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PubMed1993

[A case of pulmonary asbestosis with slightly increased serum IgE concentration and histopathological changes resembling DIP].

A 68-year-old male presented with cough and sputum. He had suffered from these symptoms for ten years prior to admission. Chest roentgenogram revealed reticulonodular shadows in the lower fields of both lungs. CT scan of the chest revealed an interstitial pattern in the lower field of both lungs. Honeycombing and bullous pattern were also present in the subpleural area. The patient had a history of dust and asbestos inhalation while working as an electrician. Eosinophilia of the peripheral blood and BALF, and a slightly increased serum IgE concentration were noted. Open lung biopsy revealed interstitial fibrosis with intra-alveolar macrophage accumulation and asbestos bodies. The histopathological features resembled UIP and DIP, although DIP is uncommon in pulmonary asbestosis. The slightly increased serum IgE concentration was considered to be an additional effect of asbestos. This is a case of pulmonary asbestosis with intriguing immunological and histopathological features.

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PubMedDate not supplied

[Cause-specific mortality of asbestos-cement workers compensated for asbestosis in the city of Bari].

The cause-specific mortality of 233 asbestos cement workers employed by the Fibronit company in Bari and compensated for asbestosis was investigated. Cohort members were enrolled on 31.12.1979 and followed through 30.4.1997; follow-up was completed for 98.3% of study subjects, and causes of death were ascertained for 96.6% of deceased subjects. Observed mortality was contrasted to that expected according to cause-sex-age- and calendar time-specific rates of the population resident in the Apulia Region. All causes observed mortality exceeded expected value (SMR: 117, 87 observed), due to a significant' increase in pneumoconiosis (SMR: 11238, 14 observed) and malignant neoplasms (SMR: 163, 38 observed)). A significant decrease of circulatory diseases was found (SMR: 64, 18 observed). Among cancer deaths, the following sites showed a significant excess: lung (SMR: 206, 17 observed), pleura (SMR: 2551, 4 observed), mediastinum (SMR: 2367, 2 observed) and peritoneum (SMR: 2877, 2 observed). The excess mortality due to asbestosis, respiratory cancer and peritoned neoplasms can be causally attributed to occupational asbestos exposure.

Asbestos↗
PubMedDate not supplied

[Asbestosis with sarcoid-like pulmonary lesions. A propos of one anatomoclinical case report].

A report of a clinico-pathological case of asbestosis with special histological lesions. The latter had a granulomatous appearance, progressing to fibrosis with Schaumann bodies organised around bodies with a ferruginous covering, apparently due to asbestosis. The histogenesis of the lesions is discussed, together with the need to take a precise professional history. The usefulness of certain simple methods of analysis is mentioned.

Asbestos↗
PubMed2000

Science or public relations? The inside story of the Asbestosis Research Council, 1957-1990.

In 1957, the leading British asbestos companies (Turner & Newall, Cape Asbestos, and British Belting & Asbestos) founded the Asbestosis Research Council (ARC). This was a response to rising asbestosis and asbestos cancer mortality in the UK and the attendant political and social problems that threatened the existence of the asbestos industry. An ARC research program was launched, that by the 1970s was mainly based within the Institute of Occupational Medicine at Edinburgh University. By the end of the 1980s, well over a hundred papers had been published with ARC support. The bulk of the work involved animal experiments and the chemical analysis of fibers, but the asbestos companies showed little enthusiasm for wider epidemiological studies or for exploring the cancer threat. The sponsoring companies dictated the ARC's research strategy and also vetted (and sometimes censored) publications; while using the ARC as a counterweight to government regulation and media attacks. The ARC's history highlights the compromises that were made by individual scientists and demonstrates the dilemmas inherent in industry-controlled research.

Asbestos↗
PubMed1985

Bronchoalveolar lavage and clearance of 99m-Tc-DTPA in asbestos workers without evidence of asbestosis.

