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The prolonged inhalation of silicon powders induces an oxidative stress at respiratory system level, due to the formation of free radicals (FR). Free radical origin is either exogenous (as a result of the chemical structure of powders) or endogenous (result of the endocytosis of silicon powders). Bivalent Fe ions are implied in FR generation, and the substances with Fe chelating and antioxidizing actions block the evolution of silicosis.
After successful animal studies since 1986, a single left lung transplantation was performed on a 35-year-old male patient with end-stage silicosis in July 1991. The surgical technique was similar to that used by the Toronto Transplant Group, except for some modification in bronchial anastomosis. The donor lung was preserved by simple surface cooling after the administration of heparin, methylprednisolone and PGE1. The ischemic time for the donor lung was 3.5 hours. A cardiopulmonary bypass through the femoral vessels was applied for a duration of 90 minutes. Immediate postoperative complications included massive bleeding, disseminated intravascular coagulation, adult respiratory distress syndrome and acute graft rejection. Fortunately, we overcame these complications through intensive care. Immunosuppression included antilymphocytic globulin, cyclosporine, azathioprine and corticosteroids. The results of this single lung transplantation were satisfactory. The patient was doing well and was able to satisfactorily breathe room air six weeks after the transplantation. Unfortunately, the patient died of opportunistic systemic aspergillosis six months after the transplantation. In conclusion, lung transplantation is an effective treatment for patients with end-stage lung diseases, and the results of this first single lung transplantation in Taiwan are encouraging and promising.
The forms of catalase modified by treatment with dextran aldehyde were obtained and studied. Efficacy of the preparations containing native and modified forms of catalase and superoxide dismutase as well as their covalent bienzyme conjugate containing catalase-dextran aldehyde-superoxide dismutase was studied in rats with simulated silicosis. The preparations were administered into rats by means of inhalation and intraperitoneal injection. Positive protective effect exhibited a mixture of native enzymes and their covalent conjugate. The most pronounced additional effect was caused by the mixture of native catalase and superoxide dismutase as compared with modified preparation of superoxide dismutase. The preparation of bienzyme containing conjugate was less effective.
The aim of this study was to determine the distribution of lung diseases in the autopsy subjects brought for medicolegal examination in the Transkei area. Two hundred histopathological slides were examined microscopically. Of them, 46 subjects (23%) showed some kind of pathology. There were four kinds of lesions observed: dust reticulation (anthracosis), necrotizing granulomatous inflammation, tuberculosis and silicosis. Dust reticulation was observed in the lungs of 16 cases (8%), 14 of them (7%) were females and 2 males (1%), the deposition of carbon with some refractive silica particles seen in the lung fields predominated. These were the rural women aged 45-75 years. Narcotizing granulomatous inflammation of lungs that was probably tuberculosis and clear tuberculosis were found in 14 (7%) and 8 (4%) cases respectively.
All admissions with diagnosis of silicosis from 1980 to 2000, in the Occupational Medicine Division of Fondazione S. Maugeri, Cassano Murge (Bari), were examined. From 586 gathered medical records we selected 106 subjects with double admissions and detected their X-rays of chest, FVC and FEV1. The stationary results of their chest X-rays and the light declines of their respiratory functions confirm the slow evolution in time of this pathology.
Silicosis is an ancient disease, but with modern understanding of safe levels of exposure, it should be a vanishing disease. Emphasis will be placed on newer concepts in the pathogenesis of the disease and the health effects of low levels of quartz dust in relation to current exposure standards. The ongoing controversy regarding the carcinogenicity of quartz is discussed.
OBJECTIVE: To study the correlation between the expression of Egr-1 and NF-kappaB and the up-regulation of TNF-alpha and TGF-beta1 in macrophages after stimulation by silica in-vitro. METHODS: Macrophages were treated with antibodies against Egr-1 and NF-kappaB and antisense oligonucleotides. The level of TNF-alpha protein in the cell supernatant was then measured using enzyme-linked immunoadsorbent assay (ELISA). The expression of TGF-beta1 protein was detected by immunocytochemistry. The expression of TNF-alpha and TGF-beta1 mRNAs was also monitored by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: Compared with silica-stimulated macrophages untreated with antibodies, the cells treated with 10 micro g/ml of Egr-1 or NF-kappaB antibodies were associated with reduced expression of TNF-alpha and TGF-beta1 proteins and mRNAs (P < 0.05). Compared with silica-stimulated untransfected group, the antisense group was associated with obvious reduction in the expression of TNF-alpha and TGF-beta1 proteins and mRNAs (P < 0.05). CONCLUSION: The expression of TNF-alpha and TGF-beta1 mRNAs and proteins are associated with activation of Egr-1 and NF-kappaB in macrophages, after stimulation by silica. It is possible that the corresponding antibodies and antisense oligonucleotides may become a potential therapeutic tool in the management of silicosis in the future.
