The American Review of Respiratory Disease

About the journal

Publisher: American Lung Association
Published: 1959–1993, United States
Language: English
ISSN: 0003-0805 (print)
Continues: American Review of Tuberculosis and Pulmonary Diseases
Continued by: American Journal of Respiratory and Critical Care Medicine
Its record in the NLM Catalog

1990s

Asbestos-related radiographic abnormalities in elevator construction workers. E.A. Bresnitz, M.J. Gilman, E.J. Gracely, et al. 1993;147(6 Pt 1):1341-4. PubMed · Publisher

Abstract

Elevator construction workers are exposed to asbestos dust during construction and refurbishment work on older buildings. We screened a cohort of workers, all with greater than 20 yr of employment in the industry, with clinical examinations, chest radiography ("B" reader interpretations), and routine spirometry. Twenty of the 91 workers (22%) had evidence of pleural disease, but none of them had an interstitial process consistent with asbestosis. Of those with pleural thickening, 15 had bilateral circumscribed plaques and five had unilateral plaque formation. There were no cases of diffuse pleural thickening, benign pleural effusions, or mesothelioma identified in our cohort. The difference in the mean body mass index of those with pleural abnormalities (29.18 +/- 3.95) and those without (27.7 +/- 3.86) was not statistically significant (p = 0.135). We conclude that elevator construction workers have an increased risk for the development of asbestos-related pleural disease.
Clinical relevance of cellular mediators of inflammation in workers exposed to asbestos. D.A. Schwartz, J.R. Galvin, K.L. Frees, et al. 1993;148(1):68-74. PubMed · Publisher

Abstract

To identify the clinical relevance of cellular mediators of inflammation in workers exposed to asbestos, we investigated the relationship between inflammatory products primarily released by alveolar macrophages and the clinical expression of asbestos-induced interstitial fibrosis. Our study population consisted of 93 white men who had been occupationally exposed to asbestos and were on average 60 yr of age. Pulmonary function tests, chest radiographs, high-resolution CT scans, and bronchoalveolar lavage (BAL) were performed on almost all study subjects; 11 (11.8%) had restrictive lung function, 22 (23.7%) had abnormal gas exchange, 30 (32.3%) had interstitial fibrosis on chest x-ray, and 24 (25.8%) had interstitial changes on high-resolution CT scan. The cellular markers of parenchymal inflammation that we examined included fibronectin in BAL fluid and alveolar macrophage release of prostaglandin E2 (PGE2), interleukin-1 beta (IL-1 beta), and tumor necrosis factor (TNF-alpha) under unstimulated and endotoxin (LPS)-stimulated culture conditions. Significantly higher concentrations of fibronectin in BAL fluid were observed among those with restrictive lung function. In addition, higher concentrations of PGE2, released from cultured but otherwise unstimulated alveolar macrophages, were associated with restrictive lung function. However, the inverse relationship with PGE2 was observed among subjects with abnormal gas exchange. Interestingly, no consistent changes in these inflammatory mediators were observed in those with interstitial changes identified on either the chest radiograph or the high-resolution CT scan.(ABSTRACT TRUNCATED AT 250 WORDS)
Correlation between respiratory symptoms and pulmonary function in asbestos-exposed workers. C.A. Brodkin, S. Barnhart, G. Anderson, et al. 1993;148(1):32-7. PubMed · Publisher

Abstract

Studies of respiratory questionnaire efficacy have emphasized reliability of responses; few have validated symptom response with objective measures of pulmonary function. To determine whether respiratory symptoms are associated with diminished pulmonary function, symptoms reported on the American Thoracic Society (ATS-DLD-78A) questionnaire were correlated cross-sectionally with measured spirometric volumes in 816 asbestos-exposed workers. Cough, phlegm, wheeze, and dyspnea were inversely related to pulmonary function. Cough, phlegm, and chronic bronchitis were associated with a 2 to 8% reduction (p < 0.001) in predicted values for forced vital capacity (FVC) and forced expiratory volume (FEV1); wheeze and dyspnea were clinically more significant, with an 11 to 17% reduction (p < 0.001). Wheeze, dyspnea, and roentgenographic fibrosis were all significant independent predictors of risk for restrictive impairment. These results support the validity of the ATS questionnaire as an epidemiologic tool and emphasize the importance of clinical history in assessing respiratory status.
Distribution of asbestos bodies in the human lung as determined by bronchoalveolar lavage. H. Teschler, N. Konietzko, B. Schoenfeld, et al. 1993;147(5):1211-5. PubMed · Publisher

Abstract

Asbestos-related lung diseases tend to have distinct local distributions, for example, asbestosis first appears and tends to be more severe in the peripheral parts of the lower lung zones. The risk for asbestosis is related to the total asbestos burden of the lung. This suggests that the lower lobes in asbestos-exposed individuals may contain more asbestos than the other lobes. To test whether such topographic differences exist, we compared the number of retrieved asbestos bodies (AB) per ml BAL fluid in three groups of occupationally asbestos-exposed subjects who underwent BAL at different sampling sites. In Group 1 (n = 24) we performed BAL at three sites, namely in a segment of the right upper, right middle, and right lower lobe, to evaluate differences in asbestos body burden from lung apex to basis. There was a distinct increase in BAL asbestos body concentrations from the upper (21.2 +/- 9.1 AB/ml BAL fluid) to the middle (30.4 +/- 12.8 AB/ml BAL fluid) and to the lower lobe (56.0 +/- 20.2 AB/ml BAL fluid), all differences being significant (p < 0.01). In Group 2 (n = 40), we found good interlobar correlations for asbestos body counts between the right middle lobe (21.0 +/- 5.8 AB/ml BAL fluid) and the lingula (22.4 +/- 5.9 AB/ml BAL fluid) (r = 0.941, p < 0.001) and, in Group 3 (n = 15), between the ventral basal segment of the right (41.2 +/- 13.6 AB/ml BAL fluid) and left lung (39.0 +/- 13.6 AB/ml BAL fluid) (r = 0.966, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Fiber burden and patterns of asbestos-related disease in chrysotile miners and millers. A. Churg, J.L. Wright, S. Vedal. 1993;148(1):25-31. PubMed · Publisher

Abstract

To examine how fiber type, fiber concentration, and fiber size correlate with the presence of asbestos-related disease in workers with heavy chrysotile exposure, we used analytic electron microscopy to determine the fiber content of the lungs of 94 long-term chrysotile miners and millers from the region of Thetford Mines, Quebec. Mesothelioma, airway fibrosis, and asbestosis were strongly associated with a high tremolite fiber concentration, whereas pleural plaques and carcinoma of the lung showed no relationship to tremolite burden. Similar patterns were seen for chrysotile concentration, but further analysis suggested that the apparent effect of chrysotile probably was due to the high correlation (r = 0.70) between chrysotile and tremolite concentration rather than to an independent effect of chrysotile. Increased tremolite-chrysotile ratio was marginally associated with the presence of pleural plaques but not with any other disease. Very high correlations (r > 0.90) between the concentrations of fibers longer or shorter than 8 microns prevented assessment of the effects of long compared with short fibers. Pleural plaques were very strongly associated with higher mean tremolite fiber aspect ratios, but no differences in mean fiber size (length, width, aspect ratio, surface area, and mass) were seen for any other disease. Total fiber size measures (total fiber length/g and others) showed differences similar to fiber concentration for mesothelioma, airways fibrosis, and asbestosis, but no one measure was clearly better than another or better than fiber concentration. We conclude that, in this population of heavily exposed chrysotile miners and millers, the presence of airways fibrosis and asbestosis and, probably, mesothelioma reflects high tremolite burden.(ABSTRACT TRUNCATED AT 250 WORDS)
The left-sided predominance of asbestos-related pleural disease. H. Hu, L. Beckett, K. Kelsey, et al. 1993;148(4 Pt 1):981-4. PubMed · Publisher

Abstract

In a series of 406 subjects with a diagnosis of asbestos-related pleural disease (ARPD), the left-right symmetry of radiographically diagnosed ARPD was assessed using the International Labour Organization (ILO) system for classifying radiographic abnormalities and three different statistical models for testing the degree of symmetry. The extent of chest disease was found to be greater on the left than on the right for a number of parameters of pleural disease, including the width and extent of localized pleural thickening, the extent of enface pleural thickening, and the extent of diaphragmatic and chest wall calcification. Current cigarette smoking significantly enhanced the observed asymmetry, with the most pronounced effect being in diaphragmatic calcification. Using a composite scale for each subject's pleural disease, the left side had 1.6 times more localized disease than did the right (p < 0.001). Asymmetry in one parameter was associated with asymmetry in another for a number of pairs. The most significant of these associations was between enface pleural thickening and chest wall calcification (Kendall's tau B = 0.42). The pathophysiologic mechanisms that explain these findings remain elusive and need further investigation.
Cellular and molecular basis of the asbestos-related diseases. A. Cosentino, M.L. Warnock. 1992;145(1):238-9. Comment · Letter PubMed · Publisher
Clinical utility of asbestos bodies in BAL fluid. P. De Vuyst, P. Dumortier, R. Vande Weyer, et al. 1992;145(6):1513-4. Comment · Letter PubMed · Publisher
Detection of dysplasia and carcinoma in situ by ratio fluorometry. S. Lam, J.Y. Hung, S.M. Kennedy, et al. 1992;146(6):1458-61. PubMed · Publisher

Abstract

Fluorescence bronchoscopy was performed in 82 volunteers recruited from occupational groups at risk of exposure to asbestos and/or diesel fumes to determine whether differences in tissue autofluorescence between normal and malignant bronchial tissues can be used to improve the sensitivity of standard fiberoptic bronchoscopy in detecting dysplasic and carcinoma in situ (CIS). This study consisted of 25 nonsmokers, 40 exsmokers, and 17 current smokers with mean ages of 52, 55, and 49 yr, respectively. Tissue autofluorescence was induced by a blue light from an He-Cd laser coupled to the illumination channel of the bronchoscope and analyzed by a ratiofluorometer. One or more sites of moderate or severe dysplasia were found in 12% of the exsmokers and current smokers but in none of the nonsmoker volunteers. CIS was found in two of the exsmokers. The sensitivity of fluorescence bronchoscopy (86%) was found to be 50% better than that of conventional white-light bronchoscopy (52%) in detecting dysplasia and CIS. Pre- and post-bronchoscopy sputum cytology failed to detect these precancerous lesions. Our results suggest that fluorescence bronchoscopy may be an important new method that can improve the ability to detect and localize precancerous and/or CIS lesions.
Immunocytochemistry and ELISA quantitation of mucin for diagnosis of malignant pleural effusions. P.C. Yang, K.T. Luh, S.H. Kuo, et al. 1992;146(6):1571-5. PubMed · Publisher

Abstract

One hundred and thirty-five pleural effusions with definite etiology were analyzed by mucin-specific monoclonal antibody (17Q2)-derived enzyme-linked immunosorbent assay (ELISA). Twenty-four effusions were transudate, 45 were nonmalignant exudate, and 66 were malignant. Among the 66 malignant effusions, 52 were adenocarcinoma, and 14 were malignancies other than adenocarcinoma. Purified mucous glycoproteins from sputa of normal subjects were used as ELISA standard. Our results showed that the mean mucin concentration in malignant pleural effusions were significantly higher than that of benign exudates (8.41 +/- 13.48 ng/ml versus 1.09 +/- 0.82 ng/ml, p < 0.01). Mucin concentration in malignant pleural effusions caused by adenocarcinoma was also significantly higher than in non-adenocarcinoma effusions (9.96 +/- 14.81 ng/ml versus 2.66 +/- 1.74 ng/ml, p < 0.01). With the use of mean +/- 2 SD of mucin concentration in benign exudates as a cut-off value (2.73 ng/ml), the sensitivity of this assay for diagnosis of malignant effusions was 66.7%, specificity was 97.1%, and accuracy was 82.2%. High levels of mucin concentration were more specifically associated with adenocarcinoma. When the mucin concentration in pleural effusions was greater than 5 ng/ml, 93.1% (27/29) of patients were adenocarcinoma. If the mucin concentration was greater than 10 ng/ml, 100% (14/14) of patients were adenocarcinoma. Immunofluorescent staining by mucin-specific monoclonal antibody 17Q2 were also carried out in diastase-treated cell preparations obtained from 22 patients with malignant pleural effusions and 16 benign exudates. Nine of 14 adenocarcinomas (64.2%) were reactive with monoclonal antibody 17Q2, while none of the benign exudates, squamous cell carcinomas, and mesotheliomas were stained.(ABSTRACT TRUNCATED AT 250 WORDS)
Influence of cigarette smoking on bronchoalveolar lavage cellularity in asbestos-induced lung disease. D.A. Schwartz, J.R. Galvin, R.K. Merchant, et al. 1992;145(2 Pt 1):400-5. PubMed · Publisher

Abstract

To investigate the influence of cigarette smoking on bronchoalveolar lavage (BAL) cellularity in asbestos-induced lung disease, we compared BAL cells in asbestos-exposed, nondiseased subjects (n = 20) with those with either asbestosis (n = 25) or asbestos-induced pleural fibrosis (n = 28). Patients with asbestosis (ILO greater than or equal to 1/0) had higher concentrations of BAL macrophages (p = 0.04), neutrophils (p = 0.003), and eosinophils (p = 0.01), while patients with asbestos-induced pleural fibrosis (circumscribed plaques and diffuse pleural thickening) had higher concentrations of BAL lymphocytes (p = 0.02). Within our study population, however, cigarette smoking (smoking status or pack-years of smoking) was strongly associated with BAL macrophages, neutrophils, and eosinophils but was not associated with the concentration of BAL lymphocytes. Using multivariate analysis, we found that although asbestosis remained associated with higher concentrations of BAL macrophages, neutrophils, and eosinophils, cigarette smoking had a far greater contribution to the concentrations of BAL macrophages and eosinophils than did asbestosis. Although cigarette smoking accounted for 17 to 18% of the variance of BAL macrophages and eosinophils, asbestosis was associated with approximately 6% of the variance associated with these cells. In contrast, the concentration of BAL neutrophils remained associated with asbestosis and was not influenced by smoking behavior. We conclude that cigarette smoking strongly influences BAL cellularity (macrophages and eosinophils) in our patients with asbestosis but does not appear to affect the type or concentration of BAL cells in patients with asbestos-induced pleural fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Lymphocytic alveolitis and pleural calcifications in nonoccupational asbestos exposure. Protection against neoplasia?. S.H. Constantopoulos, Y.A. Dalavanga, K. Sakellariou, et al. 1992;146(6):1565-70. PubMed · Publisher

Abstract

Inhabitants of the Metsovo area in Northwest Greece (population, 4,000) have been exposed to asbestos through the use of whitewash containing tremolite. This has resulted in endemic pleural calcifications (PCs) and increased incidence of malignant pleural mesothelioma (MPM). In order to evaluate the lung response to the fiber, bronchoalveolar lavage (BAL) was performed in 25 Metsovites; 14 with PCs, three with PCs and neoplasia, five without PCs, and three without PCs but with established neoplasia. There were no differences between the four groups with regard to age or exposure. Twelve Metsovites had lymphocytic alveolitis (BAL lymphocytes > 15%). Eleven belonged to the group with PCs and one belonged to the group without PCs. None of those with neoplasia had alveolitis. The lymphocytes were mainly helper T-cells, and activation markers were more frequent among those with PCs. We have previously reported on the relative absence of PCs in Metsovites with malignant pleural mesothelioma. This observation and the results of the present study suggest that lymphocytic alveolitis correlates with pleural calcifications, whereas both are rarely present in patients with neoplasia.
NHLBI workshop summary. Environmental lung diseases. Relationship between acute inflammatory responses to air pollutants and chronic lung disease. J. Crapo, F.J. Miller, B. Mossman, et al. 1992;145(6):1506-12. PubMed · Publisher

Summary

This report summarized a workshop held by the Division of Lung Diseases, National Heart, Lung and Blood Institute, on May 29 and 30, 1991, in Bethesda, Maryland, cosponsored by the National Institute of Environmental Health Sciences. Participating scientists reviewed current knowledge of how acute inflammatory responses to environmental air pollutants may contribute to chronic lung diseases such as fibrosis, emphysema, chronic bronchitis and lung cancer. They also identified gaps in knowledge. Topics included microdosimetry of inhaled gases and particles, the transfer of ozone and nitrogen dioxide across the air-tissue interface, oxidative reactions involving nitric oxide, early events leading to lung fibrosis, chronic injury in the proximal alveolar region, pollutant mixtures and diesel exhaust. For asbestos, the summary reported that fibers had a superadditive effect with radiation on transformation of C3H10T1/2 cells. It also reported that iron in asbestos accelerated hydroxyl radical production in vitro. The mechanisms linking reactive oxygen species to asbestosis, lung cancer or mesothelioma were described as unclear. The interaction of asbestos with cigarette smoke was described as particularly hazardous but poorly understood. The participants made 15 recommendations, including better anatomical and dosimetry models, studies of genetic and molecular responses, and work on reactive species and asbestos-smoke synergy. They concluded that extrapolation from animals to humans required a mechanistic understanding linking exposure, dose and response.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.
Relationship of pulmonary function to radiographic interstitial fibrosis in 2,611 long-term asbestos insulators. An assessment of the International Labour Office profusion score. A. Miller, R. Lilis, J. Godbold, et al. 1992;145(2 Pt 1):263-70. PubMed · Publisher

Abstract

Radiographic evidence of interstitial fibrosis (IF) secondary to asbestos inhalation (using the International Labour Office [ILO] profusion of small irregular opacities) was compared with FVC as an independent indicator of IF. In addition, spirometric indices of airflow (FEV1/FVC and FET25-75%) were correlated with the radiographic profusion score. A study of 2,611 long-term insulators was well designed for these analyses since all subjects were from the same trade, there were sufficient (n = 515) nonsmokers to assess the effects of asbestos exposure in the absence of smoking, most (60%, n = 1,557) of the workers had parenchymal abnormalities (scores greater than or equal to 1/0), and there was a greater prevalence of high scores than in other published series (347 workers or 13.3% had scores greater than or equal to 2/1). Looking at all subjects, the FVC decreased as profusion score increased. The FVC was abnormal (88.0% of predicted) even when the profusion score was clearly normal (0/0). The FVC was lower at any score in smokers and in workers with pleural thickening (more so with diffuse thickening). There was, however, no difference in FVC between intermediate scores 0/1 versus 1/0 and 1/2 versus 2/1. Airflow increased with greater profusion, tending to overcome a decrease seen at lesser profusion scores. These results provide a greater understanding of the relationships among profusion scores, smoking, pleural diseases, and pulmonary function.
Asbestos exposure and asbestos-related pleural and parenchymal disease. Associations with immune imbalance. N.L. Sprince, L.C. Oliver, T.C. McLoud, et al. 1991;143(4 Pt 1):822-8. PubMed · Publisher

