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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cohort study has been carried out of 2167 subjects employed between 1941 and 1983 at an asbestos cement factory in England. The production process incorporated the use of chrysotile asbestos fibre only, except for a small amount of amosite during four months in 1976. Measured airborne fibre concentrations available since 1970 from personal samplers showed mean levels below 1 fibre/ml, although higher levels had probably occurred previously in certain areas of the factory. No excess of lung cancer was observed in the mortality follow up by comparison with either national or local death rates, and analyses of subgroups of the workforce by job, exposure level, duration of employment, duration since entry, or calendar years of employment gave no real suggestion of an asbestos related excess for this cause of death. There was one death from pleural mesothelioma and one with asbestosis mentioned as an associated cause on the death certificate, but neither is thought to be linked to asbestos exposure at this factory. Other suggested asbestos related cancers, such as laryngeal and gastrointestinal, did not show raised risks. Although the durations of exposure were short in this study, the findings are consistent with two other studies of workers exposed to low concentrations of chrysotile fibre in the manufacture of asbestos cement products which reported no excess mortality.
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PMID:Follow up study of workers manufacturing chrysotile asbestos cement products. 302 95

The ability of inhaled asbestos to produce asbestosis, lung cancer, and mesothelioma in both humans and animals is well established, and asbestos exposures in the occupational and general community environment are recognized as significant hazards. However, it has not been possible to establish realistic and credible dose-response relationships, primarily because of our inability to define which constituents of the aerosols produce or initiate the pathological responses. It is generally acknowledged that the responses are associated with the fibers rather than the nonfibrous silicate mineral of the same chemical composition. Available data from experimental studies in animals exposed by injection and inhalation to fibers of defined size distributions are reviewed, alone with data from studies of fiber distributions in lungs of exposed humans in relation to the effects associated with the retained fibers. It is concluded that asbestosis is most closely related to the surface area of retained fibers, that mesothelioma is most closely associated with numbers of fibers longer than approximately 5 microns and thinner than approximately 0.1 micron, and that lung cancer is most closely associated with fibers longer than approximately 10 microns and thicker than approximately 0.15 micron. The implications of these conclusions on methods for fiber sampling and analyses are discussed.
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PMID:Asbestos exposure indices. 328 41

The presence of asbestos containing materials (ACM) in office and commercial buildings is a significant environmental problem. Asbestosis, mesothelioma and lung cancer have been linked with industrial exposure to airborne asbestos. The extensive use of asbestos products in buildings has raised concerns about the widespread exposure of the general public to asbestos in nonoccupational settings. The presence of asbestos in a building does not necessarily mean that significant exposure of the occupants of the building has occurred, but it is important that the asbestos be monitored regularly to ensure that fibers do not become airborne. If ACM are contained within a matrix and not disturbed, exposure is unlikely. However, if the asbestos becomes friable (crumbling) or if building maintenance, repair, renovation or other activities disturb ACM, airborne asbestos fibers may be a source of exposure to the occupants of the building. Currently, asbestos exposure assessment is conducted by a phase contrast light microscope (PCM) technique. Due to its inherent limitation in resolution and the generic counting rules used, analysis by the PCM method underestimates the airborne asbestos fiber concentration as compared to analysis by transmission electron microscopy (TEM). It is important that the air monitoring results analyzed by PCM be interpreted carefully in conjunction with a survey by a professional to judge the physical condition of the ACM in buildings. Exposure levels to airborne asbestos fibers vary from day to day and depend on the physical condition of the material involved and the type of operating and maintenance program in place.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessing asbestos exposure potential in nonindustrial settings. 330 96

Tracheal explants from Sprague-Dawley rats were briefly exposed to cigarette smoke or air (control) and then to amosite asbestos. Asbestos fibers in or under the tracheal epithelium were counted and extent of hyperplastic lesions was ascertained at 24 hours, 72 hours, and 1 week after exposure. Smoke-exposed cultures showed significantly greater numbers of fibers in the epithelium and greater proliferative activity compared to findings in cultures not exposed to smoke. These observations indicate that very short exposure to cigarette smoke can directly affect the response of the epithelium to asbestos fibers and that smoke exposure need not be concurrent with asbestos exposure for such event to occur. These reactions may play a role in the greater incidences of lung cancer and asbestosis seen in asbestos-exposed workers who smoke.
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PMID:Direct enhancement by cigarette smoke of asbestos fiber penetration and asbestos-induced epithelial proliferation in rat tracheal explants. 336 89

