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PubMed1985

Mortality of factory workers in east London 1933-80.

The mortality of 3000 male factory workers, 1400 laggers, and 700 women factory workers in east London has been studied. The men were first employed between 1933 and 1964, the women between 1936 and 1942. Textiles were produced until the late 1950s as well as other asbestos products. Laggers were employed on contract in increasing numbers in later years. Crocidolite asbestos was used until the late 1950s as well as asmosite and chrysotile. Exposure of workers was graded according to the job into two categories, low/moderate and severe, and subdivided by duration of employment up to two years or longer. Mesothelial tumours accounted for 7.5% of the total mortality in men, and 9% in women with their longer follow up period. Lung cancer accounted for 20% of deaths in men and 14% in women. Both mesothelial tumours and lung cancer showed a dose response relationship. Histopathological examination of a series of predominantly postmortem specimens showed 22% of adenocarcinomas of lung among men and 21% in women. There was an excess of gastrointestinal tumours but no dose response relationship could be shown. Among severely exposed male factory workers there was an excess of deaths from cancer of the larynx and among severely exposed women of carcinoma of the breast and ovary. Twenty four deaths (2%) were due to asbestosis. There is an indication that the incidence of mesothelial tumours is declining but a further period of observation is required for confirmation.

Adult↗
PubMed1986

Asbestos fibres in bronchoalveolar lavage fluid from asbestos workers: examination by electron microscopy.

The uncoated and coated fibre load in bronchoalveolar lavage (BAL) fluid was assessed using light microscopy, scanning electron microscopy, and x ray microanalysis in 15 subjects with previous, unprotected exposure to asbestos, including three with clinical and radiological evidence of asbestosis, and in 13 urban dwelling control subjects with no known occupational exposure to asbestos. The mean ferruginous body count per ml BAL fluid in asbestos exposed subjects as determined by light microscopy was 52 (range 0-333). No ferruginous bodies were detected in control subjects. The mean fibre count per ml BAL fluid in asbestos exposed subjects as determined by electron microscopy was 793 (133-3700), significantly greater than 239 (44-544) in controls (p less than 0.05). Electron microscopic counts correlated with duration of previous exposure to asbestos (r = 0.47, p less than 0.05) and with percentage neutrophil counts (r = 0.53, p less than 0.025). There was no relation between electron microscopic fibre counts and light microscopic ferruginous body counts. In 11 asbestos exposed cases x ray microanalysis confirmed the presence of asbestos and in six the asbestos fibre type was clearly identified. Of five subjects showing no asbestos bodies by light microscopy, all showed fibres by electron microscopy, and in three cases the presence of asbestos was confirmed by microanalysis. Among control subjects, fibres were either large organic fibres or smaller particles which microanalysis showed were not asbestos. In only one control case were a few fibres identified which were confirmed as asbestos fibres on microanalysis. Electron microscopic examination of BAL fluid may confirm past exposure to asbestos and probably gives a crude quantitative estimate of asbestos load.

Adult↗
PubMed1990

Comparison of chest radiograph reading methods for assessing progress of pneumoconiosis over 10 years in Wittenoom crocidolite workers.

Thirty three pairs of chest radiographs taken up to 10 years apart were obtained for 33 subjects suffering from asbestosis who had applied for compensation to the Pneumoconiosis Medical Board of Western Australia. Multiple films from the period before the first radiograph in each pair, from the intervening period between the two, and from the period subsequent to the second radiograph were also available and all films were read by two independent readers according to the 1980 ILO classification of pneumoconiosis. Films were read twice as side by side pairs ten years apart, twice as two separate randomly ordered films ten years apart, and once as part of the full series of all available chest radiographs on each subject to assess which method provided the best consistency (between reader variation) and repeatability (within reader variation). Judging by consistency, the full series method performed as well as either of the other methods when assessing radiographic changes and significantly better when assessing the level of profusion of small opacities. There was little to choose between the other two methods either judging by consistency or repeatability, which could not be estimated for the full series method. Use of all available films for a subject is recommended for assessing single films, as in a prevalence study, as well as for documenting change in a longitudinal study.

