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PubMed1999

Mineral fibre analysis and routes of exposure to asbestos in the development of mesothelioma in an English region.

OBJECTIVES: To compare the concentrations of inorganic fibres in the lungs in cases of mesothelioma and controls: to determine whether concentrations of retained asbestos fibres differ with the different exposures identified from interview; and to investigate the existence of a cut off point in concentrations of asbestos fibres that indicates occupational exposure. METHODS: Case-control study; 147 confirmed cases of mesothelioma and 122 controls identified from deaths occurring in four districts of Yorkshire between 1979 and 1991. Surviving relatives were interviewed to determine lifetime exposure history to asbestos. Mineral fibre analysis was carried out on lung tissue from postmortem examinations. RESULTS: Odds on high concentrations of retained asbestos fibres were greater in cases than controls. After excluding subjects with occupational and paraoccupational exposure, the odds on high concentrations were still greater in cases than controls, but only significantly so for amphiboles. There was only a weak relation between probability of occupational exposure to asbestos and concentrations of retained asbestos fibres, and no significant difference in fibre concentrations was found between subjects who had been exposed to asbestos through different routes: these comparisons were only based on small groups. There was considerable overlap in concentrations of retained asbestos fibres between cases and controls with and without histories of occupational exposure. CONCLUSIONS: The study has confirmed previous results of higher concentrations of asbestos fibres in cases than controls, and has shown that this is still found in subjects with little evidence of occupational and para-occupational exposure. The overlap in concentrations of retained asbestos for different groups of subjects did not suggest a clear cut of value.

Aged↗

PubMed1999

Asbestos-induced phosphorylation of epidermal growth factor receptor is linked to c-fos and apoptosis.

We examined the mechanisms of interaction of crocidolite asbestos fibers with the epidermal growth factor (EGF) receptor (EGFR) and the role of the EGFR-extracellular signal-regulated kinase (ERK) signaling pathway in early-response protooncogene (c-fos/c-jun) expression and apoptosis induced by asbestos in rat pleural mesothelial (RPM) cells. Asbestos fibers, but not the nonfibrous analog riebeckite, abolished binding of EGF to the EGFR. This was not due to a direct interaction of fibers with ligand, inasmuch as binding studies using fibers and EGF in the absence of membranes showed that EGF did not adsorb to the surface of asbestos fibers. Exposure of RPM cells to asbestos caused a greater than twofold increase in steady-state message and protein levels of EGFR (P < 0.05). The tyrphostin AG-1478, which inhibits the tyrosine kinase activity of the EGFR, but not the tyrphostin A-10, which does not affect EGFR activity, significantly ameliorated asbestos-induced increases in mRNA levels of c-fos but not of c-jun. Pretreatment of RPM cells with AG-1478 significantly reduced apoptosis in cells exposed to asbestos. Our findings suggest that asbestos-induced binding to EGFR initiates signaling pathways responsible for increased expression of the protooncogene c-fos and the development of apoptosis. The ability to block asbestos-induced elevations in c-fos mRNA levels and apoptosis by small-molecule inhibitors of EGFR phosphorylation may have therapeutic implications in asbestos-related diseases.

Animals↗

PubMed1998

Association of cigarette smoking and asbestos exposure with location and histology of lung cancer.

