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

1167 workers of Lorraine (France) iron mines, a random sample of 5600 workers aged 35 to 55 years, at work in 1975 constituted the initial cohort that was examined twice at 5-year intervals after the first examination. A questionnaire on respiratory symptoms and smoking habits (MRC questionnaire) plus questions on the work history of each participant was completed, vital capacity (VC), forced expiratory volume in one second (FEV1.0), residual volume (RV) and fractional uptake of CO (FuCO) were measured at the first examination and repeated five and ten years later. At the end of the ten year follow-up, 522 subjects were re-examined, 186 were lost to follow-up, 328 answered a mail questionnaire, and 111 had died. The total number of deaths was not different from that of the general population, but for lung cancer the standardized mortality ratio (SMR) was significantly increased (SMR = 3.7). For the miners re-examined, frequency of bronchitis and decrease of functional tests were more related to age and smoking habits than to occupation.
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PMID:Iron miners--a ten year follow-up. 139 30

Repeated measurements of dust concentrations and work loads were made at the workplaces in iron foundries (interval 10 years) and processing of asbestos (dusts 27 years and work load 8 years). The work load was mild to moderate, rarely heavy (energy output 2.0 to 5.7 MJ in the shift) with a mean heart rate 94-106. The incidence of occupational diseases was stabilized in the foundries, increased in the asset processing plants (mostly lung cancer). Two thirds of the workers were smokers, in spite of that the workers in the foundries had their mean flow-volume curve almost identical with the standards. Their age conditioned diminution was faster especially for FEF50 and 25 and accompanied with a bigger rise of FRC and RV. Exercise testing demonstrated the same fitness as in normal population (2.7 +/- 0.7 l/min). As far as asbestos processing is concerned, a diminution of dust concentrations below the limits was found. Despite of this, an increase in lung cancer incidence was observed probably as a consequence of high dust concentrations in the past and smoking habits (2/3 of workers). The flow-volume curves were obviously smaller than the normals. With the rising of exposure to asbestos and with the advancing age (more close correlation), the deterioration of respiratory parameters (measured during 6-7 years) was two times faster. The correlations were more close for women then for men. In the man group, this deterioration was greater in the last measurements. The results of ergometer testing up to anaerobic threshold were identical with those found in normal population.
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PMID:[Fibroplastic dust and cardio-respiratory functions]. 141 Dec 43

Epidemiological data have revealed significant excesses of lung cancer among workers exposed to some types of man-made mineral fibers (MMMF), but inhalation experiments performed on rats have failed to reveal the origin of these excesses. Some of these materials, however, are able, in aqueous media, to exhibit surface oxidizing properties after reduction of oxygen by a radical pathway. Tests have been carried out with 12 MMMF samples collected from various sources without prior knowledge of their origin, to determine their oxidizing surface activity in relation to their divalent iron content. Some of these fibers were obtained from factories included in an epidemiological investigation. Only fibers coming from plants where excesses of lung cancer were observed are classified as active in an oxidative process and, consequently, probably toxic in biological media by an oxidative stress mechanism. We therefore propose an hypothesis of a causal relationship between these oxidizing properties and the ability of the materials to induce lung cancer.
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PMID:Man-made mineral fibers and lung cancer: an hypothesis. 154 87

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

A prospective mortality study was conducted over a period of 5 years on a group of 13,801 iron miners, who were alive on January 1, 1982. During this 5-year period, 1813 deaths were registered. For 1222 (67.4%), the cause of death and work history are known. For 135 (7.4%), the cause of death is known, but not the work history. For 455 (25.1%), the cause of death is unknown. Proportional mortality ratio (PMR) is significantly higher than 1 for lung cancer (PMR = 2.51, p less than 0.001) and for stomach cancer (PMR = 2.31, p less than 0.001). The results are discussed in regard to occupational risks that result in these two kinds of increased mortality rates, and the hypothesis of redox activity on the surface of dust particles is advanced as a common denominator.
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PMID:Prospective mortality study among iron miners. 178 33

To investigate lung cancer risk, the authors conducted a historical cohort mortality study of 4,459 mild steel welders who had been employed at three midwestern plants which manufactured heavy equipment. Follow-up began in the mid-1950s and extended through 1988. All welders had at least 2 years welding experience (average duration, 8.5 years). This cohort had no occupational exposure to asbestos or stainless steel fumes (containing nickel and chromium), two potential confounders in previous welders studies. A comparison population of 4,286 nonwelders, all with at least 2 years employment at the same plants, was also studied. Nonwelders had never been welders and were allowed to have no more than 90 days employment as a painter, foundryman, or machinist. Sampling data collected from 1974-1987 indicated that welders were exposed to 6-7 mg/m3 of total particulate and 3-4 mg/m3 of iron oxide, while nonwelders had negligible exposures to welding fumes. When compared with the United States population, both welders and nonwelders had elevated rates for lung cancer (standardized mortality ratios (SMRs): welders, SMR = 1.07; nonwelders, SMR = 1.17), but neither SMR was significantly elevated. Limited smoking data based on a 1985 survey indicated that both welders and nonwelders smoked more than the United States population, possibly accounting for part of their elevated lung cancer rates. There was no trend of increased risk for welders with increased duration of exposure. The only other cause of death significantly elevated was emphysema among welders. Nonmalignant respiratory disease was not elevated for welders (SMR = 0.96). When welders were compared with nonwelders directly for lung cancer, the rate ratio was 0.90.
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PMID:Lung cancer in mild steel welders. 200 Aug 39

