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

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

A mortality study was carried out among the workers of a plant that had produced ferrochromium and stainless steel, and was still producing stainless steel, in order to determine whether exposure to chromium compounds, to nickel compounds, and to polycyclic aromatic hydrocarbons (PAH) could result in a risk of lung cancer for the exposed workers. The cohort comprised 2269 men whose vital status were recorded between 1 January 1952 and 31 December 1982. The smoking habits of 67% of the cohort members were known from medical records. The observed numbers of deaths were compared with the expected ones based on national rates with adjustment for age, sex, and calendar time. A low mortality, achieving statistical significance, was found from all causes (observed = 137, standardised mortality ratio (SMR) = 0.82) and from benign respiratory diseases (observed = one, SMR = 0.15). With regard to mortality from lung cancer, a non-significant excess appeared in the whole cohort (observed = 12, SMR = 1.40). Among the exposed workers, however, a significant lung cancer excess was found (observed = 11, SMR = 2.04) that contrasted with a low SMR (0.32) in the non-exposed group. This excess is unlikely to be explained by smoking, as the tobacco consumption of these two groups was similar. No trend was observed for mortality from lung cancer either according to time since first exposure, or according to duration of exposure. A nested case-control study clearly suggested that this excess of deaths from lung cancer was attributable to former PAH exposures in the ferrochromium production workshops rather than to exposures in the stainless steel manufacturing areas.
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PMID:Mortality study among workers producing ferroalloys and stainless steel in France. 239 34

Histopathological diagnoses were compiled for 100 sinonasal cancers and 259 lung cancers in nickel refinery workers, including cases from Wales, Canada, and Norway. The sinonasal cancers comprised squamous cell carcinomas (48 percent), anaplastic and undifferentiated carcinomas (39 percent), adenocarcinomas (6 percent), transitional cell carcinomas (3 percent), and other malignant tumors (4 percent). The lung tumors comprised squamous cell carcinomas (67 percent), anaplastic, small cell, and oat cell carcinomas (15 percent), adenocarcinomas (8 percent), large cell carcinomas (3 percent), other malignant tumors (1 percent), and cancers not otherwise specified (6 percent). Possible selection bias in these data cannot be excluded, since the histological diagnoses represent 63 percent, 68 percent, and 100 percent of cases of sinonasal cancer and 24 percent, 47 percent, and 86 percent of cases of lung cancer in the Welsh, Canadian, and Norwegian workers. This study suggests that (a) the sinonasal cancers in nickel refinery workers conformed to the usual distribution of histological types observed in the general population (in contrast to the predilection for adenocarcinomas in wood workers), and (b) the lung cancers in nickel-refinery workers showed preponderance of squamous cell carcinomas and deficit of adenocarcinomas, compared to prevalent proportions of these neoplasms, possibly reflecting the paucity of women in the cohorts and temporal trends during the six decades in which the tumors were diagnosed.
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PMID:Histopathology of sinonasal and lung cancers in nickel refinery workers. 253 54

This paper describes observed and expected mortality from cancers of the lung, larynx, nose, and kidney in a cohort of 54,509 nickel workers followed for 35 years. For analysis purposes the cohort was subdivided into men with and without service in one of the three high nickel dust areas of the operation: the Sinter Plants at Copper Cliff and Coniston, and the Leaching, Calcining and Sintering (LC&S) department at Port Colborne. At Copper Cliff Sinter Plant workers experienced three times the expected number of lung cancer deaths; the SMR rose steeply with increasing duration of service peaking at 943 with 10 to 15 years. A similar overall excess risk of lung cancer was seen in the smaller Coniston Sinter Plant again with an indication of an exposure risk gradient. Men in the LC&S department at Port Colborne also experienced a dose related excess risk of lung cancer death that rose to an SMR of 806 with 20 to 25 years of service. Nasal cancer deaths were increased at both the Copper Cliff Sinter Plant (6 deaths) and the LC&S department at Port Colborne (19 deaths), representing SMRs of 3,704 and 7,755, respectively, for this rare cancer. Laryngeal cancer and kidney cancer, both previously associated with nickel, were not in excess in these high risk groups. A further exploration of death from these causes in the lower exposure remainder of the cohort revealed an epidemiologically modest elevation in lung cancer death in miners (probably not nickel related) and parts of the Copper Refinery. No evidence of laryngeal cancer excess was found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A study of mortality in workers engaged in the mining, smelting, and refining of nickel. II: Mortality from cancer of the respiratory tract and kidney. 262 65

