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PubMed1985

A variable feed rate mechanism for fluidized bed asbestos generators.

A simple and inexpensive dust feed mechanism has been designed for use with a two-phase fluidized bed generator (FBG). The mechanism is especially useful for generating asbestos aerosols, but may be used with other dusts as well. Using this system, a steady state concentration (39.1 fibers/cc greater than 5 microns in length +/- 6.2%) of asbestos aerosol was maintained in an inhalation chamber for five hours. In addition, FBG output concentration was easily adjusted and quickly equilibrated (within 10 minutes). The system provides a good technique for generating asbestos aerosols for day-long animal exposures.

Aerosols↗

PubMed1986

Asbestos and disease: an industrial hygienist's perspective.

I have traced a personal thirty year journey of involvement with asbestos in the workplace and the nonoccupational environment, one still in progress, in an attempt to extract selected lessons for the industrial hygienist. Lessons for other professions, namely medicine, law and management have been studiously avoided in the interests of the scope of this presentation and permissible time. There are certainly numerous other lessons to contemplate. The movement of asbestos from the occupational to the nonoccupational environment is a case study that will undoubtedly be followed in the future by other potentially toxic materials. We must determine our position as a profession with regard to the tools we utilize, the procedures we follow, and our understanding of our moral and legal obligations to prepare for the often scientifically and technically unsupportable positions assumed by others, including governmental agencies, in their zeal to bring about change. We must discourage the opportunistic distortion of professional practices in these matters, and must issue well considered statements as a profession, statements relevant to the way these matters are addressed by society. We have a responsibility to lend perspective to these issues, to not permit understandably emotional responses to documented past severe health effects in other areas, such as the case of asbestos in the workplace, to carry over into conditions of very low exposures in the public domain. We must remind people of the relevance of dose-response and toxicological principles to assessment of risk.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollutants, Occupational↗

PubMed1985

Genotoxicity of dimethylnitrosamine in the presence of chrysotile asbestos UICC B and xonotlite.

Interactions of particulates with chemical genotoxic agents may play an important role in the induction of carcinogenesis. With respect to bronchogenic cancer, the synergism associated with combined exposure to asbestos and tobacco smoke is a well-documented phenomenon. The present work focused on chrysotile asbestos and xonotlite. The latter is a fibrous calcium silicate which is increasingly being used to replace asbestos in various industrial applications. The study was aimed at testing the possible interaction of these materials with dimethylnitrosamine (DMN), a genotoxic component of tobacco smoke. The capacity of fibers to interfere with the genotoxic response elicited by DMN in the UDS/hepatocyte assay system specifically designed for sensitive detection of short-patch DNA repair, was looked for. The properties of the selected fibers with respect to binding affinity towards DMN were also examined.

2-Acetylaminofluorene↗

PubMed1986

Apparent synergy in lung carcinogenesis: interactions between N-nitrosoheptamethyleneimine, particulate cadmium and crocidolite asbestos fibres in rats.

Environmental carcinogenesis in man is widely accepted to be a multifactorial process, and in the causation of lung cancers it is suspected that low levels of systemic carcinogens may act synergistically with inhaled particulates so that some exposed individuals are at increased risk. In the present study the carcinogenic effects of low levels of industrially and environmentally significant particulate materials (crocidolite asbestos and metallic cadmium) and a putative systemic carcinogen, N-nitrosoheptamethyleneimine (NHMI), were investigated in the laboratory rat, using this as a model of potential human exposure. The overall lung tumour incidence rate in the group of animals receiving crocidolite, cadmium and NHMI (14/45) was significantly higher than in the groups of animals receiving either crocidolite and cadmium together (2/51) or crocidolite and NHMI together (7/42). The results demonstrated an apparent synergy between cadmium and NHMI in the presence of crocidolite in the causation of lung cancer in rats, a finding which was confirmed statistically. This study helps to further evaluate and define the roles of asbestos and particulate cadmium in the causation of lung cancer. It is suggested that people who are exposed through occupation and/or environment to cadmium and asbestos and to low levels of systemic carcinogens may show a significantly elevated risk of lung cancer.

Animals↗

PubMed1988

Apparent synergy between chrysotile asbestos and N-nitrosoheptamethyleneimine in the induction of pulmonary tumours in rats.

