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PubMed2004

Asbestos and mesothelioma in South Africa.

Asbestos has been used by man since 4000 before the Christian era (BCE) in many different parts of the world and for a wide range of functions. Blue asbestos (crocidolite) was first discovered in South Africa in 1805 and within a few years was being mined there extensively. Mining reached its peak in 1977 with >380,000 tons being exported and 20,000 miners employed in the industry. South Africa also has large deposits of white asbestos (chrysotile) and brown asbestos (amosite) both of which have been mined extensively. At the turn of the 20th century, it was noted that those working with asbestos suffered lung disease and in 1960, the link between asbestosis and mesothelioma was established in the Kimberley area of South Africa. Further studies in the 1970s and 1980s showed an alarming incidence of mesothelioma based on pathology reports. The majority of the reported mesothelioma cases result from exposure to asbestos in its many uses in secondary industry although incidence of the condition among miners is also significant. A high proportion of mesothelioma in patients in South Africa is attributed to environmental origin with a high incidence of women and children affected.

Adult↗

PubMed2005

Asbestos problem in India.

Primary exposure to asbestos in India can be encountered in the form of asbestos mining, asbestos cement industries, asbestos processing unit and during renovation and demolition of old asbestos cemented roof or other structures as well as modern electrical as well as mechanical appliances in which asbestos is still found. Ultimately construction workers, electricians, vehicle mechanics and other workers in the building trades who are exposed to asbestos inhale hundreds and thousands of amphiboles, which causes lung damage. It is being mined in India at places such as Andhra Pradesh (Pulivendla), Jharkand (Roro), Rajasthan (Ajmer, Bhilwara, Udaipur, Rajsamand) and the common problem faced by the locals are asbestosis through air and fluorosis through drinking water. The problem continues to be in India as well as other developing countries. Also, India import and re-export asbestos to other countries and workers at shipyard, transport of the hazardous material on road and roadside residents all are vulnerable to this uncommon disease. The signs and symptoms generally found with the workers are shortness of breath, persistent and productive cough due to pulmonary fibrosis can show up many years after the asbestos exposure.

Asbestos↗

PubMed2000

Increased phosphorylated extracellular signal-regulated kinase immunoreactivity associated with proliferative and morphologic lung alterations after chrysotile asbestos inhalation in mice.

Activation of extracellular signal-regulated kinases (ERK) has been associated with the advent of asbestos-associated apoptosis and proliferation in mesothelial and alveolar epithelial cells and may be linked to the development of pulmonary fibrosis. The objective of studies here was to characterize the development of inflammation, cellular proliferation, and fibrosis in asbestos-exposed C57Bl/6 mice in relationship to patterns of ERK phosphorylation. Inflammation occurred after 10 and 20 days of asbestos exposure as evidenced by increases in total protein and neutrophils in bronchoalveolar lavage fluid. Increases in cell proliferation were observed at 30 days in bronchiolar epithelia and at 4, 14, and 30 days in the alveolar compartment of the lung. Trichrome-positive focal lesions of pulmonary fibrosis developed at 30 days in the absence of elevations in lung hydroxyproline or procollagen mRNA levels. Striking increases in ERK phosphorylation were observed within pulmonary epithelial cells at sites of developing fibrotic lesions after 14 and 30 days of inhalation. In addition to characterizing a murine inhalation model of asbestosis, we provide the first evidence showing activation of ERK signaling within lung epithelium in vivo, following inhalation of asbestos fibers.

Administration, Inhalation↗

PubMed1985

Thoracic surgical problems in asbestos-related disorders.

Among 1,577 persons with asbestos exposure followed up from 3 to 30 years, 113 had thoracic surgical procedures for asbestos-related disorders. Twenty-six individuals suspected of having asbestosis with atypical features underwent open-lung biopsy; a different disease was revealed in 14. Most of the 29 patients with mesothelioma had a small thoracotomy for diagnosis only; chemotherapy in half of them proved entirely ineffective. Experience with 23 patients with bronchogenic carcinoma did not differ from that in persons not exposed to asbestos. Problems of causal relationship are discussed. Most of the 68 individuals with benign asbestos pleural effusion had no symptoms, but because of recurrence, 15 were operated on for decortication or for possible mesothelioma. Hyaline plaques often were mistaken for lung, rib, or diaphragmatic tumors, and sometimes mesothelioma was suspected. Operative intervention in the 24 patients with plaques could have been avoided by obtaining a more detailed occupational history and reviewing previous chest roentgenograms, which invariably showed identical or smaller plaques from 2 to 17 years earlier.

