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Serial lung function tests were performed on 17 patients with asbestosis. A marked fall in the transfer factor often preceded any significant decline in the vital capacity. Changes in vital capacity and transfer factor did not appear to give any indication of the prognosis in these patients. Death was more commonly due to carcinoma of the lung than to the effects of the lung fibrosis.
After intratracheal injection of short chrysotile asbestos fibres in guinea-pigs an intense neutrophil alveolitis was observed within three days. Evaluation by bronchoalveolar lavage of the inflammatory and immune effector cells producing the alveolitis by three days showed an increased proportion of polymorphonuclear leucocytes, which comprised 21% +/- 3% of the total leucocytes compared with 9% +/- 2% for the controls (p less than 0.05), persisting for at least six weeks (after which time the polymorphonuclear leucocytes comprised 28% +/- 2% compared with 7% +/- 1% for the controls: p less than 0.05). One mechanism by which asbestos fibres may cause polymorphonuclear leucocytes to be attracted to the alveolar structures is by induced release of neutrophil chemotactic factor by alveolar macrophages. When exposed in vitro to short or intermediate chrysotile fibres or amosite or crocidolite fibres guinea-pig alveolar macrophages released appreciable amounts of neutrophil chemotactic factor. The release of this chemotactic factor was augmented when the asbestos fibres had been previously exposed to normal serum. The chemotactic factor was lipid soluble, and was similar to the neutrophil chemotactic factor spontaneously released by alveolar macrophages recovered from guinea-pigs exposed in vivo to short chrysotile fibres. These observations suggest that alveolar macrophages may play an important part in the early stages of asbestosis by modulating the migration of neutrophils to the lung.
One hundred and fifty five male cases of asbestosis certified by the London Pneumoconiosis Medical Panel during 1968-74 were followed up during 1978-9, 4-11 (mean 7.5) years after certification. Fifty nine patients had died, 23 (39%) from lung cancer, 6 (10%) from mesothelioma, and 11 (19%) from other respiratory causes. The number of observed deaths was 2.25 times greater than expected and 7.4 times greater than expected for lung cancer. Adenocarcinoma was the commonest histological type but other cell types were also increased. Finger clubbing (p less than 0.01) and percentage of predicted FEV1 (p less than 0.01) were of value in predicting death, but increasing profusion of small opacities greater than 1/0 (ILO/U-C international classification of radiographs of pneumoconiosis, 1971), duration of exposure to asbestos, time from first exposure to asbestos, and percentage of predicted vital capacity and transfer factor did not predict death.
The prognostic significance of finger clubbing in asbestosis has been assessed in 167 cases certified by the London Pneumoconiosis Medical Panel from 1968 to 1974. Finger clubbing developed early in the clinical course of the disease and was associated with a lower gas transfer, a higher mortality and a greater likelihood of progression in intrapulmonary fibrosis than was found among cases without finger clubbing. Finger clubbing was not associated with heavier asbestos exposure. Its presence appears to be associated with a more severe form of disease.
To determine the earliest stage at which lesions in asbestosis can be diagnosed and to assess their progression, 23 asbestos-exposed patients with minimal or no abnormalities at plain radiography were examined with high-resolution computed tomography (HRCT) twice, with an interval of 12-37 months between examinations. In 21 of the patients, parenchymal abnormalities were found. Major parenchymal features seen at CT included thickened intralobular and interlobular lines, subpleural curvilinear lines, pleural-based nodular irregularities, hazy patches of increased attenuation, small cystic spaces, and small areas of low attenuation. At paired serial CT, subpleural isolated dots or branching structures connected with the most peripheral branch of the pulmonary artery started to appear in lower subpleural zones and then became confluent to create pleural-based nodular irregularities. CT-pathologic correlation led to the conclusion that the confluence of subpleural peribronchiolar fibrosis creates subpleural fibrosis.
A case associating asbestosis and clinical lupus erythematosus (SLE), both diagnosed according to standard criteria, is described. It is suggested that such an association may bear some analogy to the well-known 'Caplan-Collinet' syndrome, associating silicosis and rheumatoid arthritis.
The authors report the case of a 65-year-old accountant whose only asbestos exposure was during a summer job 50 years earlier in a California vermiculite expansion plant. Vermiculite is a silicate material that is useful in building and agriculture as a filler and insulating agent. He developed extensive fibrocalcific pleural plaques and end-stage pulmonary fibrosis, with rapidly progressive respiratory failure. Careful occupational and environmental history revealed no other source of asbestos exposure, and the initial clinical diagnosis was idiopathic pulmonary fibrosis; open lung biopsy shortly before his death confirmed asbestosis. Electron microscopic lung fiber burden analysis revealed over 8,000,000 asbestos fibers per gram dry lung, 68% of which were tremolite asbestos. Additional asbestiform fibers of composition not matching any of the standard asbestos varieties were also present at over 5,000,000 fibers per gram dry lung. Comparison analysis of a sample of Libby, Montana, vermiculite showed a similar mix of asbestiform fibers including tremolite asbestos. This case analysis raises several concerns: risks of vermiculite induced disease among former workers of the more than 200 expansion plants throughout the United States; health effects of brief but very high-intensity exposures to asbestos; and possible health effects in end-users of consumer products containing vermiculite.