Abstract

The study hypothesis was that asbestos exposure and asbestos-related pleural plaques and interstitial disease are associated with (1) immune imbalances favoring helper-inducer T-cell subsets in blood and bronchoalveolar lavage (BAL) and (2) T-lymphocyte accumulation in BAL. One hundred twenty-two asbestos-exposed subsets (AES), including 27 nonsmokers (NS), were evaluated and compared with 10 unexposed normal subjects. Data were collected on medical, smoking, and occupational histories, physical examination, spirometry, lung volumes, single-breath DLCO, chest films read by a "B" reader, and T-lymphocyte characterization in blood and BAL using flow cytometry analysis of monoclonal-antibody-treated cells. On average, AES were 47 yr of age and had 23 yr of asbestos exposure. Fifty-eight (48%) had pleural thickening, and seven (6%) had profusion greater than or equal to 1/0. In blood, asbestos-exposed NS had lower total and percent CD8 and lower total CD3 than did normal subjects. In BAL, asbestos-exposed NS had higher total CD3 than did normal subjects. Among AES, increased asbestos exposure was associated with increased percent CD8 in BAL and decreases in both percent lymphocytes and total CD8 in blood. Increase in CD4/CD8 ratio in BAL were associated with pleural thickening. In those seven with profusion greater than or equal to 1/0, there was increased percent CD4 in blood and decreased percent CD8 in BAL. These results suggest immune imbalance favoring helper-inducer T-cell subsets in association with asbestos exposure systemically and with pleural plaques in BAL.(ABSTRACT TRUNCATED AT 250 WORDS)
Cellular and molecular basis of the asbestos-related diseases. W.N. Rom, W.D. Travis, A.R. Brody. 1991;143(2):408-22. Review PubMed · Publisher

Abstract

Asbestosis is an inflammatory and fibrotic process of the alveolar structures mediated, at least in part, by cytokines released by "activated" alveolar macrophages. The process of phagocytosis and "activation" of alveolar macrophages is poorly understood. Are all macrophages activated or only subpopulations? Which cytokines are up-regulated? How does the local milieu modulate profibrotic and antifibrotic mediators? Is protein release accompanied by up-regulation of gene transcription? Is there an ordered sequence of cytokine activity? What roles do neutrophils and lymphocytes play? How can disease progression best be quantified absent further exposure? Answers to these questions are important to direct rational strategies at interdicting the fibrotic process. The question of cancer and asbestos is more vexing. The processes of inflammation, fibrosis, and carcinogenesis appear to be closely intertwined. For example, proto-oncogenes such as c-sis (PDGF B-chain) are up-regulated in activated alveolar macrophages from fibrotic lungs; these and possibly others may play an important role in asbestos carcinogenesis. Second, asbestos can transfect DNA into cells. Furthermore, DNA can adhere to asbestos fibers, and these fibers are capable of direct transmigration into cells. The questions of the mechanisms of cigarette smoke cocarcinogenicity and latency remain. Lastly, if the bronchial epithelium is highly metaplastic throughout from cigarette smoking, what triggers a single (or several) nidus of cells to transform into carcinoma? Malignant mesothelioma poses the most challenging questions because of association with brief asbestos exposure by history. Mesothelial cells are susceptible to minute environmental manipulations, and changes occur after exposure to all fiber types. Yet epidemiologic studies point toward long amphiboles as having greater mesothelioma risk. To test this hypothesis, experimental data must be generated differentiating tumorigenesis risk from short, chrysotile fibers that can migrate to the parietal pleura from the associations of long amphiboles persisting in lung tissue. Despite the future decreasing numbers of clinical cases of asbestos-related disease, solving the important mechanistic questions remaining will contribute significantly to our understanding of fibrosis and cancer.
Idiopathic pulmonary fibrosis in asbestos-exposed workers. E.A. Gaensler, P.J. Jederlinic, A. Churg. 1991;144(3 Pt 1):689-96. Case report PubMed · Publisher

Abstract

Diffuse interstitial lung disease in asbestos-exposed workers is presumed to represent asbestosis. Among 176 asbestos-exposed persons for whom lung tissue was available, we found nine with clinical features consistent with asbestosis, but histologic sections failed to demonstrate asbestos bodies, the usual requirement for pathologic diagnosis of asbestosis (Group I). These nine were compared by analytic electron microscopy with nine persons with idiopathic pulmonary fibrosis (Group II), and with nine persons with all the criteria of asbestosis (Group III). The three groups did not differ significantly with respect to lung burden of chrysotile or tremolite and actinolite, but Group III had a lung burden of amosite and crocidolite that was three orders of magnitude greater than in Groups I and II, with no overlap. We conclude that (1) the American Thoracic Society criterion of "a reliable history of exposure" is sometimes difficult to define; (2) asbestos bodies are seen in tissue sections only when exposure has been reasonably high, and given the proper clinical setting, the presence of diffuse fibrosis and asbestos bodies in tissue sections are sensitive and specific criteria for a diagnosis of asbestosis; and (3) the prevalence here of 5.1% nonasbestos-induced interstitial lung disease among asbestos-exposed persons is artefactually high because of atypical case selection. However, because asbestosis is a disappearing disease, such cases will become more frequent. The identification of these other diseases is important because therapy and prognosis may differ from that of asbestosis.
Mica-associated pulmonary interstitial fibrosis. S.K. Landas, D.A. Schwartz. 1991;144(3 Pt 1):718-21. Case report PubMed · Publisher

Abstract

We present the clinical and biopsy findings of a 63-yr-old white male with interstitial pulmonary fibrosis and a long history of extensive exposure to mica while working in the rubber industry. The patient presented 30 yr after the initial exposure with complaints of progressive shortness of breath and a chronic nonproductive cough. Pulmonary function testing revealed restrictive lung function with a mild reduction in the total lung capacity (80% of predicted) and a moderate-to-severe reduction in the diffusing capacity of carbon monoxide (50% of predicted). The chest radiogram and high-resolution chest CT scan showed diffuse fibrosis and focal honeycombing involving the upper and lower lung zones bilaterally. Bronchoalveolar lavage revealed 20% neutrophils in the lavage fluid with abundant rectangular flaking crystals. Open-lung biopsy exhibited extensive fibrosis and architectural remodeling with abundant sheets and fragments of engulfed polarizable crystalline material. Energy-dispersive spectroscopy and electron diffraction studies confirmed the material to have the features of mica. Asbestos and other silicates were not identified. The documentation of prolonged exposure to mica, the clinical and radiographic features of severe interstitial fibrosis, and the histopathologic delineation of the interstitial lesion, including spectroscopic and crystallographic verification of crystalline mica, support the causal relationship between mica and interstitial fibrosis.
The clinical utility and reliability of asbestos bodies in bronchoalveolar fluid. D.A. Schwartz, J.R. Galvin, L.F. Burmeister, et al. 1991;144(3 Pt 1):684-8. PubMed · Publisher

Abstract

Although asbestos bodies are easily identified in bronchoalveolar lavage (BAL) fluid and are thought to be strongly associated with the asbestos body burden in the lung parenchyma, the clinical utility and reliability of this biologic measure of exposure has not been sufficiently studied. To assess the clinical relevance of BAL asbestos bodies we compared this bioassay of exposure to other measures of exposure and also indices of lung disease in asbestos-exposed workers (n = 71). The median concentration of asbestos bodies was 0.8 bodies per ml of BAL fluid (range 0 to 34.3). Seven workers or 9.9% had zero asbestos bodies identified in the BAL fluid. The concentration of BAL asbestos bodies was not associated with the duration of exposure (r = -0.02), the time from first exposure to asbestos (r = 0.12), or the time since last exposure to asbestos (r = 0.05). Moreover, radiographic and physiologic measures of asbestos-induced lung disease were not found to be associated with the concentration of BAL asbestos bodies. In fact, of the seven study subjects with zero BAL asbestos bodies, the mean duration of exposure was 32 yr, and six of these subjects had radiographic evidence of asbestos-induced lung disease. To assess the reliability of measuring BAL asbestos bodies, we performed a second bronchoscopy on 54 subjects and directly compared the concentration of BAL asbestos bodies from both the first and second BAL samples. Within these 54 subjects, the concentration of BAL asbestos bodies was found to be a very reliable measure (r = 0.76; p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
The diagnosis of asbestosis. R.N. Jones. 1991;144(3 Pt 1):477-8. Comment · Editorial PubMed · Publisher

Summary

In this editorial, the author commented on a report by Gaensler and coworkers in the same issue and reviewed how asbestosis is diagnosed. He described the diagnosis as inferential, resting on two main criteria. The first is an occupational exposure history showing substantial present risk of lung fibrosis, taking account of exposure intensity, duration and latency. The second is evidence, usually clinical and radiologic, that diffuse interstitial pulmonary fibrosis (DIPF) has developed. Drawing on the principle of prior probability, he proposed a third criterion: there should be no good reason to attribute the findings to another condition, such as connective tissue disease, chronic sarcoidosis, certain chemotherapy agents, amiodarone or lung radiotherapy. He noted that tissue examination can establish exposure through asbestos bodies, quantify fiber burdens and confirm DIPF. In the Gaensler pathology series, 9 of 176 asbestos-exposed persons (5.1%) lacked histologic asbestos bodies. Compared with 9 asbestosis cases matched for age and smoking, seven had shipyard exposures, against one in the asbestosis group. Asbestos product factory, insulator and pipe coverer trades accounted for eight of the nine asbestosis cases. Years of exposure and latency differed little between the groups. The author concluded that both intensity and duration of exposure must be considered and that yes/no exposure categories are inadequate for asbestosis. When the exposure or response criteria are deficient, or a confounder is present, asbestosis becomes a strictly pathologic diagnosis.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.
The relationship between respiratory impairment and asbestos-related pleural abnormality in an active work force. J.E. Cotes, B. King. 1991;143(5 Pt 1):1197. Letter · Comment PubMed · Publisher
Asbestos content of lung tissue, lymph nodes, and pleural plaques from former shipyard workers. R.F. Dodson, M.G. Williams, C.J. Corn, et al. 1990;142(4):843-7. PubMed · Publisher

Abstract

Autopsy samples from eight former shipyard workers were collected from lung parenchyma, tracheal lymph nodes, and pleural plaques. The tissue from each respective area was prepared by a modified bleach digestion technique, and the residue was collected on a 0.2-micron pore polycarbonate or 0.22-micron mixed cellulose ester filter. Quantitation of ferruginous bodies and uncoated fibers was done by light and transmission electron microscopy, respectively. Differences in the asbestos burden were noted for each site. Ferruginous bodies were observed in both parenchyma and nodes but not in plaques. Three subjects were found to have more ferruginous bodies per gram dry weight in their lymph nodes than in their lung parenchyma. Likewise, all subjects were found to have more uncoated fibers per gram in the nodes than in the parenchyma. Amphibole and chrysotile fibers were noted in the lung and extrapulmonary sites, with chrysotile being the predominant asbestiform in plaques. The majority of the uncoated fibers in both the nodes and the plaques were less than or equal to 5 microns in length. However, some fibers with dimensions conforming to the "Stanton hypothesis" reached both areas. These residual patterns most likely reflect the impact of clearance on lung burden as opposed to the eventual accumulation and stasis in the extrapulmonary areas.
Asbestos-induced pleural fibrosis and impaired lung function. D.A. Schwartz, L.J. Fuortes, J.R. Galvin, et al. 1990;141(2):321-6. PubMed · Publisher

Abstract

To assess the clinical significance of asbestos-induced pleural fibrosis, we evaluated the relationship between radiographic evidence of pleural fibrosis and spirometric values in 1,211 sheet metal workers. Of those with pleural fibrosis (n = 334), 78% had circumscribed plaques and 22% had diffuse pleural thickening involving the costophrenic angle. Factors that were found to be associated with the presence and type of pleural fibrosis included increased age (p less than 0.001), more years in the trade (p less than 0.0001), more years since first exposure to asbestos (p less than 0.0001), more pack-years of cigarette smoking (p less than 0.01), and the presence and degree of interstitial fibrosis (p less than 0.0001). After controlling for these potential confounders (age, years in the trade, latency, pack-years of smoking, and ILO profusion category), linear multivariate regression models demonstrated that both circumscribed plaques (p = 0.007) and diffuse pleural thickening (p = 0.008) were independently associated with decrements in FVC but not with decrements in the FEV1/FVC ratio. Furthermore, our data indicate that the effect of diffuse pleural thickening on decrements in FVC is approximately twice as great as that seen with circumscribed pleural plaques. We conclude that the presence and type of pleural fibrosis among asbestos-exposed workers is independently associated with a pattern of spirometry that is suggestive of an underlying restrictive defect in lung function.
Changes in surfactant in bronchoalveolar lavage fluid after hemithorax irradiation in patients with mesothelioma. M. Hallman, P. Maasilta, L. Kivisaari, et al. 1990;141(4 Pt 1):998-1005. PubMed · Publisher

Abstract

Experimental studies have shown that the surfactant system of the lung is affected shortly after irradiation. It is unclear, however, whether surfactant plays a role in the pathogenesis of radiation pneumonitis. In the present study surfactant components (saturated phosphatidylcholine, surfactant protein A, phosphatidylglycerol, and phosphatidylinositol) and other phospholipids of bronchoalveolar lavage fluid (BAL) were studied in four patients with pleural mesothelioma before and during hemithorax irradiation (70 Gy) as well as zero, 1, 2, 3, and 4 months following irradiation. The concentrations of these same components and of soluble proteins were also estimated in the epithelial lining fluid (ELF) using urea as a marker of dilution. After radiotherapy, the concentrations of the surfactant components in ELF decreased to 12 to 55% of the control values before radiation, whereas the concentration of sphingomyelin in ELF increased ninefold. There were small changes in the other phospholipids. The concentration of soluble protein in ELF increased sevenfold. The minimum surface activity of crude BAL increased from 12 +/- 4 to 32 +/- 6 mN/m, and that of the sediment fraction of BAL increased from 7 +/- 4 to 22 +/- 6 mN/m, p less than 0.001. The protein-rich supernatant fraction of BAL from irradiated lung had a inhibitory effect on normal surfactant. There were significant correlations between the increasing severity of the radiologic changes on the one hand and, on the other, the saturated phosphatidylcholine/sphingomyelin ratio (p less than 0.001), the concentrations of soluble protein (p less than 0.001), and the concentrations of the surfactant components (p less than 0.02-0.001) in ELF.(ABSTRACT TRUNCATED AT 250 WORDS)
Clinical features of adenosquamous lung carcinoma in 127 patients. K.S. Sridhar, M.J. Bounassi, W. Raub, et al. 1990;142(1):19-23. PubMed · Publisher

Abstract

There has been increased recognition of adenosquamous lung carcinoma since the 1982 modification of World Health Organization (WHO) histologic criteria. However, data on clinical features of this histologic subtype were nonexistent. Medical records of 127 patients with adenosquamous lung carcinoma were reviewed to determine the clinical features, namely, age, race, sex, smoking history, asbestos exposure, symptoms present at the time of diagnosis, stage, treatments, and survival. The age distribution was: less than 40 yr, 3%; 40 to 49, 17%; 50 to 59, 28%; 60 to 69, 32%; 70 to 79, 18%; greater than or equal to 80, 2%. Men constituted 72%, and 90% were smokers. Four smokers had documented asbestos exposure. The symptoms in order of decreasing frequency were cough, weight loss, expectoration, anorexia, chest pain, dyspnea, weakness, hemoptysis, pneumonia, fever, nausea, vomiting, dizziness, and chills. Stage could be ascertained in 120 (95%) patients. Local stage constituted 10%, regional constituted 30%, and distant constituted 60%. Local stage had the best survival, with a projected 5-yr survival of 62%. Median survivals in regional and distant stages were 8 and 4 months, respectively. Symptoms of adenosquamous lung carcinoma were similar to other histologies. Most patients present in regional or distant stages. Local-stage patients had a good long-term survival after surgical excision of the tumor.
Environmental Controls and Lung Disease. 1990;142(4):915-39. PubMed · Publisher
Health effects of tremolite. This official statement of the American Thoracic Society was adopted by the ATS Board of Directors, June 1990. 1990;142(6 Pt 1):1453-8. Review PubMed · Publisher

Summary

In 1988 the American Thoracic Society appointed a committee to critically assess scientific knowledge of health risks from tremolite, an amphibole that contaminates chrysotile, talc and vermiculite deposits. A draft was presented at a public forum in May 1989 and revised after comments, and the statement was adopted in June 1990. The committee reviewed epidemiologic, lung-burden, animal and mineralogic evidence and commented on OSHA regulatory issues. Because mineralogists disagreed, it largely treated cleavage fragments and asbestiform fibers together as "fibers." Montana vermiculite miners had four mesotheliomas and a dose-related excess of lung cancer (15 observed, 5.3 expected, 20 years or more from hire; SMR 2.85). Talc studies had not convincingly shown an exposure-related cancer risk. Elevated mesothelioma risk had been observed in rural areas of Turkey with naturally occurring asbestiform tremolite. Lung-burden evidence implied that long, high-aspect-ratio tremolite fibers were particularly dangerous because of their propensity to induce mesothelioma. Animal studies showed tremolite to be a powerful mesothelial carcinogen. The committee concluded that tremolite asbestos had unquestioned health effects in humans and animals, identical to those of other forms of asbestos. It found that evidence for biologic distinctions based on mineralogic parameters other than fiber dimension and fiber number was inadequate. It also concluded that appropriately sized tremolite "fibers," in sufficient exposure dose, should be regarded as capable of producing the recognized asbestos-related diseases and regulated accordingly. It recommended further research.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.
Inhibition of lung injury, inflammation, and interstitial pulmonary fibrosis by polyethylene glycol-conjugated catalase in a rapid inhalation model of asbestosis. B.T. Mossman, J.P. Marsh, A. Sesko, et al. 1990;141(5 Pt 1):1266-71. PubMed · Publisher

Abstract

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)
Mineralogic parameters related to amosite asbestos-induced fibrosis in humans. A. Churg, J. Wright, B. Wiggs, et al. 1990;142(6 Pt 1):1331-6. PubMed · Publisher

Abstract

We have previously shown that in the lungs of a group of chrysotile miners and millers, grade of interstitial fibrosis (asbestosis) is directly proportional to tremolite fiber or chrysotile fiber concentration but is inversely proportional to mean fiber length and length-related parameters. To compare the effects of the commercial amphibole asbestos amosite on parenchymal fibrosis, we histologically graded fibrosis in four different sites in the lungs of 20 shipyard and insulation workers with heavy amosite exposure and measured by analytic electron microscopy fiber concentration and size in corresponding portions of lung tissue. Fibrosis grade was found to be strongly positively correlated with amosite concentration and negatively correlated with mean fiber size parameters, including fiber length, width, surface area, and mass. A comparison of our present results with our data on the chrysotile miners and millers showed that the regression lines of fibrosis grade versus concentration for amosite, chrysotile, and tremolite were statistically different. These findings indicate that amosite concentration, like chrysotile and tremolite concentration, is closely and directly related to fibrosis at the local lung level. Furthermore, these observations again raise the possibility that short fibers may be more important than is commonly believed in the genesis of fibrosis in man. Last, the concentration comparison data indicate that, fiber for fiber, amosite is more fibrogenic than is chrysotile or tremolite, and indirectly suggest that tremolite is more fibrogenic than is chrysotile.
Pulmonary fibrosis in aluminum oxide workers. Investigation of nine workers, with pathologic examination and microanalysis in three of them. P.J. Jederlinic, J.L. Abraham, A. Churg, et al. 1990;142(5):1179-84. PubMed · Publisher

