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

Although serum CA 19-9 is considered to be a useful and specific tumor marker for pancreatic cancer, some patients with benign pulmonary diseases show elevated serum CA 19-9 levels. We measured serum CA 19-9 levels of 156 patients with benign pulmonary diseases (55 with asbestosis, 11 with bronchial asthma, 32 with bronchiectasis, 16 with idiopathic pulmonary fibrosis (IPF), 13 with healed pulmonary tuberculosis (HPT) and 29 other benign diseases). The percentage of patients with positive serum CA 19-9 was 42.3% (14.5% in asbestosis, 27.3% in bronchial asthma, 59.4% in bronchiectasis, 81.3% in IPF, 61.5% in HPT and 51.7% in others). In some patients, serum CA 19-9 levels were as high as those found in malignant gastrointestinal diseases. Serum CA 19-9 levels correlated well with disease activity. Immunohistochemically, CA 19-9 was expressed in mucous cells of the bronchial gland and surface of the bronchiolar surface epithelium cells in benign pulmonary disease. Gel filtration study suggested some difference in molecular weight between the serum CA 19-9 antigen of lung cancer and that of benign pulmonary diseases. It is suggested that serum CA 19-9 increases in the case of hyperplasia of the bronchiolar epithelium cells or the mucous cells of the bronchial gland. We conclude that benign pulmonary disease is one of the factors that affect serum CA 19-9 levels.
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PMID:[CA 19-9 in patients with benign pulmonary diseases]. 227 61

Complex hygienic, clinical and epidemiologic studies were carried out at 2 enterprises producing asbestos-technical products. It was established that the workers engaged in the production of such products were exposed to relatively low levels of asbestos-containing dust. The course, complications and outcome of asbestos-associated fibrosis were studied in 110 patients. The study revealed that asbestosis was characterized by its slowly progressing development. Asbestosis complications included lung tuberculosis, chronic intersticial pneumonia, and lung cancer. Proceesing from the epidemiologic survey higher risk of malignant neoplasms of the lungs was established in patients with asbestosis in comparison with those exposed to asbestos-associated fibrosis were studied in 110 patients. The study revealed that asbestosis was characterized by its slowly progressing development. Asbestosis complications included lung tuberculosis, chronic intersticial pneumonia, and lung cancer. Processing from the epidemiologic survey higher risk of malignant neoplasms of the lungs was established in patients with asbestosis in comparison with those exposed to asbestos-containing dust but having no occupational disease. The study findings were used for the substantiation of dispensarization principles for patients with asbestosis. The number of follow-up, laboratory and other examinations along with basic curative and preventive measures were pointed out.
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PMID:[Basic principles of mass screening of patients with asbestosis]. 252 66

There is a causal correlation between the inhaled dose of asbestos at the working place, the occurrence of asbestosis, and a 5-fold increased mortality rate of lung cancer. Mesothelioma, which appears to be very rare among the general population, is a specific sign of exposure to asbestos fibres. Malignant tumours of the urinary bladder, the gastro-intestinal tract, the larynx and the oesophagus in workers may also be ascribed to the specific exposure in some cases. After a brief outline of the epidemiology of these diseases the carcinogenic effects of asbestos on the cellular and subcellular level are described. It can be shown from most recent literature that asbestos fibres can also trigger epigenetic and genotoxic effects. Numeric mutation of chromosomes, damage of the plasma membrane, and a modification of the immune system are most significant. In the presence of PAH, asbestos acts as a cocarcinogen. Asbestos fibres are positive in the cellular transformation test. Due to its initiating and promoting effects, asbestos proves to be a complete carcinogen. Obviously, asbestos fulfils the criteria of the modern theory of carcinogenesis as a multicausal and multistep process.
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PMID:[The carcinogenic effect of asbestos]. 253 13

To estimate the effects on health of occupational exposure to crocidolite, a highly toxic form of asbestos, we studied a cohort of 33 men who worked in 1953 in a Massachusetts factory that manufactured cigarette filters containing crocidolite fibers from 1951 to 1957. Twenty-eight of the men have died, as compared with 8.3 deaths expected. This increased mortality was attributable to asbestos-associated diseases. Fifteen deaths were caused by cancer, as compared with 1.8 expected (relative risk, 8.2; 95 percent confidence interval, 4.6 to 13.4), including eight from lung cancer, five from malignant mesothelioma, and two from other types of cancer. There were seven deaths from nonmalignant respiratory disease, as compared with 0.5 expected (relative risk, 14.7; 95 percent confidence interval, 5.9 to 30.3), of which five were due primarily to asbestosis. In contrast, the mortality rates from cardiovascular diseases and all other causes were not increased. Four of the five living workers have pulmonary asbestosis; three of them have recently diagnosed cancers, including two additional lung cancers. We conclude that the extremely high morbidity and mortality in these workers were caused by intense exposure to crocidolite asbestos fibers.
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PMID:Asbestos-associated diseases in a cohort of cigarette-filter workers. 255 14

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.
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PMID:Predictions of future cases of asbestos-related disease among former miners and millers of crocidolite in Western Australia. 215 40

The mortality of workers from an Ontario factory manufacturing amosite asbestos insulation materials under poorly controlled environmental conditions is reported here. Seven (58%) of 12 deaths among exposed workers 10 or more years after first exposure were due to malignancies; four (25%) were from lung cancer, and there were two deaths from peritoneal mesothelioma. Those dying from mesothelioma were 47 and 49 years of age. Three (25%) of 12 deaths were from respiratory disease, two were attributed to asbestosis (in men 42 and 53 years of ages), and one to pneumonia in a 54-year-old male.
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PMID:Mortality among employees of an Ontario factory manufacturing insulation materials from amosite asbestos. 272 89

