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PubMed1990

Asbestosis: high-resolution CT-pathologic correlation.

High-resolution computed tomography (HRCT) was performed in seven inflated and fixed postmortem lungs from seven asbestos-exposed patients with pathologically proved asbestosis. The parenchymal abnormalities seen at in vitro HRCT included thickened intralobular lines (n = 7), thickened interlobular lines (n = 7), pleural-based opacities (n = 7), parenchymal fibrous bands (n = 5), subpleural curvilinear shadows (n = 4), ground-glass appearance (n = 4), traction bronchiectasis (n = 4), and honeycombing (n = 2). The thickened intralobular lines were shown histologically to be due to peribronchiolar fibrosis. Thickened interlobular lines were due mainly to interlobular fibrotic thickening in four lungs and edema in three. The peribronchiolar fibrosis was most severe in the subpleural lung regions, creating curvilinear line shadows and pleural-based areas of opacity. Some subpleural fibrosis extended proximally along the bronchovascular sheath to create bandlike lesions. Areas of ground-glass appearance on HRCT scans were shown to be the result of mild alveolar wall and interlobular septal thickening due to fibrosis or edema. Postmortem HRCT findings were similar to premortem HRCT findings and correlated well with the pathologic findings of asbestosis.

Aged↗

PubMed1990

Inhibition of lung injury, inflammation, and interstitial pulmonary fibrosis by polyethylene glycol-conjugated catalase in a rapid inhalation model of asbestosis.

Several in vitro studies suggest the involvement of active oxygen metabolites in cell damage caused by asbestos. To determine if lung injury, inflammation, and asbestosis could be inhibited in vivo in a rapid-onset, inhalation model of disease, a novel method of chronic administration of antioxidant enzymes was developed. In brief, Fischer 344 rats were treated with polyethylene glycol-conjugated (PEG-) superoxide dismutase or catalase in osmotic pumps over a 10-day (5 days/wk for 2 wk) or 20-day (5 days/wk for 2 wk) period of exposure to crocidolite asbestos. Control rats included sham-exposed animals and those exposed to asbestos but receiving chemically inactivated enzymes. After 10 days of exposure to asbestos, lactic dehydrogenase (LDH), alkaline phosphatase, and total protein in bronchoalveolar lavage (BAL) were measured in one group of rats. Total and differnetial cell counts in BAL also were assessed. After 20 days of exposure, lungs of an additional group of rats were evaluated by histopathology and by measurement of hydroxyproline. Asbestos-associated elevations in LDH, protein, and total cell numbers in BAL were reduced in rats receiving PEG-catalase. Decreases in numbers of alveolar macrophages, polymorphonuclear leukocytes, and lymphocytes occurred in these animals. Exposure to asbestos for 20 days caused significant increases in both the amount of hydroxyproline in lung and the severity and extent of fibrotic lesions as determined by histopathology. These indicators of asbestosis were inhibited in a dosage-dependent fashion in rats receiving PEG-catalase. Use of inactivated PEG-catalase failed to boost serum levels of catalase and did not inhibit asbestos-induced elevation of hydroxyproline in lung.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1979

Absence of synergism between exposure to asbestos and cigarette smoking in asbestosis.

To assess both independent and synergistic effects of exposure to asbestos and cigarette smoking on the development of asbestosis, survey data from 4 groups of workers exposed to asbestos were analyzed with multivariate statistical models. Survey methods were standardized and included for the 383 subjects a respiratory symptoms questionnaire, occupational history, physical examination, pulmonary function testing, and a chest radiograph. Exposure to asbestos and cigarette smoking were assessed by questionnaire. Synergism between the 2 exposures was not present for previously identified manifestations of asbestosis including bilateral fine crackles, clubbing, dyspnea, radiographic abnormality, decreased forced vital capacity, and decreased single-breath diffusing capacity of the lung for CO. However, additive, independent effects of these 2 exposures were present for each of these parameters.