Abstract

Epidemiologic surveys have indicated an excess of nonmalignant respiratory disease in workers exposed to aluminum oxide (Al2O3) during abrasives production. However, clinical, roentgenographic, histologic, and microanalytic description of these workers are lacking. This is a report of nine Al2O3-exposed workers with abnormal chest roentgenograms (profusion greater than or equal to 1/0, ILO/UC) from a plant engaged in the production of Al2O3 abrasives from alundum ore. Mean duration of exposure was 25 yr, and time since first exposure was 28 yr. in a subgroup of three, the severity of symptoms, reduction in the forced vital capacity (67% predicted) and diffusing capacity (51% predicted), and progressive roentgenographic changes (profusion greater than or equal to 2/2) prompted open lung biopsy. Lung tissue was analyzed by scanning electron microscopy and electron microprobe analysis. In each of the three biopsies, interstitial fibrosis with honeycombing was seen on routine section. In one biopsy, silica and asbestos fiber counts were at the low end of the range seen with silicosis and asbestosis; however, the absence of asbestos bodies and silicotic nodules suggested that the fibrosis was due to another cause. Metals occurred in amounts several orders of magnitude above background, and the majority was aluminum as Al2O3 and aluminum alloys. The findings in these nine workers suggests a common exposure as the possible cause. The nonspecific pathologic findings, absence of asbestos bodies and silicotic nodules, and the striking number of aluminum-containing particles suggest that Al2O3 is that common exposure. The possibility of "mixed dust" fibrosis should also be considered.
The degree of roentgenographic parenchymal opacities attributable to smoking among asbestos-exposed subjects. S. Barnhart, M. Thornquist, G.S. Omenn, et al. 1990;141(5 Pt 1):1102-6. PubMed · Publisher

Abstract

Considerable controversy surrounds the question of whether cigarette smoking has the potential to increase the prevalence of small opacities on chest roentgenographs among asbestos-exposed workers. To compare the relative contribution of smoking with other predictors of the presence of roentgenographic small opacities, we examined 661 men enrolled in a double-blind, randomized trial designed to assess the efficacy of vitamin A and beta-carotene in the prevention of lung cancer among workers with heavy occupational asbestos exposure. Subjects in the study population had a mean latency of 35 yr from first asbestos exposure and a mean of 28 yr in their trade. The prevalence of roentgenographic abnormalities consistent with asbestos exposure was 26% for pleural abnormalities alone, 10% for parenchymal abnormalities alone, and 20% for pleural and parenchymal abnormalities together. We investigated occupation, age, latency from first asbestos exposure, and smoking status as predictors of roentgenographic small opacities. Smoking history, independent of latency, contributed to the prevalence and extent of small opacities, but its effect was less than that of latency. We conclude, that in the setting of heavy occupational exposure to asbestos, cigarette smoking confers added risk for the development of roentgenographic small opacities.
The relationship between respiratory impairment and asbestos-related pleural abnormality in an active work force. J. Bourbeau, P. Ernst, J. Chrome, et al. 1990;142(4):837-42. PubMed · Publisher

Abstract

With the general improvement in environmental controls in workplaces where asbestos is used, an increasing number of workers are seen who exhibit isolated pleural plaques. The question as to whether these are associated with respiratory impairment independently of parenchymal disease remains unresolved. The question was reinvestigated using quantitative gallium-67 lung scanning to take into account early parenchymal change not evident on the chest radiograph. We carried out a cross-sectional study of 110 construction insulators all currently at work. Overall, 58.2% had pleural abnormality, 52.5% pleural plaques only, and 5.5% diffuse pleural thickening as assessed from the PA chest radiograph. Compared with those without, those with any pleural abnormality had a decrease in FEV1 and FVC on average of 222 and 402 ml (p less than 0.05), and those with isolated pleural plaques, a decrease on average of 200 and 350 ml (p less than 0.05), after taking into account age, height, smoking status, and the presence of parenchymal abnormality as assessed by chest radiography and gallium uptake. The complaint of dyspnea with strenuous activities was also significantly related to the width and extent of chest wall pleural thickening (p less than 0.05), independently of parenchymal disease. This study suggests that the most common radiographic findings in asbestos-exposed, isolated pleural plaques are associated with a significant reduction in FEV1 and FVC, which cannot be attributed to the presence of radiographic and subradiographic pulmonary fibrosis.

1980s

Alveolar macrophages from patients with asbestos exposure release increased levels of leukotriene B4. J.G. Garcia, D.E. Griffith, A.B. Cohen, et al. 1989;139(6):1494-501. PubMed · Publisher

Abstract

The alveolar influx and subsequent activation of inflammatory cells such as neutrophils and eosinophils are believed to be important in the pathogenesis of many interstitial lung disorders, including asbestosis. Indices of lower respiratory tract abnormalities detected by bronchoalveolar lavage (BAL) were investigated in 93 asbestos-exposed workers as well as in smoking (n = 12) and nonsmoking (n = 10) control subjects. Patients with clinical asbestosis (n = 12) exhibited increases in both BAL neutrophils and BAL eosinophils, expressed as both percentage of total cells and total numbers, when compared to asbestos-exposed workers without asbestosis (n = 81) and control subjects. Significantly greater numbers of BAL neutrophils were also found in asbestos-exposed workers without asbestosis than in either smoking or nonsmoking control subjects. These abnormalities correlated significantly with in vitro BAL alveolar macrophage production of the potent leukocyte chemotaxin, leukotriene B4 (LTB4). For example, basal, unstimulated LTB4 production was 3.1 +/- 0.8 ng/10(6) alveolar macrophages for patients with asbestosis, 1.05 +/- 0.2 ng/10(6) cells in asbestos workers without asbestosis, 0.9 +/- 0.2 ng/10(6) cells in control nonsmokers, and 0.2 +/- 0.05 ng/10(6) cells in control smokers. Stimulated LTB4 release from BAL alveolar macrophages (A23187 or arachidonate) was even more pronounced in asbestos workers with or without asbestosis, suggesting an in vivo priming effect on alveolar macrophage synthesis of LTB4. Cell-free BAL supernatants from asbestos-exposed patients with or without asbestosis also contained significantly greater amounts of LTB4 than did those from control subjects, indicating enhanced in vivo production of this inflammatory mediator.(ABSTRACT TRUNCATED AT 250 WORDS)
Asbestos and cancer: human natural killer cell activity is suppressed by asbestos fibers but can be restored by recombinant interleukin-2. B.W. Robinson. 1989;139(4):897-901. PubMed · Publisher

Abstract

Inhalation of asbestos fibers is associated with a marked increase in the risk of developing pulmonary malignancy, particularly bronchogenic carcinoma. As natural killer (NK) cells are specialized lymphocytes that are considered to have an important in vivo role in the recognition and destruction of malignant cells, we examined the capacity of asbestos fibers (chrysotile, amosite, and crocidolite) to interfere with the NK activity of nylon wool-nonadherent, human blood lymphocytes (51Cr-release assay, K562 target cells, 14 h effector-to-target ratio = 50:1). Final asbestos concentrations used were 1 to 1,000 micrograms/ml. None of the fibers altered spontaneous target cell lysis or lymphocyte viability. All types of asbestos suppressed NK activity in a dose-dependent fashion. This effect was most marked with chrysotile, which exerted a profound inhibitory effect on blood NK cell activity; at 100 micrograms/ml, NK activity was inhibited 84 +/- 2% (p less than 0.001). The suppressive effects of asbestos were exerted directly on the NK cells (large granular lymphocytes, 91 +/- 2% inhibition at 100 micrograms/ml; p less than 0.001). Exposure of lymphocytes to recombinant interleukin-2 (IL-2, 150 units/ml) for 24 h prior to exposure to asbestos restored the level of activity to 99 +/- 6% of the original value (p less than 0.001), and lung lymphocytes that were exposed to IL-2 in vivo (active sarcoidosis) were resistant to suppression by asbestos. Similar results were observed in a group of patients with asbestosis. This suppression of NK activity may contribute to the increased susceptibility of asbestos-exposed persons to the development of pulmonary malignancy.
Asbestos fibers and silica particles stimulate rat alveolar macrophages to release tumor necrosis factor. Autoregulatory role of leukotriene B4. C.M. Dubois, E. Bissonnette, M. Rola-Pleszczynski. 1989;139(5):1257-64. PubMed · Publisher

Abstract

Alveolar macrophages (AM) can play a crucial role in the pathogenesis of pulmonary disease via their ability to produce potent inflammatory and fibrogenic mediators. We found that rat AM cultured with 1 to 100 micrograms/ml of silica particles or asbestos fibers produced tumor necrosis factor (TNF) and leukotriene B4 (LTB4) in a concentration-dependent fashion, whereas latex beads, an inert phagocytic stimulus, failed to induce significant augmentation of either TNF or LTB4. In a time course study, AM stimulated for 2 h with silica or asbestos produced an increased amount of LTB4, which preceded the rise in TNF activity detected 7 and 24 h after culture initiation. The induction appears to involve the synthesis of new protein since actinomycin D and cycloheximide abrogate the majority of the stimulatory effect. We next examined the role of LTB4 in mineral-dust-induced TNF production. The lipoxygenase inhibitors nordihydroguaiaretic acid (NDGA) and AA861 used at 1 to 50 micrograms/ml reduced in a concentration-dependent fashion asbestos- or silica-stimulated TNF release. On the other hand, "reconstitutive" experiments in which we added exogenous LTB4 (10(-14) to 10(-8) M) to AM treated with lipoxygenase inhibitors showed partial restoration of TNF production induced by chrysotile or silica, with peak effect at 10(-10)M LTB4. The present study demonstrated that AM incubated in the presence of chrysotile A or silica can produce both LTB4 and TNF and that endogenous lipoxygenase metabolites as well as exogenous LTB4 can act to amplify TNF production. These observations suggest a common mechanism by which asbestos and silica may modulate the production of inflammatory and fibrogenic cytokines.
Bronchoalveolar lavage cell and lymphocyte phenotype profiles in healthy asbestos-exposed shipyard workers. J.M. Wallace, J.S. Oishi, R.G. Barbers, et al. 1989;139(1):33-8. PubMed · Publisher

Abstract

The cellular and lymphocyte phenotypic composition of bronchoalveolar lavage (BAL) fluid and peripheral blood (PB) from 15 healthy, nonsmoking, asbestos-exposed shipyard workers (AEW) and 10 nonsmoking, age-matched unexposed workers (UEW) were compared. None of the AEW had clinical, radiographic, or physiologic evidence of asbestosis, but six had radiographic evidence of pleural plaques and/or thickening. The mean duration of asbestos exposure was 16.3 +/- 2.3 yr, and the mean period since exposure was 10.8 +/- 0.5 yr. All but three of the AEW and none of the UEW had asbestos bodies detected in the first 20 ml of BAL fluid recovered (0.1 to 35 asbestos bodies/ml). The AEW had a significantly higher mean percentage (19.1 +/- 2.8% versus 9.7 +/- 1.6%) and concentration (31.6 +/- 5.2 x 10(3) cells/ml versus 14.7 +/- 2.5 x 10(3) cells/ml) of BAL lymphocytes compared with that in the UEW, with an increased mean concentration of each phenotype measured. In PB, the mean lymphocyte concentration was also higher in the AEW than in the UEW (2.0 +/- 0.3 x 10(3) cells/ml versus 1.5 +/- 0.3 x 10(3) cells/ml), but the difference was not statistically significant, and there was no increase of any phenotype measured. BAL lymphocytosis did not correlate with exposure history or BAL asbestos body count, but was greater in AEW with pleural abnormality (30.1 +/- 2.9% versus 11.8 +/- 1.6%). BAL concentrations of CD-20, CD-3, and CD-4, but not of CD-8 cells were significantly increased compared with those in the AEW without pleural abnormality. Further longitudinal studies are needed to determine the prognostic significance of these findings.
Effect of tobacco smoking on the presence of asbestosis at postmortem and on the reading of irregular opacities on roentgenograms in asbestos-exposed workers. A. Kraut, J. Godbold, R. Lilis. 1989;139(6):1567-9. Letter PubMed · Publisher
Evaluation of the causal relationship between crocidolite asbestos-induced lipid peroxidation and toxicity to macrophages. L.A. Goodglick, L.A. Pietras, A.B. Kane. 1989;139(5):1265-73. PubMed · Publisher

Abstract

In vitro, crocidolite asbestos toxicity to macrophages is mediated by the production of reactive oxygen metabolites. We examined whether exposure of macrophages to crocidolite asbestos induced lipid peroxidation as measured by the thiobarbituric acid assay. When elicited mouse peritoneal macrophages were exposed to crocidolite, a dose- and time-dependent increase in lipid peroxidation breakdown products accompanied cell death. Superoxide dismutase plus catalase or deferoxamine prevented both lipid peroxidation and loss of viability caused by crocidolite. We tested whether crocidolite-induced lipid peroxidation was causally responsible for cell death. Macrophages were not killed by crocidolite when incubated with 10 mM 3-aminobenzamide. The level of thiobarbituric acid-reactive material was the same, however, for cells incubated with crocidolite in the presence or absence of 3-aminobenzamide. When macrophagaes were pretreated for 24 h with 25 microM vitamin E and then incubated with crocidolite, no thiobarbituric acid-reactive products were detected. Vitamin E, however, did not prevent crocidolite cytotoxicity. These results suggest that exposure of macrophages to crocidolite asbestos produces lipid peroxidation as measured by thiobarbituric acid-reactive products. This reaction, however, is not directly responsible for irreversible injury in this model system.
Exposure to low levels of ozone results in enhanced pulmonary retention of inhaled asbestos fibers. K.E. Pinkerton, A.R. Brody, F.J. Miller, et al. 1989;140(4):1075-81. PubMed · Publisher

Abstract

Health effects associated with exposure to ozone at environmentally relevant concentrations are subject to considerable controversy. Currently, no compelling evidence exists that exposure to low levels of ozone leads to lasting impairment of pulmonary structure or function. One adverse health effect of ozone may be to change lung uptake or clearance functions for other inhaled air pollutants. As a test of this hypothesis, Fischer 344 rats were continuously exposed to 0.06 ppm ozone 7 days a week with a slow rise in ozone to a peak of 0.25 ppm and subsequent decrease to 0.06 ppm over a 9-h period five times each week for 6 wk. Three days after the end of ozone exposure, animals-were exposed to aerosolized asbestos fibers for 5 h and examined immediately after or 30 days after exposure to asbestos. Filtered air control animals were simultaneously exposed to asbestos. Immediately after the end of fiber exposure, lung asbestos fiber burden was similar in both groups. However, 1 month after exposure, fiber mass and fiber number were significantly greater (p less than 0.05) in the lungs of animals exposed to ozone than in the lungs of those exposed to air. These findings suggest that ambient levels of ozone can impair clearance of fibrogenic and carcinogenic materials such as asbestos from the lungs and represent an important adverse effect of prolonged exposure to low levels of this oxidant gas.
High resolution computed tomography and lung function in asbestos-exposed workers with normal chest radiographs. C.A. Staples, G. Gamsu, C.S. Ray, et al. 1989;139(6):1502-8. PubMed · Publisher

Abstract

Asbestos-exposed persons with normal chest radiographs can demonstrate parenchymal abnormalities on high resolution computed tomography (HRCT). We reviewed the HRCT, clinical presentation, and results of pulmonary function tests in 169 asbestos-exposed workers with normal chest radiographs (ILO less than 1/0). The HRCT was normal or near normal in 76 subjects (Group 1), abnormal but indeterminate for asbestosis in 36, and abnormal and suggestive of asbestosis in 57 (Group 2). The indeterminate subjects were excluded from further analysis. The subjects in Groups 1 and 2 were not significantly different in their duration of asbestos exposure, latency, smoking history, or in measurements of airflow obstruction (FEV1/FVC% and %FEV1). Both the vital capacity percent predicted and diffusing capacity percent predicted were significantly lower in the abnormal subjects (Group 2) than in the normal subjects (Group 1) (79.0 versus 86.2, p = 0.005; 78.2 versus 87.1, p = 0.024; independent t test). We conclude that in asbestos-exposed subjects with normal chest radiographs, HRCT can identify a group of subjects with significantly reduced lung function indicative of restrictive lung disease when compared with a group with normal or near-normal HRCT.
Increased alveolar plasminogen activator in early asbestosis. A. Cantin, C. Allard, R. Bégin. 1989;139(3):604-9. PubMed · Publisher

Abstract

Alveolar macrophage-derived plasminogen activator (PA) activity is decreased in some chronic interstitial lung diseases such as idiopathic pulmonary fibrosis and sarcoidosis but increased in experimental models of acute alveolitis. Although asbestos fibers can stimulate alveolar macrophages (AM) to release PA in vitro, the effect of chronic asbestos exposure of the lower respiratory tract on lung PA activity remains unknown. The present study was designed to evaluate PA activity of alveolar macrophages and bronchoalveolar lavage (BAL) fluid in asbestos-exposed sheep and asbestos workers. Forty-three sheep were exposed to either 100 mg UICC chrysotile B asbestos in 100 ml phosphate-buffered saline (PBS) or to 100 ml PBS by tracheal infusion every 2 wk for 18 months. At Month 18, chest roentgenograms were analyzed and alveolar macrophage and extracellular fluid PA activity were measured in samples obtained by BAL. Alveolar macrophage PA activity was increased in the asbestos-exposed sheep compared to control sheep (87.2 +/- 17.3 versus 41.1 +/- 7.2 U/10(5) AM-24 h, p less than 0.05) as was the BAL fluid PA activity (674.9 +/- 168.4 versus 81.3 +/- 19.7 U/mg alb-24 h, p less than 0.01). Among the asbestos-exposed sheep, 10 had normal chest roentgenograms (Group SA) and 15 had irregular interstitial opacities (Group SB). Strikingly, whereas Group SA did not differ from the control group in BAL cellularity or PA activity, Group SB had marked increases in alveolar macrophages (p less than 0.005), AM PA activity (p less than 0.02), and BAL PA activity (p less than 0.001) compared to the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
Mineralogic correlates of fibrosis in chrysotile miners and millers. A. Churg, J.L. Wright, L. DePaoli, et al. 1989;139(4):891-6. PubMed · Publisher

Abstract

To determine which mineral parameters relate to the degree of interstitial fibrosis (asbestosis) in the lungs of chrysotile miners and millers, we graded fibrosis histologically and correlated fibrosis grades with fiber concentration and mean size, surface area, and mass, and with total sample fiber length, surface area, and mass in 21 cases. A positive correlation of fibrosis grade with tremolite concentration and a lesser correlation with chrysotile concentration was found for whole lungs, specific sites within lungs, and, for tremolite, single microscopic fields. No correlations were found for measures of chrysotile fiber size, surface area, or mass, but tremolite mean fiber length, aspect ratio, and surface area were, surprisingly, negatively correlated with fibrosis grade. Measures based on total rather than on mean case or site parameters failed to show correlations with fibrosis. We conclude that: (1) degree of pulmonary fibrosis reflects fiber concentration at both a bulk and a microscopic level; (2) mean fiber length and parameters related to mean fiber length also correlate with fibrosis grade, but, contrary to predictions from animal studies, this correlation is negative, suggesting that short fibers may be more important in the genesis of pulmonary fibrosis than is commonly believed; (3) there is no evidence that parameters such as total fiber length, surface area, or mass provide predictors of degree of fibrosis.
Morphologic characterization of alveolar macrophages from subjects with occupational exposure to inorganic particles. T. Takemura, W.N. Rom, V.J. Ferrans, et al. 1989;140(6):1674-85. PubMed · Publisher

