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PubMed1983

Asbestos in drinking water: a status report.

The conference is briefly reviewed in the light of its impact on future regulatory decisions regarding the possible control of asbestos fiber in drinking water. The results of animal feeding studies indicate that asbestos fails to demonstrate toxicity in whole-animal lifetime exposures. The epidemiologic evidence of risk from ingestion of water containing asbestos fibers is not convincing, and in view of the lack of confirmation by animal studies, the existence of a risk has not been proven; however occupational gastrointestinal cancer may indicate ingestion risk. Whether or not there is a risk from asbestos in drinking water, however, common sense tells us to deal with an undesirable situation by employing means that are commonly and economically available. Well-known methods can minimize the presence of asbestos fibers in finished drinking water. In the case of natural fiber in raw water, standard or augmented filtration practices are extremely effective. If the source of asbestos fiber is asbestos-cement pipe that is being attacked by corrosive water, then, there is more than sufficient economic reason to correct the corrosivity of the water.

Animals↗

PubMed1989

Evidence supporting a role for active oxygen species in asbestos-induced toxicity and lung disease.

Asbestos is an important occupational and environmental toxicant that affects several cell types in the respiratory tract. In an effort to understand how asbestos causes cell injury and/or altered proliferation and differentiation of cells, this laboratory has focused on reactive oxygen species as mediators of asbestos-induced biological effects. A compendium of experimental results reported by this laboratory and others supports this hypothesis. For example, scavengers of reactive oxygen metabolites and iron chelators (i.e., desferroxamine) prevent cytotoxicity after addition of asbestos to a variety of cell lines and macrophages in vitro. DNA strand breakage associated with toxicity of crocidolite asbestos in C3H10T 1/2 cells also is ameliorated with use of desferroxamine. All types of asbestos cause lipid peroxidation in mammalian cells and artificial membranes, a phenomenon that can be prevented by removal of catalytic iron. Last, asbestos causes generation of active oxygen species after interaction with leukocytes or by reduction of oxygen on the surface of the fibers.

Antioxidants↗

PubMed1994

Asbestos and colon cancer: a weight-of-the-evidence review.

What is the evidence that exposure to asbestos causes colon cancer? This weight-of-evidence review considers epidemiologic evidence from cohort studies of asbestos-exposed workers, case-control studies of colon cancer, animal bioassays, and other corroborative evidence. The major evidence for a causal association at high exposure is a combined colorectal standardized mortality ratio (SMR) of 1.5 for asbestos cohorts where the lung cancer SMR was greater than twofold. However, misdiagnosis may spuriously elevate the SMR. The strongest evidence against a causal association between colon cancer and asbestos exposure is the lack of an exposure-response gradient in asbestos cohorts where trends for lung cancer are observed. Population-based case-control studies of colon cancer do not show any consistent risk associated with asbestos exposure. Long-term ingestion studies show no evidence of an increased incidence of colon cancer in animals by this route of exposure and do not provide biological plausibility for a causal association between asbestos exposure and colon cancer.

Alcohol Drinking↗

PubMed1997

Lung proliferative and clearance responses to inhaled para-aramid RFP in exposed hamsters and rats: comparisons with chrysotile asbestos fibers.