The association between silicosis and lung cancer mortality was estimated in 9,912 (369 silicotics and 9,543 nonsilicotics) white male metal miners. These miners were examined by the U.S. Public Health Service during 1959-1961 and were followed through 1975. Miners were excluded from this study if they were employed in a mine during 1959-1961 that used diesel equipment underground. The ores that were mined consisted of copper, lead-zinc, iron, mercury, lead silver, gold and gold-silver, tungsten, and molybenum. The standardized mortality ratio (SMR, U.S. white male rates) for lung cancer was 1.73 (95% CI: .94-2.90) in silicotics and 1.18 (95% CI: .98-1.42) in nonsilicotics. Additionally, SMRs were higher in silicotics than in nonsilicotics, even in most subgroups stratified by cigarette smoking habit, type of ore mined, years of service in an underground job, radon exposure group, or year of hire. When lung cancer mortality between silicotics and nonsilicotics was compared, the age-adjusted rate ratio (95% CI) was 1.56 (.91-2.68), and the age- and smoking-adjusted rate ratio was 1.96 (.98-3.67). Corresponding figures for miners who were employed in mines with low levels of radon exposure were 1.90 (.98-3.67) and 2.59 (1.44-4.68), respectively. These findings indicate that lung cancer mortality risk was increased in silicotics, and this probably did not result from chance or bias. However, confounding from radon exposure could not be ruled out. The findings indicate that further follow-up of this cohort is needed.
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PMID:Silicosis and lung cancer in U.S. metal miners. 200 98

A retrospective cohort mortality study was conducted among 8147 men and 627 women employed in a gray iron foundry for at least 6 months between 1950 and 1979. More than 1700 deaths occurred during a 35-year period of observation. Standardized mortality ratios (SMRs) for all causes were close to expected values based on the US general population as the standard. The mortality of nonwhite men was significantly increased for lung cancer (SMR 132) and ischemic heart disease (SMR 126). Other moderate, but nonsignificant excesses were noted among nonwhite men for cancers of the stomach, pancreas, and prostate, for diabetes mellitus and pulmonary emphysema, and among white men for cancers of the lung and stomach, gastric and duodenal ulcers, pulmonary emphysema, and suicide. Small mortality increases were observed in both racial groups for cerebrovascular disease. The lack of a trend with time since hire and duration of foundry employment suggests that lung cancer mortality may not be associated with exposure to the foundry environment. Utilizing indirect measures of smoking, it appears that virtually all excess lung cancer deaths among whites and at least some of the excess among nonwhites could be explained by smoking habits. Similarly, smoking may have been responsible for the mortality excesses from emphysema, cerebrovascular diseases, and ischemic heart disease.
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PMID:Mortality of iron foundry workers: I. Overall findings. 801 21

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
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PMID:Metal toxicity and the respiratory tract. 217 66

Cobalt metal and cobalt compounds are extensively used for the production of high-temperature alloys, diamond tools, cemented carbides and hard metals, for the production of various salts used in electroplating and as catalysts, drying agents in paints, additives in animal feeds and pigments. Cobalt oxides are used not only in the enameling industry and for pigments, but also in catalytic applications. There is no indication that cobalt metal and cobalt compounds constitute a health risk for the general population. Allergic reactions (asthma, contact dermatitis) can be induced by certain cobalt compounds. Interstitial fibrosis has also been observed in workers exposed to high concentrations of dust containing cobalt, tungsten, iron, etc., mainly in the cemented carbides and the diamond-polishing industries. Several experiments have demonstrated that single or repeated injections of cobalt metal powder or some forms of cobalt salt and cobalt oxide may give rise to injection site sarcoma in rats and in rabbits but the human health significance of such data is questionable. Intratracheal administration of a high dose of one type of cobalt oxide induces lung tumors in rats but not in hamsters. In the latter long-term inhalation of cobalt oxide (10 mg/m3) did not increase the incidence of lung cancer. The human data are too limited to assess the potential carcinogenic risk for workers. Co2+ interacts with protein and nucleic acid synthesis and displays only weak mutagenic activity in microorganisms. Some cobalt salts have been reported to enhance morphological transformation of Syrian hamster embryo cells. Cobalt chloride displays some limited mutagenic activity in yeast and some cobalt compounds are able to produce numerical and structural chromosome aberrations in plant cells. Cobalt and its salts appear to be devoid of mutagenic and clastogenic activity in mammalian cells. Cobaltous acetate and cobaltous chloride have not been found to be teratogenic in hamsters and rats respectively.
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PMID:Mutagenicity, carcinogenicity and teratogenicity of cobalt metal and cobalt compounds. 219 31


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