the presence of neutrophil alveolitis than is an abnormal chest x-ray film.

Asbestos↗

PubMedDate not supplied

Biological durability and oxidative potential of man-made vitreous fibres as compared to crocidolite asbestos fibres.

In this study we investigated relationships between redox properties and biodurability of crocidolite asbestos fibres and three different man-made vitreous fibres (MMVF): traditional stone wool fibres (MMVF 21), glass fibres (MMVF 11) and refractory ceramic fibres (RCF). Each fibre type was incubated up to 22 weeks in four different incubation media: gamble solution (GS) pH 5.0 and pH 7.4, representing blood plasma without proteins, and surfactant-like solution (SLS) pH 5.0 and pH 7.4. During incubation time aliquots of incubation mixtures were removed and analysed in a biochemical model reaction, mimicking activated phagocytes. In addition, changes of fibre morphology and chemical composition were examined using SEM- and EDX-technology. In the presence of crocidolite asbestos fibres and MMVF 21 the formation of OH*-radicals according to the Haber-Weiss sequence could be demonstrated, whereas MMVF 11 and RCF showed no reactivity. Crocidolite asbestos fibres exhibited a significant higher activity compared with the stone wool fibres at the onset of incubation. The oxidative capacities of these fibre types were shown to depend on both specific surface area and iron content. The oxidative potentials of crocidolite asbestos fibres as well as MMVF 21 were not constant during incubation over several weeks in each incubation medium. The reactivities showed sinoidal curves including reactivities much higher than those at the onset of incubation time. These irregular changes of oxidative capacity may be explained by changes of the redox state of fibre surface-complexed iron. Furthermore our results showed clear differences between incubation of fibres in GS and SLS, respectively, indicating that phospholipids play an important part in fibre dissolution behaviour and oxidative reactivity. In conclusion we suggest, that biodurability testing procedures should not exclusively concentrate on dissolution rates of fibres. They should include fibre characteristics concerning known pathogenic mechanisms to evaluate the real toxic potential of the fibre type looking at. Secondly we suggest, that phospholipids should be constituents of incubation liquids used for standardised fibre biodurability test procedures thus representing more realistic incubation conditions.

Asbestos, Crocidolite↗