The authors present clinical and X-ray data of 30 patients with "late silicosis" that occurred in 5-20 years after they had retired from dust-related occupation. Follow-up over 4-25 years demonstrated progression of nodular pneumosclerosis up to macronodular forms or silicotuberculoma formation. The diseases mostly developed gradually, usually was diagnosed by casual X-ray examination and was long considered as tuberculosis, sarcoidosis or other disseminated lesion.
The development of our studies on silica carcinogenesis and its mechanisms is reviewed. Starting from an analysis of the cellular reactions to silica in the pathogenesis of silicosis in the rat, followed by an analysis of the carcinogenic response to silica in the lungs of rats (but not in mice and hamsters), we went on to develop cellular models for culture and neoplastic transformation of rat alveolar epithelial cells. We studied the binding of silica to DNA, the generation of reactive oxygen species and the DNA damage mediated by hydroxyl radicals, showing marked differences among silica samples of varying purity. Then we investigated the role of peptides induced by silica in various cells, including cytokines and growth factors. Tumor necrosis factor (TNF)-alpha, which can cause activation of DNA transcription and is required for silica-induced fibrosis, was found to inhibit neoplastic transformation by quartz in cell cultures. Transforming growth factor (TGF)-beta was found to be produced in hyperplastic alveolar type II cells and to reach fibroblasts, macrophages and the connective tissue matrix adjacent to silicotic granulomas. Neuroendocrine cells and their peptides were found to be increased in alveolar and bronchiolar epithelia of silica lesions in rats, in contrast with mice and hamsters. Expression of adhesion molecules was found to be altered in silica-induced carcinogenesis and epithelial-mesenchymal transition was revealed by mesenchymal markers in the induced carcinomas. Promoter hypermethylation of adhesion genes in the induced carcinomas indicated a role for epigenetic mechanisms.
Exposure to silica can induce fibrosis and/or emphysema. Various factors such as proteases, other hydrolases and oxidants may be involved in the destruction of lung parenchyma. On the other hand, antiproteases play an important role in the protection of lung parenchyma against the action of proteases. We have developed an animal model of silicosis in monkey Macacus cynomolgus and followed these factors by bronchoalveolar lavage (BAL). We have studied glycosidases activities, elastase-like activity, immunoreactive alpha 1-protease inhibitor (alpha 1PI), neutrophil elastase inhibitory capacity (NEIC) and myeloperoxidase. Bronchoalveolar cells in serial BAL were also studied. Six monkeys were exposed to quartz aerosols (100 mg.m-3) for 18 wks. They were followed until they developed X-ray changes, which occurred between 21-64 wks after the end of the dust exposure. Cellular "silicotic nodules" were observed in lung biopsies. A control animal underwent serial BAL. Changes were seen in the differential cell count. The release of superoxide anion by bronchoalveolar cells obtained during the experiment was increased. Separation on a gradient of Percoll showed the presence of young macrophages, which exhibited enhanced release of superoxide anion as compared to the totality of bronchoalveolar cells. The biochemical analysis of BAL fluids obtained during and after the period of dust exposure showed an increase in glycosidases, alpha 1PI and NEIC. Some free elastase-like activity was simultaneously detected in BAL fluids from exposed animals but not from the control. This elastase-like activity was very low compared to NEIC. The increase in enzymatic and antiprotease activities occurred at different points in time for each animal, suggesting large differences in individual responses to dust, but occurred before the chest X-ray abnormalities.
The present paper dwells on biomedical study of aldehyde dextran modified superoxide dismutase. Pharmacokinetic data demonstrated that modification of superoxide dismutase increased its half-time. A rat model of experimental silicosis showed that aldehyde dextran modified superoxide dismutase inhibited evolving fibrosis in the lungs. The same dose of native enzyme produced no therapeutic effect. Thus, superoxide dismutase can be considered as a potential agent for treatment of fibrosis due to its modification.