Environmental carcinogenesis in man is widely accepted to be a multifactorial process, and in the causation of lung cancers it is suspected that low levels of systemic carcinogens may act synergistically with inhaled particulates so that some exposed individuals are at increased risk. In the present study the carcinogenic effects of low levels of industrially/environmentally significant particulate materials (chrysotile asbestos and metallic cadmium) and a putative systemic carcinogen, N-nitrosoheptamethyleneimine (NHMI), were investigated in the laboratory rat, using this as a model of potential human exposure. The overall lung tumour incidence rate in the groups of animals receiving chrysotile and NHMI together (8/50) or chrysotile, cadmium and NHMI together (6/44) was substantially higher than in the groups receiving chrysotile alone (1/86) or chrysotile and cadmium (1/94) or NHMI alone (2/48). The results demonstrated apparent synergy between chrysotile and NHMI in the induction of lung tumours. Incidence of pulmonary hyperplastic lesions paralleled the trend in tumour incidence. Cadmium had little or no influence on the incidence of either lung tumours or hyperplastic lesions. This study helps to evaluate further the role of asbestos in the causation of lung cancer. It is suggested that people who are or have been exposed to chrysotile asbestos may show a significantly elevated risk of lung cancer if concomitantly or subsequently exposed to tumour initiating agents.

Animals↗

PubMed1992

Diminution in kerosene-mediated induction of drug metabolizing enzymes by asbestos in rat lungs.

In order to determine the pulmonary toxicity of kerosene and its ignition product (soot) in asbestos exposed subjects, the activities of phase I and phase II drug metabolizing enzymes in rat lungs after single intratracheal co-exposure to Indian chrysotile asbestos and kerosene or its soot and Indian chrysotile were assayed. Exposure to kerosene or its soot resulted in a significant increase in the level of microsomal cytochrome P-450 and the activity of P-450 dependent monooxygenase, benzo(a)pyrene hydroxylase, as well as in the activities of microsomal epoxide hydrase and cytosolic glutathione-S-transferase (GST). However, in chrysotile exposed animals a reverse pattern in these parameters was recorded. The co-exposure to chrysotile and kerosene or chrysotile and soot led to a significant depletion in cytochrome P-450 level and a decrease in the activities of benzo(a)pyrene hydroxylase, epoxide hydrase and GST when compared to kerosene and soot controls, respectively. These results suggest that asbestos by altering the pulmonary drug metabolizing enzyme system may increase the toxic potential of kerosene and its ignition product in the respiratory system.

Animals↗

PubMed1983

Mortality of workers manufacturing friction materials using asbestos.

A mortality (1942-80) study was carried out on 13460 workers of a factory producing friction materials. The only type of asbestos used was chrysotile, except during two well-defined periods before 1945 when crocidolite was used, and over 99% of the population was traced. Compared with national death rates there were no detectable excesses of deaths due to lung cancer, gastrointestinal cancer, or other cancers; 11 deaths were due to pleural mesothelioma. A case-control study was carried out on deaths due to mesothelioma; this showed that eight workers had been exposed to crocidolite and another was possibly exposed intermittently to crocidolite. The other two had been employed for most of their working lives outside the factory, and their mesotheliomas could not be definitely attributed to exposure to chrysotile. Limiting the study to cases and controls who had exposure to 5 fibres/ml of chrysotile asbestos it was found that five of the six cases compared with two of the 10 controls had also been exposed to crocidolite. The probability (1:36) of this occurring were there no association with crocidolite is most unlikely. A case-control study was also carried out on deaths due to lung cancer and gastrointestinal cancer to investigate the dose-response relationships between these tumours and exposure to chrysotile. Measured and estimated fibre concentrations were available for the different jobs over the period of the study. No dose-response relationships were observed, but the exposures were low with only 5% of men accumulating 100 fibre-years/ml. The experience at this factory over a 40-year period showed that chrysotile asbestos was processed with no detectable excess mortality.

Adult↗

PubMed1984

Radiographic changes in a group of chrysotile miners and millers exposed to low asbestos dust concentrations.

Radiographic changes in 342 Quebec asbestos miners exposed to low levels of asbestos dust for an average period of 20 years were studied. Their estimated cumulative exposure ranged from 7 fibres per cubic centimeter X years (f-y/cc) to 300 f-y/cc. Of these workers, 2.1% showed a small opacity score of 1/0 or more and 2.7% showed pleural changes. No linear relationship could be established between small opacity score and any index of exposure to asbestos. Pleural changes were related to age. A referent group of office workers within the same mining industry showed a prevalence of 2.1% (1/48) for small irregular opacities 1/0 or more, and for pleural changes.