We performed BAL and measured the clearance of 99m-Tc-DTPA in 20 non-smoking subjects (mean age 50, range 36-68 years) occupationally exposed to asbestos (mean duration 14, range 3-30 years). All had normal lung function and none had clinical or radiological evidence of asbestosis. The mean BAL results were: total cells per ml 737 X 10(3) (360-1210), percentage macrophages 79 (49-96), percentage lymphocytes 13 (1-42), percentage neutrophils 8 (1-40), percentage eosinophils 0 (0-3), asbestos bodies per ml 83 (0-550). Eight subjects showed increased percentage of lymphocytes and four others showed increased percentages of neutrophils when compared with normal ranges in our laboratory. Higher percentages of neutrophils correlated with longer duration of exposure to asbestos (r = 0.54, P less than 0.025), and shorter time since last exposure to asbestos (r = -0.54, P less than 0.025). Four subjects showed faster clearance of 99m-Tc-DTPA than was observed in 31 normal non-smoking control subjects. There was a tendency for faster solute clearance to be associated with greater numbers of BAL macrophages (r = -0.39, P less than 0.10) but there were no significant relationships between solute clearance and other BAL variables. BAL profiles in asbestos workers may be abnormal in the absence of clinical or radiological evidence of asbestosis.

Adult↗
PubMed1997

The glutathione S-transferase theta and mu deletion polymorphisms in asbestosis.

The glutathione S-transferases (GSTs) catalyze the conjugation of a wide variety of reactive, electrophilic substrates with glutathione, facilitating their excretion. There is also evidence that GSTs can catalyze glutathione conjugation of lipid radicals as well as act in the generation of leukotriene inflammatory mediators. Studying construction carpenters screened for the presence of asbestos-related diseases, we have previously reported that the constitutional deletion of GSTM1 (the gene coding for glutathione S-transferase class mu) is associated with an increased risk of asbestos-related interstitial lung disease, measured radiographically. In the current work, we have further studied this group of workers, investigating the distribution of a novel deletion polymorphism in the newly described GSTT1 gene, that codes for the GST class theta enzyme. A total of 666 carpenters were studied, and 124 (19%) had the deleted genotype. There was no association between the GSTT1 deletion and the radiographic diagnosis of either asbestos-related pleural or parenchymal disease. The GSTM1 deletion remained associated with the presence of x-ray evidence of asbestosis after adjustment for GSTT1 genotype. The GSTM1 null genotype was also associated with a family history of any malignancy. These data suggest that the association of polymorphic GSTs with asbestos-induced radiographic changes is specific for substrates of the GST class mu.

Adult↗
PubMed1981

Immunoblastic lymphadenopathy and asbestosis.

Immunoblastic lymphadenopathy was diagnosed in a 71-year-old white man who had weakness, with weight loss, fever, cough, and generalized lymphadenopathy. The patient had a long occupational history of shipyard work. Diagnosis of asbestosis was made clinically by chest x-ray, and ferruginous bodies were found in the lung at autopsy. Recent reports have suggested a possible association between asbestos exposure and lymphoproliferative neoplasms. Chronic antigenic stimulation by asbestos could predispose one to the immunoproliferative disorder seen in this patient or be responsible for it. The possible significance of this relationship, previously unreported, is discussed for future consideration.

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PubMed1981

Hemodynamics of pulmonary circulation in asbestosis: study of 16 cases.

Pulmonary circulation hemodynamics was studied by microcatheterization at rest and during exercise in 16 workers with asbestosis. There was pulmonary arterial hypertension owing to increased total pulmonary resistance even in the early stages of pneumoconiosis, sometimes without impairment of lung function. In two cases, a partial reduction in pulmonary hypertension and total pulmonary resistance was obtained with aminophylline. The pathogenesis of pulmonary circulation impairment has been attributed in previous work to periarteriolar fibrosis originating in the lymphatic vessels, until now insufficiently emphasized as the anatomical basis of these physiological alterations.

Adult↗
PubMed1992

Serum oncoproteins and growth factors in asbestosis and silicosis patients.

