Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The issue of carcinogenicity among mine workers and among workers in selected nonmining industries is examined. In the late 19th century, a high frequency of lung cancers was noted among metal miners in Bohemia, which probably related to their exposure to radon. Subsequently, other substances, including arsenic, asbestos, chromates, nickel, and chloroethers, have been linked causally to lung cancer. The IARC classification of substances as carcinogens is summarized, and the epidemiologic studies of humans employed in occupations with high rates of lung cancer due to carcinogen exposures are reviewed.
 ...
PMID:Respiratory cancers in mining. 838 78

Exposure to certain industrial agents has been thought to have carcinogenic potential, both for employees who work closely with such agents and for the general population that comes in contact with them. Although case reports, laboratory studies, and epidemiologic analyses help to determine the carcinogenicity of implicated agents, each of these types of investigation has limitations and deficiencies in distinguishing causal from noncausal associations. Asbestos has been linked with bronchogenic carcinoma, but several controversial factors--the degree of risk relative to exposure dose, the synergistic effect of cocarcinogens, and the question of existence of a threshold dose--complicate the understanding of the magnitude of the risk for exposed persons. Several other physical and chemical agents (such as chromium, nickel, and radon) have also been associated with an increased incidence of lung cancer in epidemiologic and animal studies. As with asbestos, the specific type of the agent and exposure conditions are important in determining the degree of carcinogenicity. In studies of exposure to man-made mineral fibers, formaldehyde, and silica, the findings have been inconsistent. Because the degree of health hazard attributable to asbestos and other known and suspected lung carcinogens is controversial, a wide range of opinions exists about the importance of occupational exposures to the overall incidence of lung cancers. Nevertheless, attempting to prevent lung cancers by minimizing or eliminating exposure to carcinogens is preferable to treating existent cases.
 ...
PMID:Occupational lung cancer. 842 99

A mortality study was carried out in conjunction with the European mortality study among welders coordinated by the International Agency for Research on Cancer (IARC). The study was aimed at assessing risks for lung cancer in relation to exposure to asbestos, welding fumes containing chromium and nickel, and tobacco smoke. The study included a cohort of 2721 welders and an internal comparison group of 6683 manual workers employed in 13 factories in France. The mortality of the two cohorts was studied from 1975 to 1988 by the historical prospective method. Job histories of welders were traced including welding processes used, metals welded, and proportion of worktime spent in welding. Data on smoking habits were collected from medical records. The observed number of deaths were compared with those expected (standardised mortality ratio (SMR)) based on national rates with adjustments for age, sex, and calendar time. The smoking habits of 87% of the whole study population were known. The distribution of welders and controls according to smoking was not statistically different. The overall mortality was slightly higher for welders (SMR = 1.02, 95% confidence interval (95% CI) 0.89-1.18) than for controls (SMR = 0.91, 95% CI 0.84-0.99). For lung cancer, the SMR was 1.24 (95% CI 0.75-1.94) for welders, whereas the corresponding value was lower for controls (SMR = 0.94, 95% CI 0.68-1.26). The SMR for lung cancer was 1.59 among non-shipyard mild steel welders (95% CI 0.73-3.02). This contrasted with the results for all stainless steel welders (SMR = 0.92, 95% CI 0.19-2.69), and for stainless steel welders predominantly exposed to chromium VI (SMR = 1.03, 95% CI 0.12-3.71). Moreover, SMRs for lung cancer for mild steel welders tended to increase with duration of exposure and time since first exposure, leading to significant excesses for duration > or = 20 years and latency > or = 20 years. Such a pattern was not found for stainless steel welders.
 ...
PMID:A mortality study among mild steel and stainless steel welders. 845 90