Adult↗

PubMed1982

Asbestosis in long-term employees of an Ontario asbestos-cement factory.

We studied the development of compensable (certified) asbestosis among the 201 workers at an asbestos-cement factory who were first exposed to asbestos dust prior to 1980 and who had been employed at least 15 yr. By July 1980, 39% of the production workers and 20% of the maintenance workers had developed a compensable chest disability; the "latent interval" generally exceeded 20 yr. Workers with asbestosis were found to have markedly elevated mortality rates with deaths caused by malignancies and respiratory disease being primarily responsible. We combined the limited air sampling data available with individual work histories to calculate 18-yr cumulative fiber exposures. The cumulative probability of certification was related to the cumulative exposures and the exposure-response relationship was found to be sigmoidal in form.

Asbestosis↗

PubMed1984

Crackles in the early detection of asbestosis.

We studied 386 workers exposed to asbestos to assess the value of chest auscultation by a trained technician in detecting asbestosis as defined by previously reported clinical, physiologic, and roentgenologic criteria. The presence and degree of crackles were assessed at preselected basilar lung sites by a technician whose performance was validated by comparison with computer-generated time-expanded waveforms of tape recordings of lung sounds. Asbestosis was present in only 2.8% of the total population, but it was present in 8.6% of those with over 25 yr or more of employment. The technician correctly identified all the workers in whom the diagnosis was most certain, that is, those with all criteria positive. The overall true positive rate was 55%. The majority (94.8%) of those with no abnormal criteria were correctly classified. Auscultation by an objectively validated technician can be a useful noninvasive method for screening industrial populations exposed to asbestos.

Allied Health Personnel↗

PubMed1976

Computer tomography in the evaluation of pulmonary asbestosis. Preliminary experiences with the EMI general purpose scanner.

Thirteen individuals with varying lengths of exposure to asbestosis were examined by computer tomography with the EMI Scanner. Various pleuroparenchymal abnormalities were found, many not being seen on standard chest films. In some cases, with normal chest radiography, definite pleural involvement could be demonstrated, particularly that in the posterior sulci on the diaphragm and at the mediastinum. Tissue attenuation measurements in regions of parenchymal involvement reached 90 EMI units above normal lung tissue. The normal gravity effect is abolished in cases of parenchymal disease caused by asbestosis. Parenchymal disease was much more obvious on the CT scans than on conventional chest films.

Asbestosis↗

PubMed1983

Biochemical components of bronchoalveolar lavage in early experimental asbestosis of the sheep: phospholipase A2 activity, prostaglandin E2 and proteins.

Biochemical analyses of bronchoalveolar lavage (BAL) supernatants of sheep treated with weekly intratracheal instillations (for 6 months) of saline, 2 mg, or 128 mg of asbestos (chrysotile B; UICC) were performed. Our results showed that proteins (either total or its various components) and phospholipase A2 activity were unchanged in the low exposure group as compared to controls. However, in the high exposure group, with histopathological evidence of early asbestosis, there were significant increases in total proteins, albumin, alpha 2-globulin, beta- and gamma-globulins as well as phospholipase A2 activity of BAL fluid. Prostaglandin E2 activity was significantly increased in both low and high dose groups. These changes in protein and lipid components of BAL following asbestos exposure constitute early indices of lung inflammatory reactions which may contribute to the development of asbestosis.

Animals↗

PubMedDate not supplied

The occurrence of leukemia in a patient with pulmonary asbestosis.

A 77-year-old man, who had been a subway construction worker, was admitted to our hospital for surgical treatment of left cheek carcinoma and an examination for pancytopenia on November 17, 1986. Bone marrow aspiration revealed that 10% of the nucleated cells were blasts with morphological atypism. Bone marrow biopsy showed hypocellular marrow and a diffuse increase of argyrophil fibers with the presence of asbestos fibers was observed by microscope. A chest X-ray showed the findings of old tuberculosis and pulmonary asbestosis, and asbestos fibers were demonstrated in the broncho-pulmonary lavage fluid. He was diagnosed to have pulmonary asbestosis complicated with hypoplastic low percentage leukemia.