Adult↗

PubMed1997

Iron mobilization from crocidolite as enhancer of collagen content in rat lung fibroblasts.

Asbestos exposure causes pulmonary fibrosis by mechanisms that remain uncertain. There is increasing evidence that iron from asbestos is responsible for many of its effects. In this paper, we investigated the effect of iron mobilized from crocidolite asbestos on collagen content in rat lung fibroblast cultures under serum-free conditions. Crocidolite (2, 4, 6 microg/cm2 well) increased collagen content in a dose-dependent manner (+42 +/- 8, +92 +/- 10, and +129 +/- 13% vs controls). This effect was specific for collagen, since it did not alter total protein content and was inhibited by the iron chelator deferoxamine (DFO). Preincubation of crocidolite with citrate (1 mM) for 48 hr resulted in iron mobilization (51 microM) and increased collagen production (>3-fold) in treated cells. These effects occurred without the intervention of serum factors. The absence of cell damage, proliferation or lipid peroxidation leads to the supposition that iron from crocidolite per se may act as a profibrogenic agent. Although the in vivo participation of other cells and factors cannot be excluded, we conclude that iron released from crocidolite plays a role in collagen increase occurring during asbestosis.

Animals↗

PubMed2003

Respiratory impairment due to asbestos exposure in brake-lining workers.

There is extensive evidence that exposure to asbestos causes pulmonary parenchymal fibrosis, pleural disease, and malignant neoplasm in asbestos-exposed workers. However, few data concerning brake-lining workers are available in the literature. In this study, we aimed to assess the long-term effects of chrysotile asbestos exposure on lung function and the risk of asbestos-related diseases in brake-lining workers. Seventy-four asbestos-exposed workers who processed brake-lining products and 12 unexposed office workers were offered pulmonary function tests (spirometry and transfer factor) in 1992 and 1999. In 1999, the mean duration of asbestos exposure was 10.00+/-4.07 and 11.02+/-4.81 years (7-31 years) in nonsmoking and smoking asbestos workers, respectively. Transfer factor (T(L), CO) and transfer coefficient (K(CO)) decline were significant in the 7-year follow-up in both smoking and nonsmoking asbestos workers. However, lung function indices of the control group, whom were all current smokers; were also found to be decreased, including FEF(75), T(L), CO and K(CO). We found minimal reticular changes in 10 asbestos workers who were all current smokers, they underwent high-resolution computed tomography scans of the chest and we found that they had peribronchial thickening resulting from smoking. As a conclusion, even in the absence of radiographic asbestosis, T(L), CO and K(CO) may decrease after a mean 10-year duration of exposure to asbestos in brake-lining workers and this is more noticeable with cigarette burden.

Adult↗

PubMed1992

Deposition, clearance, and translocation of chrysotile asbestos from peripheral and central regions of the rat lung.

We investigated the pulmonary deposition, clearance, and translocation of chrysotile asbestos in the context of our previously developed model of asbestosis in the rat. Adult male rats were exposed for 3 hr to an aerosol of chrysotile asbestos. Subgroups were sacrificed up to 29 days postexposure and the lungs of the animals fixed. Peripheral and central regions of the left lung were resected, digested, and analyzed for fiber content by scanning electron microscopy. Pulmonary deposition did not differ between peripheral and central regions. There was no evidence of translocation of fibers from central to peripheral regions. The average diameter of retained fibers decreased over time, consistent with longitudinal splitting. The average length of retained fibers increased over time, consistent with slower clearance of longer fibers. We employed a novel counting scheme to ensure accurate fiber number measurements, allowing the calculation of clearance rates for fibers 0.5 to greater than or equal to 16 microns in length. Fibers of length greater than or equal to 16 microns were cleared slowly, if at all. These findings could have important implications for the pathogenesis of asbestos-related pleural disease. Many fibers are deposited in the peripheral region, and the longest (greater than or equal to 16 microns) will persist there for extended periods.

