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

In a previous report (Pedersen et al., 1973) an excess risk of respiratory cancer among Norwegian nickel workers was demonstrated. The number of cancer cases was relatively small for the study of temporal changes in exposure. In this report the number of cancer cases increased by 70% through an extended follow-up to 1979, and the results published previously were confirmed. Data on smoking habits of the employees at the nickel refinery have now become available. The interaction between smoking and occupational nickel exposure is assessed by comparing the excess risk of lung cancer caused by smoking in the study group and in a sample of the general population. It is shown that the interaction is closer to being additive than multiplicative. This observation has methodological implications for studying temporal changes in occupational exposure. These implications are discussed. No substantial reduction in occupational exposure at the nickel refinery can be observed as far as lung cancer is concerned. For nasal cancer, however, the risk is much smaller among those employed around 1960 than among those employed around 1930. The difference in trend of occupational risk for the two types of cancer cannot be explained by the data presented.
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PMID:Cancer of respiratory organs among workers at a nickel refinery in Norway. 716 Sep 38

Morphological transformation and induction of somatic mutation in the hamster embryo cell bioassay have been used to study whether the carcinogenicity of nickel is affected by polycyclic hydrocarbons. The transformation frequency was found to increase with increasing concentration of nickel sulphate, benz[a]pyrene (BP) and methylcholanthrene. In experiments with combinations of nickel sulphate and BP, the transformation frequencies used for all concentrations were higher than for compounds tested separately. The greatest enhancement was found using 5 micrograms/ml NiSO4 . 6H2O and 0.78 microgram/ml BP. The transformation frequency obtained with this combination was 10.7%, compared to 0.5% and 0.6% for the individual substances. No synergistic effect could be detected between nickel sulphate and methylcholanthrene (MC). In experiments measuring somatic mutation by selection for ouabain resistance, the mutation frequency was likewise found to be significantly higher than expected in mixtures of nickel sulphate and BP. The present demonstration of the synergistic effect between nickel sulphate and BP is of interest with the potentiating effect of cigarette smoking on development of lung cancer among nickel refinery workers.
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PMID:Synergistic effect on morphological transformation of hamster embryo cells by nickel sulphate and benz[a]pyrene. 722 42

The mortality of men employed in a plant manufacturing nickel alloys from metallic nickel and other metals has been examined. The plant has operated since May 1953, and 1925 men were identified who had been employed in the operating areas at the plant, other than as members of the staff, for a total of five or more years, excluding breaks. Analysis of samples of air obtained from personal samplers showed that since 1975 most of the men are likely to have been exposed to average concentrations of nickel of between 0.5 and 0.9 mg Ni/m3. All but 22 (1.1%) of the men were successfully traced to 1 April 1978 or until they died or emigrated. One hundred and seventeen had died. The numbers of deaths observed from cancers of respiratory and other sites, other respiratory disease, ischaemic heart disease, and other causes of death were compared with the numbers expected from national and local mortality rates. No evidence of the existence of any occupational hazard was obtained. The number of deaths from lung cancer (15) in men employed for five years or more is small. At 98% of the number expected at local rates it is statistically compatible with risks of between 0.5 and 2.2 times "normal."
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PMID:Mortality of nickel workers: experience of men working with metallic nickel. 727 35

Mortality and causes of death were examined among 1,059 white male welders employed between 1943 and 1973 at three plants in Oak Ridge, Tennessee. Based on deaths reported as of 1974, the standardized mortality ratio (SMR) for all causes was 87 (173 deaths observed vs. 199.0 expected on the basis of death rates for US white males). There were no deaths resulting from sinonasal cancer, and the SMR for lung cancer was 150 (95% confidence limits = 87 and 240). A subgroup of these welders (N = 536) was exposed to nickel oxides at the Oak Ridge Gaseous Diffusion (K-25) Plant; recent air concentrations of nickel (from personal air samplers) were greater than proposed standards. Standardized mortality ratios for lung cancer and diseases of the respiratory system were not higher among K-25 Plant welders than among other welders (N = 523). Welders employed for greater than or equal to 50 wk at the K-25 Plant had an SMR for lung cancer of 188 (95% confidence limits = 61 and 438) based on small numbers of deaths (5 observed vs. 2.66 expected). Further follow-up of these groups is needed.
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PMID:Mortality among welders, including a group exposed to nickel oxides. 729 87

A study was undertaken of a cohort of nickel refinery workers from a sinter plant that operated from 1948 to 1962. A complete follow-up of the 495 workers has been carried out by searching death records and other measures. Incidence cases known to the Workmen's Compensation Board of Ontario have been included. Fifty-four cases of lung cancer and eight of sinus cancer (including two in men who subsequently developed primary lung cancer) were located. The risk of lung and sinus cancer was much higher in the earlier days of operation of the plant, with an increase rate of over 40% for those employed in the first year of operation. The dose-response relationship has been examined by regressions of standardised morality ratios (SMR) and standardised incidence ratios (SIR). The SIR suggests that the risk doubled at levels of exposure of 12 months (six months in the earlier years).
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PMID:Respiratory cancer in a cohort of nickel sinter plant workers. 731 95

