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

Iron foundry workers, exposed to high levels of polycyclic aromatic hydrocarbons (PAHs), silica, and metal fumes and dusts, are at elevated risk of lung cancer. Benzo(a)pyrene and a number of structurally related PAHs are metabolically activated to diol epoxides (e.g., 7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenzo(a) pyrene) which are mutagenic, carcinogenic in experimental animals, and form covalent adducts with DNA. The levels of these adducts were measured in an enzyme-linked immunosorbent assay using a polyclonal anti-benzo(a)pyrene diol epoxide-I-DNA antibody which cross-reacts with DNA modified by diol epoxides of structurally related PAHs. DNA was analyzed from peripheral blood cells of 35 Finnish foundry workers and 10 controls. Workers were classified as having low (less than 0.05 micrograms/m3), medium (0.05-0.2 micrograms/m3), or high (greater than 0.2 micrograms/m3) exposure to benzo(a)pyrene (as an indicator of PAH). When adjustment was made for cigarette smoking and time since vacation, benzo(a)pyrene exposure was significantly related to adduct levels (P = 0.0001). Each of the three exposure groups had significantly elevated adduct levels compared to controls. Among the exposed workers, the low group differed significantly from the high and medium categories. This study supports the usefulness of monitoring adduct formation in a population occupationally exposed to carcinogens.
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PMID:Detection of polycyclic aromatic hydrocarbon-DNA adducts in white blood cells of foundry workers. 312 49

A case-control study of Japanese women in Nagoya was conducted to investigate the significance of passive smoking and other factors in relation to the etiology of female lung cancer. A total of 90 nonsmoking patients with primary lung cancer and their age- and hospital-matched female controls were asked to fill in a questionnaire in the hospital. Elevated relative risk (RR) of lung cancer was observed for passive smoking from mother (RR = 4.0; p less than 0.05) and from husband's father (RR = 3.2; p less than 0.05). No association was observed between the risk of lung cancer and smoking of husband or passive smoke exposure at work. Occupational exposure to iron or other metals also showed high risk (RR = 4.8; p less than 0.05). No appreciable differences in food intakes were observed between cases and controls.
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PMID:A case-control study of lung cancer in nonsmoking women. 318 4

Biologic evidence suggests that high body iron stores could promote development of cancer. Because a previous study had shown an association between prescribed iron medication and lung cancer risk in men, we examined recent iron use as well as 2 additional indirect measures of body iron stores, anemia and the total iron-binding capacity (TIBC) of plasma, in relation to subsequent risk of cancer in a larger cohort of 174,507 persons. Women, but not men, who reported recent iron use had a lower risk of lung cancer than those who did not [RR = 0.60, 95% confidence limits (CL) 0.37, 0.97] after adjustment for age and cigarette smoking. Women who had used iron appeared to remain relatively iron-depleted. Risk for other cancers was slightly, but not significantly, lower in women who used iron. Anemia (hemoglobin less than 12 g) was also associated with lower risk of lung cancer in women (RR = 0.61, 95% CL 0.61, 0.98), but not in men. TIBC, which is inversely related to body iron stores, was inversely related to risk of lung cancer in women in a graded fashion (RR = 0.41, 95% CL 0.23, 0.73 comparing highest with lowest quartile). In men, a protective effect of higher TIBC against lung cancer was suggested, but did not reach statistical significance. These indirect measures of body iron stores appeared to reflect iron stores better in women than in men, probably because variability in iron stores is greater in women and iron deficiency more prevalent. A possible alternative explanation for our findings is incomplete adjustment for the confounding effects of cigarette smoking. This could apply to iron use and hemoglobin level which were related to smoking, but not to TIBC, which was not. These data, which indicate lower risk of cancer in iron-depleted women, lend epidemiologic support to the hypothesis that high iron stores may increase cancer risk, at least for lung cancer.
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PMID:Epidemiologic evidence of an association between body iron stores and risk of cancer. 336 89