Aerosols↗

PubMed1992

Occupational exposure to asbestos and urinary bladder cancer.

By the use of transmission electron microscopy (TEM) and energy dispersion spectrometry the amount (mean value mean = 191 +/- 94 fibers/mg of tissue) and the type (chrysotile and tremolite) of asbestos fibers have been determined in tissue samples of four bladder cancer patients affected by pulmonary asbestosis, working in the same plant producing asbestos-cement pipes and boards. Similar measurements were carried out on samples of bladder cancers of eight control patients not professionally exposed to asbestos. Only five of them also revealed chrysotile fibers (mean = 151 +/- 196 fibers/mg of tissue). The paucity of the study and control cases and the small quantitative difference between them regarding the presence of infraneoplastic asbestos fibers does not consent us to hypothesize a causal relationship between tumor and occupational exposure.

Aged↗

PubMed1986

Effects of asbestos fibers on alveolar macrophage-mediated lymphocyte cytostasis.

Prolonged asbestos inhalation results in pulmonary inflammation and fibrosis. Since alveolar macrophages are active in regulation of immune responses in lung and appear to be involved in the pathogenesis of asbestosis, we evaluated the effects of asbestos exposure on the ability of these cells to regulate lymphocyte function. Alveolar macrophages obtained by lung lavage from BALB/C mice were treated in vitro with either UICC amosite or chrysotile asbestos and the effects on lymphocyte cytostasis compared with those of macrophages incubated with latex beads or zymosan. Macrophages (10%) incubated either alone or with latex beads for 48 hr effectively inhibited lymphocyte mitogenesis. However, alveolar macrophages incubated with either amosite or chrysotile asbestos did not demonstrate intact cytostatic activity. Decreased viability of chrysotile asbestos-treated macrophages correlated with loss of cytostatic effects, but alveolar macrophages exposed to amosite remained viable. We conclude, therefore, that exposure of alveolar macrophages to asbestos can result in loss of their ability to down-regulate lymphocyte proliferation, a finding which may be important in the pathogenesis of asbestos-related disease.

Animals↗

PubMed1983

Small-airway lesions in patients exposed to nonasbestos mineral dusts.

Small-airway lesions were identified in histologic sections from the lungs of seven workers with histories of exposure to nonasbestos dusts. The lesions consisted of deposits of fibrous tissue, often accompanied by pigment, in the walls of membranous and respiratory bronchioles and alveolar ducts. Comparison with a matched population of persons with no dust exposure revealed that the changes in the respiratory bronchioles and alveolar ducts were morphologically distinctive and could be used to diagnose the lesions. Structurally, these lesions were very similar to those described in the airways of asbestos workers, although comparison with the authors' previous results indicated that the number of severely affected airways was less in the nonasbestos dust group. Mineralogic analysis indicated that these abnormalities were produced by a variety of different dusts including silica, iron oxide, and aluminum oxide, and that occult asbestos exposure, although possible in three of the cases, was most likely not a primary cause of disease. The authors suggest that this lesion, which they call mineral dust airways disease, is a nonspecific reaction of the small airways to inorganic particulates. The presence of such changes casts considerable doubt on the theory that small-airway abnormalities in asbestos workers are the earliest form of asbestosis.

Aged↗

PubMed1984

Morphology of small-airway lesions in patients with asbestos exposure.

The morphologic changes in the small airways of 15 patients who had been exposed to asbestos and had abnormalities of the respiratory bronchioles and alveolar ducts were examined and compared with changes in the small airways of a matched group of cigarette smokers. Lesions were evaluated using a visual grading scheme to determine pathologic severity of fibrosis, inflammation, and pigmentation in these airways. The membranous bronchioles of both asbestos-exposed and cigarette exposed patients showed the deposition of fibrous tissue and pigment; the lesions were morphologically identical, although more severe in the asbestos group (67 per cent of airways) than in the smoking group (19 per cent of airways). A distinctive lesion, consisting of fibrosis often accompanied by pigment, was found in 74 per cent of the respiratory bronchioles in the asbestos-exposed patients, compared with 6 per cent of respiratory bronchioles in the smokers. Similar changes were found in 49 per cent of alveolar ducts in the asbestos group and 1 per cent of the ducts in smoking group. Asbestos bodies were found in only 11 of 15 cases. The authors conclude that a distinctive lesion of small airways exists in some asbestos workers and that it can be identified by the finding of marked fibrosis in the walls of respiratory bronchioles and alveolar ducts. Because there is no proof that this lesion actually progresses to interstitial fibrosis (asbestosis), the authors suggest that it be termed "asbestos airways disease."

