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

Bleomycin is an agent with significant antitumor efficacy whose major dose limiting toxicity is pulmonary fibrosis. Attempts have thus been made to identify congeners with reduced toxicity and with comparable or greater antitumor activity. Tallysomycin S10b is a bleomycin analogue possessing significantly greater potency, equal or reduced lung toxicity, and slightly greater antineoplastic activity when compared to the parent compound in preclinical studies. This report describes our experience with tallysomycin S10b in 30 patients with a variety of non-hematologic neoplasms. Pulmonary toxicity, occurring in 4 patients, was the major toxicity. The recommended cumulative dose of tallysomycin S10b was difficult to establish from the results of this study, as pulmonary toxicity appeared to be more idiosyncratic than dose- or schedule-dependent. The employment of more sensitive methods for detecting pulmonary toxicity in this study suggest that tallysomycin S10b may have reduced pulmonary toxicity compared to the parent compound. Both bleomycin and tallysomycin S10b have similar t1/2 beta half-lives of 2-4 h. Six patients had prolonged terminal elimination half-lives of tallysomycin S10b, but no clear relationship between this phenomenon and efficacy or toxicity was evident. No complete or partial responses occurred. Disease stabilization occurred in 4 of 15 patients with diagnoses of renal cell carcinoma, rectal cancer and lung cancer. Five of eight patients with non-measurable disease had stable disease, including one with mesothelioma, one with carcinoma of the head and neck, two with renal cell cancer and one with colon carcinoma.
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PMID:Phase I trial of tallysomycin S10b, a bleomycin analogue. 169 67

The relative risk of mesothelioma associated with different levels of exposure to asbestos was evaluated. The exposure was assessed from work histories of 51 mesothelioma cases and 51 sarcoidosis referents. The lung fiber concentration of the mesothelioma patients was compared with that of two reference groups (13 random autopsy cases and 43 male lung cancer patients). When the categories definite and probable were used as an estimated probability of occupational exposure, an odds ratio of 17.7 [90% confidence interval (90% CI) 3.4-253] and 3.0 (90% CI 0.9-10.6), respectively, was obtained. A lung fiber concentration of greater than 1 million fibers/g of dry tissue as an indicator of accumulated exposure gave an odds ratio of 14.4 (90% CI 2.5-178) for the men in comparison with the autopsy cases and 3.1 (90% CI, 1.3-7.5) in comparison with the lung cancer patients. Elevated risk of mesothelioma was shown to be associated with a lung fiber concentration of greater than 1 million fibers/g of dry tissue.
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PMID:Relative risk of mesothelioma associated with different levels of exposure to asbestos. 178 34

Selection bias is inherent in all occupational cohorts. Selection bias at entry has long been known and is commonly referred to as a "healthy worker effect." Less well appreciated is selection during the life of a cohort resulting from life-style factors (e.g., cigarette smoking); aging with accompanying chronic diseases, economic and demographic circumstances; and diseases that might result from exposures suffered by the cohort being studied, that influence whether individuals remain in a trade. These factors weigh differently at different times. Thus, at any point in time, "surviving" members of a cohort reflect an amalgam of selection factors. When such groups are studied in cross-sectional surveys there can be uncertainty whether clinical, radiological and physiological findings are necessarily representative for the trade or occupation as a whole. We analyzed the results of a large clinical field survey of long-term asbestos insulation workers to investigate whether the non-participants differed substantially from those who were examined. Five thousand three hundred and fifty-five (5,355) men, of an initial cohort of 17,800 established January 1, 1967, had reached 30 or more years from onset of their work by July 1, 1981. All were invited to come for examination. Two thousand and seventy-seven (2,077) came, and 3,278 did not. We questioned a sample of 1,393 non-responders to see why they failed to appear. The answers did not give evidence of significant health-related selection influence. Sickness only infrequently kept them away. We then followed both groups--those examined and those not examined--to the end of 1987 for their mortality experience. There was no great difference. The non-responders had somewhat fewer deaths overall and proportionately fewer of asbestos-associated cancers, such as mesothelioma and lung cancer. The results indicated that, in this cohort, there did not seem to be health-related selection bias that determined whether or not cohort members responded to invitations for examinations.
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PMID:Evaluation of selection bias in a cross-sectional survey. 179 4