Lung specimens from 39 nickel refinery workers autopsied during the period from 1978 to 1984 were analyzed for nickel. Fifteen of the workers were employed in the Roasting and Smelting Department, where exposure to nickel was predominantly in the form of nickel-copper oxides, Ni3S2 and metallic dust. The remaining 24 men worked in the Electrolysis Department. Exposure in this group was considered to be mostly to the water-soluble compounds, NiSO4 and NiCl2, but also to a lesser degree to water-insoluble nickel compounds such as nickel-copper oxides and sulphides. The arithmetic mean +/- SD for nickel concentration in lung tissues expressed in micrograms g-1 dry wt for the 39 workers was 150 +/- 280. In the workers employed in the Roasting and Smelting Department, the average nickel concentration was 330 +/- 380; for those who worked in the Electrolysis Department it was 34 +/- 48. Lung tissue from 16 autopsied persons not connected with the refinery had an average nickel concentration of 0.76 +/- 0.39. Statistical analysis based on log-normal distributions of the measured nickel concentrations allowed three major conclusions to be formulated: (1) nickel refinery workers exhibit elevated nickel levels in lung tissues at autopsy; (2) workers of the Electrolysis Department and the Roasting Smelting Department constitute distinct groups with respect to the accumulation of nickel in lung tissue; (3) workers who were diagnosed to have lung cancer had the same lung nickel concentrations at autopsy as those who died of other causes.
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PMID:Determination of nickel in lung specimens of thirty-nine autopsied nickel workers. 272 52

Using data from published studies, lung concentrations of nickel were compare for persons with and without occupational exposure to nickel. As expected, the concentrations were much higher for persons with occupational exposure. To estimate the effects of nickel-containing tobacco smoke and nickel in the ambient air on the amount of nickel accumulated in lungs over time, a model was derived that took into account various variables related to the deposition of nickel in lungs. The model predicted nickel concentrations that were in the range of those of persons without known nickel exposure. Nickel is a suspected carcinogen and has been associated with an increased risk of respiratory tract cancer among nickel workers. However, before the nickel content of cigarettes can be implicated in the etiology of lung cancer, further studies are needed to evaluate the independent effects of smoking and exposure to nickel.
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PMID:The accumulation of nickel in human lungs. 275 60

After inhalative occupational exposure to certain compounds containing nickel and chromium (mostly over many years), an accumulation of these metals may occur in the lung tissue. This is of particular importance, both from a toxicological point of view and with regard to expert reports, since certain nickel and chromium compounds may induce lung cancers. In the context of this study, samples of pulmonary tissue from 34 deceased persons from the Bergen area (Norway) were analysed by atomic absorption spectrometry with regard to their content of chromium and nickel. The deceased comprised 21 men and 13 women. In 15 cases, death resulted from lung cancer; in the other 19 deceased, there was no indication of a malignant disease of the airways. The concentrations of nickel found in the lung tissue do not differ between patients with lung cancer and patients with healthy lungs. On the other hand, the concentration of chromium in the pulmonary tissue in the patients who had died of lung cancer and who had all been inhalative smokers, are higher (statistically significant) than in the nonsmokers or in those with healthy lungs. An accumulation of these two metals in the tumor matrix could not be detected. Both the average nickel and the average chromium concentrations were higher in the persons who had probably been exposed occupationally. Considering the present state of scientific knowledge, the aspects relevant to expert reports which result from the analyses of metals in the pulmonary tissue are discussed.
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PMID:Analyses of chromium and nickel in human pulmonary tissue. Investigations in lung cancer patients and a control population under special consideration of medical expertise aspects. 280 68

Many epidemiological and experimental studies have suggested that the respiratory tract is one of the most sensitive organs to environmental carcinogens. Nevertheless there is little evidence to determine the relationship between a specific environmental carcinogen and a cell type of lung cancer, because the cell types of lung cancer and their relative frequencies are highly complex compared with those of other organs and tissues. In the present paper, occupational lung-cancer characteristics, which are the clearest in the relation between cause and effect in human lung cancers, were reviewed in comparison with the results of animal experiments concerned with occupational lung carcinogens. Through accumulation of histopathological examinations of the lung cancer cases, the following relationships between cause and cell type were conjectured: chromium and squamous cell carcinoma; asbestos and adenocarcinoma; nickel and squamous cell carcinoma; beryllium and small cell carcinoma; bis (chloromethyl) ether and small cell carcinoma; mustard gas and squamous cell or small cell carcinoma; vinyl chloride and large cell or adenocarcinoma; radionuclides and small cell carcinoma. The relation pertaining to arsenic, benzotrichloride and tar could not be conjectured because of insufficient cases and information in the histological diagnosis. On the other hand, the carcinogenicity of these substances in occupational exposure has been confirmed by animal experiments administered intratracheally or by inhalation studies under relatively higher concentration. As a result of recent refinements of inhalation study, all-day and life-span exposure to extremely low concentrations, such as microgram/m3 orders, of certain substances has been possible. The characteristics of lung tumors occurring in these animals are rather different from those of human. For example, in mouse, almost all of the malignant lung tumors developed by carcinogens are adenocarcinomas and it is rare to find the squamous cell carcinoma. Moreover, small cell carcinoma and large cell carcinoma have not known to occur in the lungs of rats and mice. Therefore, future research should focus elucidating the specific relationship between cause and cell type of human lung cancer by means of animal experiments on lung cancer that give attention to the specificities of each experimental animal and the origin of the resultant lung tumor.
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PMID:[Occupational lung cancer. A comparison between humans and experimental animals]. 283 18