Adult↗

PubMed1989

Relation between asbestosis and bronchial cancer in amphibole asbestos miners.

In a necropsy series of 339 amphibole asbestos miners heavy smoking, age, and the presence of asbestosis were significantly associated with the presence of bronchial cancer. Of the 35 cases of bronchial cancer, 24 were associated with asbestosis. Eleven cases of bronchial cancer occurred in men without asbestosis; all were smokers. Standardised proportional mortality rates indicated no excess of bronchial cancer in 302 exposed men without asbestosis whereas these rates were progressively raised in men with slight or moderate/severe asbestosis. Of the four exposure variables introduced separately into a logistic regression model, "years of exposure" made a small but significant contribution; "residence time" marginally failed to achieve a 5% level of significance. Two other exposure variables tested including cumulative fibre exposure (fibre years) made no significant contribution. In the absence of asbestosis at necropsy a bronchial cancer in a man exposed to asbestos is unlikely to be due to asbestos.

Asbestos↗

PubMed1991

Early detection of interstitial lung disease in asbestos exposed non-smoking workers by mid-expiratory flow rate and high resolution computed tomography.

Ten years of lung function and radiological findings in six non-smoking asbestos exposed subjects who had increased mid-expiratory flow rate (FEF 25-75%) as the only functional abnormality were prospectively analysed. A biphasic change in FEF25-75% was noted. It initially increased up to the fifth year, and then a decrease was seen. In the final three years of the study, FEF25-75% reduction correlated well with a decrease in pulmonary capacity for CO (DLCO). During that time high resolution computed tomography (HRCT) probability scores correlated inversely with FEF25-75% and with DLCO, whereas chest radiography was unchanged (International Labour Organisation (ILO) profusion below 1/1). For five of the six subjects HRCT probability of asbestosis was intermediate. An increase in FEF25-75% in some asbestos exposed non-smoking workers may be one of the earliest functional signs indicative of future development of parenchymal asbestosis. Early asbestos related parenchymal abnormalities are seen more frequently on HRCT than on chest radiography.

Adult↗

PubMed1988

Experimental lung tumors following specific intrabronchial application of chrysotile asbestos. Longitudinal light and electron microscopic investigations in rats.

Longitudinal light and electron microscopy investigations were previously carried out on Wistar rats to study the pathogenesis of pulmonary fibrosis due to asbestos. In the present study, the genesis of pulmonary carcinomas and pleural mesotheliomas have been investigated by light and electron microscopy on the same model after intrabronchial instillation of chrysotile B and benz(a)pyrene, as well as a combination of the two carcinogens. A single instillation of 1 mg chrysotile B with a fiber length between 0.05 and 0.2 micron in 0.1 ml tricaprylin by means of a polyvinyl catheter into the right lower lobe of the lung of 70 anesthetized 6-week-old Wistar rats caused pulmonary carcinomas or malignant pleural mesotheliomas in 18 animals (24%). The tumors occur at intervals between 12 and 31 months after the asbestos application. By electron microscopy, small asbestos fragments can be detected under the pleural mesothelium at the earliest 1 year after the intrabronchial application of chrysotile. A single combined instillation of 1 mg chrysotile and 0.5 mg benz(a)pyrene does not increase the tumor incidence. With simultaneous administration of these two substances, however, lung tumors arise very much earlier than in instillation of only one of the carcinogens. Thus, an adenocarcinoma was found in the lungs after 4.5 months, and a pleural mesothelioma was already found after 7.7 months. The intrabronchial instillation of benz(a)pyrene alone causes fewer lung tumors (tumor incidence 10%, interval between 13 and 33 months).

Adenocarcinoma↗

PubMed1989

Evaluation of the causal relationship between crocidolite asbestos-induced lipid peroxidation and toxicity to macrophages.

