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At least 289 records · Page 16Linked to original sources
PubMed1986

[Peritoneal mesothelioma in asbestosis].

The clinical and pathoanatomical findings from a 46 year old man with peritoneal mesothelioma in pulmonary asbestosis are described. The tumor arose 13 years after termination of a 10 year professional exposure to asbestos dust. The findings of asbestos bodies in the hilar and tracheobronchial lymph nodes is interpreted as evidence for transport of asbestos bodies in the lymphatic vessels from the lungs to the peritoneal cavity. In the case in question, numerous histological slides showed no asbestos bodies in the tumor tissue itself. The pathogenesis of mesotheliomas following exposure to asbestos is discussed.

Asbestos↗
PubMed1972

Phagocytic activity of the alveolar epithelial cells in pulmonary asbestosis.

In the course of pulmonary asbestosis in hamsters, alveolar epithelial cells can transform into large phagocytic cells which ingest asbestos fibers and produce asbestos bodies. In the process, the epithelial cells frequently lose their original Type I or Type II cell structure and change into a form intermediate between the epithelial cell and the alveolar macrophage. This transformation may be the result of continuous stimulation of the cells by repeated phagocytosis of asbestos, followed by rapid death of the host cell, release of the fibers and rephagocytosis by a new cell. It is suggested that some of the large macrophages in the alveolar spaces originate from the alveolar epithelial cells via the intermediate form.

Animals↗
PubMed1977

[Asbestosis. Apropos of one case].

Having reported a very complete observation of a patient with asbestosis, as well as silicosis, hitherto undiscovered tuberculosis and a pleural mesothelioma, the authors sum up our present knowledge on the consequences of inhaling asbestos dust. Clinical signs are numerous, benign or malignant, the risks of pleural and broncho-pulmonary cancer being greater in people exposed to asbestos. Diagnosis rests mainly on professional anamnesis and on the presence of great quantities of asbestos bodies in the sputum. Any pleural thickening on X ray should always suggest the development of a mesothelioma. As it now gives right to legal compensation, it is recommended to authentify the malignancy of the thickening by surgery.

Aged↗
PubMed1984

Evidence for the activation of the kallikrein-kinin system in experimental asbestosis.

Immunoreactive bradykinin (BK) and its metabolites, namely des-Arg9-BK and des (Phe8,Arg9)-BK, were measured in acidic extracts of lungs from normal and asbestos-treated guinea pigs. The development of experimental asbestosis did not change the levels of BK (0.67 ng/mg and 0.72 ng/mg) while the levels of des-Arg9-BK increased from 0.06 to 0.57 ng/mg (P less than 0.01) and those of des (Phe8,Arg9)-BK, from 0.09 to 1.48 ng/mg (P less than 0.01). These increases in the amount of the BK metabolites suggest the participation of the kallikrein-kinin system in the inflammatory reaction induced by the intratracheal administration of asbestos into guinea pigs.

Animals↗
PubMed1984

Pulmonary and systemic immunoregulatory changes during the development of experimental asbestosis.

Initial studies on the effects of low dose exposure to asbestos on pulmonary and systemic immune responses have revealed a bi-phasic pattern characterized by an early enhancement followed by inhibition of lymphocyte responses to several mitogens. In the present study, we sought to define the cellular and humoral factors, responsible for the observed effects. The early enhancement of peripheral blood and pulmonary lymphocyte responses to mitogens may be due, at least in part, to the loss of the inhibitory capacity of alveolar macrophages from asbestos exposed animals to suppress lymphocyte response. Furthermore, macrophages from low dose exposed animals actually enhanced lymphocytes responses to Con A and PHA. The latter inhibition observed following 6-12 months of exposure may be due to the in vivo generation of suppressor lymphocytes. Unfractionated lymphocytes from blood or alveolar space as well as enriched T cells from high dose exposed animals suppressed the proliferative responses of pulmonary or circulating lymphocytes to PHA and Con A, but not to PWM. Similarly, pre-incubation of normal blood or pulmonary lymphocytes in serum from high dose exposed animals for 24 h induced the appearance of suppressor cell activity in these populations when further tested in a co-culture assay with normal fresh lymphocytes. Taken together, these studies demonstrate the multi-faceted effects of asbestos on the immune system. The eventual fibrogenic process of asbestosis may result from the interplay of several mechanisms, some of which are suggested in this work.

Animals↗
PubMed1983

A murine model of asbestosis.

