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

Projections have been made of the number of mesotheliomas, lung cancers, and cases of asbestosis that might occur over the period 1987 to 2020 in former workers at the Wittenoom crocidolite asbestos mine in Western Australia. Predictions were based on the observed mortality to the end of 1986 and modelling of the mesothelioma rate. Elimination of crocidolite from the lungs was included in the model. Between the years 1987 and 2020 it is predicted that between 250 and 680 deaths will occur due to mesothelioma. This wide range is due to uncertainty on the functional form of the relation between mesothelioma rate and time, and insufficient data to estimate the elimination rate of crocidolite from the lungs. The most likely range is the lower half of this total range--that is, between 250 and 500. It is predicted that between 340 and 465 deaths will occur due to lung cancer. About 45% of these deaths would be attributable to exposure to asbestos. It is estimated that currently there are up to 200 cases of undiagnosed asbestosis. Of these about 50 will die of lung cancer or mesothelioma and are therefore also included in the figures above. Up to 60 former workers may develop the first signs of asbestosis in the future but any such cases are likely to progress to more serious disease at a much slower rate than the cases that have already been identified.
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PMID:Prediction of mesothelioma, lung cancer, and asbestosis in former Wittenoom asbestos workers. 160 35

A cohort study is presented on the mortality of blue-collar workers in an asbestos-cement production plant that has been operating since 1907. Use of both crocidolite and chrysotile is reported. The cohort includes 2608 men and 759 women who were employed in the plant on Jan. 1, 1950 and those who started to work between 1950 and 1980. Follow-up was terminated on April 15, 1986 with 97.9% traced. Expected deaths were estimated from the age- and sex-specific regional mortality rates for the years 1969 to 1981. The data have been analyzed for the period 1964 to 1986 based on person-years at risk: 43,000 for men and 14,494 for women. A statistically significant increase was found in both sexes for mortality from all causes. From 1964 to 1986, 728 men died from all causes (608 expected), 275 with cancer at any site (158 expected) 110 with lung cancer (41 expected), 28 with pleural tumors (1 expected) and 85 with asbestosis (less than 1 expected). Corresponding figures for women were--all causes: 136 deaths versus 102 expected; all cancers: 79 verses 32 expected; lung cancer: 7 versus 2 expected; pleural tumor: 15 versus 0 expected and asbestosis: 4 versus 0 expected. Deaths from digestive tract cancer were in excess only among women (18 observed versus 10 expected, p less than 0.01). No excess was found for deaths from laryngeal cancer. Standardized mortality rates (SMR) for lung cancer among males showed a clear increase in direct relationship with length of follow-up. SMR according to length of employment were 234 for length 10 to 19 years, 363 for 20 to 29 years, and 256 for 30 years or longer (p less than 0.05 and lower).
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PMID:Mortality from respiratory and digestive cancers among asbestos cement workers in Italy. 178 32

Literature published in the years 1934-1965 was reviewed to determine attitudes and opinions of scientists as to whether asbestos is a cause of cancer. In Germany, the issue was decided in 1943 when the government decreed that lung cancer, when associated with asbestosis (of any degree), was an occupational disease. In the United States, however, there was no consensus on the issue until 1964. Opinions of scientists over a 22 year period are shown and the contributions of various cultural, social, economic and political factors to these opinions are discussed. A lack of experimental and epidemiological evidence played a major role in delaying a consensus. Other important factors included a rejection of science conducted outside of the U.S. during this period, particularly a rejection of German scientific thought during and after WWII, and a rejection of clinical evidence in favor of epidemiological investigations. Individual writers rarely changed their minds on the subject of asbestos as a cause of cancer.
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PMID:Changing attitudes and opinions regarding asbestos and cancer 1934-1965. 850 74

