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

For the historical follow-up study among arc welders exposed to chromium and nickel, which was started in 1980 in Germany, a third follow-up extending the observation period to the years 1989 through 1995 has been carried out. By 1995, of the 1213 welders and 1688 turners (control group) who were originally included in the study, 274 welders and 448 turners had died. Death certificates could be obtained for approximately 96% of the deceased. Results of the evaluation presented in this article showed that cancer mortality remains significantly increased, compared with the general population and the control group, by approximately 35%. There was an elevation of approximately 50% or 60% in mortality from cancers of the respiratory tract, which is also statistically significant. However, this increase is predominantly due to a large excess in mortality from mesothelioma, which is known to be caused chiefly by asbestos exposure. Lung cancer mortality is nonsignificantly increased by approximately 20% to 30%. An indirect assessment of asbestos-related lung cancers and total cancer indicates that the observed increase of mortality might be mainly due to asbestos exposure. Beyond that, no indication of an elevated cancer risk specifically associated with the exposure to welding fumes containing chromium and nickel could be determined.
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PMID:Cancer mortality among arc welders exposed to fumes containing chromium and nickel. Results of a third follow-up: 1989-1995. 1022 96

This report presents 20 years' of cancer incidence data by occupational group for the Nordic populations. The study covers the 10 million people aged 25-64 years at the time of the 1970 censuses in Denmark, Finland, Norway, and Sweden, and the 1 million incident cancer cases diagnosed among these people during the subsequent 20 years. The project was undertaken as a cohort study with linkage of individual records based on the personal identification numbers used in all the Nordic countries. In the 1970 censuses, information on occupation for each economically active member of the household was provided in free text in self-administered questionnaires. The data were centrally coded and computerized in the statistical offices. Norway, Sweden, and Finland used the Nordic Classification of Occupations, while Denmark used a national coding scheme. However, all the data could be reclassified into 53 occupational groups and 1 group of economically inactive persons. Person-years at risk were accumulated from 1 January 1971 until the date of emigration, date of death or 31 December 1987 in Denmark, 1989 in Sweden, 1990 in Finland, and 1991 in Norway. The 4 countries all had nationwide registration of incident cancer cases during the entire study period. All incident cancer cases during the individual risk periods were included in the analysis. Despite minor differences between the countries, the International Classification of Diseases, 7th revision, formed the core basis for the diagnostic coding in all 4 countries. For the present study the incident cancer cases have been classified into 35 broad diagnostic groups. The observed number of cancer cases in each group of persons defined by country, gender, and occupation was compared with the expected number calculated from the age-, gender-, and period-specific person-years and the incidence rates for the national population. The result has been presented as a standardized incidence ratio (SIR), defined as the observed number of cases divided by the expected number and multiplied by 100. In the tables of this report, all the SIR values for which the upper limit of the 95% confidence interval is below 100 are printed in green and all those for which the lower limit of the confidence interval is above 100 are printed in red. For all cancers combined, the study showed a wide variation among the men, from an SIR of 79 for farmers to 159 for waiters. The occupations with the highest SIR values also included seamen and workers producing beverages and tobacco. Among the women the SIR values varied from 83 for gardeners to 129 for tobacco workers. Low SIR values were found for farmers and teachers. Outdoor workers such as fishermen and gardeners had the highest risk of lip cancer, while the lowest risk was found among indoor workers such as physicians and artistic workers. Almost all pleural cancers are associated with asbestos exposure. Accordingly, plumbers, welders, mechanics, and seamen were the occupations with the highest risk. There was also an excess risk of pleural cancer in the occupational group of technical, chemical, physical, and biological workers, including, among others, engineers and chemists potentially exposed to asbestos. The wood workers included in the present study had the highest risk of nasal cancer. Most studies of nasal cancer have shown increased risks associated with exposure to wood dust, both for those in furniture making and for those exposed exclusively to soft wood. Nickel refinery workers are also known for their high risk of nasal cancer. In the present study they were included in the occupational group of smelting workers. Lung cancer was the most frequent cancer among men in the present study. Tobacco smoking is the major risk factor for this disease, but occupational exposures also play an important role. Waiters and tobacco workers had the highest risk of lung cancer. Miners and quarry workers also had a high risk of lung cancer, which may be related to
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PMID:Work-related cancer in the Nordic countries. 1050 18

Mining activities in the former German Democratic Republic were documented as early as 1168 in the ore mountains (Erzgebirge) of Saxony. Silver, bismuth, cobalt, nickel and tungsten were mined from then up to the end of the 19th century. After the Second World War, the Soviet Occupation Authorities reopened the old silver mines in Saxony to mine uranium for the Soviet nuclear industry. About 400, 000 workers produced a total of 220,000 tons of uranium during the years 1946 to 1990. After the reunification of Germany, the archive of the Institute of Pathology of the mining area was opened for research. It contains protocols of 28,975 autopsy cases and about 400,000 slides collected from 1957 to 1992, about 66,000 tissue blocks, and 238 whole lungs. From the autopsy cases, 17,466 could be identified as workers of the uranium mining company. The remainder of the cases were in the population of the mining area. A comparison of the frequencies of malignancies of male workers older than 15 years with those of the population of the mining area for the years 1957 to 1989 demonstrates a significantly higher percentage of lung cancer among the uranium miners. There was no significant difference for other solid cancers and leukemias.
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PMID:German uranium miner study--historical background and available histopathological material. 1056 36