This study compared pulmonary effects of para-aramid respirable-sized, fiber-shaped particles (RFP) (p-aramid fibrils) and chrysotile asbestos fiber exposures in rats. Additional p-aramid inhalation studies were conducted in hamsters to compare species responses. The hamster results are preliminary. The parameters studied were clearance/biopersistence of inhaled p-aramid RFP or size-separated asbestos fibers as well as pulmonary cell proliferation and inflammation indices after 2-week inhalation exposures. Rats were exposed nose only to chrysotile asbestos fibers at concentrations of 459 and 782 fibers/ml or to p-aramid RFP at 419 or 772 fibrils/ml. Hamsters were exposed whole body to p-aramid RFP at concentrations of 358 and 659 fibrils/ml. Subsequently, animals were assessed immediately (time 0) as well as 5 days (10 days for hamsters), 1, 3, 6, and 12 months postexposure. Lung burdens for the p-aramid-exposed rats were 4.8 x 10(7) and 7.6 x 10(7) fibrils/lung, with similar numbers of chrysotile fibers > 5 microns recovered from the lungs of asbestos-exposed rats. In comparison, 1.4 x 10(6) fibrils/lung were recovered in the high-dose hamster group. Biopersistence studies in p-aramid-exposed rats and hamsters demonstrated an initial increase (relative to time 0) in retained p-aramid fibrils during the first month postexposure, which indicated breakage or shortening of inhaled fibrils. This result was associated with a progressive reduction, and increased residence time in the lung, in the mean lengths of the fibrils, which signified biodegradability of inhaled p-aramid fibrils in both species. In contrast, clearance of short chrysotile asbestos fibers was rapid, but clearance of the long chrysotile fibers was slow or insignificant, as evidenced by a progressive increase over time in the mean lengths of fibers recovered from the lungs of exposed rats. Two-week, high-dose exposures to p-aramid in both rats and hamsters produced transient increases in pulmonary inflammatory and cell proliferative responses. In contrast, inhalation of size-separated chrysotile asbestos fibers in rats produced persistent increases in cell labeling indices of airway, alveolar, and subpleural cells measured through a period of 1 to 3 months postexposure. These results suggest that inhaled p-aramid RFP are biodegradable in the lungs of exposed rats and hamsters. In contrast, exposures to chrysotile asbestos fibers in rats resulted in a selective pulmonary retention of long chrysotile fibers.

Administration, Inhalation↗

PubMed2004

Changing patterns in asbestos-induced lung disease.

STUDY OBJECTIVES: To determine patterns in asbestos-induced lung diseases found in older, less exposed workers. DESIGN: Review of a database evaluating lung function, smoking status, form of asbestos-induced lung disease, and radiograph abnormalities. SETTING: Outpatient clinic. PARTICIPANTS: A total of 3383 asbestos-exposed workers referred for independent medical evaluation, including control subjects who lacked asbestos-specific radiograph abnormalities (n = 243), subjects with low International Labor Organization (ILO) scores (n = 2,685), high ILO scores (n = 312), bronchogenic cancer (n = 63), and mesothelioma (n = 80). Of these, 3,327 workers have specific smoking status information and 3,312 workers have lung volume measures. INTERVENTIONS: Chest radiographs were interpreted by a certified B-reader, and abnormalities were quantified according to the ILO scoring system. Spirometry and lung volume measurement were performed. Subjects completed a self-administered questionnaire that was reviewed at the time of examination. Control subjects were screened on two separate occasions at least 10 years apart to exclude subclinical or slowly progressive asbestos-induced lung disease. MEASUREMENTS AND RESULTS: The mean age of the population was 65.1 +/- 9.9 years, and the latency was 41.4 +/- 10.1 years (+/- SD). Most subjects (41.8%) had normal pulmonary function. Obstruction was the most common pulmonary function abnormality (25.4%), followed by restriction (19.3%) and a mixed pattern (6.0%). Most subjects (79.4%) had low ILO scores. Benign pleural abnormalities were the only findings in 54% of subjects with low ILO score. Subjects with high ILO scores were older, smoked more, and had a longer latency than subjects with low ILO scores and control subjects. Smokers were younger, had a shorter latency, and had paradoxically greater ILO scores than nonsmokers. Subjects with bronchogenic cancer and mesothelioma had longer latencies than control subjects and subjects with benign asbestos-induced lung disease. CONCLUSIONS: Asbestos-induced lung disease today is characterized by low ILO scores, long latencies, greater disease magnitude in smokers, and a normal or obstructive pattern of pulmonary function abnormality. Spirometric evaluation in the absence of lung volume measurements caused misclassification that resulted in overestimation of the presence of a restrictive pattern of pulmonary function.

Adult↗

PubMed1980

Presence of asbestos bodies in organs other than the lung.

This study was designed to test the hypothesis that subjects with many asbestos bodies in their lungs at autopsy would also have asbestos bodies in various other organs. The subjects included 19 cases with diagnosis of asbestosis at death (two of these had mesothelioma, five had lung cancer) and 18 with pleural plaques but not asbestosis. Occupational histories were obtained from relatives. In subjects occupationally exposed to asbestos, large numbers of asbestos bodies were found in the lungs, and in most of these, asbestos bodies were found in many of the other organs examined. In the 18 cases with only pleural plaques found at autopsy, considerably fewer asbestos bodies were found in the lungs. The number of other organs with one or more asbestos bodies ranged from 32 percent to 62 percent of the sites examined. The findings seem to confirm the hypothesis of the study.