Abstract

Alveolar macrophages recovered by bronchoalveolar lavage from 43 nonsmoking or greater than 5-yr ex-smoking subjects with occupational exposure to inorganic particles (asbestos, n 1/2 19; silica, n 1/2 10; coal, n 1/2 14) were evaluated by light microscopy and transmission and scanning electron microscopy to determine the morphologic changes resulting in these cells from chronic inorganic particulate inhalation. Alveolar macrophages from dust-exposed subjects, including those who had been free of exposure to particles for more than 1 yr, contained particles of higher proportion than did those of normal unexposed subjects. Most of these particles were located within phagolysosomes. The frequency of multinucleated alveolar macrophages was significantly higher in the dust-exposed groups. Ultrastructural studies showed alterations of the morphologic aspects of the surfaces of alveolar macrophages from the dust-exposed subjects, including increased numbers of rufflings, filopodia, pinocytotic vesicles, subplasmalemmal linear densities, and increased frequency of macrophage-macrophage and macrophage-lymphocyte interactions. Furthermore, the numbers of lysosomes were significantly increased in alveolar macrophages from the dust-exposed subjects. Together, these morphologic changes are consistent with the sequelae of phagocytosis, and they emphasize both the role of alveolar macrophages in eliminating inorganic particles from the alveolar spaces and the consequences this role has in alveolar macrophage activation.
Pleural mesothelial cells stimulated by asbestos release chemotactic activity for neutrophils in vitro. V.B. Antony, C.L. Owen, K.J. Hadley. 1989;139(1):199-206. PubMed · Publisher

Abstract

The development of the pleural inflammatory response to asbestos remains poorly defined. Importantly, the role of the pleural mesothelial cell in recruitment of neutrophils to the pleural space is not known. We hypothesized that rabbit pleural mesothelial cells stimulated by asbestos fibers release chemotactic factor(s) for neutrophils. Primary cultures of rabbit pleural mesothelial cells were established, and their purity verified by the presence of keratin and hyaluronic acid mucin. Mesothelial cells in serum-free media, in the presence of 30 micrograms/ml of crocidolite asbestos, released chemotaxins for neutrophils. This activity was not dependent on the type of asbestos fiber or fiber length. It was dose-dependent until 30 micrograms/ml of asbestos. The chemotactic fractions had the ability to increase both directed and random migration of neutrophils. The chemotactic activity was not present in sonicated fractions of unstimulated mesothelial cells, nor in supernates of asbestos fibers alone. Characterization of the chemotactic activity showed that it was heat stable (56 degrees C per 30 min) and sensitive to digestion with trypsin and papain. On Sephadex G-50 chromatography, it had a molecular weight between 6,000 and 9,000. Production of the chemotactic activity was inhibitable by cycloheximide. These results demonstrate that pleural mesothelial cells can actively synthesize a protein fraction with chemotactic activity for neutrophils. Production of this mesothelial cell-derived chemotactic activity for neutrophils may play an important role in the initiation of the inflammatory response of the pleura to asbestos.
Rapid short-term clearance of chrysotile compared with amosite asbestos in the guinea pig. A. Churg, J.L. Wright, B. Gilks, et al. 1989;139(4):885-90. PubMed · Publisher

Abstract

Compared with amphibole forms of asbestos, chrysotile asbestos fails to accumulate in lung tissue; the mechanism of this effect is disputed. To investigate this problem, we administered a mixture of the amphibole, amosite, and chrysotile to guinea pigs by intratracheal instillation. At 1 day, 1 week, and 1 month after instillation, animals were killed, and the numbers, types, sizes, and compositions of fibers in the lungs were determined by analytical electron microscopy. Both chrysotile and amosite fiber concentrations decreased with time, but relative chrysotile clearance was significantly greater than amosite clearance. There was no evidence of magnesium leaching from chrysotile fibers of any size at any time. Analysis of fiber lengths and widths showed a time trend toward shorter and narrower fibers (particularly toward fibers of less than 2 microns long and less than 0.025 microns wide) for chrysotile. This effect was not seen for amosite. We conclude that (1) failure of chrysotile accumulation in lung results from preferential chrysotile clearance during the first few days to weeks after exposure; (2) there is no evidence that fiber dissolution plays a role in chrysotile clearance; (3) preferential clearance may be a result of fragmentation and rapid removal of chrysotile fibers.
A retrospective cohort study of lung cancer and diesel exhaust exposure in railroad workers. E. Garshick, M.B. Schenker, A. Muñoz, et al. 1988;137(4):820-5. PubMed · Publisher

Abstract

The risk of lung cancer as a result of exposure to diesel exhaust from railroad locomotives was assessed in a cohort of 55,407 white male railroad workers 40 to 64 yr of age in 1959 who had started railroad service 10 to 20 years earlier. The cohort was traced until the end of 1980, and death certificates were obtained for 88% of 19,396 deaths; 1,694 lung cancer cases were identified. Yearly railroad job from 1959 to death or retirement was available from the Railroad Retirement Board, and served as an index of diesel exhaust exposure. Directly standardized rates and a proportional hazards model were used to calculate the relative risk of lung cancer based on work in a job with diesel exhaust exposure beginning in 1959. A relative risk of 1.45 (95% CI = 1.11, 1.89) for lung cancer was obtained in the group of workers 40 to 44 yr of age in 1959, the group with the longest possible duration of diesel exposure. The cohort was selected to minimize the effect of past railroad asbestos exposure, and analysis with workers with possible asbestos exposure excluded resulted in a similarly elevated risk. Workers with 20 yr or more elapsed since 1959, the effective start of diesel exposure for the cohort, had the highest relative risk. These results taken in conjunction with other reported results support the hypothesis that occupational exposure to diesel exhaust results in a small but significantly elevated risk for lung cancer.
Asbestos bodies in bronchoalveolar lavage fluid and in lung parenchyma. P. Sebastien, B. Armstrong, G. Monchaux, et al. 1988;137(1):75-8. PubMed · Publisher

Abstract

Numerical concentrations of asbestos bodies (AB) were measured by light microscopy both in samples of bronchoalveolar lavage (BAL) fluid and in samples of lung parenchyma from 69 patients with suspected asbestos-related diseases who had had lavages and later open lung biopsies or autopsies. Objectives were to study the recovery of pulmonary AB by BAL and the ability of BAL concentrations to predict parenchymal concentrations. BAL and parenchymal concentrations were both spread over 6 orders of magnitude and were positively correlated (r = 0.74 between logarithmic values). It is believed that, by a process of progressive elution, AB firmly adherent to the alveolar wall become suspended in BAL fluid; such suspended bodies represent roughly 2% of all the bodies stored in the portion of lung lavaged. Recovery is associated with great interindividual variations. When a measured BAL concentration exceeds 1 AB/ml, it can be quite confidently predicted, however, that the parenchymal concentration is in excess of 1,000 AB/g and that the patient has experienced a nontrivial asbestos exposure.
Asbestos-induced endothelial cell activation and injury. Demonstration of fiber phagocytosis and oxidant-dependent toxicity. J.G. Garcia, L.D. Gray, R.F. Dodson, et al. 1988;138(4):958-64. PubMed · Publisher

Abstract

Vascular endothelial cell injury is important in the development of a variety of chronic interstitial lung disorders. However, the involvement of such injury in the inflammatory response associated with the inhalation of asbestos fibers is unclear and the mechanism of asbestos fiber cytotoxicity remains unknown. In the present study, human umbilical vein endothelial cells were challenged with amosite asbestos and several parameters of cellular function were examined. Electron microscopic examination revealed that endothelial cell exposure to asbestos resulted in active phagocytosis of these particulates. Biochemical evidence of dose-dependent asbestos-mediated endothelial cell activation was indicated by increased metabolism of arachidonic acid. For example, amosite asbestos (500 micrograms/ml) produced a ninefold increase in prostacyclin (PGI2) levels over those levels in non-exposed cells. Incubation of human endothelial cells with asbestos fibers induced specific 51Cr release in both a dose- and time-dependent fashion indicative of cellular injury. Injury induced by amosite asbestos was not significantly attenuated by treatment of the endothelial cell monolayer with either the iron chelator deferoxamine, which prevents hydroxyl radical (.OH) formation, or by the superoxide anion (O2-) scavenger, superoxide dismutase. However, significant dose-dependent protection was observed with the hydrogen peroxide (H2O2) scavenger, catalase. Chelation of elemental iron present within amosite asbestos fibers by deferoxamine produced a 33% reduction in asbestos cytotoxicity, suggesting a potential role for hydroxyl radical-mediated injury via the iron-catalyzed Haber-Weiss reaction.(ABSTRACT TRUNCATED AT 250 WORDS)
Effect of tobacco smoking on the presence of asbestosis at postmortem and on the reading of irregular opacities on roentgenograms in asbestos-exposed workers. E. Hnizdo, G.K. Sluis-Cremer. 1988;138(5):1207-12. PubMed · Publisher

Abstract

A statistically significant association between cigarette smoking and radiologic readings of irregular opacities was observed in a case-control study of 430 South African asbestos miners (OR = 3.03; 95% confidence interval, 1.50; 6.11). In another case-control study of 487 dead South African asbestos miners, no positive association between smoking and autopsy findings for asbestosis was observed (OR = 0.50; 95% confidence interval, 0.20; 1.29). The association between greater than slight asbestosis (moderate and marked) and smoking (yes/no) was not significant (Fisher's exact test, p = 0.44), and the adjusted odds ratio was 1.25 with 95% confidence interval (0.20; 7.78). In addition, the certification in life for asbestosis, based on chest roentgenogram readings for irregular opacities, was also found to have a tendency to be related to smoking. Thus, the findings of these studies do not support the hypothesis that smoking is associated with the presence of asbestosis at autopsy or that smoking and asbestos dust act synergistically in producing asbestosis at autopsy. But the findings of this and other studies suggest that smoking does produce some change in the lung structure that can be visible on the roentgenogram and can be wrongly interpreted as irregular opacities caused by asbestosis.
Effects of cigarette smoke on tissue uptake and retention of iron oxide in the guinea pig. B. Gilks, J. Wright, A. Churg. 1988;137(6):1382-4. PubMed · Publisher

Abstract

We have previously shown that cigarette smoke increases retention and tissue penetration of asbestos, a pathogenic dust. To determine whether these same phenomena occur with an inert dust, we administered iron oxide particles to guinea pigs by intratracheal instillation. Half of the animals were exposed to cigarette smoke. Animals were killed at 1 day, 1 wk, and 1 month. Numbers of particles in airway epithelia and walls were counted in histologic sections of one lung, and the other lung was analyzed chemically for iron content. In both smoke-exposed and nonexposed groups, the chemically determined concentration of iron in the lung tissue decreased between 1 day and 1 month; however, the concentration of iron was significantly greater in the smoke-exposed group at 1 day and 1 wk. By 1 month, there was no significant difference between the 2 groups. The number of particles in the epithelia of respiratory bronchioles also decreased in both smoke-exposed and nonexposed groups between 1 day and 1 month, but the smoke-exposed group had significantly more intraepithelial particles at 1 day and 1 wk than did the nonexposed group. The number of particles in the walls of respiratory bronchioles increased between 1 day and 1 month in both smoke-exposed and nonexposed groups; the difference between these groups was significant only at 1 wk, when airway walls of the smoke-exposed animals contained more particles.(ABSTRACT TRUNCATED AT 250 WORDS)
Lung function impairment as a guide to exercise limitation in work-related lung disorders. J.E. Cotes, J. Zejda, B. King. 1988;137(5):1089-93. PubMed · Publisher

Abstract

The hypothesis that exercise limitation of respiratory origin can be predicted accurately from the lung function impairment has been tested using maximal oxygen uptake (VO2max) as the dependent variable in a multiple regression analysis. The subjects were 157 men who met objective criteria for exercise being limited by respiratory impairment. VO2max (mean value, 1.38 L min-1) was described by FEV1 and single-breath lung transfer factor (diffusing capacity) for carbon monoxide (TL') singly or in combination, but the accuracy was poor (at best, standard error of the estimate, 0.36 L min-1; r2, 29.1%). FEV1 could be replaced by FVC and FEV1/FVC. Description of VO2max was improved by also including in the equation the variables age, fat-free mass, and submaximal exercise ventilation (VE). Transfer factor did not then contribute significantly. VO2max as percent of predicted (mean value of 60%) was described by %FVC or %FEV1, but the accuracy was poor (SEE, 16.0%; r2, 14%). Prediction was improved somewhat by the alternative use of inspiratory vital capacity and FEV1/FVC. Transfer factor did not contribute additional information; however, inclusion of VE materially improved the accuracy (SEE, 12.9%; r2, 44%). Among a subgroup of 35 men whose lung disease was due to asbestos, %TL' or transfer factor measured using a multibreath estimate of residual volume (%TLCO) made a small contribution to the explained variance, e.g.: %VO2max = 0.44% FEV1 -0.78 VE + 0.16% TLCO + 52.3 SEE 7.27%. This equation also described the %VO2max of all subjects (SEE, 13%).(ABSTRACT TRUNCATED AT 250 WORDS)
The relation among pulmonary function, chest roentgenographic abnormalities, and smoking status in an asbestos-exposed cohort. L. Rosenstock, S. Barnhart, N.J. Heyer, et al. 1988;138(2):272-7. PubMed · Publisher

Abstract

To clarify the clinical value of the International Labor Office (ILO) roentgenographic classification of pneumoconiosis in assessing asbestos-exposed persons, we determined the relationships among spirometric values, radiographic evidence of parenchymal pulmonary fibrosis and/or pleural thickening, and cigarette smoking history in 684 consecutively enrolled male plumbers and pipefitters participating in a larger cross-sectional prevalence study. The subjects were mainly marine pipefitters (35%), plumbers (24%), and steamfitters/welders (23%); 28% had never smoked, 39% were ex-smokers, and 33% currently smoked cigarettes. Mean values for FVC and FEV1 were 95.0 and 91.9% of predicted, respectively, with mean FEV1/FVC ratio 77.7%; by standard criteria, 7.8% had restrictive impairment, and 21.7%, obstructive defects. Chest radiographs were normal in 63% and showed pleural abnormalities only in 17%, parenchymal abnormalities only in 7%, and both pleural and parenchymal abnormalities in 12%. Both FVC and FEV1 correlated with the degree of small opacity profusion, as assessed by ILO grade. Pleural abnormalities were associated with lower FVC values, independently of ILO profusion grade for Grades less than or equal to 1/0, and were unexplained by smoking status. In addition, there was a positive association between smoking history and degree of ILO parenchymal abnormality, particularly in those with the heaviest cumulative smoking history. Our results suggest that the ILO classification of pneumoconiosis, although a useful epidemiologic tool, should be applied with caution in persons with asbestos exposure, and that pleural abnormalities may be associated with physiologic impairment in such persons.
A case-control study of lung cancer and diesel exhaust exposure in railroad workers. E. Garshick, M.B. Schenker, A. Muñoz, et al. 1987;135(6):1242-8. PubMed · Publisher

Abstract

A case-control study of deaths among U.S. railroad workers was conducted to test the hypothesis that lung cancer is associated with exposure to diesel exhaust. Employed and retired male workers with greater than or equal to 10 yr of service who were born on or after January 1, 1900 and who died between March 1, 1981 and February 28, 1982 were eligible. We collected 87% of the death certificates from 15,059 deaths reported to the U.S. Railroad Retirement Board (RRB). Cases of lung cancer (1,256) were matched to controls by age (+/- 2.5 yr) and date of death (+/- 31 days). Potential exposure to diesel exhaust was assigned based on an industrial hygiene evaluation of jobs and work areas. Each subject's work history was determined from a yearly job report filed by his employer with the RRB from 1959 until death or retirement. Asbestos exposure prior to 1959 was categorized by the job held in 1959, the end of the steam locomotive era, or by the last job held if retirement occurred before 1959. Smoking histories were obtained by questionnaire from next of kin. Using multiple conditional logistic regression analysis to adjust for smoking and asbestos exposure, workers 64 yr of age or younger at the time of death with work in a diesel exhaust exposed job for 20 yr had a significantly increased relative odds (odds ratio = 1.41, 95% Cl = 1.06, 1.88) of lung cancer. No effect of diesel exhaust exposure was seen in workers 65 yr of age or older because many of these men retired shortly after the transition to diesel-powered locomotives.(ABSTRACT TRUNCATED AT 250 WORDS)
Asbestos-related mesothelioma risk among railroad workers. M. Huncharek. 1987;135(4):983-4. Letter PubMed · Publisher
Changes in autacoid and neuropeptide contents of lung cells in asbestos-induced pulmonary fibrosis. R. Day, S. Lemaire, D. Nadeau, et al. 1987;136(4):908-15. PubMed · Publisher

Abstract

The purpose of this study was to determine if asbestos-induced pulmonary fibrosis in the rat can affect the levels of autacoids and peptides in freshly isolated lung cells. Lung fibrosis was experimentally induced in rats by a single intratracheal instillation of 5 mg UICC Canadian chrysotile B fibers. Isolated lung cells were prepared from normal and from asbestos-exposed rats. These cells were also fractionated on bovine serum albumin (BSA) gradients. The contents of serotonin (5-HT), histamine (HIST), vasoactive intestinal peptide (VIP), and bombesin (BN) were measured in isolated total cell preparations as well as in density-fractionated cell populations from normal and from asbestos-exposed rats. Analysis of total lung cell preparation showed the presence of heterogeneous populations in normal rat lung. After asbestos exposure, there were significant changes in these cell populations as evidenced by significant increases in lymphocyte and mast cell numbers. In addition, increased levels of 5-HT, HIST, and VIP were observed in isolated lung cells obtained from rats exposed to asbestos 1, 3, and 6 months after instillation. BN content was unchanged 3 months after treatment, but was significantly increased at the 6 month-interval, suggesting a different pattern of response for this neuropeptide. Density fractionation of various cell populations further showed selective changes in specific cell fractions of lung after asbestos exposure. At 6 months, increased levels of 5-HT, HIST, and VIP were associated with cell fraction 7, whereas changes in BN content were found in cell fractions 2 and 3. Similarly, there was a significant increase of mast cells in fraction 7 at the 6-month interval.(ABSTRACT TRUNCATED AT 250 WORDS)
Characterization of the lower respiratory tract inflammation of nonsmoking individuals with interstitial lung disease associated with chronic inhalation of inorganic dusts. W.N. Rom, P.B. Bitterman, S.I. Rennard, et al. 1987;136(6):1429-34. PubMed · Publisher