Previous studies of asbestos exposure in humans and small animals have suggested that air flow limitation associated with small airway disease may be an early manifestation of asbestosis, but the subject is still controversial. In this report, we present the airway morphologic aspects and function of our sheep model of the disease. Three groups of 6 sheep were exposed to repeated intratracheal injections of either saline (control group), 2 mg of UICC Canadian chrysotile asbestos in saline (low exposure group), or 128 mg of the same fibers (high exposure group). At the end of the twelfth month of exposure, an alveolitis had developed in the high exposure group only. Detailed pulmonary function tests were followed within 48 by lung biopsies according to methods described, to which were added air-helium flow-volume curves. Lung biopsies in control and low exposure groups did not demonstrate significant morphologic changes, whereas all biopsies in the high exposure group showed alveolitis characterized by an alveolar and interstitial accumulation of macrophages and mononuclear cells without interstitial fibrosis. On all biopsies, over half of the airways were altered by a similar peribronchiolar process, which at times compressed the peripheral airways. Functionally there was no significant difference between low exposure and control groups. However, compared with the control group, the high exposure group had significantly lower vital capacity (2.0 +/- 0.1 versus 2.9 + 0.1 L, p less than 0.01), lower static lung compliance (91 + 13 versus 132 + 9 ml/cmH2O, p less than 0.05), higher isoflow volume (2.15 + 0.08 versus 1.4 + 0.1 L, p less than 0.01), and higher upstream resistance below the isoflow volume (3.3 + 0.2 versus 1.3 + 0.3 cmH2O L/s, p less than 0.02). These data demonstrate that in the early asbestos-induced peribronchiolar alveolitis of the sheep, which restricts lung volumes, there is a concomitant small airway disease that significantly limits air flow.
A short-term inhalation model of asbestosis was developed in rodents to examine possible preventive approaches to lung disease. Fischer 344 (F344) rats were exposed for 10 and 20 days to National Institute of Environmental Health Sciences (NIEHS) crocidolite asbestos while sham controls were exposed to air only. To determine quantitative biochemical indicators of asbestos-induced lung disease, bronchoalveolar lavage (BAL) fluids were analyzed for lactic dehydrogenase (LDH), alkaline phosphatase, angiotensin-converting enzyme (ACE), and protein. Total and differential cell counts were performed on cell pellets from BAL. Lungs from additional rats were processed for histopathology, measurement of hydroxyproline, and autoradiography after injection of rats with 3H-thymidine. Exposure to asbestos for 10 and 20 days caused increases in LDH, alkaline phosphatase, and protein in BAL. In contrast, ACE was undetectable in BAL fluids from sham or asbestos-exposed rats. At both time periods, the percentages of polymorphonuclear leukocytes (PMNs) and lymphocytes in BAL were increased in asbestos-exposed rats. Total cell numbers in BAL were increased significantly at 20 days in animals inhaling asbestos. Exposure to asbestos for 10 and 20 days caused elevated amounts of hydroxyproline in lung and the development of fibrotic lesions. Asbestos-exposed rats exhibited increased numbers of interstitial cells and airspace epithelial cells incorporating 3H-thymidine, whereas labeled bronchiolar epithelial cells were not elevated significantly. The quantitative changes in asbestos-associated enzyme levels, cell types and protein in BAL, as well as increases in hydroxyproline and morphologic evidence of fibrosis, are useful indices of asbestos-related lung injury which enable preventive and therapeutic approaches to disease.
We describe herein a case report of a patient affected by pulmonary asbestosis who developed a non-Hodgkin lymphoma originating in the pleura. The case is unusual for the uncommon site and because the chronic antigenic stimulation by asbestos bodies may have locally promoted an immunologic derangement.
The purpose of the study was to evaluate the accuracy of magnetic resonance imaging (MRI) in detecting subclinical morphological changes caused by asbestos exposure. Conventional chest radiographs according to the International Labour Organisation (ILO) categories 0-11 and spirometric data were compared with MRI in 17 men with mean (+/-2SD) asbestos exposure time of 24.6+/-13.0 yrs. Mean age was 62.0+/-9.4 yrs. The inclusion criterion was an ILO score of 2 or more. Electrocardiographic registrations and antirespiratory movement artefact techniques were used in all MRI examinations to avoid movement artefacts. Mean ILO grading was found to be 7.7+/-3.8 on chest radiography and 9.8+/-2.0 with MRI (p=0.01). Five patients had a higher ILO stage as evaluated by MRI, but in nine patients the staging remained unchanged. MRI revealed mediastinal adenopathy in four patients. Forced expiratory volume in one second (expressed as a percentage of the predicted value) was negatively correlated with ILO score as assessed by MRI (r=-0.4, p=0.032). Magnetic resonance imaging seems to be more sensitive than conventional radiographs in detecting subclinical fibrosis as well as the extent of pleural asbestosis.
