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PubMed1997

Exposure and mineralogical correlates of pulmonary fibrosis in chrysotile asbestos workers.

OBJECTIVES: The relation between lifetime cumulative exposure to asbestos, pathological grade of pulmonary fibrosis, and lung burden of asbestos at death, was explored in a necropsy population of former workers in a chrysotile asbestos textile plant in South Carolina. METHODS: Estimates of cumulative, mean, and peak exposures to asbestos were available for 54 workers. Necropsy records and lung tissue samples were obtained from hospital files. Matched control cases were selected from consecutive necropsies performed at the same hospitals. The extent and severity of pulmonary fibrosis was graded on tissue sections. Mineral fibres in lung tissue were characterised by transmission electron microscopy combined with x ray spectroscopy. RESULTS: A significant positive correlation (r = 0.67, P < 0.0001) was found between lifetime cumulative exposure to asbestos and total lung burden of asbestos fibres. This relation was also found for the individual types of asbestos associated with the exposure: chrysotile and tremolite. Pulmonary fibrosis was correlated with both cumulative exposure to asbestos (r = 0.60, P < 0.01) and the concentration of asbestos fibres in the lung (r = 0.62, P < 0.0001). The concentration of tremolite fibres in the lung provided a better estimate of lung fibrosis than did the concentration of chrysotile. Asbestosis was usually present in asbestos textile workers with more than 20 fibre-years cumulative exposure. The lengths and aspect ratios of chrysotile asbestos, but not amphibole asbestos, were greater in the lungs of asbestos fibre workers than in the control population. Textile workers with lung cancer had significantly greater cumulative exposures and fibrosis scores than workers without lung cancer. CONCLUSIONS: Both cumulative exposure to asbestos and lung fibre burden are strongly correlated with severity of asbestosis. The data also support the hypothesis that the high prevalence of asbestosis and lung cancer in this population resulted from exposure to long fibres of chrysotile asbestos in the workplace.

Asbestos, Serpentine↗
PubMed1989

Conventional and high resolution computed tomography in the diagnosis of asbestos-related diseases.

High resolution CT (HRCT) can image the fine structures of the lung parenchyma and the pleura. Analysis of supine and prone HRCT scans in 300 patients with asbestos exposure shows that asbestosis is characterized the following findings; (1) parenchymal bands, (2) increased interlobular septa, (3) increased intralobular core structures, (4) subpleural lines, and (5) dependent opacity. Pleural disease is well displayed on HRCT scans. Correlated studies with whole lung sections confirm the HRCT findings. Masses in asbestosis may be benign or malignant, and CT helps in their differentiation. HRCT correlates well with radiographic and clinical criteria for asbestosis and is more sensitive than either in detecting abnormalities.

Asbestosis↗
PubMedDate not supplied

Pneumoconiosis: comparison of imaging and pathologic findings.

Pneumoconiosis may be classified as either fibrotic or nonfibrotic, according to the presence or absence of fibrosis. Silicosis, coal worker pneumoconiosis, asbestosis, berylliosis, and talcosis are examples of fibrotic pneumoconiosis. Siderosis, stannosis, and baritosis are nonfibrotic forms of pneumoconiosis that result from inhalation of iron oxide, tin oxide, and barium sulfate particles, respectively. In an individual who has a history of exposure to silica or coal dust, a finding of nodular or reticulonodular lesions at chest radiography or small nodules with a perilymphatic distribution at thin-section computed tomography (CT), with or without eggshell calcifications, is suggestive of silicosis or coal worker pneumoconiosis. Magnetic resonance imaging is helpful for distinguishing between progressive massive fibrosis and lung cancer. CT and histopathologic findings in asbestosis are similar to those in idiopathic pulmonary fibrosis, but the presence of asbestos bodies in histopathologic specimens is specific for the diagnosis of asbestosis. Giant cell interstitial pneumonia due to exposure to hard metals is classified as a fibrotic form of pneumoconiosis and appears on CT images as mixed ground-glass opacities and reticulation. Berylliosis simulates pulmonary sarcoidosis on CT images. CT findings in talcosis include small centrilobular and subpleural nodules or heterogeneous conglomerate masses that contain foci of high attenuation indicating talc deposition. Siderosis is nonfibrotic and is indicated by a CT finding of poorly defined centrilobular nodules or ground-glass opacities.

Aged↗
PubMed1993

Fiber burden and patterns of asbestos-related disease in chrysotile miners and millers.

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)

Aged↗
PubMed1983

Asbestos fiber content of the lungs in patients with and without asbestos airways disease.

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.