Asbestos fibers and ferruginous bodies (FBs) in lung parenchyma, lung cancer tissues, pleural plaques, and pleural and peritoneal mesothelioma tissues from 13 North American insulation workers were analyzed and quantified using an analytical transmission electron microscope and a polarized microscope. Diseases from which these workers suffered included asbestosis, lung cancer, and mesothelioma. They had been occupationally exposed to materials containing chrysotile and amosite; their pathological diagnoses, occupational and cigarette smoking histories, and clinical summaries have been reported. Large numbers of FBs were found in the lungs and small numbers found in extrapulmonary sites. Most of the FBs had cores of amosite fibers. In all instances, lung parenchyma and lung cancer tissues showed chrysotile and amosite fibers in high concentrations (63.1 x 10(6) and 150.2 x 10(6) fibers/g dry tissue as mean values, respectively). Crocidolite fibers were seen in seven of the 13 cases, but in much smaller numbers. Other amphiboles were rarely found. In pleural plaques and in pleural and peritoneal mesothelioma tissues, amosite fibers were markedly fewer in number, whereas chrysotile fibers were seen in similar numbers as in the lungs. No significant differences in the size distribution of asbestos fibers were seen in the different sites. However, the mean widths of chrysotile fibers were thinner than those of amosite fibers. These results strongly suggest that translocation of inhaled asbestos fibers from the lung to other tissues, such as the pleura and the peritoneum, occurs frequently, and that chrysotile may be more actively translocated from the lung, compared to amosite or amphibole asbestos. The likelihood of translocation seems to be strongly related to the thinness of the fibers. Translocated chrysotile fibers may play an important role in the induction of either malignant mesothelioma and/or hyaline plaques, since the asbestos fibers detected in both these sites were mainly chrysotile.
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PMID:Analysis of asbestos fibers in lung parenchyma, pleural plaques, and mesothelioma tissues of North American insulation workers. 180 39

Although tremolite asbestos has been well characterized since 1916, appreciation of its role in disease induction is relatively recent. It has always been understood that the morphology of tremolite is complex, and part of the slowness in recognizing it as a hazard has been definitional in nature. Reduced to simple terms the questions are, when is tremolite "asbestos-like," when is it an innocuous amorphous particle, do these forms occur together, with what confidence can they be separated for regulatory purposes, and what is the spectrum of disease potential for varying exposure? A brake on regulation is partially due to a convergence of opinion of unlikely and unintentional allies: industries producing tremolite-containing materials and some epidemiologists resisting attribution of risk to tremolite on the grounds that its known effects--pleural plaques, asbestosis, lung cancer and mesothelioma--are principally due to chrysotile, which is often contaminated with fibrous tremolite. The latter group concentrate their skepticism on internal-dose biomarker studies associating lung tremolite content with mesothelioma (but not so clearly with lung cancer or asbestosis). They ignore the basic carcinogenic quality of fibrous tremolite, shown in both animal and epidemiological studies. Evidence from the Quebec chrysotile/tremolite mining districts suggests that very low concentrations of tremolite in ambient air can be translated into high concentrations in lung, even in those without occupational exposure. Disease incidence, especially for mesothelioma, seems also to be associated with tremolite air and lung content. The risk associated with tremolite has been demonstrated in Corsica, Cyprus, the United States, and Canada. Of particular importance is an apparent increase in the proportion of mesothelioma risk attributable to tremolite, since the fibers heretofore most responsible for that disease--commercial amphiboles--have been or are being severely regulated or completely eliminated in production and use. Further, amosite and crocidolite, while still a concern, form a small fraction of "asbestos-in-place": most of this material is chrysotile and we do not really know to what degree it is contaminated with tremolite. The available evidence suggests that bulk analysis or airborne fiber analysis will not answer this question, and perhaps only animal bioaccumulation assay is sufficient. Until we know more, it seems prudent for public health to avoid dispersing chrysotile/tremolite into the environment, and, where we can, to regulate all tremolite "fibers" conservatively.
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PMID:Health effects of tremolite. Now and in the future. 180 62

Data on the health effects caused by locally mined chrysotile asbestos in Zimbabwe have been very limited. The prevailing local view has been that risk is minimal. In this report we critically reassess the cases of 51 individuals with asbestos exposure who have been compensated by the Central Pneumoconiosis Bureau since independence in 1980. Results demonstrate that the major health risks of exposure reported elsewhere--morbid asbestosis, nonmalignant pleural disease, malignant mesothelioma, and lung cancer--all occur in Zimbabwe, at least among workers in the asbestos mines and mills. It is concluded that further investigation and control measures in the industry are warranted.
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PMID:Chrysotile asbestos and health in Zimbabwe: I. Analysis of miners and millers compensated for asbestos-related diseases since independence (1980). 184 1