Balb/c mice were exposed to aerosolized chrysotile fibers and evaluated as a host for the study of asbestos-induced pulmonary disease. Histologically, an initial macrophage reaction was found to progress to "asbestos body" formation and diffuse focal interstitial fibrosis within 1 year of a chronic exposure period. This reaction was most intense in areas adjacent to respiratory bronchioles and alveolar ducts. Two morphologically distinct tumors at the pulmonary visceral surface were also discovered among a high percentage of asbestos-exposed mice. Bronchoalveolar lavage demonstrated an eventual alteration of the retrievable cell populations among the dusted animals. Evaluation of systemic B-lymphocyte activity suggested a stimulation of this cell subset following chrysotile inhalation. These results demonstrate that subsequent to chronic asbestos exposure, the mouse develops pulmonary and immunologic changes very similar to those noted in human asbestosis.

Animals↗
PubMed1983

Bronchoalveolar lavage in asbestosis.

The interstitial lung disease associated with asbestosis is unique in that the etiological agent and its effects on the pulmonary parenchyma can be studied on a serial basis using bronchoalveolar lavage. In this way both disease activity and structural derangements can be assessed and used in the treatment of the affected individual. In this review, attention has been drawn to the cascade of inflammatory changes induced by asbestos fibers. The activated inflammatory cells are responsible for the alveolitis characteristic of this condition. Like the other forms of diffuse interstitial lung disease, it is the alveolitis that precedes and predicts eventual fibrosis.

Animals↗
PubMed1981

Mortality among workers receiving compensation for asbestosis in Ontario.

Mortality among 172 workers who received workmen's compensation for asbestosis in Ontario was investigated and the causes of death were compared with those for the general male population in that province. The workers were found to have increased rates of death, relative to the general populations, for nonmalignant respiratory diseases, lung cancer and pleural and peritoneal mesothelioma. In comparison with the general population, the proportion of workers that survived was 69% of that expected 5 years after they were awarded compensation and 53% at 10 years.

Adult↗
PubMed1983

[Ultrasonic diagnosis of pleural changes in asbestosis].

One of the characteristic biological effects of the inhaled asbestos dust is the formation of hyaline thickenings on all pleurae in the form of plaques, in which calcium could be deposited. Due to the difficulties in the differentiation of the pleural hyalinosis with the conventional X-ray methods, the authors studied the potentialities of echography in 18 patients in contact with asbestos. They used two apparatuses (type "grey scale" 3401 of the firm (Brüel & Kjaër with linear scanning and "Siam" with sector scanning). Echography could establish areas of thickening on the parietal and diaphragmatic pleurae, to determine their thickness in micron and the degree of echogenicity. The comparison with the X-ray examination of the chest (face and I oblique position, lowvoltage technique) showed a positive finding with both methods in 7, suspicious X-ray finding with positive echography--in I, positive finding only with echography--in 6 and negative by both methods--in 4 subjects. The echographic examination on pleura is a rapid, cheap and harmless method, contributing not only to the early detection of its asbestosis lesions but to the elucidation of the etiology of pulmonary fibrosis.

Asbestosis↗
PubMed1983

[Pleural mesothelioma, asbestosis and silicosis following long-term exposure to talc dust].

A case report with pleural mesothelioma, asbestosis and silicosis after long time exposure to talc dust has been given. Pathological findings, professional exposure, diagnostic aspects, and medical assessment of disablement are described. The relationship between the diseases of lungs and the professional exposure to talc dust as well as the possibility of cause-distinction by co-working of pathologist and industrial hygienist are discussed.

Aged↗
PubMed1980

The value of nonradiological indicators in the early diagnosis of asbestosis.

The early pulmonary lesions due to long and to short asbestos fibres are described. The signs that such preradiological 'asbestosis' present can be used as nonradiological indicators. These are: asbestos bodies in the sputum, siderocytes in the sputum, crepitating basal rales, restrictive ventilatory insufficiency and impairment of alveolar-capillary diffusion of gases. The predictive value of combinations of these indicators was studied in 182 moderately and heavily exposed asbestos workers. The results show that the presence of pulmonary lesions due to asbestos can be diagnosed in 80-90% of cases, independently of the results of radiological examination.

Asbestosis↗
PubMed1980

Roentgenographic lung changes, asbestosis and mortality in a Belgian asbestos-cement factory.