Prior studies have suggested that lung cancers that arise in association with cigarette smoking favor an upper-lobe location while those associated with asbestos exposure favor a lower-lobe location. An excess of adenocarcinomas has also been reported among cases not exposed to cigarette smoke as well as among those exposed to asbestos. However, these studies typically have not adjusted adequately for potential confounders such as the patient's age, sex, race, or family history of cancer. To better examine the effects of cigarette smoking and asbestos exposure on location and histology of lung cancer, we analyzed data from a large case-control study that included 456 patients with stage I or II lung cancer. Patients with upper-lobe tumors tended to have had more exposure to tobacco as assessed by pack-years smoked (54.7 versus 46.2, p = 0.07) and less time since quitting smoking (3.0 versus 5.5 yr, p = 0.05). In contrast to some prior reports, asbestos exposure was also associated with an upper-lobe location of tumor. Among those with upper-lobe tumors, 14.6% had a history of significant asbestos exposure compared with 5.4% of those with lower-lobe tumors (p < 0.01). The relationship between asbestos exposure and upper-lobe location of tumor was also statistically significant whether stratified by smoking or analyzed by multivariable logistic regression modeling. Adenocarcinomas were more likely among those with less exposure to cigarette smoke based on fewer pack-years smoked (41.5 versus 61.8, p = 0.0001) and more time since quitting smoking (5.0 versus 3.0 yr, p = 0.02). The proportion of patients with significant exposure to asbestos was lower among those with adenocarcinomas but was not statistically significant (9.5 versus 15.3%, p = 0.09). In multivariable logistic regression analysis, longer time since smoking exposure remained a significant predictor of adenocarcinomas (p < 0.02), but history of asbestos exposure did not predict tumor histology. Thus, in patients with lung cancer, both cigarette smoking and asbestos exposure histories favor an upper-lobe location of tumor. Longer time since smoking exposure favors adenocarcinomas, but the history of asbestos exposure does not appear to influence the tumor histology.

Adenocarcinoma↗

PubMed1988

Asbestos-induced endothelial cell activation and injury. Demonstration of fiber phagocytosis and oxidant-dependent toxicity.

Vascular endothelial cell injury is important in the development of a variety of chronic interstitial lung disorders. However, the involvement of such injury in the inflammatory response associated with the inhalation of asbestos fibers is unclear and the mechanism of asbestos fiber cytotoxicity remains unknown. In the present study, human umbilical vein endothelial cells were challenged with amosite asbestos and several parameters of cellular function were examined. Electron microscopic examination revealed that endothelial cell exposure to asbestos resulted in active phagocytosis of these particulates. Biochemical evidence of dose-dependent asbestos-mediated endothelial cell activation was indicated by increased metabolism of arachidonic acid. For example, amosite asbestos (500 micrograms/ml) produced a ninefold increase in prostacyclin (PGI2) levels over those levels in non-exposed cells. Incubation of human endothelial cells with asbestos fibers induced specific 51Cr release in both a dose- and time-dependent fashion indicative of cellular injury. Injury induced by amosite asbestos was not significantly attenuated by treatment of the endothelial cell monolayer with either the iron chelator deferoxamine, which prevents hydroxyl radical (.OH) formation, or by the superoxide anion (O2-) scavenger, superoxide dismutase. However, significant dose-dependent protection was observed with the hydrogen peroxide (H2O2) scavenger, catalase. Chelation of elemental iron present within amosite asbestos fibers by deferoxamine produced a 33% reduction in asbestos cytotoxicity, suggesting a potential role for hydroxyl radical-mediated injury via the iron-catalyzed Haber-Weiss reaction.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

PubMed1995

Iron and reactive oxygen species in the asbestos-induced tumor necrosis factor-alpha response from alveolar macrophages.

Free radicals and other reactive oxygen species (ROS) are important mediators in asbestos-induced lung toxicity. Asbestos fibers are thought to stimulate cells to generate ROS via iron that is present on fibrous silicates. The pathophysiologic responses in the lung after asbestos exposure are characterized by the accumulation of macrophages at the site of fiber deposition and the release of growth factors and proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha). We have examined the role of iron-catalyzed ROS in asbestos induction of TNF-alpha from rat alveolar macrophages. Treatment of alveolar macrophage cultures with asbestos stimulated dose-dependently TNF-alpha secretion, which was inhibited by the addition of deferoxamine, an iron chelator. Asbestos fibers, pretreated with deferoxamine to remove iron from the fibers before addition to alveolar macrophages, also significantly reduced the TNF-alpha response. Consistent with the role of iron on asbestos fibers in catalyzing hydroxyl radical generation, membrane-permeable hydroxyl radical scavengers (tetramethylthiourea, dimethyl sulfoxide) inhibited the asbestos-induced TNF-alpha response. The asbestos-induced increase in TNF-alpha, as well as in interleukin-1 alpha, and their inhibition by tetramethylthiourea occurred at the transcriptional level. The role of ROS in signaling TNF-alpha stimulation was confirmed by use of free radical-generating systems (hypoxanthine-xanthine oxidase, hydrogen peroxide, glucose-glucose oxidase, or ferrous plus hydrogen peroxide). These results suggest that intracellularly generated ROS can stimulate TNF-alpha in alveolar macrophages and that asbestos-induced TNF-alpha gene expression and secretion are mediated by iron-catalyzed product of ROS.

