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PubMed2000

Association of concentration of asbestos and asbestos-like fibers with the patient's survival and the binding capacity of lung parenchyma to galectin-1 and natural alpha-galactoside- and alpha-mannoside-binding immunoglobulin G subfractions from human serum.

Our aim in this study was to search for lung parenchyma alterations associated with asbestos and/or asbestos-like fiber concentration. This was done by means of immuno- or glycohistochemistry. The hot-ashing technique determined the asbestos and asbestos-like fiber concentrations in the lung tissues of 100 patients of whom 52 were treated for primary lung and 25 for secondary lung tumors; fiber concentration was also measured for 23 patients whose disease was benign. The results were correlated to smoking habits, survival of the patients, and expression of binding capacities for endogenous lectins, natural carbohydrate-binding and lectin-specific antibodies. The cohort with proven asbestos exposure revealed a mean fiber concentration 114 f/g compared to 95 f/g in the non-exposed group. An increased asbestos fiber concentration was correlated to galectin-1-binding and the presence of epitopes for natural immunoglobulin G subfractions with selectivity to alpha-galactosides and alpha-mannosides. The survival of patients with primary and secondary lung tumors was negatively associated with the fiber concentration. The data indicate that increased presence of asbestos is correlated with an alteration of defined glycohistochemical features of alveolar lining cells.

Adult↗
PubMedDate not supplied

Asbestos fiber analysis in nine lung cancer cases with high asbestos exposure.

We examined the types and sizes of 100 asbestos fibers in lung tissue obtained from 9 lung-cancer cases (5 autopsy and 4 surgical) with more than 10(4) asbestos bodies per 5 g of wet lung tissue, asbestos bodies in histological sections, and the history of occupational asbestos exposure. Evaluation of asbestos fibers by transmission electron microscopy (2,000 x magnification) revealed that most fibers were longer than 3 microns (96%) and were thicker than 0.1 micron (93%). The analytical conditions we used enabled us to identify 99.7% of all asbestos fibers as being amphibole asbestos. Crocidolite fiber, which was found most frequently (73.1%), was the predominant type of fiber found in 8 of the 9 cases; crocidolite was followed by amosite (21.7%), which was the predominant type found in the remaining case. Crocidolite fibers were thin and had a high aspect ratio (mean diameter = 0.23 micron, mean aspect ratio [length/diameter] = 85.5). Amosite fibers were long, and they also had a high aspect ratio (mean length = 21.8 microns, mean aspect ratio = 66.4). It has been suggested that such fibers with a high aspect ratio are strongly carcinogenic to pulmonary parenchyma. Review of our previous and present data with respect to the ratio of amosite to crocidolite fibers in groups of subjects who had various diseases revealed that this ratio was relatively constant in some occupations. The more predominant fibers found were crocidolite in insulation workers and amosite in railroad workers. The ratio of amosite to crocidolite fibers should be considered in tissue-burden studies.

Adult↗
PubMed2006

Pleural mesothelioma in a woman whose documented past exposure to asbestos was from smoking asbestos-containing filtered cigarettes: the comparative value of analytical transmission electron microscopic analysis of lung and lymph-node tissue.

Asbestos has had many commercial applications, including its use as a major component in various types of filters. Between 1952 and 1956, crocidolite asbestos was used as a component of filters for cigarettes, reportedly greatly reducing tars and nicotine from mainstream smoke. This case report quantifies asbestos burden in lung and lymph node tissue in a 67-yr-old woman who succumbed to mesothelioma. Her only historically documented exposure to asbestos was from smoking crocidolite asbestos-containing filtered cigarettes between 1952 and 1956. Tissue digestion analysis by analytical transmission electron microscopy (ATEM) identified crocidolite fibers in lungs and thoracic lymph nodes. Combined ATEM data of lung and lymph node tissue clarified the patient's exposure to asbestos and particularly to crocidolite asbestos and thus to the presence of an entity recognized as the causal agent for mesothelioma.

Aged↗
PubMed1993

The frequency of p53 immunostaining in asbestos-associated mesotheliomas and non-asbestos-associated mesotheliomas.

It has been suggested that asbestos might have an important role in the development of p53 mutations in mesotheliomas. The objective of this study was to examine asbestos-associated mesotheliomas and non-asbestos-associated mesotheliomas to establish whether the frequency of p53 immunostaining and, by implication, p53 gene mutation is related to asbestos exposure. Immunopositivity for p53 was found in seven (44%) of the 16 mesotheliomas examined. The frequency was approximately the same in both the asbestos-associated mesotheliomas and the non-asbestos-associated mesotheliomas. It is concluded that the frequency of p53 immunostaining in mesotheliomas and, by implication, the frequency of p53 gene mutation is probably not related to asbestos exposure.

Asbestos↗
PubMed1992

Fibres and asbestos bodies in bronchoalveolar lavage fluids of asbestos sprayers.

