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

Elevated risks of lung cancer have been observed in foundry workers in a number of studies. When the levels of exposure were compared with other industries, the most probable causes of the lung cancer excess were polynuclear aromatic compounds (PACs) and silica in iron foundries and PACs, silica, as well as chromium and nickel fumes in steel foundries.
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PMID:Estimated risk of lung cancer attributable to occupational exposures in iron and steel foundries. 222 34

In order to investigate anthracosis of the human lung, especially its causal relationship with atmospheric pollution and the occurrence of lung cancer, intrapulmonary particulate pollutants (IPP) from autopsy cases and patients lobectomized because of lung cancer were separated by alkali digestion of the lung tissue, and their elemental constitution was analyzed by a wavelength-dispersive X-ray fluorescence spectrometer. Silicon was the most abundant mineral constituent of non-carbonaceous fraction of IPP, followed by calcium, magnesium, iron, aluminum and other trace elements. The levels of silicon and aluminum in IPP were significantly higher in individuals treated at Saitama Medical School Hospital than in those from Tokyo. Farmers showed higher levels of silicon and aluminum than other occupational categories, whereas male blue-collar workers showed higher levels of calcium and lead than farmers. The level of iron in IPP of male smokers tended to be higher than in non-smokers. In cases of lung cancer, especially of the hilar type, the levels of iron, calcium, copper, lead, chromium and nickel in IPP tended to be higher than in non-lung cancer cases, whereas the levels of silicon and aluminum were lower than in non-lung cancer cases. On the basis of these results, pulmonary anthracosis was considered to be etiologically related to the occurrence of lung cancer.
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PMID:Studies on pulmonary anthracosis. With special reference to the mineral constitution of intrapulmonary particulate pollutants in the human lung. 231 71

The mortality risk of iron ore (haematite) miners between 1970 and 1982 was investigated in a retrospective cohort study of workers from two mines, Longyan and Taochong, in China. The cohort was limited to men and consisted of 5406 underground miners and 1038 unexposed surface workers. Among the 490 underground miners who died, 205 (42%) died of silicosis and silicotuberculosis and 98 (20%) of cancer, including 29 cases (5.9%) of lung cancer. The study found an excess risk of non-malignant respiratory disease and of lung cancer among haematite miners. The standardised mortality ratio for lung cancer compared with nationwide male population rates was significantly raised (SMR = 3.7), especially for those miners who were first employed underground before mechanical ventilation and wet drilling were introduced (SMR = 4.8); with jobs involving heavy exposure to dust, radon, and radon daughters (SMR = 4.2); with a history of silicosis (SMR = 5.3); and with silicotuberculosis (SMR = 6.6). No excess risk of lung cancer was observed in unexposed workers (SMR = 1.2). Among current smokers, the risk of lung cancer increased with the level of exposure to dust. The mortality from all cancer, stomach, liver, and oesophageal cancer was not raised among underground miners. An excess risk of lung cancer among underground mine workers which could not be attributed solely to tobacco use was associated with working conditions underground, especially with exposure to dust and radon gas and with the presence of non-malignant respiratory disease. Because of an overlap of exposures to dust and radon daughters, the independent effects of these factors could not be evaluated.
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PMID:Mortality experience of haematite mine workers in China. 232 25

This review concerns primarily the health effects that result from indoor air exposure to radon gas and its progeny. Radon enters homes mainly from the soil through cracks in the foundation and other holes to the geologic deposits beneath these structures. Once inside the home the gas decays (half-life 3.8 d) and the ionized atoms adsorb to dust particles and are inhaled. These particles lodge in the lung and can cause lung cancer. The introduction to this review gives some background properties of radon and its progeny that are important to understanding this public health problem as well as a discussion of the units used to describe its concentrations. The data describing the health effects of inhaled radon and its progeny come both from epidemiological and animal studies. The estimates of risk from these two data bases are consistent within a factor of two. The epidemiological studies are primarily for hard rock miners, although some data exist for environmental exposures. The most complete studies are those of the US, Canadian, and Czechoslovakian uranium miners. Although all studies have some deficiencies, those of major importance include uranium miners in Saskatchewan, Canada, Swedish iron miners, and Newfoundland fluorspar miners. These six studies provide varying degrees of detail in the form of dose-response curves. Other epidemiological studies that do not provide quantitative dose-response information, but are useful in describing the health effects, include coal, iron ore and tin miners in the UK, iron ore miners in the Grangesburg and Kiruna, Sweden, metal miners in the US, Navajo uranium miners in the US, Norwegian niobian and magnitite miners, South African gold and uranium miners, French uranium miners, zinc-lead miners in Sweden and a variety of small studies of environmental exposure. An analysis of the epidemiological studies reveals a variety of interpretation problem areas. The major and almost universal problem is in estimating exposure levels. In many cases there were no direct measurements of radon or radon progeny and the exposure levels are estimates based on irregular measurements and known levels in nearby mines. Perhaps the most important variable or complicating factor in the determination of the risk due to radon exposure is the confounding factor of exposure to cigarette smoke. The general scientific concensus is that, although the interaction could be somewhere between linear and supramultiplicative, it is likely a combination, and closer to multiplicative. A number of other complexities contribute to the uncertainty in the risk estimates, likely to a lesser degree than those of exposure measurements and cigarette smoke confounding.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Indoor air radon. 240 87