Asbestos↗

PubMed1978

The hygiene standard for chrysotile asbestos.

Previous studies, including the analysis on which the current 2 fibres/cm3 hygiene standard is based, may have underestimated the risk of morbidity or mortality following exposure to low levels of asbestos dust. Accurate dose-response data at levels below 2 fibres/cm3 are unlikely to be available for the foreseeable future, and the biologically plausible assumption that excess cancer mortality is approximately proportional to dust level should be provisionally accepted. It may be reasonable, however, to postulate a safe threshold for mortality from asbestosis. If excess mortality from asbestos-related disease is proportional to dust level for each cause, approximately 10% of male asbestos workers might, under certain assumptions, eventually die of asbestos-induced disease after 50 years' exposure at 2 fibres/cm3. Peritoneal mesothelioma is usually due to crocidolite (blue asbestos) or other amphiboles, but exposure to chrysotile (white asbestos) alone may lead to a substantial risk of pleural mesothelioma. These predictions are based on rather small numbers in a single factory, and further studies in other working environments are required. Fibre counts based on optical microscopy are likely to be less relevant than total counts by electron microscopy, and excess mortality is virtually confined to men first exposed more than 20 years ago, when little or no accurate data on dust levels were collected.

Asbestos↗

PubMed2002

Manganese superoxide dismutase genotypes and asbestos-associated pulmonary disorders.

Manganese superoxide dismutase (MnSOD) activity is highly elevated in the biopsies of human asbestos-associated malignant mesothelioma. We therefore examined if polymorphism in the mitochondrial targeting sequence of the MnSOD gene modified individual susceptibility to this malignancy or related asbestos-associated pulmonary disorders. The study population consisted of 124 male Finnish asbestos insulators who were all classified as having been exposed to high levels of asbestos; 63 of the workers had no pulmonary disorders and 61 either had malignant mesothelioma or the non-malignant pulmonary disorders asbestosis and/or pleural plaques. No significant associations were found between the MnSOD genotypes and these ill-health. This study therefore suggest no major modifying role for the MnSOD polymorphism in development of asbestos-associated pulmonary disorders.

Asbestos↗

PubMed1999

Chrysotile-mediated imbalance in the glutathione redox system in the development of pulmonary injury.

A significant depletion in the content of glutathione (GSH) and alteration in GSH redox system enzymes were observed in the lung of chrysotile-exposed animals (5 mg) during different developmental stages of asbestosis. In the alveolar macrophages (AM) of exposed animals, the depletion in GSH started from day 1 and reached a maximum at day 16, whereas in lung tissue the maximum depletion was observed when fibrosis has matured. It appears that cellular GSH depletion triggers oxidative stress in the system as observed from increased thiobarbituric acid reactive substance (TBARS) production and alteration in the activities of glutathione peroxidase (GPx), glutathione reductase (GR), glucose 6-phosphate dehydrogenase (G6PD) and glutathione S-transferase (GST), the enzymes regulating oxidative tone. The depletion in GSH was also observed in red blood cells (RBC) of the exposed animals reaching a maximum when fibrosis matured. Thus the observed depletion in GSH, ascorbic acid and alteration in GSH redox system enzymes may be involved in fibrosis and carcinogenesis induced by chrysotile.

Animals↗

PubMed1986

Approaches to prevention of asbestos-induced lung disease using polyethylene glycol (PEG)-conjugated catalase.