Aged↗

PubMed1990

[Active oxygen species and asbestos toxicity].

It has been demonstrated that active oxygen species is involved in inflammation, immunologic disorders, cancer, etc. Along this line, biological effects of asbestos have been investigated. The results of these studies can be classified into two groups. The first is based on researches on hydroxy radical, the most active oxygen species which originates through the catalytic reaction of asbestos iron. It has been confirmed that cigarette smoke enhances hydroxy radical induction with asbestos exposure. This combined exposure causes greater DNA damages than exposure to them independently. The second is based on researches on release of active oxygen species due to interaction between asbestos and phagocytic cells. In addition to either alveolar or peritoneal macrophages and polymorphonuclear leukocytes, lung fibroblast and endarterial cells have been confirmed to release active oxygen species after exposure to asbestos. However, this has not been confirmed with mesothelial cells. These evidences associated with asbestos exposure and generation of active oxygen species are available for checking the safety of many kinds of synthetic mineral fibers which are recently replacing asbestos.

Animals↗

PubMed2006

Asbestos products, hazards, and regulation.

Asbestos is present in the United States in a multitude of products used in past decades, and in some products that continue to be imported and domestically produced. We have limited information on the hazards posed by some of these individual products and no information at all on most of them. Legal discovery of corporate documents has shed some light on the use of asbestos in some products and exposures from asbestos in others, sometimes adding considerably to what was in the published literature. But liability concerns have motivated corporate efforts to curtail governmental public health guidance on long-recognized hazards to workers. Liability considerations have also evidently led, in the case of asbestos brake linings, to the support of publication in the scientific literature of review articles denying in the 21st century what had been widely accepted and established in health policy in the 20th century. This report is an effort to illustrate the suppression and emergence of scientific knowledge in a climate of regulation and liability. Examples discussed are vinyl-asbestos flooring, feminine hygiene products, automotive friction materials, and asbestos contamination of other minerals such as talc and vermiculite. Global efforts to deal with the hazards of continuing marketing of asbestos products are also discussed.

Asbestos↗

PubMed2000

Asbestos exposure in a shipyard area, northeastern Italy.

The Monfalcone area, northeastern Italy, is a small industrial district (population 60,000), with a large shipyard. In order to monitor asbestos exposure in this area, a series of 3,640 necropsies, carried out at the Monfalcone Hospital between October 1979 and September 1998, were investigated. The thoracic cavities were examined for pleural plaques; these were classified into three classes (small, moderate, large). Routine histological sections of lung tissue were examined for asbestos bodies. Isolation and counting of asbestos bodies were performed in 1,075 cases. Lifetime occupational data were collected in 1,277 cases. Pleural plaques were observed in 70.5% among men and in 23.8% among women. The prevalences of pleural plaques did not show significant variations during the study period. Asbestos bodies were found on routine lung sections in 23.7% of men and 3.0% of women. The shipyard workers, the most numerous category in the series, were characterized by high prevalence of pleural plaques (total 86.7%, large 32.4%), high prevalence of asbestos bodies on routine lung sections (35.3%), and high amounts of lung asbestos bodies after isolation. The present data indicate that asbestos exposure may reach alarming levels in the shipyard areas.

Adolescent↗

PubMed2003

Clinical study of asbestos-related lung cancer.

We analyzed the characteristics of 120 patients of primary lung cancer supposed to be induced by exposure to asbestos. Most of 120 patients were male and the age ranged from 47 to 87 years with a median of 70 years. No particular tendency was observed in the histological types of the lung cancer in 120 patients. Forty of the 120 patients were heavy smokers. When the occupational history was analyzed, most of the patients had been exposed to asbestos in former Japanese naval shipyard, commercial shipyards, construction industry and ironworks. The term of asbestos exposure was 2 to 60 years with a median 27 years. Lung cancers appeared after 15 to 69 years with a median 43 years from the initial exposure to asbestos. Lung cancer was accompanied by asbestosis in 35 patients and by pleural plaques in 77. Twenty-two patients had both asbestosis and pleural plaques. The number of asbestos bodies per 5 g wet lung tissue for 72 patients whose lung tissues obtained from autopsy or surgery was more than 150 bodies which meant the number of occupational asbestos exposure. As for the kinds of asbestos fibers of 32 patients, 14 patients exposed to crocidolite, 10 patients to amosite and 8 patients to chrysotile.