Levels of 9 different oncoproteins and growth factors were assayed by immunoblotting with monoclonal antibodies in 91 serum samples collected between March 1983 and August 1987 from 46 pneumoconiosis patients (36 asbestosis, 10 silicosis) at high risk for the development of cancer. Follow-up of these patients through June 1991 showed that 18 had developed cancer (11 lung, 2 pleural mesothelioma, 2 transitional-cell carcinomas of the urinary bladder, 1 osteosarcoma, 1 non-Hodgkin's lymphoma, 1 adenocarcinoma of the gallbladder). Increased serum levels of ras oncogene-related protein (p21) were found in 7 of the 18 patients who developed cancer (5 lung, 2 pleural mesothelioma) versus 2 of the 28 patients without cancer, a statistically significant difference (p = 0.012). In addition, 6 of the 7 p21-positive cancer cases had positive serum samples prior to clinical diagnosis of disease (average = 16.3 months, range = 3-26 months prior to diagnosis), suggesting that elevated serum p21 levels may be a useful marker for earlier detection in a significant percentage of respiratory malignancies. Finally, elevated serum levels of PDGF-related protein were detected significantly more frequently in advanced pneumoconiosis cases (ILO radiographic classification of 2/1 or greater) than in less advanced cases (80% vs. 41.9%; p = 0.016), and there was a tendency for these PDGF-positive patients to have progression of their disease (68.2% vs. 41.7%; p = 0.065), suggesting that elevated serum PDGF levels may be a marker for the development of severe and progressive pneumoconioses.

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PubMed1985

Fine structural changes in cryptogenic fibrosing alveolitis and asbestosis.

Lung biopsies from 17 patients with cryptogenic fibrosing alveolitis of a cellular rather than fibrotic pattern were examined by transmission electron microscopy in the hope that such cases would show features of pathogenetic significance. Further selection was made by choosing minimally affected areas. There was no ultrastructural evidence of immune complex deposition but alveolar epithelial and capillary damage was frequently found (17 and 14 of the 17 cases respectively). Alveolar epithelial injury consisted of patchy necrosis and regenerative hyperplasia. Alveolar capillary injury consisted of cytoplasmic swelling and basement membrane thickening and reduplication. Many of these features have not been emphasized in previous reports and their prominence in early stages of the disease suggest that they may have pathogenetic significance, possible mechanisms of which are discussed. Similar findings identified during the course of this study in 8 asbestos workers suggest that similar pathogenetic mechanisms may operate in asbestosis.

Asbestosis↗
PubMed1998

An overview of the role of mineral solubility in silicosis and asbestosis.

Asbestosis and silicosis are fibrotic diseases initiated by the inhalation of silica-containing dusts, asbestos and quartz. There are various approaches for explaining the causes of these diseases. At present, our knowledge on the matter indicates that silicic acid dissolved from these minerals, contact between macrophages and minerals, highly reactive and oxidative species formed on the mineral surface, and lysosomal enzymes released upon engulfment of particulate mineral of appropriate size all contribute to various extents to the initiation of fibrosis. Among these mineral solubility seems to have a substantial contribution as a causative factor.

Asbestosis↗
PubMed1993

Quantitative analysis of 8-hydroxyguanine in peripheral blood cells: an application for asbestosis patients.

The quantitative analysis of 8-hydroxy-2'-deoxyguanosine (oh8dG) in human peripheral blood cells was carried out to find integrated biomarkers for estimating cancer risk. The change of the oh8dG levels over time in two healthy volunteers was measured to evaluate a intraindividual variance and each individual value was confirmed to be almost constant when they maintained usual life style. We applied this measurement to asbestosis patients who had worked in dockyard for 19-42 years. The oh8dG were detected in all samples and ranged from 0.77 to 1.28/10(5) deoxyguanosine (dG)8. No significant differences was observed in mean values of oh8dG between patients (1.00 +/- 0.17/10(5)dG) and hospital control group without asbestos exposure (1.03 +/- 0.20/10(5)dG) No association was found with the status of cigarette smoking. The oh8dG level in peripheral blood cells is therefore not a sensitive biomarker for past asbestos exposure at low levels.

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PubMed1989

Pulmonary inflammation and fibrosis in a murine model of asbestosis and silicosis. Possible role of tumor necrosis factor.

Prolonged asbestos and silica inhalation is associated with pulmonary inflammation and fibrosis. Several studies suggest that TNF may play a role in the development of inflammation and fibrosis. We studied TNF production in a murine model of asbestosis and silicosis. Asbestos fibers caused a significant inflammatory response at two weeks and pulmonary fibrosis beginning at one month. Pulmonary inflammation was principally caused by an accumulation of neutrophils (0.88 x 10(5) neutrophils/compared to 0.05 x 10(5) in controls). TNF production by bronchoalveolar cells was higher in asbestos-instilled mice at two weeks, but was significantly diminished in older mice. Pulmonary inflammation was observed until six months in silica-instilled mice. Neutrophils were also the principal protagonists of the inflammation. In this group, severe fibrosis was observed at two weeks. TNF production in silica-instilled mice was similar to controls, possibly due to the presence of large numbers of neutrophils (3.3 x 10(5)/lavage) that could adsorb TNF. In vitro experiments showed an augmentation of TNF production by bronchoalveolar cells in the presence of silica. Taken together, our data suggest that asbestos and silica stimulate alveolar macrophages to produce TNF, which can be involved in pulmonary inflammation and fibrosis.