Asbestos-associated damage to cells of the respiratory tract in vitro can be prevented by the simultaneous addition of scavengers of active oxygen species to cultures. To determine if administration of scavenger enzymes to animals and humans is a plausible approach to the prevention of asbestos-induced lung disease, osmotic pumps were filled with various concentrations of PEG-coupled catalase and implanted subcutaneously into Fischer 344 rats over a 28-day period. At 3, 14, and 28 days after implantation of the pumps, the animals were evaluated for levels of catalase in serum and lung. In addition, lung tissue and lavage fluids were examined at 28 days for biochemical and morphologic indications of cell injury, inflammation, and fibrotic lung disease. At all time points examined, the administration of PEG-catalase caused a dosage-dependent increase in serum levels of catalase. The levels of lung catalase were evaluated at 28 days but not at earlier time periods. In comparison to control rats, the amounts of enzymes (lactic dehydrogenase, alkaline phosphatase), protein, and cells in lavage fluids from treated animals were unaltered. Moreover, the lungs showed no evidence of inflammation or fibrotic disease as determined by differential cell counts in lavage and measurement of hydroxyproline. These studies suggest that administration of PEG-catalase does not cause injury or other alterations in lung tissue and can be pursued as a feasible approach to prevention of asbestosis.

Animals↗

PubMedDate not supplied

[Asbestos-related pleuropulmonary diseases: pictorial essay].

Pleural and pulmonary asbestos-related diseases range from benign conditions, like pleural effusion and pleural plaques, to some neoplasias, such as lung cancer and malignant mesothelioma. Pleural effusion is the earliest finding after asbestos exposure, but the imaging findings are not specific. Diffuse pleural thickening involves the visceral pleura and pleural plaques are considered to be hallmarks of exposure. Asbestosis is the pulmonary fibrosis due to asbestos. Rounded atelectasis is a peripheral lung collapse in these individuals, generally related to pleural disease. Some neoplasias, like lung carcinoma and pleural mesothelioma, are more prevalent in asbestos-exposed subjects. The aim of this essay is to illustrate the main imaging findings of asbestos-related diseases.

Asbestos↗

PubMed1990

Pleural and parenchymal fibrosis mainly affecting the upper lung lobes in persons exposed to asbestos.

From the County of Uppsala, Sweden, more than 1600 persons with pleural plaques and/or asbestos-related pleural thickening have been seen at the Uppsala University Hospital during a period of about 15 years. During the observation time, 40 patients developed lesions mainly affecting the upper lobes of the lung. They were all men, 41 to 78-years-old, and all had been occupationally exposed to asbestos. The mean latency time from the first exposure was 34 years. The mean width of the apical pleural thickening was 21 mm. In 21 patients the lesions were on the right side, in 15 they were bilateral, and in only four patients was the left side alone affected. Biopsies from the pleura were available in twelve patients and from the lung parenchyma in eight. The biopsies of the lungs all showed varying degrees of asbestosis and of the pleura nonspecific pleuritis. The lesions tended to progress and in all cases except one they were part of a diffuse pleural and parenchymal fibrosis involving the rest of the lung. Consequently, the pulmonary function was impaired, with the vital capacity reduced to an average of 62% and total lung capacity to 68% of the predicted value. In many patients there was contraction of the upper lobe and deviation of the trachea towards the same side. Upper lobe changes are a relatively rare complication of exposure to asbestos but are important to recognise. Other possible causes of upper lobe changes such as tuberculosis must always be excluded before the diagnosis is made.

Adult↗

PubMed2000

Sister chromatid exchange rate from pleural fluid cells in patients with malignant mesothelioma.

This study assessed the impact of malignant mesothelioma on the frequencies of sister chromatid exchange (SCE) in the pleural effusion cells. Ten patients with mesothelioma and 20 control subjects were included in the study. The control subjects were the patients with tuberculosis pleurisy, and the remaining 10 subjects of control group were healthy volunteers and only heparinized blood samples were collected from these subjects. The pleural effusion cells were cultured with conventional culture methods. The samples were obtained from the patients after histopathologic confirmation of the malignancy but before the initiation of chemotherapy or radiotherapy. At the end of the culture period and 48 h prior the harvesting, BrdU was added into flasks. Totally, 100 metaphases were scored for each sample. In this study, we found that the SCE frequencies of malignant pleural mesotheliomas were significantly higher than the control subjects (P<0.001). Six of 10 patients came from central Anatolia, which is of great importance due to high rate of exposure to asbestosis in this region.

Adult↗