Reducing the incidence of diseases caused by exposure to radon, lead and asbestos is a major public health challenge. Radon gas, which usually enters a home through the foundation, can cause lung cancer. Exposure to lead through paint, auto emissions and other sources can cause neurologic deficits, as well as anemia, abnormal vitamin D metabolism, nephropathy, hypertension and reproductive abnormalities. Asbestos, which is used in a vast number of products, is primarily associated with parenchymal asbestosis, pleural fibrosis, mesothelioma and lung cancer. The family physician can play a pivotal role in providing information about hazardous exposure, sources of exposure, epidemiology and disease prevention.
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PMID:Overview of radon, lead and asbestos exposure. 195 Sep 82

A prospective mortality study of 839 men employed in the manufacture of asbestos cement products in 1969 examined lung cancer risk in relation to lung fibrosis seen on chest x ray film, controlling for age, smoking, and exposure to asbestos. Twenty or more years after hire, no excess of lung cancer was found among workers without radiographically detectable lung fibrosis, even among long term workers (greater than or equal to 21.5 years); nor was there a trend in risk by level of cumulative exposure to asbestos among such workers. By contrast, employees with small opacities (greater than or equal to 1/0; ILO classification) experienced a significantly raised risk of lung cancer (nine observed deaths v 2.1 expected), even though their exposures to asbestos were similar to the exposures of long term workers without opacities. In this population, excess risk of lung cancer was restricted to workers with x ray film evidence of asbestosis, a finding consistent with the view that asbestos is a lung carcinogen because of its fibrogenicity.
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PMID:Asbestosis as a precursor of asbestos related lung cancer: results of a prospective mortality study. 202 87

Usual interstitial pneumonitis (UIP) is a chronic pulmonary process with a characteristic peripheral fibrotic pattern on gross pathologic lung sections and CT scans. This condition is often idiopathic, but asbestosis, rheumatoid arthritis, and scleroderma may cause the same peripheral fibrosis in the lungs. UIP is associated with an increased incidence of pulmonary neoplasms. The purpose of this study was to evaluate the size of mediastinal lymph nodes in patients with UIP in whom no evidence was seen of malignancy or current active infection. CT scans of 14 patients (12 with idiopathic pulmonary fibrosis and two with collagen vascular disorders) were assessed for lymph node location (American Thoracic Society mediastinal map) and size. In 13 of 14 patients, nodes measured greater than threshold size values. Nodes as large as 20 x 30 mm were identified in three patients. Nodal sites 10R, 4R, 2R, 5, and 6 were most commonly abnormal. We conclude that increase in the size of mediastinal lymph nodes as shown on chest CT scans is common in patients with UIP, occurs without superimposed infectious or malignant complications, and is thus presumably part of the chronic inflammatory process. Consequently, lymphadenopathy in these patients does not suggest that they have lung cancer also.
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PMID:Mediastinal lymph node enlargement on CT scans in patients with usual interstitial pneumonitis. 210 8

Asbestos is a mineral of special technical properties and therefore used in many products all over the world. The inhalation of asbestos causes chronic inflammation of lung--the asbestosis--and pleura--pleuraplaques and pleuritis--and is responsible for mesothelioma and lung cancer. Under normal conditions the diagnosis asbestosis is easy because of the typical x-ray findings and the history of intensive exposure of asbestos. In rare conditions the history of exposure is uncertain and the diagnosis might be difficult. The expected anuity depends on the loss of lung-function. First we find a restrictive ventilatory disorder i.e. a reduction in VC and compliance. Later after progress of the disease the gasexchange is impaired. In case of mesothelioma or lungcancer the person is generally expected to be unable to work.
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PMID:[Expert assessment of asbestos-induced lung damage]. 213 90


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