Animals↗
PubMed1991

Asbestosis, endobronchial Aspergillus infection, and bronchocentric granulomatosis presenting with hemoptysis.

A patient with pulmonary asbestosis developed hemoptysis and a lesion on chest radiograph secondary to bronchocentric granulomatosis (BG) associated with Aspergillus fumigatus. Although pulmonary Aspergillus infection is a known complication of asbestos exposure. BG has not been previously reported in this disorder. This patient's case further documents that Aspergillus hyphae may be present in BG unassociated with allergic bronchopulmonary aspergillosis. A wide range of processes affecting airways, including asbestos exposure, may be associated with bronchocentric granulomatosis.

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PubMed2002

Mechanisms of colchicine effect in the treatment of asbestosis and idiopathic pulmonary fibrosis.

The objective of this study was to evaluate the mechanisms of colchicine action in pulmonary fibrosis. The study included 10 patients with pulmonary fibrosis (idiopathic pulmonary fibrosis 5, asbestosis 4, and scleroderma 1) who had been admitted to Bellevue Hospital Center, a tertiary care public hospital in New York City. We administered colchicine 0.6 mg orally for 12 weeks to patients with pulmonary fibrosis. Symptoms, high resolution CT scans, pulmonary function tests, and bronchoalveolar lavage parameters were compared prior to and after treatment. Results showed declines in dyspnea index, selective improvement in several CT scans, but no statistically significant change in BAL cells, cytokines, fibronectin, or hydroxyproline. However, there was a decline in hydroxyproline in the BAL fluid in 8/10 patients. We concluded that colchicine has a mild antifibrotic effect which may be in inhibiting collagen formation since there was no effect on the inflammation that accompanies fibrosis.

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PubMed1975

The diagnosis of asbestosis.

Lung biopsy in 16 patients with abnormal lung function and who had been exposed to asbestos revealed asbestosis in 4 with considerable radiological evidence of the disease, in of 4 with minimal radiological changes and in none of 8 with completely clear radiographs. Thus biopsy for the diagnosis of this condition should be avoided if the chest radiograph shows no evidence of it.

Adult↗
PubMed1986

Experimental lesions in rats corresponding to advanced human asbestosis.

Rats inhaling chrysotile asbestos developed a progressive interstitial fibrosis similar in most respects to human asbestosis. The earliest lesions were focal deposits of fibrous tissue in the walls of respiratory bronchioles and alveolar ducts. Later alveolar septa between adjacent bronchioles became progressively thickened to produce lesions with similarities to human honeycombing. The thickened septa between alveoli or "micro-honeycomb" spaces were mainly surfaced with cuboidal epithelial cells although some spaces lined by ciliated columnar epithelium were also found. Transmission electron microscopy of these advanced lesions showed that the cuboidal epithelial cells retained most of the characteristics of type 2 pneumocytes but that they frequently exhibited apical cytoplasmic blebs normally associated with the apocrine secretion of Clara cells. Columnar cells exhibited all stages from fully cilitated to cells with only an occasional cilium among the normal cell surface microvilli. Alveolar or micro-honeycomb spaces frequently contained clusters of pulmonary macrophages with their surface processes interdigitated but with no signs of fusion to giant cells. At more than 18 months after the end of dust inhalation these macrophages contained no chrysotile asbestos. The basement membranes beneath the epithelial layers of thickened septa were irregular and often convoluted as well as being much thicker than normal. Microscopic deposits of calcification were frequently found within the basement membrane material. Some thickened septa were relatively acellular, consisting mainly of masses of collagen fibrils but others were cellular and contained many macrophages, fibroblasts, plasma cells and mast cells. In these advanced lesions extremely little chrysotile asbestos was found and this was present in two sites only. Some chrysotile, always as individual fibrils and usually of short length, was present among collagen fibrils in areas of fibrosis and some was present within the thickened basement membranes.

Animals↗