In vitro, crocidolite asbestos toxicity to macrophages is mediated by the production of reactive oxygen metabolites. We examined whether exposure of macrophages to crocidolite asbestos induced lipid peroxidation as measured by the thiobarbituric acid assay. When elicited mouse peritoneal macrophages were exposed to crocidolite, a dose- and time-dependent increase in lipid peroxidation breakdown products accompanied cell death. Superoxide dismutase plus catalase or deferoxamine prevented both lipid peroxidation and loss of viability caused by crocidolite. We tested whether crocidolite-induced lipid peroxidation was causally responsible for cell death. Macrophages were not killed by crocidolite when incubated with 10 mM 3-aminobenzamide. The level of thiobarbituric acid-reactive material was the same, however, for cells incubated with crocidolite in the presence or absence of 3-aminobenzamide. When macrophagaes were pretreated for 24 h with 25 microM vitamin E and then incubated with crocidolite, no thiobarbituric acid-reactive products were detected. Vitamin E, however, did not prevent crocidolite cytotoxicity. These results suggest that exposure of macrophages to crocidolite asbestos produces lipid peroxidation as measured by thiobarbituric acid-reactive products. This reaction, however, is not directly responsible for irreversible injury in this model system.

Animals↗

PubMed1983

Lung structure as a risk factor in adverse pulmonary responses to asbestos exposure. A case-referent study in Quebec chrysotile miners and millers.

To investigate the hypothesis that lung structure may predispose to the development of asbestos-related pulmonary fibrosis, we carried out a case-referent study using data gathered in a cross-sectional study of Quebec chrysotile asbestos miners and millers. Tracheal and thoracic measurements were derived from the routine chest radiographs of 44 men with established radiologic fibrosis and compared with similar measurements for 88 men matched for age and cumulative exposure in the same industry who had not developed pulmonary fibrosis. Intrathoracic tracheal lengths were, on the average, shorter, and transthoracic diameters narrower in cases compared with those in referents. In addition, cases were shorter than the referents, suggesting that height might be an indirect measure of the structural characteristics relevant to the response to inhaled asbestos particles. Our findings are thus consistent with the hypothesis outlined, and they suggest a line of investigation that might be useful in relation to other inhaled pollutants.

Adult↗

PubMed1993

Induction of metaphase and anaphase/telophase abnormalities by asbestos fibers in rat pleural mesothelial cells in vitro.

The cytogenetic effects of asbestos fibers on rat pleural mesothelial cells were studied in vitro. Crocidolite UICC significantly enhanced aneuploidy and produced few structural chromosome aberrations, whereas anatase, an isomorphic particle, induced no numerical or structural changes. Mitomycin C (300 nM) produced a tenfold increase in abnormal anaphases compared with controls. Asbestos produced anaphase/telophase abnormalities in a concentration-dependent manner. The majority of the abnormalities involved lagging chromosomes. Crocidolite UICC induced abnormalities at a dose of 7.0 micrograms/cm2, whereas Canadian chrysotile did so at 1.0 to 2.0 micrograms/cm2. When the response was assessed by the number of long and thin fibers per cm2 (length > 8 microns; diameter < or = 0.25 microns), crocidolite UICC produced more abnormalities than Canadian chrysotile at all concentrations. On a per-weight basis, these findings differ from those obtained after intrapleural inoculation, as crocidolite induced more mesotheliomas than chrysotile; however, on a per-fiber basis, the in vitro and in vivo effects were similar. These results show that anaphase/telophase analysis is sensitive and complementary to metaphase analysis, and suggest that asbestos might produce cell transformation by inducing chromosome missegregation and aneuploidy.

Anaphase↗

PubMed1984

Changes in numbers and dimensions of chrysotile asbestos fibers in lungs of rats following short-term exposure.

Previous studies from this laboratory have demonstrated that in rats exposed briefly to aerosolized chrysotile asbestos, fibers initially deposited in the distal lung impact primarily at bifurcations of alveolar ducts. Subsequently, there is a progressive decrease in the numbers of fibers seen by scanning electron microscopy at the bifurcations with increasing time from initial exposure. The purpose of the present study was to assess the number and dimensions of fibers deposited in the lungs of these rats and to determine how these parameters changed at various intervals after the termination of exposure. This was accomplished using a sodium hypochlorite digestion-concentration technique to recover the fibers on a membrane filter. The numbers and dimensions of the fibers were then assessed using scanning electron microscopy. Utilizing these data, the mass of asbestos retained in the lung was calculated with a newly developed formula. Twenty-three percent of the respirable fraction was deposited in the lungs, and 19% of this amount was still present 31 days after exposure. Over the 31 days, there was a progressive increase (p less than 0.05) in mean fiber length and a significant decrease (p less than 0.05) in the diameter of the population of fibers retained in the lung. Such data should prove useful in attempting to understand the progressive pathogenesis of asbestos-induced interstitial lung disease, which seems to be related, at least in part, to the dimensions of the inhaled fibers.