Aged↗

PubMed1985

Pulmonary bombesin in experimentally induced asbestosis in rats.

The pulmonary levels of immunoreactive bombesin in normal rat lungs and rat lungs exposed to asbestos were determined. Experimental asbestosis was induced in rats by a single intratracheal injection of 5 mg or 10 mg UICC standard Canadian Chrysotile B while sham-operated control rats received only the saline carrier. At 1, 3, 6, and 9 months following instillation, 5 animals of each group were sacrificed and the lungs removed. A section was kept for morphologic analysis, while the remaining portion was submitted to acid extraction and later measured for bombesin content by radioimmunoassay (RIA). The Chrysotile B-exposed tissues displayed the characteristic features typical of the fibrotic state associated with asbestosis one month following exposure and thereafter. The pulmonary bombesinlike immunoreactivity ranged from 4.5-7.5 pmoles/g tissue in normal rat lung, and these levels remained unchanged at 1 and 3 months after asbestos exposure. However at 6 and 9 months, significant increases ranging between 2 and 2.5 fold were observed. The initial increases in bombesin levels occurred at a later time (6 months) than those already observed for vasoactive intestinal peptide (VIP) (3 months). However, VIP levels plateaued at 9 months, while those of bombesin were still increasing. High-pressure liquid chromatography (HPLC) coupled with RIA demonstrates the presence of two bombesin-immunoreactive peaks in normal rat lung, the major one coeluting with the mammalian bombesinlike peptide gastrin-releasing peptide (GRP) and the other one being presumably a C-terminal portion of GRP. These data indicate that immunoreactive bombesin and VIP are selectively increased at different times following asbestos instillation and that these changes occur after the onset of fibrosis and the appearance of well-defined fibrotic lesions.

Animals↗

PubMed2005

[Asbestosis].

Asbestosis is a diffuse interstitial pulmonary fibrosis, secondary to the inhalation of asbestos fibres. There is a dose-response relationship between exposure to asbestos and the risk of developing asbestosis, in such a way that the greater the exposure, the greater the risk of developing the disease. The time of clinical latency is inversely proportional to the level of exposure. Dyspnoea upon exertion and a dry cough together with end-inspiratory crackles are the most frequent symptoms and signs. Chest radiography is a basic tool in identifying the disease, however high resolution CAT has added greater sensitivity. Tests of the respiratory function show alterations and restrictive ventilations with a reduction of pulmonary spread. Determination of asbestos bodies in BAL is an indicator of exposure, although their absence does not rule out the disease. A histopathological diagnosis is the most reliable, although in the majority of cases the diagnosis is established on the basis of the existence of an antecedent of exposure to asbestos together with suggestive clinical, radiological and functional findings, and a suitable time of latency, without having recourse to a pulmonary biopsy.

Asbestosis↗

PubMed1978

Radiographic and physiological findings in patients with asbestosis.

Radiographic and respiratory functional findings are reported for a series of 133 Finnish patients with asbestosis. Of these patients, 65 (49%) were found to have radiographically mild diffuse pulmonary fibrosis (profusion 0/1, 1/0 or 1/1), 48 (36%) moderate fibrosis (1/2, 2/1 or 2/2) and 20 (15%) diffuse fibrosis in an advanced stage (2/3 or more). The type of fibrosis was mostly irregular (110 = 83%). Fibrosis was typically the most advanced in the lower zones of the lungs. Of the 133 patients, 88 (66%) showed pleural changes and 78 (59%) pleural calcifications. The more severe the fibrosis, as seen in the radiographs, the greater the decrease in vital capacity (VC) and expiratory volume in 1 s (FEV1.0). Transfer factor was generally impaired only in advanced cases of asbestosis (fibrosis 2/3 or more). In general, obstruction was not observed in this series. Pleural changes seemed to decrease VC and FEV1.0 when the fibrosis was mild (0/1, 1/0 or 1/1). They had no effect on diffusion capacity (TLco).