The mortality of 1947 Cumbrian iron ore miners has been studied over the period 1939-82 in relation to that among other groups of men in England and Wales: (a) all men, (b) men of similar social class, and (c) men living in similar types of (mainly rural) area. Significant excesses were found for deaths from tuberculosis and respiratory diseases compared with each of the reference populations. Lung cancer showed an excess over that in comparable (mainly rural) areas of England and Wales, as reported in a previous study using a proportionate method of analysis and which covered the period 1948-67 but no appreciable excess after 1967. Reasons for this decline are discussed.
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PMID:Decline in the lung cancer hazard: a prospective study of the mortality of iron ore miners in Cumbria. 337 97

Purified recombinant human ferritin composed solely of H subunit was radiolabeled and incubated with proerythroleukemic K562 human cells. A specific binding was detected, and it could be displaced only by ferritins, natural or recombinant, containing large proportion of the H subunit. The specific ferritin H-chain binding was saturable, and cells showed 17,000 to 23,000 binding sites per cell. The affinity constant measured at 37 degrees C was of 3 x 10(8) M-1. Treatment with pronase eliminated the specific binding. The binding sites were expressed in a high number during the cellular exponential phase of growth and progressively decreased to disappear when cells reached the plateau phase. Treatment of the cells with desferrioxamine increased recombinant H-ferritin binding, while iron had little effect. K562 cells induced to differentiate by hemin failed to bind ferritin H. Ferritin H-chain binding capacity is present on various cell lines such as HL60, lung cancer, and hepatoma cells. Analysis of the binding sites by western blotting showed a peptide with apparent mol wt of about 100 kd.
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PMID:Characteristics and expression of binding sites specific for ferritin H-chain on human cell lines. 342 30

A cohort study of 8,487 workers employed between 1948 and 1980 at a uranium mine in Saskatchewan, Canada, has been conducted. A total of 65 lung cancer deaths was observed (34.24 expected, P less than 10(-5)). There was a highly significant linear relationship between dose and increased risk of lung cancer giving estimates for the relative and attributable risk coefficients of 3.28% per working level month (WLM) and 20.8 per WLM per 10(6) person-years. Age at first exposure had a significant modifying effect on risk. The interaction of exposure with age at observation fits a relative risk model well. The similarity of these results to a recent study of Swedish iron miners with similar levels of relatively low exposure suggests that exposure to radon daughter products may be a major contributory factor to lung cancer occurring among nonsmokers in the general population. The results also reinforce concerns as to the appropriateness of present occupational exposure standards.
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PMID:Lung cancer mortality (1950-80) in relation to radon daughter exposure in a cohort of workers at the Eldorado Beaverlodge uranium mine. 346 Nov 98

A proportional mortality study of 1,075 iron ore miners in Lorraine, France, who died between 1960 and 1976 showed a significant excess of lung cancer mortality (proportionate mortality ratio = 2.25). Moreover, proportionate lung cancer mortality increased with the duration of work underground (proportionate mortality ratio = 4.24 for subjects who worked underground for more than 30 years) and was higher among pneumoconiotic (siderotic) miners (proportionate mortality ratio = 3.85) than among nonpneumoconiotic miners. These results were confirmed by a case-control study nested in the mortality study. Smoking habits could not be estimated retrospectively with sufficient accuracy to be taken into account. Although the proportion of smokers among contemporary iron ore miners is larger than in the French male population, occupational factors may also play a role; radiation exposure can be ruled out because there is no detectable radioactivity in the Lorraine mines, but dust exposure may be considered as an etiologic factor owing to the relationship between siderosis and lung cancer.
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PMID:Risk of lung cancer among iron ore miners: a proportional mortality study of 1,075 deceased miners in Lorraine, France. 368 11