Abstract

The pneumoconioses, interstitial lung disorders resulting from the inhalation of inorganic dusts, are associated with chronic inflammatory processes in the lower respiratory tract. To characterize these inflammatory processes in relation to the pathogenesis of these disorders, we studied 39 nonsmoking individuals with long-term occupational exposures to inorganic dust and functional evidence of interstitial disease (asbestosis, n = 18; coal workers' pneumoconiosis, n = 15; silicosis, n = 6). In all 3 disorders, the inflammation was dominated by alveolar macrophages. Because a common feature of these interstitial lung diseases is concurrent injury and fibrosis of alveolar walls, we assessed whether these alveolar macrophages were spontaneously releasing mediators capable of giving rise to these changes. Alveolar macrophages from the study population were spontaneously releasing increased amounts of superoxide anion and hydrogen peroxide (both p less than 0.01 compared to normals), oxidants capable of injuring lung parenchymal cells. The alveolar macrophages were also spontaneously releasing significantly increased amounts of fibronectin and alveolar macrophage-derived growth factor (both p less than 0.01 compared to normals), mediators that act synergistically to signal fibroblast replication. Taken together, these findings define a major role for the alveolar macrophage in mediating the alveolar wall injury and fibrosis that characterize the common pneumoconioses and suggest that the alveolar macrophage is an important "target" for developing strategies designed to prevent loss of lung function in these individuals.
Cigarette smoke makes airway and early parenchymal asbestos-induced lung disease worse in the guinea pig. V. Tron, J.L. Wright, N. Harrison, et al. 1987;136(2):271-5. PubMed · Publisher

Abstract

In order to assess the effects of cigarette smoke and asbestos exposure, we divided guinea pigs into 4 groups: smoking or nonsmoking, and asbestos-exposed or not asbestos-exposed groups. Asbestos-exposed animals were given a single intratracheal instillation of 5 mg UICC amosite, a dose and method of administration that we have previously shown produces morphologic changes in the small airways as well as minimal interstitial fibrosis. Animals were smoked 5 days per week for 6 months. By itself, smoking did not affect lung collagen content, small airways wall thickness, or the volume fraction of tissue surrounding airways, but it did cause a significant increase in alveolar mean linear intercept (Lm). Asbestos alone increased collagen content, airway wall thickness, and tissue volume fraction surrounding airways, the latter measure used to assess interstitial fibrosis. An unexpected finding was that asbestos also increased Lm. The two agents administered together caused more severe changes of all types than were produced by either agent alone, and the interaction between the 2 was generally synergistic. Smoke-exposed animals retained 3 times the asbestos fiber burden of those not smoke-exposed; the increase in retention was greater for short than for long fibers. We conclude that cigarette smoke can potentiate the fibrosis induced by asbestos, possibly because of increased fiber retention. As well, in this model, asbestos or asbestos plus cigarette smoke produces increases in alveolar size.(ABSTRACT TRUNCATED AT 250 WORDS)
Diagnostic value of asbestos bodies in bronchoalveolar lavage fluid. P. De Vuyst, P. Dumortier, E. Moulin, et al. 1987;136(5):1219-24. PubMed · Publisher

Abstract

Asbestos bodies (AB) were counted by light microscopy in bronchoalveolar lavage (BAL) fluid obtained from 563 subjects. The presence of AB was found to reflect occupational exposure to asbestos and was rarely found in unexposed control subjects at concentrations above 1/ml of fluid (6.9% of white collar workers and 17.8% of blue collar workers). The overlap of results observed between subjects with definite exposure and those without underlines the difficulty in assessing exposure by questioning alone, which leads to underestimations or even overestimations of the risk. The highest counts (log mean, 120.5 AB/ml; range, 0 to 42,600) were found in patients with radiologic evidence of asbestosis, most likely reflecting the known association of this disease with retention of large amounts of long amphiboles, rather than in patients with pleural disease. A considerable overlap of results was also observed between groups with different diseases or without any apparent disease. Apart from uncertainties in the radiologic diagnosis, this may be explained by differences in latency since first exposure, in individual response to asbestos inhalation, or in pathogenic properties of different asbestos types. Because the presence of AB in BAL fluid appears to be a marker of exposure and not of disease, AB are more likely to be detected in patients presenting with asbestos-related diseases but in whom exposure is not confirmed by the occupational history (65 of 78 cases).
Evaluation of breathlessness in asbestos workers. Results of exercise testing. P. Agostoni, D.D. Smith, R.B. Schoene, et al. 1987;135(4):812-6. PubMed · Publisher

Abstract

We studied 120 asbestos-exposed workers seeking compensation for asbestos-related ventilatory impairment who were referred to us for evaluation of their complaint of dyspnea. We reviewed history, chest radiographs, pulmonary function studies, and exercise tests. The workers were 59.9 +/- 9.5 (mean +/- SD) yr of age and their first asbestos exposure had been 34.4 +/- 10 yr prior to the study; 63% were smokers, 19% were ex-smokers, and 18% were nonsmokers. Chest radiographs were normal in 4%, showed only pleural disease in 35%, only parenchymal diseases in 5%, and pleuroparenchymal disease in 56%. Restrictive pulmonary function abnormalities were present in 25% of the workers, and obstructive abnormalities were present in 27%. Because the impairment of one of several organ systems (i.e., ventilatory, cardiac, pulmonary vascular, or peripheral circulatory) may limit exercise performance, we designed an exercise test score in an attempt to identify the system causing the limitation. No abnormal limitation was detectable in half (49.2%) of the subjects. Only 26% had a ventilatory limitation, which was much more frequent in smokers (32%) than in nonsmokers (9%) (p less than 0.05). Unexpectedly, rather more (37%) had a cardiac rather than a ventilatory limitation. We conclude that the complaint of dyspnea in these asbestos-exposed workers was usually not caused by a ventilatory dysfunction.
Mechanisms of macrophage accumulation in the lungs of asbestos-exposed subjects. J.R. Spurzem, C. Saltini, W. Rom, et al. 1987;136(2):276-80. PubMed · Publisher

Abstract

Chronic asbestos exposure is associated with the accumulation of mononuclear phagocytes in the lower respiratory tract. This process can be both protective and injurious, since macrophages can aid in asbestos clearance yet also modulate structural derangements of the alveolar walls. To understand why macrophages accumulate in the lungs of asbestos-exposed persons, 2 possible mechanisms were evaluated using alveolar macrophages from subjects with histories of chronic high exposure to airborne asbestos: enhanced recruitment of blood monocytes to the lung, and an increased rate of replication of macrophages in situ. Monoclonal antibody analysis with antibodies that detect surface antigens on the majority of circulating blood monocytes but only on a minority of mature alveolar macrophages demonstrated that an increased proportion of alveolar macrophages of asbestos workers expressed monocyte lineage antigens, suggesting the presence of "young" newly recruited macrophages and thus enhanced recruitment. Culture of the alveolar macrophages from these subjects with [3H]thymidine followed by autoradiography demonstrated an increased proportion of alveolar macrophages synthesizing DNA, suggesting the macrophages are replicating at an increased rate in situ. These observations are consistent with the concept that both enhanced recruitment of blood monocytes and increased local proliferation of alveolar macrophages contribute to the accumulation mononuclear phagocytes in the lung of persons with chronic asbestos exposure.
Sialic acid mediates the initial binding of positively charged inorganic particles to alveolar macrophage membranes. J.E. Gallagher, G. George, A.R. Brody. 1987;135(6):1345-52. PubMed · Publisher

Abstract

Pulmonary macrophages phagocytize inhaled particles and are postulated to play a role in the development of pulmonary interstitial fibrogenesis. The basic biologic mechanisms through which inhaled particles bind to macrophage membranes and subsequently are phagocytized remain unclear. We hypothesize that positively charged particles bind to negatively charged sialic acid (SA) residues on macrophage membranes. Alveolar Macrophages (AM) were collected by saline lavage from normal rat lungs. The cells adhered to plastic coverslips in serum-free phosphate buffered saline at 37 degrees C for 45 min and then were maintained at 4 degrees C for the binding experiments. Even distribution of SA groups on AM surfaces was demonstrated by scanning electron microscopy of wheat germ agglutinin (WGA) conjugated to 50 nm gold spheres. The WGA is a lectin that binds specifically to sialic acid, and pretreatment of AM with this lectin prevented the binding of positively charged carbonyl iron (C-Fe) spheres, aluminum (Al) spheres, and chrysotile asbestos fibers to AM surfaces. Limulus protein, another lectin with binding specificity for SA, similarly blocked the binding of positively charged spheres and chrysotile asbestos fibers but not negatively charged glass spheres or crocidolite asbestos fibers. Con A and ricin, lectins that bind to mannose and galactose residues, respectively, did not block particle binding. When both positively charged iron spheres and negatively charged glass spheres were prebound to AM membranes, subsequent treatment with WGA displaced only the positively charged spheres from macrophage surfaces. Con A and ricin had no effect on prebound positively charged C-Fe and Al spheres.(ABSTRACT TRUNCATED AT 250 WORDS)
The diagnosis of nonmalignant diseases related to asbestos. R.L. Murphy. 1987;136(6):1516-7. Letter PubMed · Publisher
The diagnosis of nonmalignant diseases related to asbestos. A. Franzblau, R. Lilis. 1987;136(3):790-1. Letter PubMed · Publisher
The role of exercise testing in impairment evaluation. A. Oren, D.Y. Sue, J.E. Hansen, et al. 1987;135(1):230-5. PubMed · Publisher

Abstract

To examine the usefulness of exercise testing in impairment evaluation, we reviewed the evaluation of 348 asbestos-exposed shipyard workers. We compared work capacity predicted from history, physical examination, chest roentgenogram, resting electrocardiogram, and resting pulmonary function tests with measured work capacity during an incremental cycle exercise test. The predicted work capacity was often incorrect when compared with measured maximal oxygen uptake (VO2). One third (22 of 66) of those predicted to have reduced work capacity had normal measured work capacity, and 46 of 148 workers (31%) predicted to have normal work capacity were found to have low maximal VO2 during exercise. Of 134 men for whom predicted work capacity was uncertain, maximal VO2 during exercise was low in 49 (37%), normal in 81 (60%), and remained indeterminate in 4 (3%). Thus, of the 138 workers who had low measured VO2, 43 were correctly predicted to have normal work capacity, 46 were incorrectly predicted, and the prediction was uncertain in 49. Only a few were limited by respiratory disease, and cardiovascular disorders limited 69% of those with a low maximal VO2 during exercise. Accordingly, resting VC, FEV1, and DLCO had a poor correlation with exercise performance. Finally, we found that resting DLCO was a poor predictor of abnormal exercise AaPO2, dead-space/tidal volume ratio, or arterial end-tidal PCO2 difference. We conclude that exercise testing is needed for accurate work capacity assessment in impairment evaluation. Exercise testing also facilitates the identification of the major limiting system in those with low work capacity.
A population-based case-control study of mesothelioma deaths among U.S. railroad workers. M.B. Schenker, E. Garshick, A. Muñoz, et al. 1986;134(3):461-5. PubMed · Publisher

Abstract

We have completed a case-control analysis of mesothelioma deaths among current and retired U.S. railroad employees. Cause-specific death certificates were obtained for 87% of 15,059 deaths reported by the railroad retirement board, and 20 mesotheliomas were identified according to death certificate diagnosis. A 10:1 matched analysis with railroad workers dying of nonmalignant, nonaccidental causes yielded a very strong association with prior railroad work in jobs with potential asbestos exposure (odds ratio = 7.2, 95% lower confidence limit = 3.3). Consideration of railroad occupations with regular asbestos exposures (e.g., skilled trades, steam locomotive repair) yielded an odds ratio of 21.4 (95% lower confidence limit = 8.7), but the occupations with potential intermittent exposure (e.g., engineers, firemen, carmen) yielded a nonsignificant odds ratio of 2.3 (95% lower confidence limit = 0.5). Applying mesothelioma mortality rates from this study to the population of U.S. railroad workers at risk yields an estimate of 416 cases of mesothelioma occurring among U.S. railroad workers between 1981 and 2000.
Alternative partial respiratory disability rating schemes. P. Harber. 1986;134(3):481-7. PubMed · Publisher

Abstract

There is no standardized method for rating "percentage partial disability" for persons with respiratory impairment of a degree less than totally disabling. Twelve alternative schemes for using results of clinical physiologic testing for "rating" partial respiratory disability are compared by examining their effects on "ratings" of 650 actual asbestos lung disease compensation claimants. The schemes differ by basis (function remaining or function lost), presence of a quantitative "threshold," and "standard" for comparison; some estimate future disability rather than current. Large differences in performance between schemes were noted. The average ratings ranged from 17 to 57 "% Disability." The relative effects on subjects with high versus low degree of physiologic impairment differed between rating schemes. The ratings were different for subjects with different patterns of physiologic abnormality.
American Thoracic Society. Medical Section of the American Lung Association: The diagnosis of nonmalignant diseases related to asbestos. 1986;134(2):363-8. PubMed · Publisher
Asbestos exposure and retention as determinants of airway disease and asbestos alveolitis. R. Bégin, S. Massé, P. Sébastien, et al. 1986;134(6):1176-81. PubMed · Publisher

Abstract

To evaluate the relationships of asbestos exposure, retention, airway response, and the asbestos alveolitis, we exposed 2 groups of sheep every 2 wk for 3 yr to either 100 ml phosphate-buffered saline (PBS) or 100 mg UICC chrysotile fibers in 100 ml PBS. The sheep were evaluated periodically by pulmonary function tests (PFT), chest radiograph (CR), bronchoalveolar lavage (BAL), and transbronchial lung biopsy (TLB). At Month 24 of the study, all asbestos-exposed sheep had significant increases in lung resistance and upstream resistance. However, only 9 of the 16 asbestos-exposed sheep had significant changes in TLB, CR, Cst, and VC, which clearly separated them from the other 6 sheep in these parameters. The 2 groups, however, had similar air-flow limitation. At lung biopsy, all asbestos-exposed sheep had significant peribronchiolar fibrosis, with significant alveolitis only in the group of 9 sheep with radiographic and functional changes of early asbestosis. The 9 sheep also had significant changes in BAL cellularity and biochemical profile, which differentiated them from the other 6 asbestos-exposed sheep. Analysis of BAL fiber content at that point revealed that despite identical exposure, the group with interstitial lung disease had significantly more fiber retention (p less than 0.01). The data demonstrate that whereas asbestos airway disease appears to be primarily an exposure-dose-related response, the lung response appears to be more closely related to alveolar retention of the dust.
Asbestos exposure--quantitative assessment of risk. J.M. Hughes, H. Weill. 1986;133(1):5-13. Review PubMed · Publisher

Abstract

Methods for deriving quantitative estimates of asbestos-associated health risks are reviewed and their numerous assumptions and uncertainties described. These methods involve extrapolation of risks observed at past relatively high asbestos concentration levels down to usually much lower concentration levels of interest today--in some cases, orders of magnitude lower. These models are used to calculate estimates of the potential risk to workers manufacturing asbestos products and to students enrolled in schools containing asbestos products. The potential risk to workers exposed for 40 yr to 0.5 fibers per milliliter (f/ml) of mixed asbestos fiber type (a permissible workplace exposure limit under consideration by the Occupational Safety and Health Administration (OSHA) ) are estimated as 82 lifetime excess cancers per 10,000 exposed. The risk to students exposed to an average asbestos concentration of 0.001 f/ml of mixed asbestos fiber types for an average enrollment period of 6 school years is estimated as 5 lifetime excess cancers per one million exposed. If the school exposure is to chrysotile asbestos only, then the estimated risk is 1.5 lifetime excess cancers per million. Risks from other causes are presented for comparison; e.g., annual rates (per million) of 10 deaths from high school football, 14 from bicycling (10-14 yr of age), 5 to 20 for whooping cough vaccination. Decisions concerning asbestos products require participation of all parties involved and should only be made after a scientifically defensible estimate of the associated risk has been obtained. In many cases to date, such decisions have been made without adequate consideration of the level of risk or the cost-effectiveness of attempts to lower the potential risk.
Correlation of bronchoalveolar lavage and clinical and functional findings in asbestosis. J.C. Yernault, P. De Vuyst, P. Dumortier. 1986;134(6):1335-6. Letter PubMed · Publisher
Cytokine regulation of lung fibroblast proliferation. Pulmonary and systemic changes in asbestos-induced pulmonary fibrosis. I. Lemaire, H. Beaudoin, C. Dubois. 1986;134(4):653-8. PubMed · Publisher

Abstract

A complex series of interactions between immunocompetent cells and fibroblasts exists. Because pulmonary fibrosis may result from an increased number of collagen-producing fibroblasts, we studied the production of fibroblast growth factors derived from alveolar macrophages (AM) and peripheral blood mononuclear leukocytes (PBML) during the development of asbestos-induced fibrosis. Three groups of rats received, respectively, a single intratracheal injection of saline (control), 5 mg of asbestos, and 10 mg of asbestos. Bronchoalveolar lavage (BAL) and PBML isolation were performed on each animal 1, 3, and 6 months after instillation. Differential cell analyses revealed no significant change in the BAL cell populations except for a small but significant increase in the proportion of lymphocytes in the 10-mg group at 1 month and in both asbestos groups at 3 months. Similar analyses of PBML revealed only a small reduction in total PBML in the 10-mg group at 6 months. Bronchoalveolar cells (98% AM) from control rats spontaneously released a fibroblast growth factor (FGF), whereas Con-A-stimulated PBML of the same animals produced fibroblast growth inhibitory activity (FGIF). One month after asbestos exposure, when fibrotic lesions were apparent, AM production of FGF was significantly enhanced, and such increase persisted for as long as 6 months. By contrast, no significant change in FGIF production by Con-A-stimulated PBML was seen at the 1-month interval. However, 3 months after exposure, there was a significant suppression of FGIF production by PBML from rats in the 10-mg group and at 6 months by PBML from rats in both asbestos groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Dental technician's pneumoconiosis. A report of two cases. P. De Vuyst, R. Vande Weyer, A. De Coster, et al. 1986;133(2):316-20. Case report PubMed · Publisher

Abstract

Diagnosis of pneumoconiosis was made in 2 dental technicians presenting with interstitial lung disease. The occupational origin of inhaled dust was confirmed by mineralogic analyses, which disclosed mainly large amounts of chromium-cobalt-molybdenum particles originating from Vitallium prostheses, but also showed abrasives (silica and silicon carbide) and asbestos in 1 patient. The presence of Vitallium and its chemical stability in bronchoalveolar lavage and lung several years after cessation of exposure confirm the resistance of this alloy to corrosion by body fluids. This contrasts with the high solubility of cobalt described in cobalt or hard metal disease. We suggest that dental technician's pneumoconiosis is a complex pneumoconiosis distinct from silicosis, asbestosis, or hard metal disease and that Cr-Co-Mo alloys play a role in its pathogenesis.
Lung asbestos content in long-term residents of a chrysotile mining town. A. Churg. 1986;134(1):125-7. PubMed · Publisher