The alveolar content of fibres and asbestos bodies was assessed by bronchoalveolar lavage (BAL) in 21 asbestos sprayers. Transmission and scanning electron microscopy (TEM and SEM) and two light microscopical (LM) methods, cytocentrifugation, and Millipore filtration were used. The subjects had been exposed mainly to crocidolite asbestos for an average of 2.8 (range 0.2-13) years in 1950-75. The mean (median) total fibre count (of asbestos bodies and uncoated fibres) per ml of BAL fluid was 5500 (2800) by TEM and 2900 (1000) by SEM. The mean (median) count of asbestos bodies per ml with LM was 810 (500) with cytocentrifugation and 750 (480) with Millipore filtration, 840 (320) by TEM, and 1750 (420) by SEM. The mean proportion of coated fibres was 35% by TEM and 45% by SEM. The mean length of the coated fibres was 22 (range 4-65) microns by TEM and 34 (range 4.5-170) microns by SEM. The total fibre count exceeded 1000 fibres per ml in 70% of the cases by TEM. Asbestos body counts exceeded 1 per ml in 95% of the cases by LM. The fibre counts by SEM were in good accordance with counts by TEM except in a few cases in which the TEM result was considerably higher. In these cases the proportion of coated fibres was also low. All four counting methods appeared to give consistent results in heavily exposed cases when fibre load in the lungs was high. The counting of asbestos bodies may, however, underestimate the total alveolar fibre load in some cases.

Adult↗
PubMed1979

Analysis of the cores of asbestos bodies from members of the general population: patients with probable low-degree exposure to asbestos.

Asbestos bodies were isolated from the lungs of 21 patients who had 300 to 9,000 of such bodies/g of lung tissue, a concentration frequently found in manual laborers in the general population who are not primary asbestos workers. All of the 123 bodies examined by electron diffraction produced diffraction patterns consistent with amphibole varieties of asbestos. Electron microprobe analysis (energy dispersive x-ray spectroscopy) of 46 bodies revealed that 38 of the cores were composed of the commercial amphiboles, amosite and crocidolite, whereas only 8 were composed of the noncommercial amphiboles, anthophyllite and tremolite. Review of the occupations of these patients revealed that all but one had blue-collar jobs. For many of these persons, putative sources of asbestos exposure such as construction work could be defined, but for some, the source could not be determined. One woman was apparently exposed to asbestos in the practice of her hobby of ceramics, in which she used anthophyllite-contaminated clay. We concluded that commercial amosite/crocidolite asbestos forms the cores of most asbestos bodies in manual laborers in the general population and that the source is usually occupational.

Adult↗
PubMed1988

Natural killer cell activity in asbestos workers. Interactive effects of smoking and asbestos exposure.

Both the numbers and function of natural killer (NK) cells in 60 were evaluated in asbestos cement workers grouped by smoking history and chest roentgenogram findings (ILO profusion scores less than 1/0 or greater than or equal to 1/0, or isolated pleural plaques). Worker and control subjects who smoked had smoking histories of less than 27 pack-years, a level of smoking lower than that previously determined to adversely affect NK function. Asbestos workers who did not smoke had percentages and total numbers of NK cells and NK function not different from that of nonsmoker control subjects. Workers who smoked and had evidence of asbestosis (ILO profusion category greater than or equal to 1/0) had significantly lower total numbers of NK cells and mononuclear cell NK activity than did smoker control subjects or smokers with pleural plaques only (p less than or equal to 0.05). Numbers of NK cells and NK cell function were not decreased in either of the asbestos-exposed smoking groups without asbestosis when compared to nonsmoker controls. We conclude that smoking and asbestos exposure interact to decrease mononuclear cell NK function in workers with levels of asbestos exposure sufficient to induce asbestosis. This finding may explain in part the previously reported synergistic effect of smoking and asbestos exposure on the risk of lung cancer. Furthermore, the data presented here clarify previous conflicting reports on NK function where asbestos exposed groups have not been stratified for analysis of data.

Adult↗
PubMed1989

Asbestos fibre release by corroded and weathered asbestos-cement products.

A description is given of portable equipment and a method of sampling and measuring asbestos fibre emissions from solid plane surfaces of asbestos-cement products (roofs and facades). Asbestos-cement products, e.g., roof tiles, contain as much as 11-12% of chrysotile asbestos. As a result of continuing exposure to the weather and to acid rain, the surface of asbestos-cement products becomes corroded and weathered. Cement particles, asbestos fibres and agglomerates of particles and fibres are therefore released from the surface and dispersed in air and water. The method described has been used to measure asbestos fibre emissions and ambient air concentrations in the Federal Republic of Germany over the period 1984-1986.

Air Pollutants↗
PubMed1986

Studies on surface properties of asbestos. III. Interactions between asbestos and polynuclear aromatic hydrocarbons.

