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

A case-control mortality study was performed at an aircraft engine factory to assess the possible association between exposure to nickel-containing compounds and death from lung cancer. Forty-two non-salaried male workers who died of lung cancer from 1966 to 1976 were identified from a chronological registry of death certificates that has been maintained by the company's medical department. Each of the decedents was matched with the next two non-salaried decedents in the registry who were of the same sex and comparable age (+/- 10 years), and who died of causes other than cancer. Without knowledge of the workmen's identities or causes of death, one of the authors classified the deceased workmen as exposed or non-exposed to nickel compounds during their employment. The proportion of workmen who died of lung cancer and were exposed to nickel (11/42) was found to be equal to the proportion of workmen who died of non-cancerous causes and were exposed to nickel (22/84). This study indicates that workers in an aircraft engine factory who were chronically exposed to low atmospheric concentrations of presumably weakly carcinogenic nickel compounds did not have any apparent increase in the relative risk of mortality from lung cancer prior to treatment.
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PMID:Investigation of exposure to nickel and lung cancer mortality: case control study at aircraft engine factory. 65 7

Continuing observations on cadmium-exposed workers have failed to yield evidence of an increased mortality from prostatic cancer, as initially suspected. There is, however, evidence of an increased mortality from lung cancer and, in at least two of the studies, of a dose-response relationship, but interpretation of these studies with regard to the role of cadmium is complicated by concurrent exposure to other known or suspected carcinogens, including arsenic, nickel, beryllium, chromium and heated mineral oils. An update of a long-term cohort mortality study from 17 plants in England employing a wide range of cadmium processes, while confirming an increased lung cancer risk related to intensity of cadmium exposure, shows some evidence of this risk also being associated with exposure to arsenic. It is thus not possible at present to attribute the excess mortality from lung cancer to cadmium owing to the presence of multiple confounding factors in the populations studied. Their role in the 17-plant study is currently being further investigated.
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PMID:Is cadmium a human carcinogen? 130 71

The Contribution of Occupational Exposures to Lung Cancer. The overall importance of occupational agents as a cause of lung cancer has been a controversial subject since the 1970s. A federal report, released in the late 1970s, projected a surprisingly high burden of occupational lung cancer; for asbestos and four other agents, from 61,000 to 98,000 cases annually were attributed to these agents alone. Many estimates followed, some much more conservative. For example, Doll and Peto estimated that 15% of lung cancer in men and 5% in women could be attributed to occupational exposures. A number of population-based case-control studies also provide relevant estimates. In a recent literature review, Vineis and Simonato cited attributable risk estimates for occupation and lung cancer that ranged from 4% to 40%; for asbestos alone, the estimates ranged from 1% to 5%. These estimates would be expected to vary across locations and over time. Nevertheless, these recent estimates indicate that occupation remains an important cause of lung cancer. Approaches to Prevention. Prevention of lung cancer mortality among workers exposed to agents or industrial processes that cause lung cancer may involve several strategies, including eliminating or reducing exposures, smoking cessation, screening, and chemo-prevention. For example, changes in industrial processes that have eliminated or reduced exposures to chloromethyl ethers and nickel compounds have provided evidence of reduced risk of lung cancer following these changes. Although occupational exposures are important causes of lung cancer, cigarette smoking is the most important preventable cause of lung cancer. For adults, the work site offers an important location to target smoking cessation efforts. In fact, the work site may be the only place to reach many smokers. As many as 70% of smokers participating in a work site program reported that they would not seek out other programs for smoking cessation. Furthermore, these programs may be as effective as other smoking cessation programs, with abstinence approaching 30%. By creating a supportive social environment, policies restricting smoking in the workplace may also assist smokers trying to quit. Screening of workers at high risk of lung cancer, with periodic chest radiography and sputum cytology, offers potential methods for early detection that may improve prognosis. However, the failure of those procedures to improve outcome from lung cancer among high-risk smokers makes screening of workers of doubtful value. Both epidemiologic and experimental evidence suggest that dietary factors may modify the risk of lung cancer. To date, attention has been focused on vitamin A and carotenoids.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Occupational lung cancer. 151 58

A total of 1,388 workers employed for at least 3 months at a copper/nickel smelter and nickel refinery were followed up for cancer from 1953 to 1987 through the Finnish Cancer Registry. There were 1,339 male and 49 female workers, making a total of 27,130 and 706 person-years, respectively. All of the women worked in the refinery, which opened in 1960, the same year the smelting of nickel began. A total of 67 cancers were diagnosed among the men, the standardized incidence ratio for all cancers being 1.0. No cancer was found among the women (1.8 expected). The risk of cancer among men was analysed according to primary site, exposure to nickel, type of work, years since first exposure and age at diagnosis. In the subcohort of nickel refinery workers, one case of sinonasal cancer was observed, against 0.02 expected, but otherwise no significantly increased risks of cancer were found. In addition to the small size of the cohort, the non-positive finding concerning lung cancer might be related to the relatively low arsenic exposure and, perhaps, to the late commencement of nickel production.
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PMID:Cancer risk among workers at a copper/nickel smelter and nickel refinery in Finland. 158 30

A retrospective industrial hygiene investigation was undertaken to explain the cause of a statistically significant excess lung cancer mortality observed in a subset of a large cohort of nickel workers involved in mining, smelting, and refining of nickel and copper in Ontario. The focus of this paper is to demonstrate how an industrial hygiene follow-up assessment of an epidemiologic finding can help to identify a likely cause. Polycyclic aromatic hydrocarbons (PAHs) alone or in association with particulate and gaseous contaminants (e.g., SO2) were likely the causative agents of the excess lung cancer observed among the lead welders, cranemen, and arc furnace workers of the copper refinery.
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PMID:Polycyclic aromatic hydrocarbons (PAHs): a possible cause of lung cancer mortality among nickel/copper smelter and refinery workers. 160 42