A general method is presented for the use of mathematical modeling in the design, execution, and interpretation of toxicology experiments. To illustrate the use of mathematical modeling toxicology, a case study is presented of how a dosimetry model for inhaled nickel was developed for use in cancer risk estimation. A physiologically based pharmacokinetic (PB-PK) dosimetry model is used to plan animal experiments and to extrapolate nickel kinetics from animals to humans. These data are then used to estimate human lung cancer risks from human exposure to nickel aerosols. To achieve this goal, a PB-PK dosimetry model for the lung was integrated with a PB-PK dosimetry model for the internal organs. Nickel removal from the lung was found to be saturable and to follow Michaelis-Menten kinetics. The PB-PK lung dosimetry model was used to design both short-term (single exposures) and long-term (multiple intermittent exposures) needed to validate the parameters (Km and Vmax) of the lung dosimetry model. A constant infusion experiment was planned using the PB-PK modeling approach to measure the distribution and elimination of intravenously administered nickel. The two PB-PK models were integrated to estimate the fate of nickel after inhalation and are being used to plan experiments for other routes of exposure such as ingestion of drinking water and dermal contact. The integrated model has been used to calculate a human cancer risk estimate in combination with short-term genotoxic experiments. Using PB-PK models in toxicology, as illustrated here, conserves experimental animals, aids in understanding new physiological phenomena (such as saturable clearance from the lung), incorporates in vitro tests with in vivo experiments, and provides a means of extrapolation to human health risks from multiple routes of exposure. Introducing the concepts of mathematical modeling into toxicity experiments at the beginning of the experiment improves the usefulness of the experiments in risk estimation. PB-PK models are suggested as a new basis for experimental design in toxicology.
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PMID:Planning and using PB-PK models: an integrated inhalation and distribution model for nickel. 317 72

Nickel (Ni) and some of its relatively insoluble compounds as well as chromates may be able to induce cancer in the region of the lungs, as well as in the nose and paranasal sinuses after occupational exposure. Latency periods may amount to 20 years and more. The results of recent investigations have shown that these metals cumulate in the lung tissue after inhalation of relatively insoluble chromium and nickel compounds. The quantitative detection of these heavy metals in samples of pulmonary tissue hence permits the amount of past exposure to be estimated. To establish the normal values, samples of pulmonary tissue from 30 normal subjects were investigated for chromium and nickel content. The samples were taken from different segments and lobes of the lungs, taking topographical anatomical criteria into consideration. In addition, 15 persons who had formerly been exposed to nickel and/or chromium (11 nickel refinery workers, of whom 10 had died of lung cancer, 2 stainless steel welders, 1 foundry worker, 1 electrical technician) were also investigated. From the results of 495 tissue samples from the normal group, median chromium concentrations between 130 and 280 ng/g were calculated, with median nickel concentrations of 20-40 ng/g (wet weight). If these values are related to the nickel concentrations measured in refinery workers, values 112-5,860 times higher were found. The concentrations were about 500 times higher than normal for nickel, and about 60 times higher than normal for chromium in the stainless steel welders. For the foundry workers who died of lung cancer, chromium and nickel concentrations in the normal range were calculated, with the exception of the nickel concentrations in the upper and lower lobes of the right lung. The very high nickel concentrations found in the samples of lung tissue from former nickel refinery workers should be regarded as a guideline with regard to the appraisal of the causal relationship between lung cancer and occupational exposure to relatively insoluble nickel compounds. This result is also supported by epidemiological investigations on this subgroup and must thus be considered etiologically conclusive. For the welders, chromium and nickel concentrations were found that were markedly above normal, but as yet there is no epidemiologically reliable verification for the increased occurrence of malignancies in this occupational group.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Investigations on the quantitative determination of nickel and chromium in human lung tissue. Industrial medical, toxicological, and occupational medical expertise aspects. 335 Jun 5


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