Adult↗

PubMedDate not supplied

[High resolution computerized tomography in the diagnosis of asbestosis].

The clinical observation, the work history, the analysis of pulmonary function tests and, mainly, the conventional x-ray chest radiograms have represented, til now, the diagnostic basis for pneumoconiosis (silicosis, mixed dust pneumoconiosis, asbestosis). Recently, the high resolution chest tomography (HRCT) has been introduced into the diagnostic procedures: such method seems to have its main application in the assessment of incipient clinical pictures of pneumoconiosis, particularly when characterized by normal pulmonary function tests. Asbestos fibers exposed workers were submitted to both radiologic methods. The great majority of them had already been recognized to be affected by asbestosis. A considerable statistical agreement (Cohen K) was observed between radiographic and tomographic I.L.O. classes. In conclusion, high resolution chest tomography doesn't appear to be an indispensable test for the diagnosis in admitted subjects, but we underline its importance in the evaluation of pleural thickenings.

Aged↗

PubMed1999

[Risk assessment of benign asbestosis (dose-effect relationship, time-effect relationship, co-factors)].

Despite the lack of precision of asbestos exposure assessments and the limitations of the main diagnostic epidemiological tool for asbestos-related diseases (i.e. standard X ray films), several issues concerning the risk of development of asbestos-related diseases are well established. For asbestosis, now a rare disease, the existence of a positive dose-response relationship, with a threshold or no-effect level, has been clearly demonstrated. The slope of the relationship curve is steeper for amphiboles than for chysotile, as it is for increased fiber length. Asbestosis is associated with an increased risk of bronchial carcinoma, however it is now known that exposure to asbestos of itself increases the risk of cancer even in the absence of any radiographic signs of pulmonary fibrosis. Pleural plaques occur even when the level of asbestos exposure is low. They are not only dose-dependent but are also latency-related. They have no prognostic significance in asbestos-exposed workers, but are associated with an increased risk for the subsequent development of mesothelioma and bronchial carcinoma when compared to the risk of the general population. Diffuse pleural thickening is associated with higher levels of asbestos exposure than those associated with pleural plaques. It usually follows a benign pleural effusion, which is a less frequent but earlier consequence of asbestos exposure than the other asbestos-related diseases documented above.

Asbestosis↗

PubMed2000

Asbestos exposure, lung cancer and asbestosis.

The relationship between asbestos exposure, lung cancer and asbestosis is reviewed. Studies have demonstrated the risk of lung cancer to be raised in asbestos-exposed workers whether asbestosis is present or not. Although increasing exposure increases the risk of disease, variability in estimation of fibre levels and in subject susceptibility should be borne in mind. Consensus opinion recommends that attribution of lung cancer to asbestos exposure should be based on clinical and occupational histories. The risk of lung cancer in those who both smoke and are exposed to asbestos is increased in a multiplicative way, putting subjects at very great risk.

Animals↗

PubMed1999

Asbestosis in Malaysia: report on first two cases.

The first two cases of asbestosis in Malaysia are reported. Both had considerable occupational exposure to asbestos dust in the past, with a long latency period exceeding 30 years. One case presented with distinctive clinical and radiological features, while the other case was only confirmed by histological diagnosis. The usefulness of modern investigation techniques such as CT scan in the diagnosis of asbestosis is also illustrated.

Asbestosis↗

PubMed1975

[Reflections on 19 cases of asbestosis discovered by chance in the population of an industrial region in the Basse-Sambre].