We conducted a population-based study of diet and lung cancer among the multiethnic population of Hawaii in 1983-1985. We completed interviews for 230 men and 102 women with lung cancer and 597 men and 268 women controls, frequency-matched to the patients by age and sex. A quantitative dietary history assessed the usual intake of foods rich in vitamins A and C and carotenoids. A clear dose-dependent negative association was demonstrated between dietary beta-carotene and lung cancer risk in both sexes. After adjusting for smoking and other covariates, the men in the lowest quartile of beta-carotene intake had an odds ratio of 1.9 (95% confidence interval, 1.1-3.2) compared to those in the highest quartile of intake. The corresponding odds ratio for women was 2.7 (95% confidence interval, 1.2-6.1). No clear association was found for retinol, vitamin C, folic acid, iron, dietary fiber, or fruits. All vegetables, dark green vegetables, cruciferous vegetables, and tomatoes showed stronger inverse associations with risk than beta-carotene. This observation suggests that other constituents of vegetables, such as lutein, lycopene, and indoles, and others, may also protect against lung cancer in humans.
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PMID:Vegetable consumption and lung cancer risk: a population-based case-control study in Hawaii. 254 91

The purpose of this ongoing study is to determine whether thoracic radiotherapy for lung cancer produces an early increase in serum copper (Cu) concentration, an increase which might predict clinical outcome. Copper and iron concentrations were measured in serum obtained from nonsmall cell lung cancer patients at 0, 1, 2, 4, and 6 weeks after the start of radiotherapy. Control groups included patients irradiated for breast cancer (low dose of radiation to the lung), for endometrial, cervical or prostatic cancer (no dose to lung), and patients with congestive heart failure, pulmonary hypertension, chronic obstructive pulmonary disease (COPD), and cutaneous burns with or without smoke inhalation (no irradiation). Serum Cu concentration increased at least 10 micrograms/dl from the pretreatment level in approximately 75% of the adenocarcinoma and squamous cell lung cancer patients, but in only 1 of 4 undifferentiated lung cancer cases. In virtually all of these responders, serum Cu increased to a maximum at 2 weeks after the start of therapy, then plateaued or decreased slightly despite continuing irradiation. Within the subset of squamous cell lung cancers, there was a direct correlation between the degree of histologic differentiation and both baseline serum Cu concentration and the probability of an early increase therein. In contrast, only 33% of breast cancer patients and 15% of endometrial, cervical and prostate cancer patients exhibited an increase in serum Cu concentration at 2 weeks after the start of radiotherapy. Serum Cu concentration was within normal limits in virtually all patients with congestive heart failure, pulmonary hypertension, and COPD. Burn patients exhibited a significant reduction in serum Cu, although concomitant smoke inhalation increased serum Cu back to low-normal levels. Serum iron concentration did not change significantly in any category of patients. These data suggest that thoracic radiotherapy for well differentiated non-small cell lung cancer is accompanied by an early increase in serum Cu concentration. This increase is partly but not wholly related to lung dose in particular rather than tissue dose in general, and specifically reflects radiation-induced lung injury rather than pneumopathy in general. In lung cancer patients, the change in serum Cu concentration during the first 2 weeks of radiotherapy exhibits a sufficiently broad range (+60 to -13 micrograms/dl) to permit testing this parameter as a predictor of tumor response and pulmonary complications.
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PMID:Serum copper concentration as an index of clinical lung injury. 262 91