This presentation reviews occupational epidemiology as a foundation for workplace disease prevention activities. By examining descriptive, etiologic and intervention occupational epidemiology studies, a range of opportunities are illustrated where epidemiology has played, or could play a principal role in guiding preventive efforts. Descriptive studies presented include ones based on vital records, on epidemic investigations, cross-sectional surveys, and surveillance. Etiologic studies review the largely successful development of knowledge for lung cancer and asbestos exposure for pulmonary effects of isocyanate exposures. However, attention is also directed to the need for etiologic studies of work environment risks for both cardiovascular and musculoskeletal disease. Finally importance is placed on the too infrequent epidemiologic studies of intervention. Historical examples of control of large risks from nickel cancers and silicosis are balanced with more recent examples of successes at reducing smaller risks of cardiovascular disease and oil acne. Throughout, emphasis is placed on the importance of reintegrating the academic discipline of epidemiology into the application of study findings to prevention of workplace risks.
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PMID:The potential impact of epidemiology on the prevention of occupational disease. 160 14

A cohort of 54,128 men who worked in Ontario mines was observed for mortality between 1955 and 1986. Most of these men worked in nickel, gold, or uranium mines; a few worked in silver, iron, lead/zinc, or other ore mines. If mortality that occurred after a man had started to mine uranium was excluded, an excess of carcinoma of the lung was found among the 13,603 Ontario gold miners in the study (standardised mortality ratio (SMR) 129, 95% confidence interval (95% CI) 115-145) and in men who began to mine nickel before 1936 (SMR 141, 95% CI 105-184). The excess mortality from lung cancer in the gold miners was confined to men who began gold mining before 1946. No increase in the mortality from carcinoma of the lung was evident in men who began mining gold after the end of 1945, in men who began mining nickel after 1936, or in men who mined ores other than gold, nickel, and uranium. In the gold mines each year of employment before the end of 1945 was associated with a 6.5% increase in mortality from lung cancer 20 or more years after the miner began working the mines (95% CI 1.6-11.4%); each year of employment before the end of 1945 in mines in which the host rock contained 0.1% arsenic was associated with a 3.1% increase in lung cancer 20 years or more after exposure began (95% CI 1.1-5.1%); and each working level month of exposure to radon decay products was associated with a 1.2% increase in mortality from lung cancer five or more years after exposure began (95% CI 0.02-2.4%). A comparison of two models shows that the excess of lung cancer mortality in Ontario gold miners is associated with exposure to high dust concentrations before 1946, with exposure to arsenic before 1946, and with exposure to radon decay products. No association between the increased incidence of carcinoma of the lung in Ontario gold miners and exposure to mineral fibre could be detected. It is concluded that the excess of carcinoma of the lung in Ontario gold miners is probably due to exposure to arsenic and radon decay products.
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PMID:Carcinoma of the lung in Ontario gold miners: possible aetiological factors. 166 86

An extended follow-up from 1977-84 was achieved in a cohort of 11,567 nickel workers engaged in mining, milling and smelting originally studied from 1950-76. Exposure data were incorporated into the analysis. One nasal cancer occurred. The lung cancer Standardized Mortality Ratio beyond 15 years from first exposure was significantly high overall (128) and in miners (153). However, detailed analyses by era of first mining and duration of mining, as well as cumulative exposure to different nickel species, did not appear consistent with an occupational etiology since significant trends were not observed. At the levels of exposure incurred, large increases in lung and nasal cancer, observed in nickel refineries elsewhere, did not occur.
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PMID:Mortality of 11,500 nickel workers--extended follow up and relationship to environmental conditions. 177 58

The inhaled tobacco smoke is the most important determinant in the etiology of lung cancer and there is a clear dose-effect relation between lung cancer risk and the duration of smoking, the number of cigarettes and the intensity of inhalation. The opinions about lung cancer risk from passive smoking are divided and the published data are still in discussion. Occupational substances include chromates, nickel, beryllium, alkylated compounds, vinylchloride, arsenic compounds and in particular asbestos. Fortunately air pollution has no or small part in the etiology of lung cancer.
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PMID:[Etiology of bronchial cancer: smoking, passive smoking, environment and occupation]. 187 88

Concentrations of nine metals (Fe, Ca, Mg, Zn, Cu, Co, Ni, Pb and Cr) concentrations in lung tissues from 224 lung cancer cases were compared with those in other cases to achieve an understanding of their contribution to the development of lung cancer and the varieties after the development of cancer. Comparisons of metal concentrations in each cell type of lung cancer were also performed. All cases were collected from routine autopsies in Tokyo and Saitama, Japan. The copper concentration in tissue from lung cancers was significantly higher than that in other specimens, although calcium, magnesium, zinc and cobalt concentrations in lung cancers were significantly lower than those in other cases. There were no significant differences in the 99% intervals (excluding extremely high values for occupationally exposed cases) for chromium, nickel and lead concentrations between lung cancers and other cases, although these values were lower in lung cancers. However, in comparisons of men only, the chromium concentration, the degree of lung contamination and the severity of pulmonary emphysema in lung cancer cases were significantly higher than those in other specimens. Moreover, percentages of lung cancer in men at each degree of contamination and each severity of emphysema increased with increasing grades. Thus, this finding could be evidence that the exposure to contaminants other than chromium and nickel in the air had affected the development of lung cancer, except for occupationally exposed individuals. Therefore, almost all chromium and nickel in lung tissue might not deposit in carcinogenic forms such as hexavalent chromium or nickel subsulfide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metal concentrations in lung tissue of subjects suffering from lung cancer. 191 70


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