Asbestos↗
PubMed2004

Effects of asbestos and smoking on the levels and rates of change of lung function in a crocidolite exposed cohort in Western Australia.

BACKGROUND: Increased rates of death from asbestos related diseases have been reported in former workers and residents exposed to crocidolite (blue asbestos) at Wittenoom, Western Australia. Exposure to asbestos is associated with reduced static lung volumes, gas transfer and lung compliance, and a restrictive ventilatory abnormality. METHODS: The effects of crocidolite exposure and smoking history on levels and rates of change of lung function were evaluated using a linear mixed model. Lung function was measured as forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and FEV1/FVC. RESULTS: Cumulative doses of asbestos and the presence of radiographic asbestosis were associated with lower levels of FEV1 and FVC and a steeper decline during the period of observation. Subjects exposed to asbestos at a younger age had lower levels of FEV1 and FVC. Current smokers had lower levels and a steeper decline in lung function than never smokers. No significant interactions between crocidolite exposure and smoking on the levels or rates of change of lung function were found. CONCLUSIONS: The deleterious effects of crocidolite exposure on lung function persist in this population, despite asbestos exposure having ceased more than 30 years ago. No significant interactions were found in this population between asbestos and smoking at the first visit or longitudinally.

Asbestos, Crocidolite↗
PubMed1977

Regional lung function in asbestos workers.

Regional lung function was measured using radioactive xenon-133 in a group of normal subjects and in two groups of asbestos workers. When compared with the normal group, patients with pulmonary asbestosis showed impaired ventilation of the lower zones. Subjects with calcified pleural plaques without radiological evidence of lung parenchymal fibrosis did not show this abnormality.

Aged↗
PubMed1993

Liposarcomatous differentiation in diffuse pleural mesothelioma.

A case history is presented of a woman who died eight hours after hospital admission with severe breathlessness. At necropsy the right lung was encased in a thickened pleura with a large tumour. Histological examination of the tumour showed pleural mesothelioma with liposarcomatous differentiation. The lungs showed changes of asbestosis and the asbestos fibre count was significantly raised. Liposarcomatous differentiation in pleural mesothelioma has not been reported previously.

Aged↗
PubMed1979

The serratus anterior muscle on chest radiographs.

The radiographic appearance of the serratus anterior muscle shadow is analyzed. In frontal and near-frontal views, it produces a "bowling-pin" silhouette. When the muscle is well developed, the medial edge of this silhouette may be superimposed upon the air shadow of the lung in a variety of ways. When it overlies the apex of the lung, it gives rise to the companion shadow; when overlying the midlateral lung edge and costophrenic angle it may mimic pleural and/or extrapleural disease. Recognition of the various possible patterns is important to prevent overdiagnosis of disease, particularly asbestosis.

Asbestosis↗
PubMed2002

Asbestos: when the dust settles an imaging review of asbestos-related disease.

Asbestos-related neoplastic and nonneoplastic diseases of the lungs and pleura range from pleural effusion and pleural plaques to lung cancer and malignant mesothelioma. Pleural effusions are typically hemorrhagic exudates of mixed cellularity but do not typically contain asbestos bodies. The classic distribution of pleural plaques seen on chest radiographs is the posterolateral chest wall between the seventh and tenth ribs, lateral chest wall between the sixth and ninth ribs, the dome of the diaphragm, and the mediastinal pleura. Computed tomographic (CT) findings support this distribution but also show anterior and paravertebral plaques not well shown at chest radiography. Imaging features of diffuse pleural thickening include a continuous sheet, often involving the costophrenic angles and apices, that rarely calcifies. The typical CT features of round atelectasis are of a round or oval mass that abuts the pleura, a "comet tail" of bronchovascular structures going into the mass, and thickening of the adjacent pleura. Features of asbestosis on chest radiographs include ground-glass opacification, small nodular opacities, "shaggy" cardiac silhouette, and ill-defined diaphragmatic contours. CT, however, is more sensitive in their detection. Chest radiography in patients with malignant mesothelioma may show an effusion, pleural thickening, and as the tumor progresses, a more lobulated outline. CT can help identify the disease in its early stages. Asbestos-related cancers can occur anywhere in the lungs. Recognition of the clinical, radiologic, and pathologic features of these diseases will be important for some years to come.