Animals↗

PubMed1996

Asbestos induces apoptosis of human and rabbit pleural mesothelial cells via reactive oxygen species.

Mesothelial cells, the progenitor cell of the asbestos-induced tumor mesothelioma, are particularly sensitive to the toxic effects of asbestos, although the molecular mechanisms by which asbestos induces injury in mesothelial cells are not known. We asked whether asbestos induced apoptosis in mesothelial cells and whether reactive oxygen species were important. Pleural mesothelial cells (rabbit or human) were exposed to asbestos (crocidolite, amosite, or chrysotile) or control particles at moderate doses (1-10 microg/cm2) over 24 h and evaluated for oligonucleosomal DNA fragmentation, loss of membrane phospholipid asymmetry, and nuclear condensation. Asbestos fibers, not control particles, induced apoptosis in mesothelial cells by all assays and induction of apoptosis was dose dependent for all types of asbestos, with crocidolite (5 microg/cm2) inducing 15.0+/-1.1% (mean+/-SE; n = 12) apoptosis versus control particles < 4%. Apoptosis induced by asbestos, but not by actinomycin D, was inhibited by extracellular catalase, superoxide dismutase in the presence of catalase, hypoxia (8% oxygen), deferoxamine, 3-aminobenzamide [an inhibitor of poly(ADP-ribosyl) polymerase], and cytochalasin B. Only catalase and cytochalasin B decreased fiber uptake. We conclude that asbestos induces apoptosis in mesothelial cells via reactive oxygen species. Escape from this pathway could allow the abnormal survival of mesothelial cells with asbestos-induced mutations.

Animals↗

PubMed2001

Asbestos-related lung cancer and mesothelioma in Japan.

In Japan, crocidolite had been used for asbestos cement pipe and spraying, and amosite had been used for building board and spraying. These two types of asbestos had stopped to use in Japan in the late 1970s. An extreme increase in imported asbestos (all 3 commercial types) was observed between 1960 and 1974. In 1960, 77,000 tons of asbestos were imported, and reached the peak as 352,316 tons in 1974. This extreme rise of asbestos imports corresponds with the recent rapid increase in mortality of malignant pleural mesothelioma. Between 1995 and 1999, an estimated mean annual death from pleural mesothelioma was about 500. The annual number of compensated occupational respiratory cancers due to asbestos exposure has also been increasing. Up to the end of March 2000, 162 cases with malignant mesothelioma and 197 cases with lung cancer were compensated. As for lung cancer, epidemiological studies are scanty in Japan. Limited environmental data of the working places in asbestos textile factories suggests that heavy asbestos exposure in the past made deaths from respiratory diseases. Less asbestos exposure will enable exposed workers to survive enough to reach cancer age. Even now smoking rate among males in Japan are over 50%. So lung cancer deaths caused by the interaction between smoking and asbestos exposure will be continuing.

Asbestos↗

PubMed1997

Relationship between asbestos bodies in sputum and the number of specimens.

OBJECTIVES: This study investigated the relationship between asbestos body identification and the number of sputum specimens obtained from each subject. METHODS: The presence of asbestos bodies in sputum was studied in 142 asbestos workers with former low-exposure levels; the number of specimens collected during 1-3 weeks varied from 2 to more than 4. Furthermore the persistence of asbestos bodies in the sputum of 15 asbestos workers was studied during a long-time follow-up. RESULTS: Asbestos bodies were present in at least 1 specimen in 44.4% of the 142 subjects. The cumulative percentage of asbestos body presence increased linearly, from 20% to 68%, as the number of specimens increased. CONCLUSIONS: Five specimens did not seem to be sufficient to obtain satisfactory sensitivity in a group with low exposure to asbestos. Neither the type of exposure (to chrysotile only or to chrysotile plus amphibole) nor the presence of an asbestos-related disease clearly influenced the probability of finding asbestos bodies.