Age of Onset↗

PubMed1986

Pathophysiologic correlations in asbestos-induced airway disease in the guinea pig.

To determine whether asbestos-induced changes in the structure of the walls of small airways might be associated with abnormalities of pulmonary function, guinea pigs were given 10 mg of amosite asbestos (test group) or saline (control group) by intratracheal instillation. Pulmonary function tests performed 6 months later revealed significant increases in FRC, RV, and TLC in the test group. Measurement of airway wall thickness showed that both membranous and respiratory bronchioles were significantly thickened in the test group; this group also had airways of smaller internal diameter than the controls. Analysis for lung collagen content as hydroxyproline showed a 50% increase in the asbestos exposed animals. There was, however, only minimal and very focal interstitial fibrosis (asbestosis) in the lung parenchyma. Analysis of fiber size indicated that the fibers obtained by digestion of the tissue or from the lavage fluid were significantly longer and wider than those in the original asbestos sample; however, the tissue contained considerably larger fibers than the lavage fluid. We conclude that: Asbestos can produce airway fibrosis and narrowing causing air trapping on pulmonary function examination; this process occurs in the absence of significant interstitial fibrosis of the parenchyma (asbestosis), implying that abnormalities of pulmonary function which are consistent with airflow obstruction in asbestos exposed animals can be caused by pathologic changes in the small airways alone; long asbestos fibers are preferentially retained in the lung, and the longest fibers appear to be in a compartment inaccessible to lavage, presumably, in this model, in airway walls. Enhanced penetration of long fibers into tissue may be one reason why long fibers are more pathogenic than short ones.

Animals↗

PubMedDate not supplied

Chrysotile asbestos and H2O2 increase permeability of alveolar epithelium.

The alveolar epithelium contains tight junctions and provides a barrier to passage of potentially injurious substances into the pulmonary interstitium. Alveolar epithelial injury is hypothesized to be an important early event in the pathogenesis of asbestosis. Mechanisms that may contribute to alveolar epithelial cell injury following asbestos exposure include the physicochemical interactions between asbestos fibers and cells, and the generation of reactive oxygen species such as hydrogen peroxide (H2O2). The present study examined changes in transepithelial resistance (Rt) (a measure of barrier function) and permeability of alveolar epithelium after chrysotile asbestos and H2O2 exposure. Alveolar epithelial cell monolayers, obtained from isolation of rat alveolar type II cells and grown on porous supports, were exposed to chrysotile asbestos or polystyrene beads (control) at concentrations of 5, 10, and 25 micrograms/cm2 for 24 h. In separate experiments, monolayers were exposed to H2O2 at concentrations of 50, 75, and 100 microM for 1 h Rt was measured using a voltohmmeter. Prior to treatment, monolayers had a high Rt (> 2000 ohms.cm2). Permeability was assessed by measuring flux of [3H]sucrose from apical to basolateral compartments. Cytotoxicity was evaluated by lactate dehydrogenase (LDH) and preincorporated [14C]adenine release. The morphological integrity of the monolayers was evaluated by scanning electron microscopy. Chrysotile asbestos and H2O2 exposure resulted in dose-dependent decrease in alveolar epithelial Rt and increases in permeability under conditions that did not result in over cytotoxicity. These results demonstrate that both chrysotile asbestos and H2O2 have effects on alveolar epithelial Rt and permeability and suggest a potential role for the alveolar epithelium in mediation of asbestos-induced pulmonary interstitial disease.

Animals↗

PubMed1994

Asbestos exposure and pulmonary fiber concentrations of 300 Finnish urban men.