Asbestos↗
PubMed2006

Asbestos-induced and smoking-related disease: apportioning pulmonary function deficit by using thin-section CT.

PURPOSE: To retrospectively correlate the extent of individual diseases seen at thin-section computed tomography (CT) with pulmonary function in an initial group of patients with asbestos-related parenchymal disease (asbestosis) and to test these findings in a subsequent group of patients whose CT scans were retrospectively identified. MATERIALS AND METHODS: This retrospective study had Institutional Review Board approval; informed consent was not required. The study included 133 individuals who had been exposed to asbestos. In the initial study group (81 patients; 79 men, two women; median age, 67 years), two observers used a CT scoring system to quantify the extent of pulmonary fibrosis, diffuse pleural thickening, small-airways disease, and emphysema. Multivariate equations were formulated by using independent CT variables to predict changes in total lung capacity (TLC) and carbon monoxide diffusing capacity (Dlco). The validity of these equations was then tested in a subsequent group of patients (52 patients; all men; median age, 60 years). RESULTS: At thin-section CT, the extent of asbestos-induced pleuropulmonary disease and emphysema correlated significantly with physiologic impairment (P<.001). Combined CT variables predicted 58% and 57% of the variability in TLC and Dlco, respectively, despite considerable variation in the proportion of coexisting pathologic conditions. When predictive equations with CT variables derived from the initial study group were applied to the subsequent study group, predicted TLC (rho=0.75, P<.001) and Dlco (rho=0.64, P<.001) correlated strongly with measured values. CONCLUSION: The proposed CT system provides a semiquantitative method for assessing the relative contribution of asbestos-induced pleuropulmonary disease and smoking-related emphysema to functional impairment.

Aged↗
PubMed1993

End-stage lung disease: CT findings in 61 patients.

PURPOSE: To determine whether the cause of end-stage lung disease could be determined on the basis of pattern and distribution of abnormalities at computed tomography (CT). MATERIALS AND METHODS: The CT scans from 61 consecutive patients with end-stage lung disease were independently assessed by two observers without knowledge of clinical or pathologic data. End-stage lung disease was defined by the presence of honeycombing, extensive cystic changes, or conglomerate fibrosis. The observers listed the three most likely diagnoses and recorded the degree of confidence in the first-choice diagnosis on a three-point scale. RESULTS: The observers made a correct first-choice diagnosis in an average of 87% of cases. A correct first-choice diagnosis was made most often in silicosis (100%), Langerhans cell histiocytosis (100%), asbestosis (90%), usual interstitial pneumonia (88%), extrinsic allergic alveolitis (87%), and sarcoidosis (83%). There was good agreement between the two observers on the first-choice diagnosis (kappa statistic, 0.89). CONCLUSION: The pattern and distribution of abnormalities in end-stage lung disease are determined by the underlying cause. In most cases, a specific diagnosis can be made on the basis of the CT findings.

Alveolitis, Extrinsic Allergic↗
PubMed1994

High-resolution CT-derived measures of lung density are valid indexes of interstitial lung disease.

To assess the validity of computer-assisted methods in analyzing the lung parenchyma imaged with high-resolution computed tomography (HRCT), we compared computer-derived estimates of lung density to other, more traditional, measures of parenchymal injury in 24 subjects with idiopathic pulmonary fibrosis (IPF) and 60 subjects with extensive occupational exposure to asbestos. Gray scale density histograms were constructed from the HRCT images. The gray scale histogram of both study groups was of a skewed unimodal distribution. However, compared with the asbestos-exposed subjects, the patients with IPF had a gray scale distribution that was significantly shifted to the right (greater density) and flatter. In a multivariate analysis, after controlling for age and cigarette smoking, we found that the mean and median gray scale densities were independently associated with the presence of moderate-to-severe dyspnea, a higher International Labour Office chest X-ray category, a lower forced vital capacity, and a higher concentration of macrophages and eosinophils in the bronchoalveolar lavage fluid. These factors accounted for > 70% of the variance of the mean and median gray scale densities. Interestingly, no differences in gray scale density measures were noted between patients with IPF and patients with asbestosis when these other factors were taken into account. Our results suggest that computer-derived density analysis of the lung parenchyma on the HRCT scan is a valid, clinically meaningful, and objective measure of interstitial lung disease.