Asbestos↗

PubMed2000

Asbestos content of lung tissue and carcinoma of the lung: a clinicopathologic correlation and mineral fiber analysis of 234 cases.

The aim of this study was to investigate the asbestos content of lung tissue in a series of patients with lung cancer and some history of asbestos exposure. This information was then correlated with demographic information, occupational and smoking history, presence or absence of pathologic asbestosis or pleural plaques, and pathologic features of the cancer. The pulmonary concentration of asbestos fibers in 234 cases of primary carcinoma of the lung was determined by means of a tissue digestion technique. Asbestos body counts were performed in 229 cases and fiber analysis by scanning electron microscopy in 221 cases. Asbestos content was recorded as total asbestos fibers, commercial amphibole fibers, noncommercial amphibole fibers, and chrysotile fibers 5 microm or greater in length per gram of wet lung tissue. The study group included 70 patients with asbestosis (Group I), 44 patients with parietal pleural plaques but without asbestosis (Group II), and 120 patients with neither (Group III). The median asbestos body content of Group I was more than 35 times greater than Group II and more than 300 times greater than Group III. The total asbestos fiber count for Group I was nearly 20 times greater than Group II and more than 50 times greater than Group III. The difference was due almost entirely to commercial amphiboles. In a series of primary lung cancer cases with some history of asbestos exposure, a markedly elevated asbestos content was identified among those with pathologic asbestosis as compared with patients with pleural plaques alone or with neither plaques nor asbestosis.

Aged↗

PubMedDate not supplied

Asbestos-induced alveolar epithelial cell apoptosis: role of mitochondrial dysfunction caused by iron-derived free radicals.

Asbestos causes asbestosis and malignancies by mechanisms that are not fully understood. Alveolar epithelial cell (AEC) injury by iron-derived reactive oxygen species (ROS) is one important mechanism implicated. We previously showed that iron-catalyzed ROS in part mediate asbestos-inducedAEC DNA damage and apoptosis. Mitochondria have a critical role in regulating apoptosis after exposure to agents causing DNA damage but their role in regulating asbestos-induced apoptosis is unknown. To determine whether asbestos causes AEC mitochondrial dysfunction, we exposed A549 cells to amosite asbestos and assessed mitochondrial membrane potential changes (delta(psi)m) using a fluorometric technique involving tetremethylrhodamine ethyl ester (TMRE) and mitotracker green. We show that amosite asbestos, but not an inert particulate, titanium dioxide, reduces delta(psi)m after a 4 h exposure period. Further, the delta(psi)m after 4 h was inversely proportional to the levels of apoptosis noted at 24 h as assessed by nuclear morphology as well as by DNA nucleosome formation. A role for iron-derived ROS was suggested by the finding that phytic acid, an iron chelator, blocked asbestos-induced reductions in A549 cell delta(psi)m and attenuated apoptosis. Finally, overexpression of Bcl-xl, an anti-apoptotic protein that localizes to the mitochondria, prevented asbestos-induced decreases in A549 cell delta(psi)m after 4 h and diminished apoptosis. We conclude that asbestos alters AEC mitochondrial function in part by generating iron-derived ROS, which in turn can result in apoptosis. This suggests that the mitochondrial death pathway is important in regulating pulmonary toxicity from asbestos.

Apoptosis↗

PubMed1992

Occupational exposure and respiratory morbidity among asbestos workers in Taiwan.