This paper, updating the findings of an earlier study, provides additional evidence that sheet metal workers in the construction trades are at increased risk for asbestos-related disease. A proportional analysis of cause of death among 331 New York sheet metal workers found a significantly elevated PMR for lung cancer (PMR = 186). In addition, there were six deaths attributable to mesothelioma (three classified as lung cancer deaths) and three death certificates mentioned asbestosis or pulmonary fibrosis, although none of these three deaths were attributed to these diseases.
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PMID:Asbestos disease in sheet metal workers: proportional mortality update. 338 68

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.
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PMID:Natural killer cell activity in asbestos workers. Interactive effects of smoking and asbestos exposure. 340 24

Lung cancer originates most commonly in the upper lobes in the general population but among workers with asbestosis it is most common in the lower lobes. Published data on lobar distribution were used to estimate the probabilities that lung cancer among asbestos workers is attributable to exposure to asbestos. This attribution varies directly with the relative risk. Critical values of the relative risk at which attribution of lung cancer to asbestos equalled its attribution to other causes, mainly smoking, were calculated. At a relative risk above 2.81 upper lobe cancers were more likely to be due to asbestos than not. For middle and lower lobe cancers, the critical relative risk was 1.55. These critical values were compared with published standardised mortality ratios reported for cohorts of workers with asbestosis. Since the ratios ranged from 6.3 to 9.1, the probability that lung cancer in such cases is due to asbestos is high regardless of lobe of origin. In many cohorts unstratified by the presence or absence of asbestosis the risk ratios are below one or both of these critical values. Since risk ratios are so high among workers with asbestosis, the ratios must be lower for workers without asbestosis than the overall ratios for unstratified cohorts. Therefore, the critical values may be useful in workers without asbestosis among such cohorts to estimate the upper limit of the probability that lung cancer in a given lobe is due to exposure to asbestos.
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PMID:Lobe of origin in the attribution of lung cancer to asbestos. 341 20

One hundred and fifty five male cases of asbestosis certified by the London Pneumoconiosis Medical Panel during 1968-74 were followed up during 1978-9, 4-11 (mean 7.5) years after certification. Fifty nine patients had died, 23 (39%) from lung cancer, 6 (10%) from mesothelioma, and 11 (19%) from other respiratory causes. The number of observed deaths was 2.25 times greater than expected and 7.4 times greater than expected for lung cancer. Adenocarcinoma was the commonest histological type but other cell types were also increased. Finger clubbing (p less than 0.01) and percentage of predicted FEV1 (p less than 0.01) were of value in predicting death, but increasing profusion of small opacities greater than 1/0 (ILO/U-C international classification of radiographs of pneumoconiosis, 1971), duration of exposure to asbestos, time from first exposure to asbestos, and percentage of predicted vital capacity and transfer factor did not predict death.
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PMID:Mortality in cases of asbestosis diagnosed by a pneumoconiosis medical panel. 343 33

Current topics for occupational and environmental medicine and physiology in the U.S.A., especially in the National Institute for Occupational Safety and Health (NIOSH), and the University of California, San Francisco, are reviewed. Reduction of the rate for occupational lung diseases is one of the national objectives for occupational safety and health in the U.S.A., and NIOSH has rated it as the top disease of ten-leading work-related diseases and injuries. Current topics for occupational lung diseases--asbestosis, byssinosis, silicosis, coal worker's pneumoconiosis, lung cancer, and occupational asthma & hyperreactivity, and for pathophysiology of airway hyperreactiveness and pulmonary edema are discussed.
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PMID:[Current topics for occupational and environmental medicine and physiology in the U.S.A.--with special reference to occupational lung diseases]. 352 79

Upon autopsy, asbestos was found in the lungs of 7 primary lung cancer patients out of 70. These seven-patients were men over 60 years old. All of them had occupational histories of exposure to asbestos. In histological classification, 4 of the cases were adenocarcinoma and the others were squamous. Six of them were in the peripheral area. According to chest X-rays two of the patients showed lung fibrosis (asbestosis), and all of them showed pleural plaque. Thus, we concluded that ten percent of the primary lung cancer cases autopsied in our hospital might be induced by exposure to asbestos.
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PMID:[Clinical evaluation of primary lung cancer induced by exposure to asbestos]. 357 10


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