Asbestosis↗
PubMed2001

Radicular involvement and medullary invasion from a malignant mesothelioma.

We present the case of a 57-year-old patient who had worked at a fiber-cement factory for 28 years. The patient developed an epithelioid-type pleural mesothelioma 5 years after retiring, after he was diagnosed with asbestosis. Only 5 months after the diagnosis of mesothelioma, a medullar section appeared to be totally invaded by a tumor in the medullar canal, thus causing paraplegia and affecting the bladder and anal sphincters. The patient underwent radiotherapy and chemotherapy, and achieved partial recovery, but died 9 months after the diagnosis.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1986

What every surgeon should know regarding asbestos-related disease.

Long-lasting occupational exposure to asbestos dust may cause pleural disease, asbestosis, bronchogenic carcinoma and mesothelioma. Many years elapse from first exposure to the appearance of symptoms. Almost all these diseases are the result of dusty working conditions 20-40 years ago. The pathological sequelae are usually irreversible and can progress after exposure ceases. There is no satisfactory treatment. Prevention is the only practical way. In spite of the fact that the general public is invariably exposed to small amounts of the material, asbestos is not a public health problem. Exemptions are the buildings not properly cared for containing sprayed asbestos. But even living in such buildings is calculated to produce a negligible risk of death. Asbestos-related diseases occur where long-lasting inhalation of high amounts of fine asbestos dust has occurred. There is no evidence to indicate that ingested asbestos fibers represent a major health problem. Industry is now replacing asbestos in many products by other fibers. Natural and synthetic organic materials used in fiber cement products are unable to reach the alveoli. They are not cancerogenic and there is no reason to believe that such fibers cause chronic pulmonary disease.

Asbestos↗
PubMed1984

Small airways changes in workers exposed to asbestos.

Although restriction is considered the classic pulmonary function profile of asbestosis, studies suggest that obstruction of the peripheral airways not revealed by standard spirometry is equally frequent and indicative of peribronchiolar fibrosis. We recorded flows and volumes from maximal expiratory flow volume (MEFV) curves, closing volume data and the phase III slope of the alveolar plateau for 610 litigants, 575 men and 35 women, exposed to asbestos for varying periods in a single workplace in northern New Jersey. Smokers (260) included current smokers and subjects who had stopped within the previous 10 years; nonsmokers (350) had either never smoked or had given up for more than 10 years. Analyses were made for both groups according to years worked. Compared to predicted, smokers and nonsmokers had significantly higher closing capacities (p less than 0.01) and delta N2% (p less than 0.001) means, and lower forced vital capacity (FVC), forced expiratory volume for the first second (FEV1.0, maximal expiratory flow rate (MEFR) and peak expiratory flow rate (PEFR) functions (p less than 0.05); the flow rate after 75% of the FVC had been exhaled (FEF75%) values were significantly reduced (p less than 0.01) only for workers exposed for more than 30 years. The change from predicted was significantly more rapid for smokers, compared with nonsmokers, for FVC, FEV1.0, PEFR, MEFR and FEF75% means, while the increase in closing capacity (CC) was twice as rapid for nonsmokers and the two groups did not differ in their mean rates of rise for delta N2%. CC and the slope of the alveolar plateau appeared to be the measures best able to discriminate between the data for both smoking and nonsmoking asbestos workers and their lung function prediction means.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Multinuclear giant cells in bronchoalveolar lavage in interstitial lung diseases.