To determine the prevalence of asbestos-related lung disease and the impairment of lung function among asbestos workers, we conducted a cross-sectional health survey of 459 workers in 33 asbestos-related factories in Taiwan. Each worker was asked about his medical and occupational history and was given a medical examination, chest roentgenogram and pulmonary function test. Manufacturing processes included production of asbestos cements, textiles, friction materials and insulation products. Exposure assessments were based on asbestos sampling and counting using a phase contrast microscope. The average age of the participants in the study was 41.6 years. They had an average of 8.1 years of dust exposure, with a range of one to 42 years. The majority had a cumulative asbestos exposure of less than 20 fiber years/mL. No case of asbestos-related lung disease was found during our investigation. No roentgenogram showed unequivocal changes of asbestosis. However, a multiple linear regression analysis of the pulmonary function test showed that both FVC and FEV1 decreased significantly with an increasing cumulative dose of exposure after controlling for age, height and smoking effects during analysis. FEV1/FVC and FEF25-75% were not affected by exposure dose. The absence of asbestosis and other asbestos-related lung diseases may be due to an inadequate induction time of asbestos exposure and a possible healthy selection of workers. We conclude that among workers in Taiwan, there is a significant effect on the respiratory system, especially pulmonary function, due to asbestos exposure.

Adolescent↗

PubMedDate not supplied

[Asbestos risk in the textile industry: final confirmation of data from the Lombardy Mesothelioma Registry].

BACKGROUND: Cases of mesothelioma in non-asbestos textile workers have been frequently reported but the identification of asbestos dispersion sources in the workplaces has never been adequately performed. During 3 years of activity of the Mesothelioma Register for Lombardy, 40 cases (10.8% of all cases) were collected in textile workers engaged in all types of productive activities. The hypothesis that a significant asbestos risk for textile workers appeared not negligible. OBJECTIVES: The research was aimed at the identification of asbestos dispersion sources in textile factories. METHODS: Specific information was collected by technicians, maintenance personnel and other experts and direct inspections were carried out in numerous workplaces that had not yet undergone significant changes with respect to the past. Also the industrial machinery utilised in the previous 40-50 years was thoroughly examined. RESULTS: Epidemological evaluation of the recorded cases showed a widespread distribution in the different phases of textile production. Inspections also showed that a large amount of asbestos had been regularly used applied to the ceilings and also to the walls of factories in order to avoid both condensation of steam and reflection of noise. In addition, asbestos had also been widely used to insulate water and steam pipes. The braking systems of most of the machines also had asbestos gaskets, and on several looms some brakes operated continuously in order to keep the warp in constant tension. CONCLUSIONS: Our observations confirmed that since production techniques in the textile industry required working in damp and warm conditions with the noise of the rapidly moving machines, asbestos was very often used because of its absorbent and soundproofing qualities and its resistance to friction. We demonstrated that asbestos was thus widely used in the industry and this certainly produced considerable fibre dispersions in the atmosphere of the workplaces. Asbestos risk must therefore be recognised for all those who have worked in the textile industry in the recent past and, as a result, cases of mesothelioma must be considered occupational diseases.

Asbestos↗

PubMed2004

[Pleural mesothelioma in women is associated with environmental exposure to asbestos].

OBJECTIVE: To determine whether local environmental exposure to asbestos in the community of Hof van Twente, The Netherlands (which houses a large asbestos cement facility and has a serious environmental asbestos pollution problem), is accompanied by an increased mortality due to pleural mesothelioma among women. DESIGN: A descriptive, ecologic-epidemiological study. METHOD: Twenty-nine women with a verified diagnosis of pleural mesothelioma were selected from 810 requests for compensation submitted to a specialised lawyers' office in the period 1990-2002. Information on asbestos exposure from occupational, household, environmental or unknown sources was obtained. The place of residence was compared to information on sources of asbestos in the immediate environment derived from the settlement 'Asbestos removal in the environment'. The expected number of cases of pleural mesothelioma among women was estimated on the basis of the observed mortality in The Netherlands in the period 1996-2002. A standardised mortality ratio (SMR) was calculated as the ratio of observed cases divided by the number of expected cases of pleural mesothelioma x 100. RESULTS: In total, 5 cases of pleural mesothelioma were identified among women without occupational or household exposure to asbestos. The age at diagnosis varied from 38 to 81 years. Each case was exposed to asbestos in the direct vicinity of the residence through walking and cycling over local roads metalled with asbestos cement scrap material. The expected number of cases of mortality due to pleural mesothelioma in the town of Hof van Twente for the period 1996-2002 was about 0.46. The SMR was 1090 (95% CI: 465-2551), indicating a 10-fold increase in risk. CONCLUSION: The increased mortality of pleural mesothelioma was most probably due to environmental exposure to asbestos. This finding agrees with comparable studies in other countries.