The purpose of this study is to reveal the nature of the physicochemical interactions between asbestos and polynuclear aromatic hydrocarbons (PAH) in an organic liquid medium, and to assist in the understanding of synergistic effects between asbestos and PAH in bronchopulmonary cancers. The adsorption curves of three PAH (phenanthrene, fluorene, dimethyl-7,12-benzanthracene) on chrysotile and crocidolite are multistep isotherms and show the formation of bidimensional condensed layers (2D) of PAH. This phenomenon is observed with solids having a dominant basic character (asbestos, magnesia) but is not detected with acidic solids (alumina, silica-alumina). The elimination of water and dissolved gases (O2, CO2) in the liquid medium increased the affinity of asbestos for PAH. The coadsorption CO2-phenanthrene on the substrate decreased the adsorbed quantities of solute but did not inhibit the formation of layers (2D). The adsorption is weaker on leached chrysotile, than on original chrysotile; the amorphous silica coating the fibers has no affinity for PAH; the adsorption is only due to some active sites present on the surface of residual chrysotile which is accessible to phenanthrene. The formation of layers (2D) is due to strong interactions between PAH having an induced or permanent dipole moment and the active electron donor sites present on the mineral surface. The equilibrium equation between the adsorbed layer and the PAH in solution is established by reference to theoretical studies, and the results allowed us to classify the charge density of the mineral surface. The interactions between PAH and asbestos allowed us to explain the differences introduced in the kinetics of PAH uptake toward the cells when PAH is preadsorbed on asbestos. This fact could, in part, explain the synergistic effects observed in carcinogenesis.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1993

Absence of amosite asbestos in airway mucosa of non-smoking long term workers with occupational exposure to asbestos.

There is considerable experimental evidence that asbestos fibres are taken up by epithelial cells, and that uptake of fibres is associated with various deleterious, particularly mutagenic, effects. It is not known, however, if asbestos fibres are taken up by human bronchial epithelial cells in vivo. To investigate this question, the amosite asbestos content of the mucosa of seven different airways and four parenchymal sites supplied by these airways in six necropsy lungs from heavily exposed never-smoking long term shipyard and insulation workers without asbestosis was examined. Amosite asbestos was readily found in moderately high concentration in all parenchymal samples, but 33 of 40 airway samples that could be evaluated showed no amosite fibres. The seven positive airways had fibre concentrations that were always much lower than the parenchymal concentrations, and these very few fibres may have been contaminants from the parenchyma. These data suggest that, at least in non-smokers, amosite asbestos either does not penetrate into or does not accumulate in human airway mucosa. These findings also call into question the idea that asbestos acts as a direct airway carcinogen in humans.

Aged↗
PubMed1980

Asbestos body content of the larnyx in asbestos workers. A study of five cases.

Occupational exposure to asbestos has been epidemiologically associated with carcinoma of the larynx; however, no search for or quantitation of laryngeal asbestos bodies has been performed. This report concerns an autopsy study of five patients with occupational asbestos exposure and proven asbestos-associated pulmonary disease in whom histologic sections of the larynx were examined and a digestion-concentration technique was used to isolate and quantitate the asbestos bodies in the remaining laryngeal tissues. No dysplastic epithelial changes were present in the mucosa. Asbestos bodies were recovered from two of the five larynges but from none of ten larynges obtained from autopsy controls.

Aged↗
PubMed1993

[The content of asbestos bodies in the bronchoalveolar fluid as a parameter of an increased pulmonary asbestos load].

Pulmonary asbestos burdens are usually determined by quantitative pulmonary dust analysis. The aim of this study was to investigate the value of bronchoalveolar lavage (BAL) for this purpose. First, the upper limit of normal for asbestos bodies (AB) in BAL fluid was established using a reference group of 371 patients with no evidence of increased exposure to asbestos. 99% of these patients had less than 0.5 AB/ml. In order to see whether BAL fluid AB concentration reflected pulmonary tissue content, BAL fluid and lung tissue from a further 64 patients with diverse histories of asbestos exposure were investigated. There was a positive association between AB concentration in BAL fluid and lung tissue only for the overall group of 64 patients (r = 0.86; P < 0.001). Twelve of 13 patients with more than 1 AB/ml and ten patients with more than 5 AB/ml had more than 1000 AB/cm3 lung tissue, a value that is usually exceeded in asbestosis. When the upper concentration limit was set at 0.5 AB/ml for BAL fluid and 50 AB/cm3 for lung tissue, only two out of 64 patients had a false positive value (specificity 95%), but eleven patients had false negative results (sensitivity 58%). These investigations establish that concentrations of > or = 0.5 AB/ml are a reliable indicator of increased asbestos exposure and concentrations > 1 AB/ml are associated with a higher probability of having more than 1000 AB/cm3 lung tissue. However, exclusion of increased asbestos exposure is not possible on the basis of negative BAL findings, since the sensitivity of the method is too low.