The presence of multinuclear giant cells (MGC) is a pathological feature of interstitial lung diseases produced either by some organic and inorganic dust or by granulomatous disorders. In order to assess the diagnostic significance of the presence of MGC in bronchoalveolar lavage (BAL), the percent of MGC in the BAL of 52 subjects exposed to asbestos (26 with asbestosis) as well as from 79 with several interstitial lung diseases (idiopathic pulmonary fibrosis, pulmonary fibrosis associated with collagen vascular disorders, hypersensitivity pneumonitis and sarcoidosis) was compared with that of a control group of 14 subjects with no evidence of diffuse pulmonary disease. The results of this study suggest that MGC are present in the BAL of subjects with no pulmonary disease, and the quantification of these cells does not aid in the diagnostic evaluation of interstitial lung diseases.

Alveolitis, Extrinsic Allergic↗
PubMed1982

In vitro effect of asbestos fibers on polymorphonuclear leukocyte function.

Incubation of chrysotile and amphibole asbestos fibers with normal human peripheral blood polymorphonuclear leukocytes (PMN) resulted in a significant stimulation of PMN metabolic activity and generation of toxic oxygen by-products as measured by chemiluminescence (CL). Although all asbestos fibers tested were cytotoxic to PMN, cytotoxicity and CL varied disproportionately with fiber type. Anthophyllite asbestos produced the greatest PMN cytotoxicity. It also depressed PMN phagocytosis of latex beads the most and induced the greatest PMN CL response of the fiber types examined. We postulate that asbestos-induced release of toxic oxygen by-products from PMN which have infiltrated into the pulmonary alveoli may contribute to disease pathogenesis in asbestosis.

Asbestos↗
PubMed1994

Dose-responsive increases in pulmonary fibrosis after inhalation of asbestos.

We focused here on steady-state mRNA levels of genes involved in antioxidant defense, i.e., manganese superoxide dismutase and copper-zinc superoxide dismutase, and in cell proliferation, i.e., ornithine decarboxylase, c-jun, and glyceraldehyde-3-phosphate-dehydrogenase in whole-lung homogenates from Fischer 344 rats at 3 h to 20 d after exposure to crocridolite asbestos. Changes in gene expression were correlated with histopathologic findings, total and differential cell counts in bronchoalveolar lavage, and levels of hydroxyproline in lung. Dosage-dependent increases in mRNA levels of antioxidant enzymes and proliferation-related genes were observed. Differential cell counts revealed a dose-related infiltration of neutrophils that preceded elevations in gene expression. Neutrophil infiltration into lung and focal lesions of fibrosis as well as increased levels of hydroxyproline were observed only at high concentrations of asbestos. These results indicate that high airborne concentrations of asbestos cause molecular changes in lung that may be related to antioxidant defense and the triggering of cell proliferation, a feature of asbestosis and lung cancer.

Administration, Inhalation↗
PubMed1994

Fiber burden and patterns of asbestos-related disease in workers with heavy mixed amosite and chrysotile exposure.

To attempt to determine the mineralogic factors that relate to the appearance of specific types of asbestos-related disease in workers with heavy mixed exposure to amphiboles and chrysotile, we analyzed the pulmonary asbestos fiber burden in a series of 144 shipyard workers and insulators from the Pacific Northwest. Amosite was found in all lungs, and tremolite and chrysotile in most lungs, but the vast majority of fibers were amosite. Tremolite and chrysotile concentrations were significantly correlated, indicating that the tremolite originated from chrysotile products, but no correlation was found between tremolite or chrysotile concentration and amosite concentration. Time since last exposure was correlated with decreasing amosite concentration and the calculated clearance half time was about 20 yr. In a multiple regression analysis that accounted for the presence of more than one disease in many subjects, a high concentration of amosite fibers was correlated with the presence of airway fibrosis and asbestosis, whereas subjects with mesothelioma, lung cancer, pleural plaques, or no asbestos-related disease had about the same, much lower, amosite concentration. No relationship was found between the concentration of chrysotile or tremolite and any disease. Analysis of fiber size measures (length, width, aspect ratio, surface, mass) showed that pleural plaques were strongly associated with high aspect ratio amosite fibers and suggested that mesotheliomas were associated with low aspect ratio amosite fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