A proportional mortality and case-referent analysis of 238 deaths among hourly employees in an automobile hardware manufacturing plant was conducted. The major operations of the plant were zinc die casting and electroplating. Chemical exposure included die-casting emissions and mists from chrome and nickel plating. The chief proportional mortality finding was a significant excess of lung cancer among both white men and women. A case-referent analysis indicated a possible association between lung cancer and work in certain departments. The findings support the hypothesis of a work-related carcinogenic risk. Follow-up recommendations have been made.
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PMID:Mortality among workers in a die-casting and electroplating plant. 733 Jun 27

In view of the historic importance of smelter workers in the field of occupational medicine, it is surprising that until very recently little data was available on the mortality experience of these workers. The problem in most studies lies in identifying the smelter workers, because smelting, strictly speaking, refers to the melting of ores for the purposes of recovering metals, whereas smelters sometimes perform the operations of roasting, calcining, sintering, converting, and refining. These distinctions are not made in most mortality studies. Most mortality studies of smelter workers conducted to date have shown some excess in lung cancer. For lead, copper, cadmium, and nickel smelters a different etiologic agent has been proposed for each. These different explanations arise partly from different initial perspectives in conducting the studies. In this paper, data are presented on a current historical-prospective study of males who worked a year or more during the period January 1, 1940 to December 31, 1964 at a copper smelter in Tacoma, Washington. This smelter (and refinery) handled a copper ore with a relatively high arsenic content and produced arsenic trioxide as a by-product. Overall 97.2% of the original study population was traced through 1976. Of the 1,061 who were found to have died, death certificates were obtained for 1,018, or 96%. For all causes of death, the mortality rates in this cohort, expressed as a Standardized Mortality Ratio (SMR), were 3.5% higher than that expected based on the United States white male mortality experience. A total of 104 respiratory system cancers were observed compared to 54.6 expected (SMR = 190.5, p less than .05). Respiratory cancer rates were found to be elevated in both smokers and nonsmokers. Overall, a gradual rise in SMR's for respiratory cancer was observed with increasing duration of exposure but not with an increasing interval from onset of exposure. This observation is consistent with the notion that the effects of arsenic on cancer incidence disappear with time. This phenomenon has also been observed for cigarette smokers and chromate workers. Additional analyses are planned for the Tacoma cohort, which will examine mortality according to process as well as by exposure to arsenic and other contaminants. The importance of studies of workers at other kinds of smelters and refineries is stressed.
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PMID:Mortality studies of smelter workers. 734 69

An overview of published information on occupational cancer and recorded ongoing occupational cancer research in developing countries is presented. The main cancers reported, of possible occupational origin, are skin carcinoma, leukemia due to exposure to benzene, asbestos-caused mesothelioma, vinyl chloride-induced hepatic angiosarcoma, carcinoma of bilharzial urinary bladder, stomach cancer reportedly associated with nitrogen fertilizers, lung cancer of nickel smelters, and nasopharyngeal and pulmonary carcinoma in workers exposed to the dust of hard wood. The difficulties of developing efficient occupational cancer prevention are discussed. Some options are analyzed regarding legislative, technological, environmental, medical, administrative, and educational cancer control applicable under conditions of developing countries.
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PMID:Problems of occupational carcinogenesis in developing countries. 734 83

It has been widely assumed, especially in the absence of other explanations, that lung cancer and nasal sinus cancers observed among nickel smelter workers are the result of the carcinogenicity of nickel. Although there may be such influence, supplementary hypotheses are also possible. The nickeliferous ores from at least one major smelter in New Caledonia (excess numbers of cancers have been found in these smelter workers) are derived from serpentinized host rocks which contain large amounts of chrysotile asbestos. Analysis indicates that nickel ores from this area are heavily contaminated by these fibers. The deposits are mined for their nickel content, but workers may be exposed to the asbestos fibers contained in the deposits. Hygiene measures limited to the avoidance of nickel may be inadequate under such circumstances and should be reevaluated so as to prevent the inhalation of asbestos-containing dusts.
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PMID:Asbestos as a cofactor in carcinogenesis among nickel-processing workers. 738 17

An increased risk of cancer associated with nickel refining and with chromate production has been known for some decades. The occupational exposure pattern of both nickel and chromium is very complex. Even though nickel carbonyl is an experimental carcinogen, there are no data supporting its carcinogenicity in humans. Nickel subsulfide may be the most potent carcinogen among the different nickel compounds. A correlation between lung cancer and exposure to chromates has been shown in several studies. As yet, there are no epidemiologic data indicating carcinogenicity of chromium(III) salts. Hexavalent chromium, however, has been suggested as the causative carcinogen among platers and ferrochromium workers. There is an urgent need for careful dose registration before a quantitative cancer risk analysis can be performed for the nickel and chromium industry.
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PMID:Cancer hazards caused by nickel and chromium exposure. 746 13


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