Adult↗
PubMed1987

Asbestos and asbestos-related disease: the South African case.

The asbestos industry in South Africa has suffered a decline in production, employment, and sales over the last few years. This mirrors the state of the industry internationally. In South Africa this has more to do with the economic recession than with legislative restrictions on asbestos use. New information has become available on the extent of asbestos-related diseases in South Africa. In this article, we outline developments in labor organization in the asbestos industry, and discuss the marked lack of control of asbestos, the inadequate state compensation system, and the difficulties facing labor. After describing recent improvements won by trade unions, mainly in the transnational corporation sector, we discuss the implications for industry, labor, and control of the asbestos hazard.

Asbestos↗
PubMed1981

Prevalence of asbestos related lung disease among employees in non-asbestos industries.

Employees from two non-asbestos industries wee examined to assess the prevalence of asbestos-related lung disease. Of the 214 employees, one suffered from a malignant mesothelioma of the pleura and in 13 (6.1%), pleural plaques were diagnosed radiologically. the plaques were symptomless and not associated with any disturbance in respiratory function. The sole source of asbestos fibre in one factory was the asbestos insulation surrounding steam and hot water pipes similar to that found throughout industry. Exposure occurred as the result of the way in which this insulation has been handled routinely in industry by people who have commonly been unaware either of their exposure or of its significance. In the second factory there was the possibility of additional exposure originating from a neighbouring industry that was a major consumer of asbestos. The results suggest that maintenance workers may be particularly at risk and that the presence of pleural plaques may be under-reported in the absence of a history of asbestos exposure to direct attention towards them. The presence of pleural plaques has important consequences for the individual and for others who have shared the work environment.

Adult↗
PubMed2004

Navy Asbestos Medical Surveillance Program (1991-1999): linear regression analysis for the effect of asbestos exposure on pulmonary function testing.

The effect of asbestos exposure on pulmonary function was studied using data from the Navy Asbestos Medical Surveillance Program. Records were selected for Caucasian men from 1991 to 1999 (N = 89,318) and were analyzed using a cross-sectional, linear regression model. Dependent variables were forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC), with independent continuous variables of age, height, weight, smoking, and asbestos history. Overall, the continuous variable for asbestos exposure demonstrated significant protection of +1.1 cm3/year (t = 3.278, p = 0.001) for FEV1 and +1.6 cm3/year (t = 4.225, p = 0.000) for FVC. There was significant interaction between asbestos exposure and smoking history (FEV1, -0.09 cm3/year2, t = -6.467, p = 0.000; FVC, -0.097 cm3/year2, t = -5.663, p = 0.000). This study suggests that workers within the program demonstrated minimal additional pulmonary function changes during the period, particularly if they do not smoke tobacco. The study also supports continuing smoking cessation efforts for all asbestos-exposed workers.

Adult↗
PubMedDate not supplied

Asbestos bodies in bronchoalveolar lavage fluid. A study of 20 asbestos-exposed individuals and comparison to patients with other chronic interstitial lung diseases.

We studied the asbestos body (AB) content of bronchoalveolar lavage fluid from 20 patients with a history of occupational asbestos exposure, 31 patients with sarcoidosis and 5 patients with idiopathic pulmonary fibrosis. The cellular lavage pellet was digested in sodium hypochlorite and filtered onto Nuclepore filters for AB quantification by light microscopy. ABs were found in 15 of 20 asbestos-exposed individuals, 9 of 31 sarcoidosis cases and 2 of 5 patients with idiopathic pulmonary fibrosis. There was a statistically significant difference in the number of ABs per million cells recovered or per milliliter of recovered lavage fluid in the asbestos-exposed group as compared to the other categories of chronic interstitial lung disease. The highest levels occurred in patients with asbestosis. Large numbers of asbestos bodies in the lavage fluid (greater than 1 AB/10(6) cells) were indicative of considerable occupational asbestos exposure, whereas occasional bodies were a nonspecific finding.

Adult↗
PubMed1994

Air samples from a building with asbestos-containing material: asbestos content and in vitro toxicity on rat pleural mesothelial cells.

Buildings equipped with asbestos-containing material may release asbestos fibers, the toxicity of which remains uncertain because of the generally low dose level. In 22 air samples collected in a building the asbestos level ranged between 0 and 0.027 f/ml. Both chrysotile and amphiboles were found. There was no association between in vitro cytotoxicity on rat pleural mesothelial cells and asbestos content, but there was a significant correlation with the total amount of particulate material. Four samples exhibited an enhancement of DNA synthesis in cells arrested in G1 with 5 mM hydroxyurea. This is more likely related to the particulate matter associated with asbestos fibers.

Air Pollution, Indoor↗