Abstract

The effects of long-term exposure to very small amounts of chrysotile asbestos are controversial. To examine this problem, the lung asbestos content from 7 long-term (25 yr and greater) residents of Thetford Mines, Quebec, who were never employed in the chrysotile mining and milling industry, was analyzed. Thetford Mines is a chrysotile mining town with a demonstrated ambient atmospheric concentration of chrysotile asbestos approximately 200 to 500 times that in urban areas of North America. Data on the residents' lungs were compared with those obtained from 20 long-term (25 yr and greater) chrysotile industry workers from Thetford Mines and 20 members of the general population of Vancouver. The median concentrations of chrysotile and tremolite in the Thetford residents were only about one fiftieth of those of the chrysotile workers, but about 10 times that of the population of Vancouver. Because long fibers of asbestos are generally thought to be more dangerous than short ones are, the sizes of fibers from these 3 groups were also examined. The fiber size distribution of the asbestos from the Thetford residents was significantly longer than that of the Vancouver population, and resembled that of the chrysotile workers. Because epidemiologic studies have consistently failed to find an increased respiratory disease incidence in lifelong residents of Quebec chrysotile mining towns who were never employed in the chrysotile industry, these findings imply that even asbestos burdens much higher, and fiber size distributions much longer, than those of the general population of most North American cities, are not associated with demonstrable pathologic effects.
Smoking inhibits asbestos clearance. D. McFadden, J.L. Wright, B. Wiggs, et al. 1986;133(3):372-4. PubMed · Publisher

Abstract

To determine whether smoking affects the clearance of asbestos fibers, guinea pigs were given amosite asbestos by intratracheal instillation and divided into 3 groups: (1) nonsmokers, (2) animals exposed to smoke only after asbestos instillation, and (3) animals exposed to smoke both before and after asbestos instillation. Asbestos fiber concentrations and sizes were measured at 1 wk and 1 month after exposure. Between 1 wk and 1 month the asbestos burden in nonsmokers decreased on average 6-fold, whereas both smoking groups failed to show a significant decrease. Over this time period, the mean length of retained fibers increased in the nonsmokers but decreased in both smoking groups. This phenomenon was seen in tissue samples and lavage samples, although lavaged fibers were consistently shorter than tissue fibers. We conclude that in this model, cigarette smoking impedes asbestos clearance, largely by increasing retention of short fibers. This increased pulmonary fiber burden may be important in the increased disease rate seen in asbestos workers who smoke.
The natural history of asbestosis in former crocidolite workers of Wittenoom Gorge. W. Cookson, N. De Klerk, A.W. Musk, et al. 1986;133(6):994-8. PubMed · Publisher

Abstract

The course of pulmonary asbestosis and its determinants have been examined in 280 applicants for compensation among former workers of the crocidolite mine and mill at Wittenoom Gorge, Western Australia. Serial chest radiographs accrued over more than 3 decades were graded for parenchymal disease separately by two observers according to the 1980 ILO Classification of Radiographs for Pneumoconioses and without knowledge of exposure histories or compensation details. In 136 subjects whose median duration of exposure was 37 months, radiographic asbestosis appeared between 1 and 34 yr after initial exposure and then progressed continuously. Total exposure to asbestos and time from first exposure to the appearance of definite radiographic asbestosis were significant determinants of the rate of progression of profusion of radiographic abnormality. Asbestosis should be considered to be an active disease even 3 decades after exposure has ended.
Time course of chemotactic factor generation and the corresponding macrophage response to asbestos inhalation. D.B. Warheit, L.H. Hill, G. George, et al. 1986;134(1):128-33. PubMed · Publisher

Abstract

Inhalation of asbestos fibers causes a progressive fibrotic lung disease in humans and animals. Pulmonary macrophages are associated with asbestos exposure and have been implicated as significant mediators of the pathogenic process. In previous studies, we showed that macrophages are attracted to sites of asbestos fiber deposition, i.e., alveolar duct bifurcations. We also showed that macrophages accumulated at these sites as the result of asbestos-induced activation of complement proteins on alveolar surfaces, consequently producing C5a, a chemotactic factor for macrophages. In the present study, we have demonstrated the time course of chemotactic factor generation and the corresponding macrophage response in vivo. A complement-dependent chemotactic factor for macrophages was activated during a 3-h exposure to asbestos and reached maximal activity by 3 h postexposure. Macrophage accumulation followed and reached a maximal amount by 24 h postexposure. Rats decomplemented with cobra venom factor exhibited a significant reduction in macrophage accumulation, but the macrophage response ensued when serum complement returned to normal. Approximately 30% of the macrophages lavaged from complement-normal, asbestos-exposed animals contained fibers, whereas only half as many macrophages from decomplemented rats contained asbestos. A small but significant increase in lavaged lung protein was measured in asbestos-exposed animals. Evidence supports the concept that complement proteins on alveolar surfaces are derived from normal transudation of serum components from the pulmonary vasculature. Increased serum transudation could provide a source of alveolar complement that sustains the generation of a chemotactic factor for macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)
A comparison of the ferruginous body and uncoated fiber content in the lungs of former asbestos workers. R.F. Dodson, M.G. Williams, M.F. O'Sullivan, et al. 1985;132(1):143-7. PubMed · Publisher

Abstract

Tissue samples from 12 former asbestos workers were digested and analyzed for ferruginous body and uncoated fiber populations. It was noted that there were large numbers of nonasbestos fibers in each of the samples. In some samples, these fibers constituted over 80% of the total uncoated fibers, and they could greatly influence the data as to asbestos content of the tissue unless differentiated by light and electron microscopic techniques, such as X-ray energy-dispersive analysis. There were great variations in the numbers of uncoated fibers per ferruginous body between the individual workers. The digested samples from lungs of 2 workers yielded no ferruginous bodies by light microscopy, even though these samples by electron microscopy contained respective loads of 780,000 and 1.2 million uncoated amphibole fibers per gram. Light microscopy examination of adjacent tissues confirmed mild fibrosis in both workers. Ferruginous bodies serve as a general marker for asbestos exposure. However, our data suggest that their absence in tissue with interstitial fibrosis from a worker with previous occupational exposure may not be sufficiently conclusive to rule out asbestos-induced disease. Rather, as shown by our data, individual exceptions may require correlated analysis by analytical electron microscopy in order to define particulate load and support the diagnosis of the disease.
Asbestos-related disease in railroad workers. A cross-sectional study. L.C. Oliver, E.A. Eisen, R.E. Greene, et al. 1985;131(4):499-504. PubMed · Publisher

Abstract

A cross-sectional prevalence study of 377 railroad workers was carried out. The purpose was to investigate the prevalence of asbestos-related disease. We compared conventional with more recently adopted criteria for defining abnormal lung function. We compared the test results of those who performed reproducibly on spirometry with those who did not. Medical and occupational histories, flow-volume loops, and posteroanterior and lateral chest radiographs were obtained. Single-breath carbon monoxide diffusing capacity (DLCO) was measured, and chest auscultation was performed. Related to time since onset of exposure, pleural plaques occurred in 22.9%. There was radiographic evidence of interstitial disease in 1.6%. Reduced single-breath DLCO (12.4%), crackles (18.4%), and dyspnea (49.6%) were significantly associated with asbestos exposure. The prevalence of restriction and obstruction was 5.1 and 12.4%, respectively, but differed (p = 0.0001) with the definition criteria selected. The proportion with each of these abnormalities was higher in the nonreproducible group. That group was older, with more pleural plaques and chronic bronchitis. Railroad workers are a group at risk for asbestos-related disease. Extent of disease and assumptions about causality are likely to vary with definitions of normalcy and the use of reproducibility criteria.
Characterization of the bronchoalveolar cellular response in experimental asbestosis. Different reactions depending on the fibrogenic potential. I. Lemaire. 1985;131(1):144-9. PubMed · Publisher

Abstract

Analysis of bronchoalveolar cell types and structure was performed during the development of asbestos-induced lung injury in the rat. Animals received single intratracheal injections of one of the following: saline (control), UICC chrysotile B asbestos (5 mg), or very short 4T30 chrysotile fibers (5 mg). Bronchoalveolar lavage (BAL) was performed at various intervals after instillation. Analysis of BAL fluid showed significant increase in inflammatory cells in response to asbestos, which persisted longer in animals treated with chrysotile B. Presence of numerous mitotic figures in BAL fluid of treated animals suggests that macrophage replication may contribute in part to this response. Differential cellular analysis indicated that after injection of long chrysotile fibers, which causes fibrotic lesions within 7 days, polymorphonuclear leukocytes (PMN) appear as early as Day 1 in significant concentration (40%) in the bronchoalveolar compartment and persist through Day 7 after treatment. From Day 7 to Day 21, multinucleated cells (MGC) were found in lavage fluid (5 to 8%). Most of these cells were binucleated, and none had more than 3 nuclei. By contrast, exposure to very short chrysotile fibers caused only a very transient influx of PMN on Day 1. By Day 7, there was a significant increase in MGC, which persisted through Day 21, at which time no fibrosis was apparent. Although most of these cells were binucleated, many cells had 3 or more nuclei. The giant cells were predominantly of the foreign body type, with MGC of the Langhans type also present.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of spirometry standards in two occupational cohorts. E.A. Eisen, L.C. Oliver, D.C. Christiani, et al. 1985;132(1):120-4. PubMed · Publisher

Abstract

Characteristics of subjects with nonreproducible lung function tests (test failures) are described in two studies of occupational respiratory disease. According to current guidelines for spirometry, subjects with test failure are excluded from analyses of epidemiologic pulmonary function data. Among 415 Chinese cotton textile workers, the prevalence of byssinosis was 5.8% for subjects with repeatable tests and 13.3% for subjects with test failure. In regression analysis, the estimate of the association between cotton dust exposure and FEV1 decreased when subjects with test failure were excluded. In a second cohort of 378 asbestos-exposed machinists, the prevalence of chronic bronchitis was significantly greater among those with test failure. Considering only subjects with repeatable measurements, FEV1 was lower among textile workers with byssinosis and machinists with chronic bronchitis than among their asymptomatic coworkers. This suggests that, on average, subjects with poor test performance had lower (unobserved) FEV1 values, and therefore that the exclusion of subjects with test failure may cause selection bias.
Lung function and exercise performance in smoking and nonsmoking asbestos-exposed workers. D.Y. Sue, A. Oren, J.E. Hansen, et al. 1985;132(3):612-8. PubMed · Publisher

Abstract

Evaluation of impairment caused by exposure to an occupational toxin can be complicated by additional exposure to other injurious agents. Because cigarette smoking is common and cigarettes are implicated in obstructive lung disease and cardiovascular diseases, we assessed the contribution of smoking to functional abnormalities in a group of asbestos-exposed shipyard workers. Seventy-three workers who never smoked were paired with 73 current smokers by age and asbestos exposure. Pulmonary function and performance during cycle incremental exercise were compared between the 2 groups. Nonsmokers had significantly higher VC, FEV1, FEV1/VC, and diffusing capacity for carbon monoxide than did smokers. Only 3 of the 73 nonsmokers but 23 of the 73 smokers had a FEV1/VC below the 95% confidence limit of predicted value. The FEF25-75%, on the other hand, failed to identify additional subjects with obstruction not found by the FEV1/VC. During exercise, despite no difference in maximal heart rate, the maximal O2 uptake (VO2max) and oxygen-pulse were lower among smokers. In addition, smokers more frequently had abnormal AaPO2 at maximal exercise. Of 33 smokers who had a VO2max less than 80% of predicted, 16 were judged to have cardiac disease, whereas only 2 appeared to be limited by obstruction. Only 15 of the 73 nonsmokers had a VO2max less than 80%. We conclude that cigarette smoking was the major contributing factor to the obstructive lung disease observed in asbestos workers, and it also had a strong influence on the occurrence, nature, and magnitude of exercise limitation. The history of cigarette smoking has an important effect on the assessment of impairment from asbestos.
Lymphocyte subpopulations in bronchoalveolar lavage fluid in asbestos workers. A.R. Gellert, M.G. Macey, S. Uthayakumar, et al. 1985;132(4):824-8. PubMed · Publisher

Abstract

We examined peripheral blood and bronchoalveolar lavage (BAL) fluid lymphocyte subpopulations in 29 asbestos workers, 10 with and 19 without clinical or radiologic evidence of asbestosis. Peripheral blood lymphocyte subpopulations were also measured in 13 control subjects. The mean OKT4:OKT8 (T-helper/inducer:T-suppressor/cytotoxic lymphocyte) ratio in BAL fluid in the 29 asbestos workers was 0.96 (range, not detected to 3.33), significantly less than 1.76 (1.33 to 2.67) in peripheral blood (p less than 0.001). There were no significant differences in OKT4:OKT8 ratios in peripheral blood between the 10 patients with asbestosis, the 19 asbestos workers without asbestosis, and the 13 normal control subjects or in the OKT4:OKT8 ratios in BAL fluid between patients with asbestosis and asbestos workers without asbestosis. In the group as a whole, 83% of those who had suffered more than 5 yr of exposure to asbestos showed OKT4:OKT8 ratios less than 1.2, whereas in those who had suffered fewer than 5 yr of exposure, 80% showed ratios greater than 1.2 (p less than 0.02). No other relationships between OKT4:OKT8 ratios and clinical, radiographic, or physiologic variables were observed.
Natural killer cell activity in cigarette smokers and asbestos workers. L.C. Ginns, J.H. Ryu, P.R. Rogol, et al. 1985;131(6):831-4. PubMed · Publisher

Abstract

In order to evaluate the effects of cigarette smoking and asbestos exposure on cellular immunity, we tested a group of cigarette smokers and asbestos workers for natural killer (NK) activity in the peripheral blood. The mean NK activity in cigarette smokers was lower than in normal subjects (13.7 +/- 1.6 versus 29.0 +/- 3%; p less than 0.05). As a group, the mean NK activity for the asbestos-exposed group was also reduced compared with that of the nonsmoking control group (22.6 +/- 3.2%; p less than 0.05). When divided according to the smoking status, the asbestos workers who were nonsmokers or ex-smokers showed similar decreases in NK activity compared with normal subjects (19.5 +/- 6.2 and 21.2 +/- 4.5%, respectively; p less than 0.05). A subgroup of asbestos-exposed subjects who currently smoked showed no decrease in NK activity. The data show that NK activity is reduced in the peripheral blood of cigarette smokers and asbestos workers. The relatively normal NK activity found in asbestos workers who also smoked is unexplained. Impairment of NK activity is a potential mechanism for the increased incidence of infection and cancer in smokers and neoplasia in asbestos workers.
Pathogenesis of pleural plaques. J.A. Elias, M.D. Rossman, R.P. Daniele. 1985;131(6):965-6. Letter PubMed · Publisher
Production of arachidonic acid metabolites by macrophages exposed in vitro to asbestos, carbonyl iron particles, or calcium ionophore. S. Kouzan, A.R. Brody, P. Nettesheim, et al. 1985;131(4):624-32. PubMed · Publisher

Abstract

Consequent to asbestos deposition, alveolar macrophages (AM) accumulate at alveolar duct bifurcations where they phagocytize fibers. Because phagocytosis can stimulate the release of arachidonic acid (AA) metabolites, the possibility that secretion of these powerful mediators of inflammation might be induced by chrysotile asbestos was investigated in vitro. Rat AM were treated in vitro with chrysotile asbestos, and the cyclooxygenase products--prostaglandins, thromboxane B2 (TXB2), 12-hydroxy-5,8,10-heptadecatrienoic acid (HHT)--and lipoxygenase products--leukotrienes (LT), hydroxyeicosatetraenoic acids (HETE)--secreted in the medium were isolated by high-performance liquid chromatography. Composition of the AA metabolites released was compared with that from those stimulated by the calcium ionophore A 23187 (20 microM) and by another particulate phagocytic stimulus, i.e., carbonyl iron beads. Calcium ionophore stimulation induced a marked release of various AA metabolites in the medium from both the cyclooxygenase pathway (HHT, TXB2, and PGE2, in decreasing quantities, respectively) and the lipoxygenase pathway (LTB4, 5-HETE, 12-HETE, and LTC4). The major product was LTB4. Treatment of the macrophages with asbestos fibers induced the release of a similar array of AA metabolites, although there were smaller amounts of LTC4 and 12-HETE, but increased quantities of PGF2 alpha. A time course study showed a steady increase in metabolite production for 1 h, followed by a plateau. In addition, the amount of metabolites released was dependent on asbestos concentrations. Phagocytosis of iron beads induced the secretion of the same metabolites as asbestos stimulation, but in larger quantities, probably reflecting the lack of cytotoxicity of the particle.(ABSTRACT TRUNCATED AT 250 WORDS)
Small airways disease and mineral dust exposure. Prevalence, structure, and function. A. Churg, J.L. Wright, B. Wiggs, et al. 1985;131(1):139-43. PubMed · Publisher

Abstract

Previously we described a lesion of the small airways that appears related to mineral dust exposure and is found in asbestos and nonasbestos dust-exposed populations. To determine the usefulness of this lesion as a marker for mineral dust exposure, and to determine whether it produces functional consequences, we examined a group of 53 workers who had been either hard rock miners or in the asbestos, construction, and shipyard industries. The specific lesion (mineral dust airways disease (MDAD] consists of marked fibrosis and pigmentation of the respiratory bronchioles and was found in 13 of 53 workers with dust exposure, but only in 1 of 121 without dust exposure. Compared with age and smoking-matched dust-exposed control subjects, patients with this lesion had significant abnormalities of forced expiratory volume in one second (FEV1), forced expiratory flow during the middle half of the forced vital capacity (FEF25-75), vital capacity (VC), and nitrogen washout. In addition to fibrosis in the walls of respiratory bronchioles, these patients also had significant increases of fibrosis in the walls of membranous bronchioles, indicating that changes in the small airways are widespread in this subset of workers. We conclude that markedly abnormal small airways are present in some workers with mineral dust exposure; pathologic observation of this lesion is a good indicator of dust exposure, and its presence is associated with abnormalities of air flow greater than those induced by smoking alone. The presence of this lesion in only a portion of dust-exposed workers may account for contradictory results in past studies that attempted to demonstrate air flow abnormalities associated with mineral dust exposure.
Cigarette smoke, asbestos, and small irregular opacities. W. Weiss. 1984;130(2):293-301. Review PubMed · Publisher

Abstract

The long-term inhalation of cigarette smoke is associated with the appearance of diffuse small irregular opacities of mild profusion on chest roentogenograms of some subjects in a limited number of reports. Human histologic and experimental animal studies have shown the presence of pulmonary interstitial fibrosis. The radiographic abnormalities may be explained by interstitial fibrosis, although bronchiolar wall thickening may also be involved. Because asbestos causes diffuse pulmonary fibrosis, the literature was reviewed for evidence concerning an interaction between cigarette smoke and asbestos in the frequency of pulmonary asbestosis. A majority of 14 prevalence studies and 7 cohort studies of asbestos workers with information on smoking habits have shown a positive interaction between the 2 agents. The interaction appears to be additive rather than synergistic. Smoking may exert an effect on the frequency of pulmonary asbestosis by increasing the effective fiber dose retained in the lungs through interference with clearance.
Crackles in the early detection of asbestosis. R.L. Murphy, E.A. Gaensler, S.K. Holford, et al. 1984;129(3):375-9. PubMed · Publisher

Abstract

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.
Interstitial pulmonary fibrosis induced in hamsters by intratracheally administered chrysotile asbestos. Histology, lung mechanics, and inflammatory events. J.L. Glassroth, J. Bernardo, E.C. Lucey, et al. 1984;130(2):242-8. PubMed · Publisher