The authors describe 19 cases of definite or highly probable asbestosis which were observed among unselected out-patients at a hospital in the industrial area of the "Basse-Sambre". These cases were of various types and were, almost exclusively, of occupational origin. The variety and severity of the asbestosis in many of the cases justify a more thorough survey in this area. Those people who have handled and inhaled asbestos fibres at work will be examined in the first place. A radiological pulmonary survey will also be organized among the people living in the neighbourhood of factories using asbestos. Precise information about the origin, quality and characteristics of the inhaled dust as well as the intensity and duration of exposure will be obtained. Cases discovered in the survey will be investigated systematically by means of an extensive range of techniques: frontal and oblique X-rays with an appropriate kilovoltage for the detection of pleural calcifications and of the reticular thickening of the parenchyma; spirometry and measurement of the transfer factor for CO; arterial blood gases at rest and during exercise; search for ferruginous bodies in sputum; pathological studies of pulmonary and pleural tissues and of the ultrastructure of pleural tumours.

Aged↗

PubMedDate not supplied

In vivo bioassays of acute asbestosis and its correlation with ESR spectroscopy and imaging in redox status.

In vivo electron spin resonance (ESR) spectroscopy and whole body imaging were used to investigate the toxicity of biological reactions and organ specific oxidative changes associated with the development of acute asbestosis. Pathogen-free mice were exposed to 100 microg of crocidolite asbestos suspended in 50 microL of a 0.9% NaCl solution by aspiration. The bio-assay group had broncho-alveolar lavage (BAL) and serum draws performed on control and treated mice at 1, 3, and 7 days post-instillation. The ESR spectroscopic measurements and whole body imaging were performed with a separate group of mice at the same time points. Bio-assays included measurements of albumin, lactate dehydrogenase (LDH), N-acetyl-beta-D-glucoaminidase (NAG), and catalase in acellular lavage fluids, and total antioxidants status in blood serum. ESR spectroscopic and imaging measurements were performed after intraperitoneal injection of 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-15N-1-oxyl (TEMPOL) or 3-carbamoylproxyl (3-CP) nitroxides at a final concentration of 344 mg/kg body weight. Albumin showed a significant increase in BAL fluid at the 3 day exposure time point. The presence of this protein in lavage fluid indicates that the gas/blood barrier has been damaged in the lung. LDH in BAL fluid also exhibited a significant increase at 3 days post-exposure, an indication of enhanced cell membrane damage in the lung. Similar results were observed for NAG, a lysosomal enzyme, implying activation of phagocytic cells. Contemporaneously with the development of acute asbestosis at day 3 post-exposure, there were significant increases in the levels of total antioxidants in the serum and catalase in the BAL fluid. Significant impairment in the ability of asbestos exposed animals to clear TEMPOL radical during acute disease progression was evident at days 1 and 3 post exposure. ESR image measurements provided information on the location and distribution of the 3-CP label within the lungs and heart of the mouse and its clearance over time. Bioassays in concert with ESR spectroscopy and imaging presented in this study provide congruent data on the early acute phase of pulmonary injury and oxidant generation in response to asbestos exposure and their decline after 7 days. The increased levels of total antioxidants in the serum and catalase in BAL fluid correlated with the reduction in the clearance rate for TEMPOL, suggesting that a change in the redox status of the lung is associated with lung injury induced by asbestos.

Acute Disease↗

PubMed1975

The immunology of asbestosis.

Forty-one employees with varying degrees of asbestosis have been tested for any alteration in the immunological profile. Of these, twenty-two employees showed evidence of pleural thickening and nineteen parenchymal asbestotic fibrosis. Those employees showing pleural thickening gave a strong reaction to different skin tests and a few of those with a parenchymal asbestotic fibrosis showed depressed cutaneous reactivity. Lymphocytotoxic antibodies were present in the sera of 60% of those with pleural thickening and 94% of those with parenchymal asbestosis. An immunological screening schedule is suggested for those employees who show pleural thickening.

Asbestosis↗