OBJECTIVES: The aim of the study was to determine the pulmonary concentrations of mineral fibers in the Finnish male urban population and to evaluate the analysis of pulmonary fiber burden by scanning electron microscopy (SEM) as an indicator of past fiber exposure. METHODS: The pulmonary concentration of mineral fibers was determined by SEM and compared with occupational history for a series of 300 autopsies of urban men aged 33 to 69 years. RESULTS: The concentration of fibers (f) longer than 1 micron ranged from < 0.3 to 163.10(6) per gram of dry tissue (f.g-1). Asbestos fiber concentrations exceeding 1.10(6) f.g-1 were observed in 33% of the cases with probable occupational exposure to asbestos and 1% of the cases with unlikely occupational exposure. Even asbestos fiber concentrations of 0.3 to 1.10(6) f.g-1, especially of crocidolite-amosite fibers, were rare among the men with unlikely occupational exposure. Fiber concentrations exceeding or equaling 1.10(6) f.g-1 were 10 times more frequent among the men more than 60 years of age as compared with those less than 40 years of age. Inorganic fibers other than asbestos had a weaker correlation with occupational history and age. Smoking habits had no significant effect on the pulmonary fiber counts. CONCLUSIONS: Asbestos fiber concentrations exceeding 1.10(6) f.g-1 are highly indicative of past occupational exposure to asbestos. The distribution of fiber concentrations in the different age groups of this study indicated decreasing asbestos exposure in Finland since the 1970s.

Adult↗

PubMed1995

Radiographic small lung opacities and pleural abnormalities as a consequence of asbestos exposure in an adult population.

OBJECTIVES: The purpose of this study was to estimate the role of past asbestos exposure as a cause of radiographic small lung opacities and pleural abnormalities in the Finnish adult population. METHODS: The study was conducted in 1978-1981 and was based on a population sample (N = 8000) representative of the Finnish population aged 30 years or over. Full-size chest radiographs and a complete job title history were available for 3811 women and 3274 men. The radiographs were classified according to the 1980 classification of radiographs of pneumoconioses published by the International Labour Office and the work histories according to the probability of occupational asbestos exposure. Age- and smoking-adjusted relative risks of radiographic parenchymal and pleural abnormalities were calculated with the analysis of covariance according to the probability of asbestos exposure. RESULTS: About 13% of the men and 0.8% of the women were classified as probably exposed to asbestos. There was more than 90% agreement in the repeated work history evaluations. The risk of small lung opacities was significantly increased among the probably exposed men [risk ratio (RR) 1.7 for ILO profusion category 1/1 or more and RR 1.6 for profusion category 1/0]. The risk of pleural plaques was increased both among the men (RR 3.0) and the women (RR 4.8) with probable exposure. The risk of thickened horizontal interlobar fissure was also increased among the probably exposed men (RR 1.7). Among the men, the etiologic fraction attributable to occupational asbestos exposure was about 30% for small lung opacities, about 40% for pleural plaques, and about 20% for thickened horizontal fissure. Among the women the etiologic fractions for asbestos were similar for pleural abnormalities, but much lower for parenchymal ones. CONCLUSIONS: Occupational asbestos exposure has been common among Finnish men, and it plays a significant role in the etiology of both pleural and parenchymal abnormalities also at the level of the general population.

Adult↗

PubMed2003

Diffuse pleural fibrosis--an unreliable indicator of heavy asbestos exposure?

OBJECTIVES: This study aimed at testing the hypothesis that diffuse pleural fibrosis is associated with a heavier exposure to asbestos than that of benign pleural plaques, and hence diffuse pleural fibrosis can be used as a marker of heavy exposure. METHODS: Asbestos burden was estimated for 192 naval dockyard workers (96 with diffuse pleural fibrosis, 96 with plaques) by calculating the exposure ratings from the trade and the years spent in that trade. In 53 cases the diffuse pleural fibrosis was bilateral. RESULTS: No difference was found in the mean estimated asbestos burden between all diffuse pleural fibrosis and plaques, nor between plaques and unilateral and bilateral diffuse pleural fibrosis, analyzed separately by a one-factor analysis of variance. The mean asbestos burden was significantly greater for bilateral than for unilateral diffuse pleural fibrosis. A wide spread of asbestos exposure was noted among the men with diffuse pleural fibrosis. CONCLUSIONS: Diffuse pleural fibrosis may arise after widely varying exposure to asbestos. The mean exposure ratings for diffuse pleural fibrosis do not differ from those for pleural plaques, although the ratings are significantly higher for men with bilateral diffuse pleural fibrosis than for those with unilateral diffuse pleural fibrosis. Diffuse pleural fibrosis cannot be used as a reliable marker of heavy asbestos exposure.