Abstract

The development of interstitial pulmonary fibrosis (IPF) is associated with persistent cellular infiltration and progressive connective tissue accumulation in the alveolar walls. To develop and characterize an animal model of IPF in which pulmonary fibrosis evolves slowly, as well as to develop an inexpensive, easily produced, model of asbestosis, Syrian golden hamsters received single intratracheal injections of either UICC chrysotile asbestos or saline. Animals were then examined at time points up to 180 days for pulmonary histologic and physiologic changes, cytologic characteristics of cells recovered by bronchoalveolar lavage, and spontaneous release of neutrophil chemoattractant activity by alveolar macrophages. Within days after asbestos treatment, hamsters developed a patchy bronchopneumonia centered around terminal airways, which progressed peripherally with time to involve the alveolar walls with persistent inflammation and the gradual development of interstitial and peribronchiolar fibrosis. These histologic changes were accompanied by physiologic findings of air-flow obstruction with air trapping. Bronchoalveolar lavage revealed a persistent neutrophilia that began within 24 h of asbestos treatment; this was associated with the spontaneous release of neutrophil chemotactic activity by cultured alveolar macrophages. In this animal model, pulmonary inflammation and fibrosis can be predictably produced by a single intratracheal instillation of chrysotile asbestos. It represents a useful tool for studying both asbestosis and pulmonary fibrosis in general.
Lung asbestos content in chrysotile workers with mesothelioma. A. Churg, B. Wiggs, L. Depaoli, et al. 1984;130(6):1042-5. PubMed · Publisher

Abstract

The role of chrysotile asbestos in the genesis of mesotheliomas in humans is disputed. We analyzed the asbestos content of the lung in 6 long-term chrysotile miners and millers who had pleural mesotheliomas. In five patients, only chrysotile ore components (chrysotile and tremolite/actinolite/anthophyllite types of amphibole asbestos) were found, while the sixth patient presented both chrysotile ore components and amosite, a type of asbestos that is not derived from the mining process. The mean number of fibers/g dry lung for the 5 patients with mesothelioma containing only chrysotile ore components was higher (chrysotile 64 X 10(6) and tremolite group 540 X 10(6] than in a group of long-term chrysotile miner control subjects who had no asbestos-related disease (chrysotile 23 X 10(6), tremolite group 58 X 10(6], but some patients with mesothelioma had fiber burdens near the mean of the control range. Fiber sizes and aspect ratios in the mesothelioma group were approximately the same as those in the control subjects, and analysis of fiber distribution failed to show any preferential localization in the periphery of the lung. However, the concentration ratio of tremolite in the lungs of the mesothelioma cases compared to the control cases was 9.3, while the ratio of chrysotile was only 2.8. Our findings provide strong evidence that chrysotile mine dust (chrysotile and amphibole components) can produce mesotheliomas in humans; the greater relative amounts of tremolite group amphiboles present in the patients with mesothelioma raise the possibility that these fibers may be important in the pathogenesis of the tumors.
Mortality among employees of an Ontario asbestos-cement factory. M.M. Finkelstein. 1984;129(5):754-61. PubMed · Publisher

Abstract

Mortality among 535 asbestos-exposed and 205 nonexposed employees of an asbestos-cement factory was investigated. In the period beyond 20 yr from first exposure, the exposed workers had standardized mortality ratios of 175 for all causes of death, 370 for all malignancies, 480 for lung cancer, 240 for gastrointestinal cancers, and 17 deaths from mesothelioma; the factory control subjects had mortality rates similar to the general population. The cell-type distribution of the lung cancers was similar to that occurring in middle-aged smokers. Cumulative fiber exposures were calculated for the production workers, and mortality rates for the asbestos-associated malignancies were found to have significant trends with exposure. Exposure-related lung cancer risks were noted, with a large margin of uncertainty, to be similar to those observed in an American study of manmade mineral fiber workers.
Pathogenesis of pleural plaques. Relationship of early cellular response and pathology. S.A. Sahn, V.B. Antony. 1984;130(5):884-7. PubMed · Publisher

Abstract

To study the initial pleural cellular response to asbestos and to determine the relationship between this response and the development of pleural plaques, a model of asbestos pleurisy was developed in both normal and nitrogen-mustard-treated (neutropenic) New Zealand white rabbits. Animals were rendered neutropenic, as it has been shown that neutropenic rabbits do not develop a macrophage influx in the pleural space after the administration of either BCG or bacteria and that the pathology is different from that in normal rabbits treated in a similar fashion. Intrapleural asbestos induced an exudative effusion in normal animals within 4 h, and there was increased metabolic activity through 120 h, with a fall in pleural fluid pH and PO2 and a rise in pleural fluid PCO2. Neutropenic animals similarly developed an exudative pleural effusion but showed no change in metabolic activity of pleural fluid. Normal rabbits showed a marked cellular influx into the pleural space after asbestos treatment, with a peak total cell count of 27,208/microliters at 24 h; the majority of these cells were polymorphonuclear leukocytes. A macrophage influx occurred at 48 h and peaked at 72 h. By 120 h, lymphocytes were the predominant cell. Nitrogen-mustard-treated animals reached a peak of only 5,442 cells/microliters in the pleural space at 24 h, with a small percentage of polymorphonuclear leukocytes. A macrophage peak did not occur in these animals. There was a marked contrast between groups noted at autopsy. Normal animals developed pleural plaque formation, which was evident by 7 days and completely developed by 1 month.(ABSTRACT TRUNCATED AT 250 WORDS)
Pulmonary changes after exposure to vermiculite contaminated with fibrous tremolite. J.E. Lockey, S.M. Brooks, A.M. Jarabek, et al. 1984;129(6):952-8. PubMed · Publisher

Abstract

Workers exposed to vermiculite contaminated with fibrous tremolite were surveyed for the presence of respiratory symptoms by questionnaire, and for pneumoconiosis by chest radiograph. Pulmonary function was measured by spirometry and single-breath carbon monoxide diffusing capacity ( DLCOsb ). Fiber exposure indexes, expressed as fiber/ml-yr, were derived for each worker from available industrial hygiene data and work histories. The estimated cumulative exposure for the work force ranged from 0.01 to 39 fiber/ml-yr. Discriminant analysis demonstrated significant correlates with shortness of breath and pleuritic chest pain to cumulative fiber exposure. The radiographic changes were limited to pleural changes and involved 4.4% of the population. Parametric and discriminant analysis demonstrated a significant correlation with radiographic changes and cumulative fiber exposure. There were no correlations between spirometry or DLCOsb and fiber exposure. Exposure to vermiculite contaminated with fibrous tremolite can cause pleural changes in occupationally exposed workers. This is supported by the previously identified 12 cases of benign pleural effusions in this working population and the association of pleural radiographic changes and pleuritic chest symptoms with cumulative fiber exposure. The lack of significant parenchymal radiographic, spirometric, and DLCOsb changes most likely reflects the low cumulative fiber exposure.
Radiographic abnormalities among asbestos-cement workers. An exposure-response study. M.M. Finkelstein, J.J. Vingilis. 1984;129(1):17-22. PubMed · Publisher

Abstract

We studied the development of small irregular opacities and bilateral pleural thickening in a longitudinal study of 181 asbestos-cement workers. The relationships between the 32-yr risks of developing abnormalities and cumulative exposure to asbestos dust could be described with log-normal curves. Smokers had higher risks of both abnormalities than did nonsmokers. In this cohort, men leaving asbestos exposure had a risk of radiographic progression similar to men continuing in exposure, and men with abnormal radiographs had higher mortality rates than did men with normal ones.
Asbestos fiber content of the lungs in patients with and without asbestos airways disease. A. Churg. 1983;127(4):470-3. PubMed · Publisher

Abstract

I analyzed the total pulmonary asbestos burden in the lungs of 9 chrysotile miners who had asbestos airways disease (so-called "early asbestosis") but no evidence of classic asbestosis (interstitial fibrosis) on pathologic examination. The results were compared with values found for 9 miners matched for age, sex, smoking, and work length who had no histologic evidence of asbestosis or asbestos airways disease. The mean value for chrysotile fibers in the airway disease group was 47 X 10(6)/g dried lung, compared with 23 X 10(6) in the group without lesions (p less than 0.04). For contaminant amphiboles, probably derived from the chrysotile ore (tremolite, actinolite, anthophyllite), the corresponding values were 106 X 10(6) versus 58 X 10(6) (p less than 0.06), and for total asbestos fibers, 153 X 10(6) versus 81 X 10(6) (p less than 0.06). There was a strong correlation between amount of chrysotile and amphibole for each case, suggesting that the amphibole was probably a good measure of the original (but no longer present) chrysotile burden. No differences were seen between the 2 groups with regard to fiber size distribution, aspect ratios, or fiber widths. I conclude that the overall differences in fiber concentration between the 2 groups, although significant, are sufficiently small enough to suggest that other factors may be involved in the genesis of small airway lesions.
Benign asbestos pleurisy in the rabbit. A model for the study of pathogenesis. B.L. Shore, C.C. Daughaday, I. Spilberg. 1983;128(3):481-5. PubMed · Publisher

Abstract

Benign asbestos pleurisy is a manifestation of asbestos-induced disease that is not uncommon but often ignored. We developed an animal model to study the pathogenesis of this syndrome. Crocidolite asbestos injected into the rabbit pleural space resulted in the appearance of chemotactic activity in an exudative effusion, characterized by a polymorphonuclear leukocyte (PMN) response that peaked 4 h after the injection. The chemotactic activity and the PMN responses occurred equally in normal animals and in animals that had been depleted of complement with cobra venom. Neutropenia, induced with vinblastine, did not alter the appearance of chemotactic activity but abrogated the PMN response. Treatment with colchicine failed to block the release of chemotactic activity into the pleural fluid, but decreased the PMN response without affecting the ability of peripheral blood PMN to respond to pleural fluid chemotactic activity. When pleural fluid containing chemotactic activity was injected into the pleural space of another rabbit, a PMN response was observed. These studies suggest that the acute exudative response seen in the rabbit model of benign asbestos pleurisy results from the release of chemotactic activity from sources other than complement. The response probably depends on interaction between the asbestos and the pleural tissue. Asbestos-PMN interaction may release chemotactic factors that amplify the response secondarily. Colchicine blocked the acute response to intrapleural asbestos by a mechanism yet to be understood.
Deposition pattern of inorganic particles at the alveolar level in the lungs of rats and mice. A.R. Brody, M.W. Roe. 1983;128(4):724-9. PubMed · Publisher

Abstract

The early pathogenesis of particle-induced lung disease is likely to be determined in large part by the initial pattern of dust deposition at the alveolar level. We have studied the deposition pattern of 5 aerosolized dusts (chrysotile and crocidolite asbestos, fiber glass, alpha-quartz, and ash from Mt. St. Helens) in the lungs of rats. Mice were exposed to chrysotile asbestos. Quantitative electron microscopy was carried out on tissues fixed by vascular perfusion. Immediately after a brief exposure, significantly (p less than or equal to 0.01) greater numbers of particulates had deposited on alveolar duct bifurcations when compared with the number of particles on duct surfaces adjacent to the bifurcations. Few particles were counted at midpoints between bifurcations, and particles rarely were observed within alveoli. Our data show that regardless of mineral nature, shape, or concentration, inhaled particulates small enough to pass through the conducting airways are deposited primarily at alveolar duct bifurcations. We proposed that the alveolar deposition patterns observed are the result of air-flow characteristics that cause enhanced deposition of particles at alveolar duct bifurcations intersecting the flow. This is similar to deposition patterns that occur at bifurcations of conducting airways.
Enhanced release of a chemoattractant for alveolar macrophages after asbestos inhalation. E. Kagan, Y. Oghiso, D.P. Hartmann. 1983;128(4):680-7. PubMed · Publisher

Abstract

Alveolar macrophage supernatants from 2 groups of asbestos-exposed rats and a group of sham-exposed rats were tested for chemoattractant activity towards rat alveolar macrophages. Enhanced chemotaxin release was observed in culture supernatants from both crocidolite and chrysotile asbestos-exposed rats when compared with supernatants from sham-exposed rats. These between-group differences persisted for as long as 15 months after exposure had ceased. Chemotactic factor release was maximal after 24 h of culture in all animal groups. Partial characterization of the chemoattractant from each of the 3 rat groups revealed that it was thermolabile, nondialyzable, and trypsin-sensitive. Separation on SDS-polyacrylamide gel electrophoresis revealed 3 major peaks of activity. The production of the chemotaxin in supernatants from asbestos-exposed rats was partially inhibited by both actinomycin D and puromycin. These agents had no appreciable effect on the production of chemoattractant in cultures from sham-exposed animals. The enhanced release of an alveolar macrophage chemoattractant after asbestos inhalation may explain why macrophages accumulate at sites of asbestos deposition in the lungs.
Environmental associations and histopathologic patterns of carcinoma of the lung: the challenge and dilemma in epidemiologic studies. J.C. Ives, P.A. Buffler, S.D. Greenberg. 1983;128(1):195-209. Review PubMed · Publisher

Abstract

An update of histopathologic classification schemes is provided for carcinoma of the lung and factors that influence proportional distributions of cell types, i.e., sources and preparations of tissue specimens, observer variability, and use of secondary sources of information. Consideration is given to the natural history and to current knowledge of the demographic characteristics of cell types of carcinoma of the lung. A review of studies reporting histopathologic associations with environmental exposures suggests that no single type of carcinoma of the lung is specifically associated with exposure to tobacco smoke, arsenic, or beryllium. Furthermore, studies concerned with exposure to asbestos, chloroethers, chromates, nickel, vinyl chloride, and radioactivity lack sufficient information to conclude definitively that only one specific lung cancer cell type is associated with these exposures. In conclusion, an exclusive association of a single cell type of carcinoma of the lung with exposure to the physical or chemical agents reviewed has not been demonstrated.
Lung structure as a risk factor in adverse pulmonary responses to asbestos exposure. A case-referent study in Quebec chrysotile miners and millers. M.R. Becklake, B. Toyota, M. Stewart, et al. 1983;128(3):385-8. PubMed · Publisher

Abstract

To investigate the hypothesis that lung structure may predispose to the development of asbestos-related pulmonary fibrosis, we carried out a case-referent study using data gathered in a cross-sectional study of Quebec chrysotile asbestos miners and millers. Tracheal and thoracic measurements were derived from the routine chest radiographs of 44 men with established radiologic fibrosis and compared with similar measurements for 88 men matched for age and cumulative exposure in the same industry who had not developed pulmonary fibrosis. Intrathoracic tracheal lengths were, on the average, shorter, and transthoracic diameters narrower in cases compared with those in referents. In addition, cases were shorter than the referents, suggesting that height might be an indirect measure of the structural characteristics relevant to the response to inhaled asbestos particles. Our findings are thus consistent with the hypothesis outlined, and they suggest a line of investigation that might be useful in relation to other inhaled pollutants.
Pleural thickening: its significance and relationship to asbestos dust exposure. T. Rodman, M.S. Rodman. 1983;127(5):656-7. Letter PubMed · Publisher
Pulmonary uptake of gallium-67 in asbestos-exposed humans and sheep. R. Bégin, A. Cantin, G. Drapeau, et al. 1983;127(5):623-30. PubMed · Publisher

Abstract

To evaluate the 67Ga lung uptake as an indicator of inflammatory activity in asbestosis, we obtained 67Ga lung scans in 58 long-term asbestos workers. The 67Ga localized excessively in the lungs of 17 of the 21 workers with asbestosis. Among workers without sufficient criteria for the diagnosis of asbestosis, the 67Ga scan index was significantly increased in 43% (16 of 37). Among the 16 with positive 67Ga scan, abnormal pressure-volume curve and/or gas exchange data were found in 87%, whereas in the 21 workers with negative 67Ga scan, similar abnormalities were found in only 29%. In the sheep model of the disease, bronchoalveolar analysis after 67Ga scan demonstrated that the excessive uptake of 67Ga in asbestosis is caused by enhanced serum protein leakage and macrophage accumulation in the lung. Thus, 67Ga scanning in asbestos workers may be a useful indicator of early lung damage.
Asbestos bodies in bronchoalveolar lavage. P. De Vuyst, J. Jedwab, P. Dumortier, et al. 1982;126(6):972-6. PubMed · Publisher

Abstract

Asbestos bodies (AB) were counted in bronchoalveolar lavage (BAL) fluid from 62 patients with suspected asbestos related diseases, 2 patients with known exposure to asbestos but without related disease, and 40 control subjects. BAL fluid contained AB in all patients with obvious exposure (28 of 28), including the 2 without related disease, in most patients with suspected exposure (26 of 28), as well as in 5 of 8 patients without known exposure but with suspicion of asbestos related disease (mesothelioma or pleural plaques). Among the 40 control subjects, the results in 5 were positive but to a low degree (less than 1 AB/ml of fluid). Quantitative analysis correlated with the type of disease: AB counts were higher in patients with interstitial lung disease than in those with benign (p less than 0.02) or malignant (p less than 0.01) pleural disease. Only 9 of 13 patients with mesothelioma had a positive lavage. In conclusion, the finding of AB in BAL fluid correlates with the occupational risk and can disclose unknown exposure better than a questionnaire, but a positive lavage is not a proof of disease. Quantitative differences in AB counts suggest a different pathogenesis for pleural and parenchymal disease.
Asbestos-related diseases of the lungs and pleura: current clinical issues. M.R. Becklake. 1982;126(2):187-94. Review PubMed · Publisher
Asbestosis in long-term employees of an Ontario asbestos-cement factory. M.M. Finkelstein. 1982;125(5):496-501. PubMed · Publisher

Abstract

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.
Fly ash lung: a new pneumoconiosis?. E.B. Golden, M.L. Warnock, L.D. Hulett, et al. 1982;125(1):108-12. Case report PubMed · Publisher

Abstract

A laborer who worked in a steel mill and in a shipyard developed a nonspecific pulmonary interstitial fibrosis. Postmortem samples of his lung were digested, and the inorganic material present was extracted and examined using transmission electron microscopy, electron diffraction, and electron microprobe analysis. Uncoated asbestos fibers were present (1.4 X 10(5)/g wet lung), but the surprising finding was the presence of a large number of fly ash particles (6 X 10(6)/g wet lung). Fly ash, the particulate material produced during coal combustion, has not previously been reported to be present in human lung tissue. Although the contribution of the asbestos to this man's lung disease is uncertain, we believe, based on previous studies implicating aluminum silicates in pneumoconiosis, that the fly ash, an aluminum silicate, may be a contributing factor.
Morphologic features and function of the airways in early asbestosis in the sheep model. R. Bégin, S. Massé, M.A. Bureau. 1982;126(5):870-6. PubMed · Publisher

Abstract

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.
Pleural thickening: its significance and relationship to asbestos dust exposure. S.M. Albelda, D.M. Epstein, W.B. Gefter, et al. 1982;126(4):621-4. PubMed · Publisher

Abstract

The admission chest radiographs of 824 were screened for the presence of bilateral pleural thickening. Those patients with pleural thickening were scored according to the ILO classification of radiographs of the pneumoconioses. The prevalence of bilateral pleural thickening was high (6.2%) in these patients, of whom 67% had an environmental or occupational history suggestive of asbestos exposure. The predictive value of bilateral pleural thickening alone as an indicator of previous asbestos exposure was 67%. If one excludes known medical or surgical etiologies of pleural thickening then the predictive value increased to 81%. The radiographic detection of bilateral pleural thickening has a strong association with prior asbestos exposure.
The association of pleural mesothelioma and tuberculosis. G.C. Roviaro, F. Sartori, F. Calabrò, et al. 1982;126(3):569-71. Case report PubMed · Publisher

Abstract

The relationship between pleural mesothelioma and asbestosis is universally accepted. Less importance has been given to its connection with chronic pleural disease, particularly tuberculosis. In a group of 35 patients affected with mesothelioma, neoplasm arose in 3 patients with calcific pleural tuberculosis, at a ratio of 1:8.5. The cause may have been indirect chronic stimulation or even direct action from oncogenic substances contained in the pleura.