The aim of this study was to investigate by computed tomography (CT) whether asbestosis, diffuse pleural thickening and/or pleural plaques are statistically associated. We also tried to find criteria to differentiate between diffuse and circumscribed pleural thickening. From 231 exposed workers, only those subjects whose radiograph showed neither bilateral calcified pleural plaques nor small pulmonary opacities higher than 1/1 grade according to the 1980 International Labour Office (ILO) Classification were considered. Scans were assessed for the presence of subpleural curvilinear lines, septal and intralobular lines, parenchymal bands, honeycombing, rounded atelectasis, pleural plaques and diffuse pleural thickening. CT scans revealed pleural and/or lung abnormalities in 99 workers. Pleural plaques were unilateral in one-third of cases with plaques. Diffuse pleural thickening, parenchymal bands and rounded atelectasis were unilateral in, respectively, 62 and 69 and 75% of cases with the abnormality. Septal and intralobular lines, and honeycombing were always bilateral. CT signs could be grouped into three patterns: 1) septal and intralobular lines, and honeycombing corresponding to pulmonary fibrosis; 2) pleural plaques corresponding to parietal pleural fibrosis; and 3) diffuse pleural thickening, rounded atelectasis and parenchymal bands corresponding to visceral pleural fibrosis. In these workers with a normal or near-normal radiograph, three groups of subjects with different responses were distinguished. Crow's feet and rounded atelectasis help to differentiate plaques from diffuse thickening.
Mixed pneumoconiosis is pulmonary disease due to two or more inhaled mineral irritants. Chronic disease due to beryllium has not been a component of any described mixed pneumoconiosis. A man with occupational exposure to a combination of dusts developed severe pulmonary disease. Silicosis, talcosis, asbestosis, and berylliosis were all documented by an open biopsy of the lung. The varieties of mixed pneumoconiosis are summarized.
Significant concentrations of asbestos fibers have been found in samples of laryngeal tissue from two patients with past exposure to asbestos and associated asbestosis. In one case, there was a polyp on a vocal cord and in the other one a laryngeal carcinoma. These findings could provide an indication of a local carcinogenic effect of asbestos fibers in laryngeal tissue.
A 73-year-old man with silico-asbestosis responded to steroid therapy. Chest CT scans showed diffuse micronodular opacities and ground glass opacities bilaterally throughout the entire lung fields, as well as progressive massive fibrosis in the bilateral upper lung fields. Diagnostic thoracoscopic biopsy revealed mixed dust pneumoconiosis with silicotic nodules, as well as fibrosis similar to that of Usual Interstitial Pneumonia (UIP) with many fibroblastic foci and alveolitis. Many asbestos bodies were also detected by iron staining.
Pathology standards for asbestos-associated diseases of the lungs and pleural cavities were recently developed by the Pneumoconiosis Committee of the United States College of American Pathologists under contract to the US National Institute for Occupational Safety and Health (NIOSH). The purpose of the contract was to develop standardized criteria for the pathological diagnosis of these diseases and to develop a system for grading the severity and extent of asbestosis. The results of a preliminary reading trial and the NIOSH statistical analysis of the trial are presented. These results indicate that the proposed grading schema has acceptable inter- and intra-observer variability. The variability is similar to that observed for radiologists in radiographic reading trials.
Rats inhaling chrysotile asbestos contracted asbestosis and fibrosis of the lungs. Studies of biochemical and morphological changes (between normal and treated animals) show that chrysotile induces an increase in the lung free cell population and pulmonary surfactant levels. Lysosomal enzyme levels are elevated in both the whole lung and free cell population and there are considerable changes in macrophage morphology. It is suggested that the primary response of the lung to chrysotile is an increase in surfactant production coupled with an increase in free cell numbers, in order to prevent the cytotoxic effect of the dust.
The paper considers the possibilities of applying telemedicine, a relatively new branch combining medicine and telecommunications, in diagnosing occupational asbestosis. Nowadays, telemedicine has been extensively used in an ever-increasing number of areas such as dermatology, oncology, radiology, surgery, cardiology, and psychiatry. The paper gives an example of possible applications in Croatia. Telemedicine is expected to significantly reduce absenteeism and travel expenses incurred by various laboratory tests. Furthermore, the diagnostic procedure would be considerably quicker, thereby improving the overall health condition of the population living in the immediate vicinity of asbestos factories. Our research has been conducted in the southern Croatian town of Ploce with an asbestos plant, but possible application refers to places distant from major hospitals, such as rural areas and the islands.