Animals↗

PubMedDate not supplied

[Sedimentation method for measuring dispersion of fibers from asbestos cement roofs].

In order to define the need for removal versus conservative interventions regarding asbestos-cement roofs and the possible priorities, visual judgement of the state of deterioration or assessments based on the weight of the superficial friable material that can be removed with adhesives are not sufficient. Since in similar deterioration conditions the dispersion of fibres may vary considerably from case to case, only counting of the dispersed fibres will ensure a correct assessment of the pollution potential of an asbestos-cement weathered surface. The paper describes a simple method for measuring the atmospheric dispersion of fibres based on the well demonstrated fact that primary dispersion from the covering, as from many other sources of asbestos pollution, consists of course bundles that are subject to rapid sedimentation. By means of aluminium boxes containing object-holder slides installed under the edge of the covering for about one month, it is possible, using optical phase-contrast microscopy, to count the fibres that have sedimented and calculate the number of fibres/m2/day. If the method is used with the standardized criteria described, it gives reproducible results, involves low costs and has the advantage of balancing the possible variations in primary dispersion intensity due to changes in the local weather conditions over the relatively long sedimentation sampling period.

Air Pollutants↗

PubMed1992

Expression of antioxidant enzymes in rat lungs after inhalation of asbestos or silica.

Several studies indicate that active oxygen species play an important role in the development of pulmonary disease (asbestosis and silicosis) after exposure to mineral dust. The present study was conducted to determine if inhaled fibrogenic minerals induced changes in gene expression and activities of antioxidant enzymes (AOE) in rat lung. Two different fibrogenic minerals were compared, crocidolite, an amphibole asbestos fiber, and cristobalite, a crystalline silicon dioxide particle. Steady-state mRNA levels, immunoreactive protein, and activities of selected AOE were measured in lungs 1-10 days after initiation of exposure and at 14 days after cessation of a 10-day exposure period. Exposure to asbestos resulted in significant increases in steady-state mRNA levels of manganese-containing superoxide dismutase (MnSOD) at 3 and 9 days and of glutathione peroxidase at 6 and 9 days. An increase in steady-state mRNA levels of copper, zinc-containing superoxide dismutase (CuZnSOD), was observed at 6 days. Exposure to asbestos also resulted in overall increased enzyme activities of catalase, glutathione peroxidase and total superoxide dismutase in lung. In contrast, silica caused a dramatic increase in steady-state levels of MnSOD mRNA at all time periods and an increase in glutathione peroxidase mRNA levels at 9 days. Activities of AOE remained unchanged in silica-exposed lungs. In both models, increases in gene expression of MnSOD correlated with increased amounts of MnSOD immunoreactive protein in lung and the pattern and extent of inflammation. These data indicate that the profiles of AOE are dissimilar during the development of experimental asbestosis or silicosis and suggest different mechanisms of lung defense in response to these minerals.

Animals↗

PubMedDate not supplied

Correlation between radiological and functional findings in workers exposed to chrysotile asbestos.

The relationship between the extent of respiratory disease from chest radiographs and the severity of functional impairment was assessed in 185 workers with long-term exposure to asbestos in an asbestos-cement factory. The workers were divided into seven subgroups according to functional abnormality findings (restrictive, obstructive, mixed restrictive-obstructive, reduced diffusion capacity, increased diffusion capacity, small airway disease and normal). Restrictive functional abnormality was present in 29% of the workers, obstructive and mixed in 3% small airway disease in 4%, reduced diffusion capacity in 4% increased diffusion capacity in 7%, while the remaining 49% were normal. The subjects with radiological diffuse pleural disease were characterized by FVC reduction, whereas in those with mixed pleural-parenchymal radiological abnormalities both FVC and DLCO were reduced. FVC and DLCO decrements correlated well with the increasing grades of profusion according to the ILO classification. In the group of workers with normal chest radiographs and normal spirometry, a decrease or increase in lung diffusion capacity for CO (DLCO) was an isolated finding. In addition, a correlation existed between the length of exposure and functional parameters (reduced FVC and DLCO, while FEV1/FVC increased with longer exposure). The study shows that reduced lung function indices can be found in subjects without radiological evidence for parenchymal asbestosis (ILO grade 1/1 profusion or greater). The results suggest that asbestos exposure, in addition to lung diffusion capacity decrease, can be accompanied by an increase in lung diffusion capacity.

Adult↗