Pathological changes of lung cancer in miners of Yunnan Tin Mine were studied, and additionally, mineral dust in the miners' lung were also investigated by using scanning electronic microscope, energy disperse X-ray spectrometer and electronic probe. The results showed: 1. mineral dust caused active hyperplasia, atypical hyperplasia, metaplasia and atypical metaplasia of the epithelial of alveoli and bronchi, which was able to induce cancer. 2. Pneumoconiosis-like changes in the miner's lung are correlated with the high incidence of lung cancer. 3. Correlated also with copper, lead, zinc and iron may be the high incidence of lung cancer. 4. Transition form from hyperplasia and atypical hyperplasia of alveolar epithelia to malignancy was observed. It suggests that lung squamous cell carcinoma probably originates from the alveolar epithelia of the lung.
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PMID:[Pathological survey of lung cancer induced by tin mine dust in Yunnan]. 263 64

Copper, zinc, magnesium, calcium and iron were measured in serum and lung tissue - tumor mass and histologically nonneoplastic tissue - from lung cancer patients and compared with serum concentrations in healthy subjects and control lung tissue obtained from patients with nonmalignant lung disease. Lung cancer patients showed a significant increase in serum Cu and Cu/Zn ratio levels and decrease in serum Zn and Fe concentrations. These findings were correlated with TNM stage of the disease, but not with histologic type of tumor. Malignant lung tissue showed a higher level of Cu, Ca, Mg, and Cu/Zn ratio and lower Zn level than that found in control samples, as well as an increase in Cu, Mg and Cu/Zn ratio concentrations with regard to histologically nonneoplastic tissue samples from the same patient. Tissue concentration of trace metals was not significantly influenced either by histologic type of tumor or clinical TNM stage. Significant correlation coefficients between serum and tissue trace metal levels were not found.
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PMID:Serum and tissue trace metal levels in lung cancer. 274 65

The mechanism by which cigarette smoking and asbestos exposure synergistically increase the incidence of lung cancer is unknown. We hypothesized that cigarette smoke and asbestos might synergistically increase DNA damage. To test this hypothesis we exposed isolated bacteriophage PM2 DNA to cigarette smoke and/or asbestos, and assessed DNA strand breaks as an index of DNA damage. Our results supported our hypothesis. 78 +/- 12% of the DNA exposed to both cigarette smoke and asbestos developed strand breaks, while only 9.8 +/- 7.0 or 4.3 +/- 3.3% of the DNA exposed to cigarette smoke or asbestos, respectively, developed strand breaks under the conditions of the experiment. Our experimental evidence suggested that cigarette smoke and asbestos synergistically increased DNA damage by stimulating .OH formation. First, significant amounts of .OH were detected by electron paramagnetic resonance (EPR) in DNA mixtures containing both cigarette smoke and asbestos, but no .OH was detected in mixtures containing cigarette smoke alone or asbestos alone. Second, the .OH scavengers, dimethylsulfoxide (DMSO), mannitol, or Na benzoate decreased both .OH detection by EPR and strand breaks in DNA mixtures exposed to cigarette smoke and asbestos. Third, the H2O2 scavenger, catalase, and the iron chelators, 1,10-phenanthroline and desferrithiocin, decreased both .OH detection and strand breaks in DNA mixtures exposed to cigarette smoke and asbestos. These latter findings suggest that iron contained in asbestos may catalyze the formation of .OH from H2O2 generated by cigarette smoke. In summary, our study indicates that cigarette smoke and asbestos synergistically increase DNA damage and suggests that this synergism may involve .OH production.
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PMID:Role of oxidants in DNA damage. Hydroxyl radical mediates the synergistic DNA damaging effects of asbestos and cigarette smoke. 282 Oct 73

A case-referent study on lung cancer was conducted in Cracow, Poland. Men dying of lung cancer within a 6-year period (1980-1985) formed the case group. The reference series was selected from death registers and was frequency-matched with the cases by sex and age. Deaths due to other respiratory diseases were excluded. Information on the occupation, smoking habits, and residency of 901 cases and 875 referents was collected from their next-of-kin. The combined effect of smoking and industrial exposure, in particular employment in steel or iron foundries, was investigated by multivariate analyses and was very well fitted by a multiplicative model. Foundry employment, in particular in the younger age (less than 70 years) group, occupational exposure to known carcinogens in other industries for more than 20 years, and smoking were found to be risk factors.
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PMID:Lung cancer, smoking, and employment in foundries. 292 87


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