Mortality analyses were carried out for 278 male hourly workers who were employed for at least 10 years at a gray iron foundry and who died between January 1, 1970 and December 31, 1981. Statistically significant excess proportional mortality due to non-malignant respiratory disease (SPMR = 177), lung cancer (SPMR = 148), and leukemia (SPMR = 284) was found among the 221 white males. Among nonwhite males there was a significant excess in proportional mortality due to circulatory diseases (SPMR = 143). White males in the Finishing classification experienced a significant excess of proportional mortality due to nonmalignant respiratory disease (SPMR = 279) and lung cancer (SPMR = 179). White males in the Core Room classification experienced an excess of proportional mortality due to nonmalignant respiratory disease (SPMR = 321). Case-control studies demonstrated a significant association between nonmalignant respiratory disease and the Finishing classification after controlling for the effects of age, prior occupations in coal mining or foundries, and smoking. A positive but nonsignificant association between lung cancer and Finishing was also found after controlling for age, prior work history, and smoking in case control studies.
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PMID:Mortality among ferrous foundry workers. 374 65

This is a study of cancer mortality, cancer incidence, and incidence of lung tuberculosis among cases of silicosis reported to the National Swedish Pneumoconiosis Register during 1959-1977. Two occupational categories were extracted--"mining, tunneling, and quarrying" (n = 284) and "iron and steel foundries" (n = 428), respectively. Control groups were drawn from a national register of persons undergoing periodic health examinations with regard to silicosis risk. The controls were matched for occupation, age, and time of first exposure. The follow-up was performed through record-linkage operations to computerized information in Swedish Death Statistics, Swedish Cancer Register, and the Swedish Tuberculosis Index. End of follow-up was set at December 31, 1980. In cases drawn from mining, quarrying, and tunneling workers seven deaths in lung cancer were observed and two among the controls. Among iron and steel foundry workers the corresponding numbers were 10 and 6. The values for expected numbers, based on general population statistics, were 1.3 and 2.6, respectively, for these two occupational groups. When cancer incidence statistics were used, the case/control ratio for lung cancer was 2.1 for "mining, quarrying, and tunneling" and 0.6 for "iron and steel foundries." There were 29 cases of lung tuberculosis registered among the silicosis cases during the follow-up period. Only one tuberculosis case was observed among the controls. The results demonstrate that persons with silicosis contracted in the mining, quarrying, and tunneling occupations are subject to an increased risk of lung cancer. The risk is observed when both the general population and a closely matched control population from the same occupations are used for values of reference. The results also demonstrate the high risk of persons with silicosis to contract lung tuberculosis.
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PMID:Silicosis and risk of lung cancer or lung tuberculosis: a cohort study. 375 78

The increased risk of lung cancer among foundry workers is assumed to be associated with the inhalation of gaseous and particle bound polycyclic aromatic hydrocarbons (PAH). These compounds are produced during pyrolysis of carbon containing loading material in the moulding sand. The concentrations of 20 PAH, some of which are carcinogenic, have been determined in the dusty casting area of an iron foundry by means of gas chromatography and mass spectrometry. The total dust was fractionated by means of a precision cascade impactor. It was possible to differentiate the PAH load in microgram/mg dust in seven particle size fractions ranging from 0.36- greater than or equal to 24.95 microns. Initially, there was an increase of the adsorbed PAH mass concentration with increasing particle diameter up to a maximum of 1.1 microgram/mg in the dust of the 1.57 micron fraction. Thereafter there was a continuous decrease of PAH mass concentration with increasing particle size. When the differing weights of the seven fractions are taken into account, however, the total PAH load of the individual fractions increases steadily with increasing particle size. The inhalable fine dust, 31.4% of the total dust, contains 49.9% of the total adsorbed PAH. The gas phase contained on average three times more carcinogenic PAH with four and five rings than was adsorbed on the dust. Thus the percentage of the gaseous substances amounts to 77% of the total PAH load at the place of work in an iron foundry.
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PMID:Gaseous and adsorbed PAH in an iron foundry. 380 35


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