Aged↗
PubMed1990

Effects of fiber characteristics on lung deposition, retention, and disease.

There is abundant epidemiologic evidence that asbestos fibers can cause lung fibrosis (asbestosis), bronchial cancer, and mesothelioma in humans, as well as limited evidence for such effects in workers exposed to slag and rockwool fibers. Epidemiological evidence for human disease from inhalation exposures to conventional fibrous glass is negative. While health concerns based on the morphological and toxicological similarities between man-made fibers and asbestos are warranted, it is important to note that most of the toxicological evidence for glass fiber toxicity in laboratory animals is based on nonphysiological exposures such as intratracheal instillation or intraperitoneal injection of fiber suspensions. Man-made fibers have produced lung fibrosis and mesotheliomas in such tests, albeit at much lower yields than asbestos. For all durable mineral fibers, critical length limits must be exceeded to warrant concern about chronic toxicity; i.e., 2 microns for asbestosis, 5 microns for mesothelioma, and 10 microns for lung cancer. Fiber width must be less than 0.1 microns for mesothelioma, and larger than this limit for asbestosis and lung cancer. The human health risks for most fibrous glass products are either low or negligible for a variety of reasons. First, most commercial fibrous glass products have mean fiber diameters of approximately 7.5 microns, which results in mean aero-dynamic diameters approximately 22 microns. Thus, most glass fibers, even if dispersed into the air, do not penetrate into the lung to any great extent. Second, the small fraction of smaller diameter fibers that do penetrate into the lungs are not persistent within the lungs for most fibrous glass products due to mechanical breakage into shorter lengths and overall dissolution.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

COX-2 is widely expressed in metaplastic epithelium in pulmonary fibrous disorders.

Idiopathic usual interstitial pneumonia/idiopathic pulmonary fibrosis (UIP/IPF) and asbestosis represent progressive and often fatal pulmonary fibrous disorders, whereas cryptogenic organizing pneumonia (COP), desquamative interstitial pneumonia (DIP), and respiratory bronchiolitis-interstitial lung disease (RB-ILD) usually are reversible or nonprogressive conditions. Prostaglandin E2 (PGE2) inhibits fibroblast proliferation and myofibroblast transition, its production depending on cyclooxygenase-2 (COX-2). In patients with UIP/IPF, levels of PGE2 and COX-2 are reduced in fibroblasts, and levels of PGE2 in bronchioalveolar lavage fluid may be lowered. We analyzed the immunohistochemical expression of COX-2 in UIP/IPF, asbestosis, COP, DIP, and RB-ILD. Our results show that the metaplastic epithelium in UIP/IPF, asbestosis, and COP is widely COX-2+, whereas COX-2 positivity is scant in DIP and RB-ILD. The mesenchymal cells remained negative. Our results suggest that irrespective of the underlying disease, lung injury that causes extensive fibrosis induces wide expression of COX-2 in the regenerating metaplastic epithelium.

Asbestosis↗
PubMed1993

The relationship between HLA-A, B, DQ, and DR antigens and asbestos-induced lung disease.

To evaluate the relationship between human leukocyte antigen (HLA) and both asbestos-induced pulmonary fibrosis and pleural fibrosis, we obtained HLA-A, B, C, DQ, and DR phenotypes in 42 long-term asbestos-exposed workers. Among these exposed workers, 15 had asbestosis (ILO > or = 1/0) on the chest radiograph and 18 had asbestos-induced pleural fibrosis. We found that there was an increased percentage of HLA-A29, HLA-B44, and HLA-Bw4 in the subjects with asbestosis. In addition, we observed a marginally positive relationship between HLA-A29 and the severity of pulmonary fibrosis. Similarly, there was a higher prevalence of HLA-DRw53 and DQ2 in the subjects with asbestos-induced pleural fibrosis. The presence of HLA-DQ2 was significantly related to the extent and type of asbestos-induced pleural fibrosis while HLA-DRw53 was not consistently related to the type or extent of pleural disease. Importantly, we observed that HLA-A29, HLA-B44, HLA-Bw4, HLA-DRw53, and HLA-DQ2 do not have a significantly shorter duration or latency of asbestos exposure. Moreover, none of the HLA haplotypes (A29, B44, Bw4, DRw53, and DQ2) that we found to be associated with radiographic manifestations of asbestos-induced lung disease were associated with the physiologic abnormalities that have been traditionally associated with asbestos-induced lung disease. The only exception was an isolated decrease in the residual volume associated with the presence of HLA-A29. These results suggest that the HLA-A29 phenotype may be associated with the development of asbestosis and the HLA-DQ2 phenotype may be associated with the development of asbestos-induced pleural fibrosis. However, these associations are not particularly strong, physiologic correlation is lacking, and previous studies do not support our findings.