PubMed has no abstract for this study. This is the authors' abstract, copied from the article.
Chrysotile asbestos inhalation in rats: deposition pattern and reaction of alveolar epithelium and pulmonary macrophages. A.R. Brody, L.H. Hill, B. Adkins, et al. 1981;123(6):670-9. PubMed · Publisher

Abstract

The initial deposition and subsequent translocation of chrysotile asbestos were studied in the lungs of rats exposed for 1 h in inhalation chambers. Using scanning and transmission electron microscopy of tissue fixed by vascular perfusion, we determined that the majority of fibers that pass through the conducting airways deposits at the bifurcations of alveolar ducts. The farther an alveolar duct bifurcation was from its terminal bronchiole, the less asbestos were observed. The amount of asbestos present on the alveolar duct surfaces was significantly decreased 5 h after cessation of the 1-h exposure. Some fibers were taken up by Type I epithelial cells during the first hour of dusting, and this process continued through the 8-day period in which the animals were studied. As early as 24 h after exposure, there was an accumulation of macrophages at the sites of initial asbestos deposition. This may be a significant cellular response in the early pathogenesis of asbestosis.
Asbestos fibers in the general population. A. Churg, M.L. Warnock. 1980;122(5):669-78. PubMed · Publisher
Comparison of sputum and lung asbestos body counts in former asbestos workers. V.L. Roggli, S.D. Greenberg, J.W. McLarty, et al. 1980;122(6):941-5. PubMed · Publisher

Abstract

The asbestos (ferruginous) body content of lung tissues was compared to the number of asbestos bodies (AB) in sputum from 6 former amosite asbestos workers. Lung tissue was obtained at autopsy (5 subjects) and lobectomy (1 subject), and AB content was determined by a digestion-concentration technique. The sputum obtained was collected by both spontaneous cough (a pooled, 3-day specimen) and aerosolized hypertonic saline induction. Four slides treated with Papanicolaou's stain were prepared from each cytologic specimen and scored from 0 to 3 + on the basis of the total number of AB counted on the 4 slides. A significant correlation (P < 0.02) was found between the number of AB per gram of lung tissue and the percentage of sputum specimens from each worker than were positive for AB. Asbestos bodies were identified in 46% of sputum specimens from the 4 workers whose lungs contained 900 or more AB/g of lung tissue.
Determination of severe impairment (disability) in interstitial lung disease. G.R. Epler, F.A. Saber, E.A. Gaensler. 1980;121(4):647-59. PubMed · Publisher

Abstract

Physicians trained primarily to recognize and treat disease are being asked more frequently to quantify impairment of health. Criteria for defining impairment due to chronic obstructive pulmonary diseases are widely accepted, but it has been difficult to establish guidelines for interstitial diseases. To develop and validate criteria, we selected 2,420 patients with airflow obstruction; 821 had interstitial disease, and 938 were employees of asbestos industries. We found that clinical and roentgenographic criteria were inappropriate for defining impairment. The forced vital capacity and single-breath diffusing capacity, each expressed as a percentage of the predicted value, were selected for analysis. Sensitivity studies using response to standard exercise as an independent criterion suggested that the limits reflecting severe impairment were a forced vital capacity 50% of predicted and a single-breath diffusing capacity 40% of predicted. Applying these criteria, 35.6% of patients with interstitial pneumonia, 12.1% with sarcoidosis, and 13.6% with pneumoconioses, but only 1.1% of the workers exposed to asbestos were severely impaired. In more than one half of patients the single-breath diffusing capacity was the only test that indicated severe impairment.
Respiratory effects of exposure to dust in taconite mining and processing. T.C. Clark, V.A. Harrington, J. Asta, et al. 1980;121(6):959-66. PubMed · Publisher

Abstract

Taconite is a low-grade iron ore consisting of iron, quartz, and numerous silicates. Taconite from the eastern tip of the Mesabi Iron Range contains the amphibole silicate cummingtonite-grunerite, which is a mineral relative of amosite asbestos. In the present study, data were collected from 249 men with 20 or more years of exposure to taconite dust and 86 men without history of intimate exposure to taconite dust. Bronchitic symptoms and impairment of expiratory flow correlated significantly with history of cigarette smoking, but not with exposure to dust. Chest radiographs revealed three cases of possible silicosis. No case of definite interstitial fibrosis, ill-defined diaphragm, pleural calcification, or mesothelioma was found. We conclude that (1) cigarette smoking is significantly correlated with bronchitic symptoms and impairment of expiratory flow; (2) taconite workers are at risk of silicosis; (3) if dust containing cummingtonite-grunerite has biologic activity comparable to that of dust from asbestos, it is not evident after 20 years of low-level exposure.

1970s

Absence of synergism between exposure to asbestos and cigarette smoking in asbestosis. J.M. Samet, G.R. Epler, E.A. Gaensler, et al. 1979;120(1):75-82. PubMed · Publisher

Abstract

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.
An epidemiologic study of a group of talc workers. J.F. Gamble, W. Fellner, M.J. Dimeo. 1979;119(5):741-53. PubMed · Publisher

Abstract

Chest roentgenograms, pulmonary function assessment by spirometry, respiratory symptoms, smoking history, and occupational history by questionnaire were obtained from 121 male talc miners and millers exposed to talc containing tremolite and anthophyllite asbestiform fibers. Ninety-three of the employees had worked in talc only at the plant under study. Symptoms were only slightly more prevalent in talc workers when compared to potash miners. Mean pulmonary function (forced expiratory volume in one sec, forced vital capacity, and maximal expiratory flow at 50 and 75 per cent of vital capacity) of talc workers was significantly decreased in comparison to that of potash miners. The prevalence of pleural calcification and pneumoconiosis in talc workers with 15 or more years of employment was higher than in potash miners. The prevalence of pleural thickening was 31 per cent in those who worked more than 15 years and was significantly increased as compared to that in potash miners. Workers with pleural thickening had decreased pulmonary function in comparison to those who did not. Decreased one-sec forced expiratory volume and forced vital capacity were associated with exposure to respirable particulate and asbestiform fibers.
Analysis of the cores of asbestos bodies from members of the general population: patients with probable low-degree exposure to asbestos. A. Churg, M.L. Warnock. 1979;120(4):781-6. PubMed · Publisher

Abstract

Asbestos bodies were isolated from the lungs of 21 patients who had 300 to 9,000 of such bodies/g of lung tissue, a concentration frequently found in manual laborers in the general population who are not primary asbestos workers. All of the 123 bodies examined by electron diffraction produced diffraction patterns consistent with amphibole varieties of asbestos. Electron microprobe analysis (energy dispersive x-ray spectroscopy) of 46 bodies revealed that 38 of the cores were composed of the commercial amphiboles, amosite and crocidolite, whereas only 8 were composed of the noncommercial amphiboles, anthophyllite and tremolite. Review of the occupations of these patients revealed that all but one had blue-collar jobs. For many of these persons, putative sources of asbestos exposure such as construction work could be defined, but for some, the source could not be determined. One woman was apparently exposed to asbestos in the practice of her hobby of ceramics, in which she used anthophyllite-contaminated clay. We concluded that commercial amosite/crocidolite asbestos forms the cores of most asbestos bodies in manual laborers in the general population and that the source is usually occupational.
Influence of dose and fiber type on respiratory malignancy risk in asbestos cement manufacturing. H. Weill, J. Hughes, C. Waggenspack. 1979;120(2):345-54. PubMed · Publisher

Abstract

This investigation provides information concerning the risk or respiratory malignancy in relation to duration, degree, and fiber type of exposure to asbestos in a manufacturing cohort of 5,645 with long-term follow-up. Excess mortality for this cause was found in groups with moderate and high cumulative exposure (standard mortality ratios of 290 and 226). Analysis of the influence of components of total exposure dose (duration, average concentration) revealed no detectable excess risk in persons employed for less than 2 years or with low-degree average exposure. Exposure to corcidolite (blue) fiber in addition to the predominantly used chrysotile in pipe making appeared to be associated with higher risk than was exposure to chrysotile alone.
Aryl hydrocarbon hydroxylase in asbestos workers. S.M. Naseem, P.V. Tishler, H.A. Anderson, et al. 1978;118(4):693-700. PubMed · Publisher

Abstract

Aryl hydrocarbon hydroxylase (AHH) activity and inducibility were studied in the lymphoblasts of 47 asbestos workers and 31 control subjects. Mean inducibility (3-methylcholanthrene [MC]-or dibenz(a,h,)anthracene [DBA]-induced divided by basal enzyme activity) was greater in the occupationally exposed subjects than in the control subjects. The estimated estimated change in mean value (+/- SE) of MC inducibility was 0.88 +/- 0.21 (P less than 0.001), and that of DBA inducibility was 1.59 +/- 0.56 (P less than 0.01). Differences in inducibility values were particularly apparent in 12 pairs of spouses, in all of whom the inducibility values of the occupationally exposed subjects exceeded those of their spouses. The differences in inducibility of AHH resulted from increases in induced activity, not from any appreciable change in basal activities. They were independent of subject age, sex, smoking status, year of first exposure to asbestos, yield of lymphoblasts, or the rate of blastogenesis as measured by the incorporation of tritiated thymidine into nucleic acid. Increased AHH inducibility may bear some relation to the greatly increased risk of bronchogenic carcinoma in asbestos workers who smoke cigarettes.
Asbestos and cancer: the international lag. P.E. Enterline. 1978;118(6):975-8. Historical article PubMed · Publisher
Malignant mesothelioma arising after direct application of asbestos and fiber glass to the pericardium. A. Churg, M.L. Warnock, K.G. Bensch. 1978;118(2):419-24. Case report PubMed · Publisher

Abstract

A case of mesothelioma, apparently arising in the pericardium, is reported in a patient who, 15 years previously, had been treated for angina pectoris by dusting of the pericardial cavity with a mixture of fibrous dusts. At autopsy, transparent fibers and ferruginous bodies were present within the pericardium. Electron diffraction and microprobe analysis indicated that approximately two thirds of the fibers were tremolite and anthophyllite asbestos, and the remainder, fiber glass. Development of mesothelioma in laboratory animals has been reported after intrapleural deposition of asbestos and other fibers, but in humans, the link between exposure to asbestos and mesothelioma has always been based on epidemiologic data and the retrospective finding of asbestos in tissues. To our knowledge, this is the first example of a malignant mesothelioma in a human associated with direct mesothelial contact with fibrous dusts.
Mesothelioma associated with the syndrome of inappropriate secretion of antidiuretic hormone. W.H. Perks, J.C. Crow, M. Green. 1978;117(4):789-94. Case report PubMed · Publisher

Abstract

A patient with a malignant mesothelioma developed the syndrome of inappropriate secretion of antidiuretic hormone. The electrolyte abnormalities were corrected by treatment with demethylchlortetracycline. Arginine vasopressin concentrations were increased in serum and urine. It is suggested that the syndrome might have been mediated by secretion of antidiuretic hormone from the posterior pituitary, because arginine vasopressin was not detected in the patient's tumor using a sensitive radioimmunoassay.
Mortality after long exposure to cummingtonite-grunerite. J.C. McDonald, G.W. Gibbs, F.D. Liddell, et al. 1978;118(2):271-7. PubMed · Publisher

Abstract

Ore containing cummingtonite-grunerite has been mined to extract gold since 1876 in Lead, South Dakota. Each of the 1,321 men who were recorded as having worked 21 years or more with the Homestake Mine was allocated to one of 5 dust-exposure categories on the basis of work history and available information on environmental conditions. All except 9 men were traced to the end of 1973, when 652 were still living; the cause of death was ascertained for 657 of the 660 men who had died. Deaths from cerebrovascular accidents and malignant disease were close to the numbers expected and from accidents and other causes were fewer than expected, but in each of the 3 diagnostic groups--pneumoconiosis (mainly silicosis), tuberculosis, and heart disease--there were more than 30 excess deaths. A clear dust-exposure relationship was found for pneumoconiosis and respiratory tuberculosis--with relative risks for the 2 groups with greatest exposure to dust as compared to the 2 with least exposure, of 19.9 and 16.0, respectively, but there was no convincing evidence of an increase in respiratory cancer.
Diagnosis of asbestosis by transbronchial biopsy. A method to facilitate demonstration of ferruginous bodies. P.B. Kane, S.L. Goldman, B.H. Pillai, et al. 1977;115(4):689-94. Case report PubMed · Publisher

Abstract

The diagnosis of asbestos-associated pulmonary fibrosis was established in 3 patients by finding ferruginous bodies in transbronchial lung biopsies. Ferruginous bodies may be difficult to identify in histologic preparations when they are not oriented parallel to the plane of tissue section or when camouflaged by anthracotic pigment. We describe a simple method to enhance diagnostic sensitivity by digesting biopsy tissue and examining the filtered residue for ferruginous bodies.
The significance of asbestos exposure in the diagnosis of mesothelioma: a 28-year experience from a major urban hospital. F.M. Hasan, G. Nash, H. Kazemi. 1977;115(5):761-8. PubMed · Publisher

Abstract

A continued increase in the incidence of diffuse mesothelioma has been attributed to greater industrial use of asbestos but is also due in part to wider acceptance of this tumor by pathologists. In this retrospective study, the epidemiology, clinical presentation, and pathology of asbestos and non-asbestos-related mesothelioma from a major urban hospital were reviewed. Of the 36 cases of mesothelioma on file, 19 were not associated with exposure to asbestos. Although a retrospective study raises the possibility of inadequate occupational histories, the lack of history of asbestos exposure correlated with postmortem histology by light microscopy. When postmortem material was reviewed, evidence of asbestos exposure was present in all cases of mesothelioma with history of exposure to asbestos, and in no cases in which the patient denied history of asbestos exposure. Using strict histologic and histochemical criteria, the diagnosis of mesothelioma was confirmed in 8 of 9 patients with asbestos-related mesothelioma but in only 4 of 13 cases of non-asbestos-related mesothelioma. The diagnosis of diffuse methelioma is often difficult to make even wtih complete autopsy examinations. It should be entertained only with adherence to strict clinical and pathologic criteria, especially in women with no history to exposure to asbestos dust.
Asbestos-related diseases of the lung and other organs: their epidemiology and implications for clinical practice. M.R. Becklake. 1976;114(1):187-227. Review PubMed · Publisher
Estimating health risks in studies of the health effects of asbestos. P.E. Enterline. 1976;113(2):175-80. PubMed · Publisher

Abstract

Epidemiologic studies of respiratory cancer hazards associated with asbestos exposure in working populations should provide some estimate not only of whether an excess in cancer exists but of the magnitude of this excess. While most studies seem to be in agreement as to the existence of an excess, there is considerable disagreement as to its magnitude. For 11 studies, estimates of relative risk for respiratory cancer range from about 1.2 to 9.2. Four features of these 11 studies can be identified that account for some of the variation in results: some studies include workers whose exposure to asbestos was too recent to be likely to produce cancer by the end of the follow-up period, and results are diluted by the presence of these workers; in most studies, the wrong population was used for estimating expected numbers of deaths; in some studies, death certificates for the study population were corrected based on a review of other medical records, but then comparisons were made with expected deaths derived from uncorrected death certificates; finally, in most studies, level and duration of exposure is unknown, and this is clearly a factor that determines the magnitude of the respiratory cancer risk. For 6 of the 11 studies it was possible from published material to correct results roughly for the first 3 of these factors and much of the variation disappeared. Problems in the 11 studies reviewed here should be considered in planning and reporting on epidemiologic investigations in the future.
Asbestos exposure and multiple primary tumors. V.A. Dohner, R.G. Beegle, W.T. Miller. 1975;112(2):181-99. PubMed · Publisher

Abstract

Recently we observed 5 patients with multiple primary tumors who also had a history of occupational asbestos exposure. Two patients had a lung carcinoma and a colon carcinoma and 3 others had 2 distinct pulmonary carcinomas. Most of the attending physicians were unaware of the patient's occupational risk for asbestos exposure and the resultant health hazards. Therefore, we review the uses of asbestos and occupations at risk for asbestos exposure.
Biochemical characterization of hyaluronic acid from a case of benign, localized, pleural mesothelioma. M. Motomiya, M. Endo, H. Arai, et al. 1975;111(6):775-80. PubMed · Publisher

Abstract

The tissue of a benign, localized, pleural mesothelioma was digested with protease, and the crude polysaccharide was fractionated by a column of Dowex-1 (Cl-form). The eluate from the column was electrophoresed and incubated with various mucopolysaccharide lysases. Based on the results of column chromatography, electrophoresis, and enzymatic digestion, it was found that hyaluronic acid was the major constituent of the glycosaminoglycans in pleural mesothelioma. The hyaluronic acid from pleural mesothelioma seemed to be identical in structure with that from human umbilical cord; however, the hyaluronic acid from mesothelioma was eluted before that from human umbilical cord when fractionated by the column of Sepharose 4B, suggesting a differnence in molecular size between the two. Also, evidence was obtained for the presence of dermatan sulfate and heparan sulfate.
Cigarette smoking, asbestos, and pulmonary fibrosis. W. Weiss. 1971;104(2):223-7. PubMed · Publisher
Early effects of asbestos exposure on lung function. G. Jodoin, G.W. Gibbs, P.T. Macklem, et al. 1971;104(4):525-35. PubMed · Publisher
Floor tile installation as a source of asbestos exposure. R.L. Murphy, B.W. Levine, F.J. al-Bazzaz, et al. 1971;104(4):576-80. PubMed · Publisher

Abstract

Asphalt or vinyl-asbestos floor tile contains fifteen to twenty-five per cent asbestos, but the mineral fibers are firmly embedded in the binding material. Installation of these tiles would, therefore, seem to be an unlikely source of a hazardous dust exposure. Case reports of two installers of floor tile, one with biopsy-proved mesothelioma and another with extensive pleural calcifications are presented. Both workers had frequently sanded asphalt and vinyl tile floors prior to installation of new floor covering. An investigation of the work process revealed that under simulated conditions of work, asbestos dust concentrations as large as 1.3 fibers per ml were found in air samples passed through membrane filters worn by a person engaged in sanding vinyl asbestos. Characteristic asbestos fibers were seen in electron photomicrographs of these samples. These findings suggest that before the tile sanding procedure is performed adequate respiratory protection should be provided or alternate, available installation methods should be used.

PubMed has no abstract for this study. This is the authors' abstract, copied from the article.
Two cases of malignant mesothelioma after exposure to asbestos. P. Champion. 1971;103(6):821-6. PubMed · Publisher
Pulmonary talc granulomatosis. A complication of drug abuse. G.B. Hopkins, D.G. Taylor. 1970;101(1):101-4. PubMed · Publisher

1960s

Asbestos and health in 1969. G.W. Wright. 1969;100(4):467-79. Review PubMed · Publisher

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