Because very recent data on asbestos in the environment are available, some fairly firm conclusions can now be drawn regarding current exposure to asbestos fibres. If account is taken of occupational exposure data (where past exposure levels were very high indeed, leading to a very significant risk to workers at the time), it is possible to make some reasoned estimates of the risk from ambient air. In the past, there was considerable confusion regarding the degree of risk for both occupational and environmental conditions. In estimating the risk, account needs to be taken, in particular, of the fact that: (a) occupational exposures in the past were frequently higher than reported; (b) asbestosis (a disease only associated with very heavy occupational exposures) would seem to be mechanistically involved in the development of lung cancer associated with asbestos exposure; (c) chrysotile asbestos is now the commonest form of fibre used unlike in the past, when greater quantities of crocidolite and amosite were used, the latter types being much more closely associated with mesothelioma than chrysotile; (d) overall levels of asbestos in environmental ambient air are lower than they used to be; (e) ingested asbestos seems to be associated with a negligible degree of risk as indicated by animal and human studies. The estimated values of risk provided here are smaller than those published some years ago but are similar to those given in very recent key publications. The level of environmental lifetime risk from exposure to airborne asbestos would appear to be about 1 in 100,000 or even lower. Such a level of risk is exceedingly low, and bearing in mind the criteria of both WHO and the Royal Society of London, it would appear to represent an acceptable 'rare-event' extremely low-level risk, like the cancer risk from the cosmic radiation adsorbed when flying across the Atlantic or from eating charcoal broiled meat, or the risk of being killed by lightning.
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PMID:Estimations of risk from environmental asbestos in perspective. 274 43

Although mesothelioma is generally considered to be caused by asbestos, epidemiologic studies indicate that some cases have another cause. In order to determine whether pulmonary asbestos burden can be used to define asbestos-related mesotheliomas, asbestos burden was quantified in 27 shipyard or construction workers with diffuse malignant mesothelioma of the pleura or peritoneum and a history of asbestos exposure. Their burden was significantly greater than the burden found in 19 unexposed men (P less than 0.001). The burdens were also compared to those of previously reported subjects with asbestosis or lung cancer. The median concentration for total amphibole fibers (2.7 million/g dry lung) in subjects with mesothelioma did not differ significantly from our previously reported median values for 14 subjects with asbestosis (1.3 million/g dry lung) or for 60 asbestos workers with lung cancer (1.3 million/g dry lung). Fiber size distribution for amosite, the most prevalent fiber type, was similar in all three subject groups. Fifteen of 25 (60%) subjects with mesothelioma had mild asbestosis. Asbestos body (AB) concentrations were greater than or equal to 1900/g dry lung, and total amphibole fiber concentrations were greater than or equal to 390,000/g dry lung. Counts of ABs greater than or equal to 0.5/cm2 in histologic sections always signified both of these concentrations in extracts. Thus, histologic sections showing greater than or equal to 0.5 ABs/cm2 or extracts containing asbestos body or amphibole fiber concentrations of at least 1900 or 390,000/g dry lung, respectively, will confirm an asbestos-related mesothelioma.
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PMID:Lung asbestos burden in shipyard and construction workers with mesothelioma: comparison with burdens in subjects with asbestosis or lung cancer. 279 62

A cohort of 820 men in a Paterson, New Jersey, amosite asbestos factory which began work during 1941-1945 was observed from 5 to 40 years after start of work. Most of the cohort had limited duration of work experience (days, weeks, months), though some men worked for several years until the factory closed in 1954. With white males of New Jersey as the control population, Standardized Mortality Ratios (SMRs) of 500 are evident for the cohort for lung cancer and for noninfectious pulmonary diseases (including asbestosis), while being almost 300 for total cancer and about 170 for all causes of death. A statistically significant SMR of almost 200 is seen for colon-rectum cancer. Mesothelioma incidence initially shows a strong relationship with advancing time since onset of exposure and then tails off. The main concern of the study is with dose-response patterns. Response is measured by the mortality for relevant causes of death, while the direct asbestos dosage was measured in two ways. One way was the length of time worked in the factory and the other was the individual's accumulated fiber exposure, calculated by multiplying the aforementioned length of time worked by the estimated fiber exposures associated with the particular job that the worker had in the factory. Whichever measure of dosage is used, it was found that, in general, the lower the dose, the longer it took for adverse mortality to become evident and, also, the smaller the magnitude of that adverse mortality.
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PMID:Mortality experience of amosite asbestos factory workers: dose-response relationships 5 to 40 years after onset of short-term work exposure. 288 May 2

Cytology and histology material from 46 bronchogenic carcinomas occurring in ex-workers from the Wittenoom crocidolite mine and mill in Western Australia and a matched random sample of 234 other bronchogenic carcinomas occurring in Western Australia over the same period were reviewed by a single histopathologist without knowledge of asbestos exposure status. Squamous-cell carcinomas formed 45.7% of the cancers in the asbestos-exposed group but only 32.5% of the cancers in the comparison group. This difference could not be explained by differences in smoking history between the two groups of lung cancer patients or in the type of histopathological material available for review. The excess of squamous-cell cancers was observed in subjects both with and without parenchymal asbestosis.
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PMID:Morphology of bronchogenic carcinoma in workers formerly exposed to crocidolite at Wittenoom Gorge in Western Australia. 300 73


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