Asbestosis↗
PubMed1981

Exercise performance and functional impairment in asbestos-exposed workers.

Eighty-eight shipyard workers with extensive asbestos exposure were evaluated in terms of dyspnea, smoking history, x-ray film abnormalities, static pulmonary function, and exercise performance. Pulmonary function abnormalities and roentgenographic pleuropulmonary disease were more frequent in smokers. Significant dyspnea was present in 41 percent of the workers and did not correlate with smoking history, pulmonary function, or exercise performance. Despite this high frequency of dyspnea, 70 percent of all workers had normal exercise tolerance by history of exercise testing. Of the 26 workers with exercise impairment, only nine had pulmonary mechanical or gas exchange limitation. Two of these workers had asbestosis, while the other had airways obstruction without asbestosis. The prevalence of both asbestosis and asbestos-related exercise impairment in this population was 2.3 percent.

Aged↗
PubMed1988

Natural killer cell activity in asbestos workers. Interactive effects of smoking and asbestos exposure.

Both the numbers and function of natural killer (NK) cells in 60 were evaluated in asbestos cement workers grouped by smoking history and chest roentgenogram findings (ILO profusion scores less than 1/0 or greater than or equal to 1/0, or isolated pleural plaques). Worker and control subjects who smoked had smoking histories of less than 27 pack-years, a level of smoking lower than that previously determined to adversely affect NK function. Asbestos workers who did not smoke had percentages and total numbers of NK cells and NK function not different from that of nonsmoker control subjects. Workers who smoked and had evidence of asbestosis (ILO profusion category greater than or equal to 1/0) had significantly lower total numbers of NK cells and mononuclear cell NK activity than did smoker control subjects or smokers with pleural plaques only (p less than or equal to 0.05). Numbers of NK cells and NK cell function were not decreased in either of the asbestos-exposed smoking groups without asbestosis when compared to nonsmoker controls. We conclude that smoking and asbestos exposure interact to decrease mononuclear cell NK function in workers with levels of asbestos exposure sufficient to induce asbestosis. This finding may explain in part the previously reported synergistic effect of smoking and asbestos exposure on the risk of lung cancer. Furthermore, the data presented here clarify previous conflicting reports on NK function where asbestos exposed groups have not been stratified for analysis of data.

Adult↗
PubMed1995

[Computed tomography of pneumoconiosis].

This review describes the usefulness of computed tomography (CT) and high-resolution computed tomography (HRCT) in image evaluation in pneumoconiosis. For pneumoconiosis, in the same way as for other diffuse lung diseases, conventional CT includes 10 mm collimation scans at 1 cm intervals from the apex to the base of the lung, whereas HRCT uses five to six 1.2 to 3 mm collimation scans at predetermined representative locations including the aortic arch, the tracheal carina, and 2 cm above the dome of the right hemidiaphragm. The CT scans are performed in the supine position in silicosis and coal workers' pneumoconiosis, and both in the supine and prone position in asbestosis. In silicosis, CT is superior to chest radiography in detecting coalescence of nodules and early stage formation of large opacities. There are good correlations between HRCT findings and histological changes, especially in secondary pulmonary lobules. With HRCT, small nodules are found to be located in the center of the secondary pulmonary lobule in silicotic lungs. The mild emphysematous change associated with silicosis can also be found with HRCT. In coal workers' pneumoconiosis, the HRCT is useful in detecting nodules located in the subpleural and fissural subpleural areas. In asbestosis, the conventional CT can detect pleural plaques more sensitively than chest radiography. HRCT is also especially useful in detecting earlier fibrotic change in asbestosis in lung parenchyma, apparent as subpleural lines, parenchymal bands, subpleural curvilinear line shadows and so on.(ABSTRACT TRUNCATED AT 250 WORDS)

Asbestosis↗
PubMed1990

Effects of individually motivating smoking cessation in male blue collar workers.