Adult↗

PubMed1976

Effect of changed working techniques on asbestos dust levels in the working environment.

The methods are presented for correcting the working environment when asbestos dust concentrations are too high. Asbestos dust, being fibrous, remains suspended longer than most industrial dusts, and has a tendency to pack and cling together. Sophisticated monitoring techniques have made possible the attainment of standards that are effective in controlling risks of asbestos related diseases. The most difficult situation to control is the dust produced in stripping old asbestos lagging, but predamping has greatly reduced the contamination. Special attention has been paid to the special needs of people working with asbestos on building sites. Special hoods have been designed to protect workers drilling, cutting and sanding asbestos material. The Environmental Control Committee has prepared a series of Control and Safety Guides and a Code of Practice for the Disposal of Asbestos Waste Material as part of activities to promote new and improved methods of dust control.

Asbestos↗

PubMedDate not supplied

[A report of 3 cases of pleural mesothelioma with unusual asbestos exposure].

The occurrence of malignant pleural mesothelioma (MT) is a sentinel event in occupational and environmental medicine. The association of pleural MT and asbestos exposure is well documented and it is well known that no threshold can be demonstrated below which there is no risk of developing MT. During the period 1994-1998, 3 patients were referred from the Pneumology Division to the Occupational Medicine Department of the Spedali Civili in Brescia. They had MT and they had a peculiar asbestos exposure. A thorough occupational and environmental history was taken by means of a standardized questionnaire. The first patient was environmentally exposed to crocidolite when she lived near an asbestos mine in Australia. The second was a teacher and the third was a goldsmith and both were occupationally exposed to asbestos. The case descriptions revealed the importance of a standardized evaluation of occupational and environmental exposure to asbestos. In this way otherwise ignored asbestos exposures can be identified therefore avoiding an underestimation of MT attributable to asbestos. The role of the occupational physician, both in hospital referrals and while taking standardized histories, is also stressed along with the importance of this contribution on the one hand to the epidemiological recording of sentinel events and on the other to the etiological definition of the cases, which was in fact our principal aim.

Aged↗

PubMedDate not supplied

[The incidence of malignant mesothelioma (1977-1996) and asbestos exposure in the population of an area neighboring Lake Iseo, northern Italy].

The study was stimulated by the occurrence of malignant mesotheliomas among the workers of two adjacent factories located in Sarnico, near Lake Iseo (province of Brescia, northern Italy), one of which manufactured crocidolite and chrysotile ropes and gaskets until 1993. The aim of the study was: identification of malignant mesotheliomas occurring between 1977 and 1996 among the residents of 11 villages, which constituted the recruitment area of the work-force; estimation of the incidence of malignant pleural mesothelioma; collection of working histories of all cases to evaluate previous exposure to asbestos and radiation therapy. 21 cases of mesothelioma were detected (20 pleural, 1 peritoneal; 9 among males), and 20 were supported by histopathologic diagnosis. The incidence (x 100,000 person-years, standard: European population) was 2.5 (0.7-4.2) and 2.8 (1.2-4.3) among males and females, respectively, corresponding to a three-fold increase among males and a more than ten fold increase among women in comparison with the incidence reported by the Lombardy Cancer Registry. No cases had been exposed to radiation therapy, whereas all cases had been occupationally exposed to asbestos. Occupational exposure to asbestos had occurred in work on the production of crocidolite and chrysotile ropes and gaskets (6 males); in work in a textile factory producing cotton garments that was adjacent to and polluted by the former, where, in addition, chrysotile blankets were used for fireproofing in the weaving area and pipes were insulated using amosite-containing materials (10 cases, 6 among females); 5 cases occurred among women working in silk factories, where asbestos exposure was possible because of the presence of pipes insulated with asbestos and because women were handling temperature-controlled trays insulted with asbestos. In conclusion, the study demonstrated that the occurrence of mesothelioma was higher among females than males in the study area and that all cases of mesotheliomas had been occupationally exposed to asbestos.

Age Distribution↗