Adult↗

PubMed2006

Association between polymorphisms of DNA repair gene XRCC1 and DNA damage in asbestos-exposed workers.

OBJECTIVE: To compare the asbestos-induced DNA damage and repair capacities of DNA damage between 104 asbestos-exposed workers and 101 control workers in Qingdao City of China and to investigate the possible association between polymorphisms in codon 399 of XRCC1 and susceptibility to asbestosis. METHODS: DNA damage levels in peripheral blood lymphocytes were determined by comet assay, and XRCC1 genetic polymorphisms of DNA samples from 51 asbestosis cases and 53 non-asbestosis workers with a similar asbestos exposure history were analyzed by PCR/RFLP. RESULTS: The basal comet scores (3.95 +/- 2.95) were significantly higher in asbestos-exposed workers than in control workers (0.10 +/- 0.28). After 1 h H2O2 stimulation, DNA damage of lymphocytes exhibited different increases. After a 4 h repair period, the comet scores were 50.98 +/- 19.53 in asbestos-exposed workers and 18.32 +/- 12.04 in controls. The residual DNA damage (RD) was significantly greater (P<0.01) in asbestos-exposed workers (35.62%) than in controls (27.75%). XRCC1 genetic polymorphism in 104 asbestos-exposed workers was not associated with increased risk of asbestosis. But compared with polymorphisms in the DNA repair gene XRCC1 (polymorphisms in codon 399) and the DNA damage induced by asbestos, the comet scores in asbestosis cases with Gln/Gln, Gln/Arg, and Arg/Arg were 40.26 +/- 18.94, 38.03 +/- 28.22, and 32.01 +/- 11.65, respectively, which were higher than those in non-asbestosis workers with the same genotypes (25.58 +/- 11.08, 37.08 +/- 14.74, and 29.38 +/- 10.15). There were significant differences in the comet scores between asbestosis cases and non-asbestosis workers with Gln/Gln by Student's t-test (P<0.05 or 0.01). The comet scores were higher in asbestosis workers with Gln/Gln than in those with Arg/Arg and in non-asbestosis workers exposed to asbestos, but without statistically significant difference. CONCLUSIONS: Exposure to asbestos may be related to DNA damage or the capacity of cells to repair H2O2-induced DNA damage. DNA repair gene XRCC1 codon 399 may be responsible for the inter-individual susceptibility in DNA damage and repair capacities.

Adult↗

PubMed1990

The formation of asbestos bodies by mouse peritoneal macrophages. An in vitro study.

For studies on the mechanism of asbestos body formation, Union Internationale Contre Cancer (UICC) crocidolite asbestos fibers were added to a culture of mouse peritoneal macrophages. Small asbestos fibers were totally ingested by the macrophages, but fibers too long to be taken up completely remained as a consequence extracellular. These long asbestos fibers became the basis for asbestos body formation. The basic mechanism underlying asbestos body formation was found to be the exocytotic activity of macrophages. The number of iron-rich inclusion bodies was dependent on the availability of iron in the culture media, and the same holds for the amount of iron in the asbestos body coat. This means that asbestos body formation is a phenomenon that occurs accidentally when macrophages come into contact with long fibers in an iron-rich environment. A time-dependent increase in the number, average size, and rate of segmentation of the asbestos bodies was observed. The present report is the first to describe asbestos body formation in vitro.

Acid Phosphatase↗

PubMed1989

Tritiated thymidine incorporation and the development of an interstitial lesion in the bronchiolar-alveolar regions of the lungs of normal and complement deficient mice after inhalation of chrysotile asbestos.