Adverse demonstrable health effects linked to the individual's smoking were shown to 2,689 American workers to motivate cessation during routine examinations to detect asbestosis. This intervention was evaluated six to 25 months later by a mailed questionnaire and by telephone to non-responders. Results were compared to yearly quit rates of 2.5 percent to 5 percent for 736 workers who were ex-smokers at the initial examination. Of the 504 men who responded by mail, 29.8 percent had quit smoking, 35.9 percent had cut down from a mean of 28 to 13 cigarettes per day, and 34.3 percent were smoking as before. Subsequent follow-up at one year showed that 25.6 percent remained quit, and that 23 percent of those who cut down had quit, for an overall quit rate of 34 percent. Of 101 non-responders contacted by telephone, 17 percent had quit and 53 percent had reduced smoking. In both samples, those who quit were more likely to have had lower alveolar carbon monoxide (COa) levels, to be older, and to have had asbestosis. Responders by mail were the same age as non-responders but had smoked longer, had higher prevalences of asbestosis, emphysema, chronic bronchitis and higher COa. Demonstration of the adverse personal effects of smoking appear to have contributed to the quit rates or reduced smoking rates in 65 percent of the responding workers.

Adult↗
PubMed1996

Non-ischemic myocardial fibrosis after long-term asbestos exposure.

To determine whether or not myocardial fibrosis in the left ventricle increases after exposure to asbestos fiber, we studied myocardial fibrosis in 42 autopsied hearts; 17 of asbestosis (AS) and 18 of chronic pulmonary disease (CP) without pneumoconiosis. Seven patients with extracardiopulmonary disease were used as a control group (CONT). The extent of myocardial fibrosis in the left ventricle was significantly greater in the AS group compared to the other groups (AS 3.6 +/- 1.3% vs. CP 2.4 +/- 1.0% vs. CONT 1.6 +/- 0.8%). There was a significant difference in the appearance ratio of focal fibrosis between the asbestosis group and the other groups. Focal fibrosis was observed in none of 7 control patients, in 3 of 18 patients with chronic pulmonary disease and in 9 of 17 patients with asbestosis. We concluded that characteristic myocardial fibrosis was observed in humans after long-term asbestos exposure.

Adult↗
PubMed2002

Apportionment in asbestos-related disease for purposes of compensation.

Workers' compensation systems attempt to evaluate claims for occupational disease on an individual basis using the best guidelines available to them. This may be difficult when there is more than one risk factor associated with the outcome, such as asbestos and cigarette smoking, and the occupational exposures is not clearly responsible for the disease. Apportionment is an approach that involves an assessment of the relative contribution of work-related exposures to the risk of the disease or to the final impairment that arises for the disease. This article discusses the concept of apportionment and applies it to asbestos-associated disease. Lung cancer is not subject to a simple tradeoff between asbestos exposure and smoking because of the powerful biological interaction between the two exposures. Among nonsmokers, lung cancer is sufficiently rare that an association with asbestos can be assumed if exposure has occurred. Available data suggest that asbestos exposure almost invariably contributes to risk among smokers to the extent that a relationship to work can be presumed. Thus, comparisons of magnitude of risk between smokers and nonsmokers are irrelevant for this purpose. Indicators of sufficient exposure to cause lung cancer are useful for purposes of establishing eligibility and screening claims. These may include a chest film classified by the ILO system as 1/0 or greater (although 0/1 does not rule out an association) or a history of exposure roughly equal to or greater than 40 fibres/cm3 x y. (In Germany, 25 fibres/cm3 x y is used.) The mere presence of pleural plaques is not sufficient. Mesothelioma is almost always associated with asbestos exposure and the association should be considered presumed until proven otherwise in the individual case. These are situations in which only risk of a disease is apportioned because the impairment would be the same given the disease whatever the cause. Asbestosis, if the diagnosis is correct, is by definition an occupational disease unless there is some source of massive environmental exposure; it is always presumed to be work-related unless proven otherwise. Chronic obstructive airways disease (COAD) accompanies asbestosis but may also occur in the context of minimal parenchymal fibrosis and may contribute to accelerated loss of pulmonary function. In some patients, particularly those with smoking-induced emphysema, this may contribute significantly to functional impairment. An exposure history of 10 fibre x years is suggested as the minimum associated with a demonstrable effect on impairment, given available data. Equity issues associated with apportionment include the different criteria that must be applied to different disorders for apportionment to work, the management of future risk (eg. risk of lung cancer for those who have asbestosis), and the narrow range in which apportionment is really useful in asbestos-associated disorders. Apportionment, attractive as it may be as an approach to the adjudication of asbestos-related disease, is difficult to apply in practice. Even so, these models may serve as a general guide to the assessment of asbestos-related disease outcomes for purposes of compensation.

Asbestos↗
PubMed1993

Lobe of origin of lung cancer among asbestos-exposed patients with or without diffuse interstitial fibrosis.