A series of biochemical and immunological investigations was performed in a group of 33 silicosis patients and in 34 controls. The results obtained suggest future prospects of utilizing the following tests as silicotic-fibrosis markers: alpha 2-globulin and ceruloplasmin levels, activity of certain lysosomal enzymes (beta-galactosidase and beta-acetylglucosaminidase), IgM and IgG immunoglobulins, elastases, and the C4 component of the complement.
We could identify, via bronchoalveolar lavage, crystals in the lavage fluid and in the alveolar macrophages. Thus, BAL could be another method for diagnosing silicosis patients.
A 43-year-old stone cutter with 13 years of exposure to silica developed a pulmonary silicosis and a glomerulonephritis with moderate renal failure. Renal biopsy demonstrated in light microscopy a segmental and focal mesangial proliferation and in electron microscopy distinct alterations of the proximal tubular cells. Renal histology suggest silica may play a part in the pathogenesis of renal damage. Clinicians should therefore include silica exposure in the differential diagnosis of unexplained glomerulonephritis.
A patient is described who had been--as a cutter of crystal--for 40 yrs exposed to the silica dust. At regular medical examinations at out-patients' department for pulmonary diseases first stage of pulmonary silicosis had been found and confirmed at the Institute for Occupational Health. Nine years after the retirement the clinical symptoms of febrility, cough, joint and muscular pains appeared together with the difficulties in swallowing and dyspnea even at minor physical activities. During the treatment the systemic vasculitis, probably visceral erythematodes, was established with satisfactory response to the corticosteroid therapy.
Three family members who had worked as sandblasters in their own sandblasting factory showed innumerable small nodularities in both lung fields of their chest radiograms. One of those showed conglomerate shadows in the upper lung fields. Those shadows seemed to be consistent with those of silicosis. One of the patients was examined by transbronchial lung biopsy (TBLB) and showed typical silicotic nodules. Mineralogical studies were done on the abrasive particles and the deposited particles in the lung tissue specimen obtained via TBLB and bronchoalveolar lavage fluid sample (BALF) using polarized microscopy, X-ray diffraction and analytical electron microscopy. The particles which had accumulated on the floor of the factory mineralogically consisted of mostly (over 90%) silica quartz containing small amount of chlorite, and the deposited particles in the lung tissue and those in the BALF showed similar composition.
A high concentration of silica dust in the air many workstands in ceramic plants is a serious risk for the health of exposed workers. It can cause the development of silicosis. The aim of this paper is to evaluate a fibrogenic activity of dusts containing 98% crystalline silica. The ceramic masses have about 25% of Quartz. The samples of 2 lode quartz and 4 sand quartz originated from different mines in Poland were used for the experiment. Their physical properties were analysed by X-ray diffraction and SiO2 content was determined by colorimetry. Their biological aggresiveness was characterised by wet weight, hydroxyproline content, lipid level in the lungs and wet weight of mediastinal lymph nodes of rats which were intratracheally given of the dusts. The results show that the tested dusts have a moderated fibrogenic activity. At short time (3 months) after their administration the fibrogenic changes in lungs were different depending on the kind of dusts, but at the 6th month of the experiment they did not differ at all. The exposition of workers to silica dusts is a great occupational hazard.
Silicate substitutes for phosphate in the transitory uncoupling of rat liver mitochondria induced by hydrazine when beta-hydroxy-butyrate is the substrate. Uncoupling is blocked by rutamycin. Just as in the case when phosphate is combined with hydrazine, ATP, ADP, PPi, and Mg++ protect against hydrazine when silicate is combined with hydrazine. A high level of ADP in the absence of added phosphate, but in the presence of silicate, induces a pseudo state three of the mitochondria. Silicate, like sulfate and arsenate which have been reported previously, is activated by the enzymes which mediate oxidative phosphorylation. These results serve to explain a role for silicate in silicosis, black lung disease, and cancer. In addition, since there is suggestive evidence in the literature that lung tissue solubilizes asbestos fibers, these results not only expand the confluence between oxidative phosphorylation and chemical carcinogenesis but are correlated with the synergistic carcinogenicity of asbestos and smoking observed by epidemiologists.