The main objective of this study was to analyze the risks associated with occupational exposures in an industrializing country where lung cancer is the primary neoplastic cause of death in men. A full occupational history was collected through interviewing 199 men with lung cancer and 393 control subjects. Exposure to arsenic, asbestos, chromium, dust, nickel, and polynuclear aromatic hydrocarbons was assessed by means of a job-exposure matrix. Elevated odds ratios were observed for employment in the alcoholic beverages industry (5.2; 95% confidence interval [CI], 1.1 to 23.1), sawmills and wood mills (4.8; 95% CI, 1.2 to 19.0), water transport (3.3; 95% CI, 1.1 to 12.1), and chemicals/plastics manufacturers (1.9; 95% CI, 1.1 to 3.3). A small, non-significant increased risk was observed after long-term exposure to arsenic and chromium, with a dose-response for chromium. Although some of the present results may result from chance, most are consistent with those of previous investigations in other countries.
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PMID:Occupational exposures and lung cancer in Buenos Aires, Argentina. 1087 59

The authors present the most essential data on physical and chemical properties of chrysotile, sources of its emission, the extent of occupational exposure, and biological effect, used in setting MAC values for chrysotile-containing dusts. Exploitable asbestos deposits do not exist in Poland, but admixtures of asbestos minerals have been found in some deposits of mineral raw materials located in the area of Lower Silesia (melafir, gabbro, dolomite. ore, nickel, magnesite, serpentinite). In the 1970s, about 100,000 tonnes of asbestos, containing 90% of chrysotile, were used annually in Poland. This figure decreased to 30,000 tonnes in 1991. In 1985 the use of crocidolite asbestos was stopped, and in 1999, the use of asbestos-containing products was banned by the virtue of the legal act. At present, the Minister of Economy in agreement with the Minister of Environmental Protection sets regularly the list of asbestos-containing products permitted for the production or in the customs area. Nowadays, the range of dust concentrations in plants which use asbestos products amounts to 0.1-0.6 mg/m3 for total dust and 0.002-0.07 f/cm3 for respirable mineral fibres; and during exploitation of rock raw material deposits 0.7-280 mg/m3, and 0.01-3.3 f/cm3, respectively. During the years 1976-96, 1520 cases of asbestos-related occupational diseases were diagnosed. This figure included 1314 cases of asbestosis, 154 cases of lung cancer and 52 cases of pleura mesothelioma. MAC values for chrysotile and chrysotile-containing dusts are: 0.2 f/cm3 and 1 mg/m3.
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PMID:[Chrysotile asbestos: biological effects, the work environment highest allowable concentration and neoplasm risk]. 1100 75

Differential display polymerase chain reaction (DD-PCR) was used to analyze the differentially expressed genes from nickel-transformed human embryonic lung (HEL) cells (MRC-9 and IMR-90) and their control counterparts (non-treated). Two genes, MS515 and IC82, were confirmed by Northern blot analysis. MS515 was detected in control and nickel oxide (NiO)-transformed MRC-9 cells, as well as in non-small cell lung cancer (NSCLC) EBC-1 cells, while very weak expression was observed in nickel subsulfide (Ni(3)S(2))-transformed MRC-9 cells and small cell lung cancer (SCLC) SBC-2 cells. IC82 could not be detected in control IMR-90 cells, while it was expressed in EBC-1 cells and NiO- and Ni(3)S(2)-transformed IMR-90 cells. These findings indicate that individual nickel compounds have their own target gene(s) in inducing lung cancer. Sequencing analyses showed that the MS515 gene shared a high degree of homology (over 80%) with the gene Mena, which is involved in actin polymerization. IC82 showed 99% homology with human chromosome 4 clone C0440E08 and a coding sequence in the brain. The roles of these two genes in nickel carcinogenesis will be discussed.
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PMID:Cloning of differentially expressed sequence tags from nickel-transformed human embryonic lung cells. 1107 13