Inhaled asbestos causes the proliferation of bronchiolar-alveolar epithelial and interstitial cells in rats and mice 19 to 72 hours after a single 5-hour exposure. This condition is associated with rapid macrophage accumulation and development of an interstitial fibrotic lesion at alveolar duct bifurcations. In an attempt to define the mechanisms mediating asbestos-induced cell proliferation and fibrogenesis, we studied mice exposed to chrysotile asbestos for five hours. The mice were normal (strain B10.D2/nSn)(C5+) and a congenic strain (B10.D2/oSn), deficient in the fifth component of complement (C5-). We knew that the latter exhibit a depressed asbestos-induced macrophage response and wanted to learn whether the depressed response correlated with measurements of cell proliferation and progression of an interstitial lesion. Sections of first alveolar duct bifurcations were prepared for light microscopic autoradiography and ultrastructural morphometry at varying times after animal exposure to asbestos. In sham-exposed C5+ and C5- animals, less than 1% of epithelial and interstitial cells of the terminal bronchioles and alveolar ducts incorporated tritiated thymidine (3H-TdR) at any time after exposure to asbestos. Between 19 and 72 hours after exposure, epithelial and interstitial cells in both strains of mice exhibited significantly increased levels of 3H-TdR incorporation. The response decreased by eight days postexposure, and 3H-TdR incorporation was normal one month after exposure. Similarly, morphometry showed that both the C5+ and C5- asbestos-exposed mice exhibited significant increases in the volume density of epithelial and interstitial cells 48 hours after exposure. However, one month after exposure, the normal C5+ asbestos-exposed mice developed a fibrotic lesion, whereas the C5- asbestos-exposed animals were no different from sham-exposed C5- controls. The depressed macrophage response in the C5- animals does not appear to change the early mitogenic response to asbestos but may be central to the apparent attenuation of fibrogenesis.

Administration, Inhalation↗

PubMed1989

Comparative studies of airborne asbestos in occupational and non-occupational environments using optical and electron microscope techniques.

We have compared asbestos fibre and general fibre counts from scanning electron microscopy (SEM) and transmission electron microscopy (TEM) with fibre counts from phase-contrast optical microscope (PCOM) methods. Three different types of sample have been evaluated: laboratory-prepared samples of different fibre types; chrysotile asbestos textile factory samples; and non-occupational and environmental samples from sites where asbestos might be found. TEM produced total fibre number assessments which were greater than those found with SEM which, in turn, produced fibre counts greater than those obtained with the PCOM. However, when fibres longer than 5 microns were alone counted, the two electron microscope (EM) methods provided similar results. This indicates that TEM is advantageous in comparison with SEM when counting or sizing short fibres and has no advantage for fibres longer than 5 microns. For fibres longer than 5 microns in both the laboratory-prepared and asbestos factory samples, the EM asbestos counts were higher than the PCOM fibre counts, the ratios depending on the fibre type in the case of the former. The PCOM fibre counts in samples from the non-occupational situations were shown to be poor predictors of airborne asbestos fibre concentrations determined by EM. This was mainly due to the presence of high and variable proportions of non-asbestos fibres in these samples. It is concluded that, in order to convert EM asbestos fibre concentrations (greater than 5 microns) to equivalent PCOM asbestos concentrations, they should be divided by 4.0 for chrysotile and 1.7 for amphibole asbestos.

Air Pollutants↗

PubMed1989

Airborne asbestos fibre levels in buildings: a summary of UK measurements.

The UK Health and Safety Executive, in conjunction with the Department of the Environment, has carried out a number of surveys of airborne asbestos fibre concentrations in buildings. All samples have been collected on membrane filters and analysed by analytical transmission electron microscopy. Four categories of buildings under normal occupation have been investigated; non-domestic buildings containing sprayed or trowelled asbestos, domestic buildings containing sprayed asbestos or asbestos plaster, buildings with warm air heaters containing asbestos and buildings without asbestos materials. A number of buildings have also been surveyed during and after the removal of asbestos materials. The choice of measurement indices and analytical procedures is reviewed, before measurements are compared in terms of the concentration of asbestos fibres greater than 5 microns long. The decision whether to remove asbestos from occupied buildings is discussed with reference to the associated cost and risk. In the present survey, management of undamaged asbestos appeared preferable to large-scale removal.

Air Pollutants↗