Annual chest radiographs, work history and mortality of 1,973 workers in an asbestos-cement factory were correlated with age and with duration and level of dust exposure. Degree of radiographic lung change was significantly related to fibre-years of exposure in the case of small lung opacities, pleural adhesions and pleural thickening. For 29 cases of asbestosis diagnosed between 1963 and 1977, a highly significant dose-response relationship was found. In comparison with national mortality rates, there was an excess of deaths due to cancer of the gastrointestinal tract, although there was no relationship to fibre-years.

Adolescent↗
PubMed1994

[A case of asbestosis with long survival by artificial ventilation].

We treated a 63-year-old man in whom asbestosis developed after he had sprayed asbestos for 24 years. He was admitted with the chief complaint of dyspnea and was managed for 4 years with artificial ventilation. We believe that he survived for this long because he was free of severe pneumonia and because the lower lung, which is primarily affected by asbestos, was relatively intact so his pulmonary function did not deteriorate rapidly. Pathological findings included plate-like atelectasis in both upper lung fields and marked thickening of the pleura. Lung fibrosis was centrilobular but showed no honeycombing. The lung tissue contained 265 X 10(6) asbestos particles and 910 X 10(6) asbestos fibers per gram (dry weight), and the pleura also had 805 asbestos particles and 3,035 asbestos fibers. Most of these asbestos fibers were 20 microns or longer and were crocidolite.

Asbestos, Crocidolite↗
PubMed1993

[Detection of asbestos in thoracic lymph nodes in patients with asbestosis].

To detect a possible lymph transport of inhaled asbestos fibres and fragments from the human lung we examined via light and scanning electron microscope a total of 224 intrapulmonary, extrapulmonary and paratracheal lymph nodes of 6 postmortem cases and 3 lung resectates from patients with histologically proven pulmonary asbestosis. The lymph nodes were subdivided into 3 groups and examined separately. We found partly sharp-edged staff-shaped and partly amorphous dust particles that were mostly embedded in phagolysosomes of macrophages, using energy-dispersive x-ray microanalysis; these particles yielded a spectrum like that of asbestos, which means they must be identified as asbestos fragments. Besides these, typical asbestos bodies and asbestos needles were also identified.

Aged↗
PubMed1993

Concurrent mesothelioma and adenocarcinoma of the lung in a patient with asbestosis.

We report the apparently unique simultaneous development of a mesothelioma and an adenocarcinoma of the lung in a patient with asbestosis. Pathologists should be aware that very rarely these two malignancies may occur concurrently, an event with potential prognostic, therapeutic, and medical-legal implications for the patient and his family. Although occupational asbestos exposure is well recognized as a risk factor in the development of both mesothelioma and lung carcinoma, this case report emphasizes the rarity of the synchronous occurrence of these tumors in asbestos exposed individuals suggesting that the mechanism by which asbestos fibers induce lung carcinoma is different from that by which they induce mesothelioma.

Adenocarcinoma↗
PubMed1995

[Standardization of diagnostic criteria for occupational asbestosis of the lungs and lung parenchyma].

A reliable method for evaluation of asbestosis-related non-malignant respiratory impairment as occupational disease is described. The method is based on an algorithm which consists of the following elements: a positive full work history, chest radiography (International Labour Organisation), ventilatory lung function measurement, determination of diffusing capacity for carbon monoxide, histopathological examination, computerized tomography, and high resolution computerized tomography for persons with a negative differential diagnosis. The algorithm is meant to contribute to the standardization of diagnostic criteria for assessment of occupational lung diseases. Its use is also proposed for assessment of other occupational diseases.

Algorithms↗
PubMed1977

Immunological studies of patients with asbestosis. I. Studies of cell-mediated immunity.

A variety of cancers have been documented in patients exposed to asbestos dust. Since a deranged immune system may play a rôle in cancer development, the general level of immunocompetence was studied in a group of twenty-six patients with radiographically defined asbestosis, who might be at risk of developing asbestos-related neoplasms. Statistical comparisons were made with a comparable control group. A disproportionate number of the patients displayed cutaneous energy to certain recall antigens and to 2,4-dinitrochlorobenzene. In vitro studies of cellular immunity, as evaluated by phytohaemagglutinin-induced proliferative and cytotoxicity assays, showed significantly lower values amongst the patient group. Serum inhibitors of mitogen-induced lymphocyte transformation were also detected in several of the patients. The possible significance of these findings is discussed.

Adult↗