Lung cancer continues to be the leader in cancer deaths in the United States. The incidence of lung cancer in men has slowly decreased since the late 1980s, but has just now begun to plateau in women at the end of this decade. Despite modest advances in chemotherapy for treating lung cancer, it remains a deadly disease with overall 5-yr survival rates having not increased significantly over the last 25 years, remaining at approximately 14%. Tobacco smoking causes approximately 85-90% of bronchogenic carcinoma. Environmental tobacco exposure or a second-hand smoke also may cause lung cancer in life-long non-smokers. Certain occupational agents such as arsenic, asbestos, chromium, nickel and vinyl chloride increase the relative risk for lung cancer. Smoking has an additive or multiplicative effect with some of these agents. Familial predisposition for lung cancer is an area with advancing research. Developments in molecular biology have led to growing interest in investigation of biological markers, which may increase predisposition to smoking-related carcinogenesis. Hopefully, in the future we will be able to screen for lung cancer by using specific biomarkers. Finally, dietary factors have also been proposed as potential risk modulators, with vitamins A, C and E proposed as having a protective effect. Despite the slow decline of smoking in the United States, lung cancer will likely continue its devastation for years to come.
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PMID:The epidemiology of lung cancer. 1122 93

In 1997, the International Agency for Research on Cancer (IARC) upgraded its evaluation of crystalline silica to a Group 1 human carcinogen. Criticism against such decision is based on the lack of consistency in experimental results across animal species, violation of an important principle for causality, such as the replication of findings under different circumstances of exposure, and the lack of a clear dose-response curve. The most recent epidemiological literature on the silica-silicosis-lung cancer link replicates the inconsistent findings that have been characterising 50 years of scientific debate in the occupational arena. Exposure circumstances capable of modifying the silica-lung cancer association include chronic bronchitis, composition of the dust mixing, particularly concerning co-occurrence of other known or probable lung carcinogens, total respirable dust, concentration of silica in respirable dust, type of crystalline silica and particle surface characteristics. The hypothesis of a silicosis-mediated pathway points toward an unspecific mechanism shared with other fibrotic conditions, for which silica might be just one of the triggers. In envisaging a multivariate multistep model of lung cancer among silica-exposed workers, silica might be considered as a "passive components of the sufficient cause", i.e., one of the associated risk factors, concurrent or subsequent to the "active component(s) of the sufficient cause" (including, for instance, smoking, asbestos, radon-daughters, arsenic, hexavalent chromium, nickel, polycyclic aromatic hydrocarbons (PAH), and diesel exhausts among the external risk factors; and DNA repair enzymes polymorphism and spontaneous inactivation of tumour suppressor genes among the internal risk factors), which adds up in modulating the tumoral development in not easily predictable directions. If silica acts as a human lung carcinogen depending on certain occupational exposure circumstances, perhaps those circumstances and not silica itself should be classified for their human carcinogenicity potential.
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PMID:Multifactorial aetiology of lung cancer among silica-exposed workers. 1160 27

Lung cancer is the most common thoracic malignancy caused by exposures at work and in the environment. The most unique thoracic malignancy is mesothelioma, because it is relatively rare and one of only a few neoplasms for which one specific inciting agent-asbestos-has been identified. Based on epidemiologic studies, approximately 15% of lung cancers in men and 5% of lung cancers in women are caused by occupational exposures. The International Agency for Research on Cancer has devised a rating system by which, based on animal and human data, they assign an agent, mixture, or exposure circumstance to one of five categories, ranging from group 1 (agent is carcinogenic to humans) to group 4 (agent is probably not carcinogenic to humans). Group 1 pulmonary carcinogens reviewed in this article include arsenic, asbestos, beryllium, bis (chloromethyl) ether, cadmium, chromium (IV), mustard gas, nickel, radon, and silica. The clinical presentation and pathology of lung cancers and mesothelioma caused by such exposures do not differ from those of cancers caused by other factors. The key to the recognition of a thoracic malignancy caused by workplace or environmental exposures is clinical suspicion and consideration of all causes for the disease present. Recognition of an exposure-related case of lung cancer or mesothelioma can aid in the identification of excess risk for a whole workforce or community and can lead to actions to reduce exposure, thus preventing future cases. In addition, such recognition allows the individuals struck by devastating illness to exercise their legal rights to compensation if so desired.
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PMID:Occupational and environmental thoracic malignancies. 1208 70

The International Agency for Research on Cancer has classified nickel compounds as carcinogenic to humans, but it is still not known with certainty which forms of nickel pose the risk. In a case-control study of Norwegian nickel-refinery workers, the authors examined dose-related associations between lung cancer and cumulative exposure to four forms of nickel: water-soluble, sulfidic, oxidic, and metallic. A job-exposure matrix was based on personal measurements of total nickel in air and quantification of the four forms of nickel in dusts and aerosols. Data on smoking habits were collected for 213 cases identified in the Cancer Registry of Norway between 1952 and 1995 and 525 age-matched controls (94% participation rate). The nickel exposures were moderately to highly correlated. A clear dose-related effect was seen for water-soluble nickel (odds ratio = 1.7 per unit in the log(e)-transformed exposure, ln[(cumulative exposure) + 1], originally given in (mg/m(3)) x years (95% confidence interval: 1.3, 2.2)). A general rise in risk from other types of nickel could not be excluded, but no further dose-dependent increase was seen. Smoking was a weak to moderate confounder. The study suggests an important role of water-soluble nickel species in nickel-related cancer.
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PMID:Exposure to different forms of nickel and risk of lung cancer. 1248 Jun 57


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