The effect of asbestos exposure and asbestos-associated fibrosis on the lobe of origin of lung cancer was studied among 108 lung cancer patients. The asbestos-exposed patients had significantly more lower lobe tumors than the unexposed patients. Similar results were obtained when occupational history or lung fiber concentration was used as an indicator of past occupational exposure to asbestos. The predominance of lower lobe tumors occurred even among exposed patients with no histological signs of asbestosis in their lung specimens. Both bronchial and peripheral cancers showed a lower lobe predominance among the exposed patients. Smoking history did not affect the lobar distribution of the tumors. No significant differences occurred for the histological cell types of the tumors between the exposed and unexposed patients. Patients with asbestosis had, however, more adenocarcinomas than the unexposed patients. The results indicate that asbestos may increase the risk of lung cancer even in the absence of asbestosis.

Adult↗
PubMedDate not supplied

Predictions of future cases of asbestos-related disease among former miners and millers of crocidolite in Western Australia.

In a cohort of 6502 male and 410 female former workers from the crocidolite (blue asbestos) mining and milling works at Wittenoom, Western Australia, there were 94 cases of malignant mesothelioma (12 cases of peritoneal mesothelioma), 141 cases of lung cancer and 356 successful compensation claims for asbestosis to the end of 1986. After adjusting for measured covariate effects by means of proportional hazards regression analysis, smooth curves were fitted to the resulting "underlying" incidence rates for malignant mesothelioma, lung cancer and asbestosis, separately, and for mortality of any cause. By the use of these curves and individual risk estimates, predictions have been made of the future incidence of these diseases to the year 2020. With the assumption that all subjects who were not known to be dead or departed overseas still were alive at December 31, 1986, and excluding persons of more than 85 years of age, the number of new cases of mesothelioma is expected to rise to a peak of around 25 cases per year in 2010, with an expected total number of 692 cases of mesothelioma (95% confidence interval [CI], 394-990 cases) between 1987 and 2020. A total of 2898 deaths (95% CI, 2284-3511 deaths) of any cause is expected in the same period. New cases of lung cancer and asbestosis are expected to continue at roughly the current rates of eight and 17 cases per year, respectively, before declining after the year 2000, leading to totals of 183 cases (95% CI, 34-335 cases) and 482 cases (95% CI, 236-728 cases), respectively, being expected by the year 2020. Predictions that were based on the censoring of subjects at the date that they last were known to be alive resulted in slightly higher, but probably less accurate, estimates.

Adult↗
PubMed2004

[Diseases caused by asbestos dust and the trend of their development in exposed workers in 1951-2003].

The paper summarizes the principal information on the properties and effects of asbestos and a survey of diseases which can be recognized in the Czech Republic as occupational diseases according to the List of Occupational Diseases (Government Order 290/1995 Coll.). The paper lists possible diagnostic means and criteria for evaluation and presents a survey of developmental trends of the disease in exposed workers of the plant under study. In the period of years 1951-2003, 87 cases of occupational diseases were reported. The first asbestosis occurred in 1955, the first lung cancer in a patient with a previously reported asbestosis in 1962, the first pleural mesothelioma in 1976, the first asbestosis of the lung with concurrent lung cancer in 1981, and the first pleural hyalinosis in 1999. A very serious fact is that 56, i.e. 64.4% of diseases, particularly lung cancer and mesothelioma, were diagnosed after the termination of working in risk and many years of latency. A long-term folow-up of workers, even of those with a short exposure, is therefore necessary.

Adult↗
PubMed1991

[Maximum permissible levels of asbestos and other natural minerals with fibrous structure--necessity of verification].

MACs of asbestos are from 2 to 20 times higher in Poland than in other Western Europe countries. The analysis of occupational diseases reported between 1983 and 1988 among workers of asbestos-cement plants has showed that Polish MAC values do not protect people from work-related asbestosis. Asbestosis was frequently diagnosed in workers employed at mining and processing of nickel ore containing admixtures of fibrous antigorite. The risk of asbestosis in workers of a nickel++ metallurgical plant was 8 times higher that in those employed at an asbestos-cement plant. In an animal study, fibrogenic, carcinogenic and mutagenic activity of antigorite was similar to the biological aggressiveness of crocidolite. Based on own studies and literature data, the following MACs for asbestos and other natural fibrous minerals were established: a) for dusts containing asbestos and other fibrous minerals except crocidolite and fibrous antigorite, total dust concentration equals 1 mg/m3 and concentration of fibres longer than 5 microns = 0.5 fibre/cm3 b) for dusts containing crocidolite and fibrous antigorite total dust concentration = 0.5 mg/m3 and concentration of fibres longer than 5 microns = 0.2 fibre/cm3.

Air Pollutants, Occupational↗