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

Cancer mortality excess has been reported repeatedly over the past hundred years to occur in merchant seamen. More recently lung cancer has been found to account for some of this excess and the question of the contribution made by cigarette smoking raised. In the one study where there was some information on smoking habit, it did not appear that cigarettes would have accounted for all the excess cancer observed. In other mortality studies, where excess cancer mortality was observed, the other cigarette-linked causes of death were not prominent. In a preliminary mortality analysis of a small population of merchant seamen, two cases of malignant mesothelioma have so far been identified, and in a national mesothelioma register 28 cases have been reported in seamen: both instances constitute abnormal occurrences. The presence of substantial amounts of asbestos-containing materials in naval construction which are continuously subjected to vibration and intermittently disturbed during servicing, and the detection of radiological stigmata consistent with asbestos exposure, add plausibility to the hypothesis that occupational asbestos exposure contributes to the apparent excess cancer mortality in merchant seamen. Methodologic deficiencies in epidemiologic studies reported to date make for uncertainty. Properly designed studies will be needed to quantify disease excess and to identify potentially causal associations. Even in the absence of such data it would be prudent to contain the asbestos currently installed and to promote smoking cessation programs.
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PMID:Cancer mortality in merchant seamen. 180 46

In in vitro test systems, chrysotile is markedly toxic, causes chromosomal aberrations, and is capable of inducing morphological and preneoplastic transformation. In carefully designed animal experiments, chrysotile produces lung cancer and mesothelioma as effectively as do the amphiboles tested. Human population studies do not refute these experimental results. Chrysotile asbestos is carcinogenic to humans, especially for the induction of lung cancer and mesothelioma in exposed populations. For cancers of other sites, with the exception of laryngeal and possibly gastrointestinal cancer, the evidence for association with exposure to all forms of asbestos, including chrysotile, is not yet adequate for evaluation.
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PMID:The carcinogenicity of chrysotile asbestos. 180 60

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

In the oil refining and petrochemical industries exposure to cancer-causing asbestos particles, especially during equipment repair and maintenance, is very high. Up to 90% of workers in the oil refining industry had direct and/or indirect contact with asbestos, and more than half of this contact occurred without the use of any kind of precaution, thus these workers are in high risk of developing lung cancer and mesothelioma, both fatal diseases. The hazards include: inadequate health and safety training for both company personnel and workers, failure to inform about the dangers and diseases (cancers) resulting from exposure to asbestos; excessive use of large numbers of untrained and uninformed contract workers; lack of use of protective equipment; and archaeological approaches and responses to repairing asbestos breaks and replacement of asbestos in oil refining facilities. For a better understanding of practices and policies in the oil refining industry, refer to Rachel Scott's Muscle and Blood, in particular the chapter "Oil" (E.P. Dutton, New York, 1974), as well as to an editorial which appeared in the Oil and Gas Journal, April, 1968.
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PMID:Dangerous and cancer-causing properties of products and chemicals in the oil refining and petrochemical industry: Part V--Asbestos-caused cancers and exposure of workers in the oil refining industry. 185 54

The constitutive cell types of the two lung cancer cell lines CaLu1 and CaLu3 have been investigated by immunocytochemical staining with markers for cytokeratins, vimentin, carcinoembryonic antigen and the epithelial cell epitope recognized by the monoclonal antibody Ber-EP4. The cells of both lines reacted with vimentin, with CAM 5.2, which is a marker for cytokeratins 8, 18 and 19, and with a specific marker for cytokeratin 19. CaLu3 cultures showed patchy staining, and CaLu1 none, when treated with a monoclonal antibody reactive with cytokeratins 13, 14 and 17. CaLu3 cells all reacted strongly with Ber-EP4 and the antibody to carcinoembryonic antigen, whereas CaLu1 gave a negative reaction with both these reagents. These results indicate that the CaLu3 line has retained antigens characteristic of some bronchial adenocarcinomata, and that the CaLu1 line was derived from a mesothelioma rather than a pleural metastasis of a squamous carcinoma.
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PMID:Immunocytochemical investigation of the tissue of origin of two lung cancer cell lines. 188 40

Workers in developing countries face as many, if not more, work-related health problems as their counterparts in industrialized nations. This paper concentrates on occupational health problems in the sugar industry, which exists in 40 countries, mostly in the Third World. Sugar cane workers have a high level of occupational accidents and are exposed to the high toxicity of pesticides. They may also have an increased risk of lung cancer, possibly mesothelioma. This may be related to the practice of burning foliage at the time of cane-cutting. Bagassosis is also a problem specific to the industry as it may follow exposure to bagasse (a by-product of sugar cane). The workers may also be affected by chronic infections which reduce their productivity. The legal framework for their protection is often inadequate. In conclusion, areas of future research are suggested.
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PMID:Aspects of occupational health in the sugar cane industry. 192 44


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