p53 mutations are frequent in malignant lung tumors. Of 88 surgically treated lung cancers from cigarette smokers previously evaluated for p53 mutations, 45 tumors (51.1%) had mutations in exons 5-8 (D. G. Guinee, Jr. et al., Carcinogenesis (Lond.), 16: 993-1002, 1995). We report here the examination of 13 occupational exposures and 13 high-risk occupations in relation to these p53 mutations. Two molecular abnormalities were associated with occupational exposures: (a) G:C-->T:A transversions on the coding (nontranscribed) strand (n = 13) were associated with chromate exposure and employment in the metal industry (P < 0.05) and marginally associated with nickel exposure (P = 0.056); and (b) G:C-->A:T transitions at non-CpG sites (n = 9) were associated with work in the petrochemical industry (P = 0.05). No association was found between p53 mutations and gender, cigarette pack-years, tumor histology, age at diagnosis, or family history of lung cancer. Because all three chromate-exposed subjects had large cell carcinomas exhibiting G: C-->T:A coding-strand transversions, follow-up of a cohort with this exposure should clarify the association with the p53 gene.
 ...
PMID:p53 mutations and occupational exposures in a surgical series of lung cancers. 895 23

A 57-year-old man was admitted because of dysphagia. Two year earlier, endoscopic ND-YAG laser treatment had been performed for squamous cell carcinoma of the tracheal carina. The esophagus was compressed and narrowed by invasion of lung cancer. After ballooning, under endoscopic and fluoroscopic control, a self-expanding nitinol stent (SENS, Ultraflex, Microvasive) was implanted in the esophagus. Immediately after esophageal prosthesis implantation, severe dyspnea and stridor developed because of tumor strictures in the left main bronchus. Under fluoroscopic and guide-wire control, SENS (Accuflex, Microvasive) was implanted in the tracheobronchial tree. Dyspnea, dysphagia and stridor were markedly improved after placement of two nitinol stents. Highly flexible, knitted, self-expanding nitinol stent is made of a nickel titanium alloy. Although the implantation of SENS in tracheobronchial stenosis has not previously been reported, it should be useful for prevention of airway obstruction.
 ...
PMID:[Self-expanding nitinol stents for treatment of tracheobronchial and esophageal stenosis caused by lung cancer]. 899 Aug 98

About 20% of al lung cancers among men are attributable to occupational exposure. During the years 1991 through 1993, Norwegian doctors reported 161 (4.6%) of 3.510 incidents of cancer in Norwegian men to the Labour Inspection as probably caused by occupational exposure. The proportion of such assumed occupational lung cancer cases varied with geographical region from 0.7% to 6.7%. Notification of an occupational cancer can be justification for economic benefits to the patient and his/her family. The most common assumed causes of the 161 cases notified as occupational lung cancers were asbestos dust exposure (148 cases), exposure to nickel (21 cases), and exposure to stone dust containing crystalline silica (18 cases). The predominating occupations of the patients at the time of the assumed carcinogenic exposure were machinist, industrial worker in metallurgical or chemical industry, mechanic, or metal worker (metal sheet worker, welder).
 ...
PMID:[Incidence and physicians' registration of assumed occupational lung cancer in Norway]. 906 34

The early epidemiological data indicated different carcinogenic risks from inhalation of different nickel compounds, but it was not clear what characteristics governed the intrinsic carcinogenic hazard of the various nickel compounds. Based on the earlier results, all soluble and insoluble nickel compounds were assumed to have the same carcinogenic mechanism albeit different potencies. Recent in vivo and in vitro studies challenged this assumption. In this paper an attempt is made to integrate the most relevant human, animal, and in vitro data into a general model that can help understand the different carcinogenic potentials of the various nickel compounds. In this perspective, it is recognized that there are two main components that could contribute to the development of lung cancer via exposure to certain nickel compounds. The first component corresponds to the heritable changes (genetic or epigenetic) derived from the direct or indirect actions of nickel compounds. The second component may be the promotion of cell proliferation elicited by certain nickel compounds. The different contributions of three nickel compounds to these two components are presented. This paper emphasizes the importance of recognizing the individuality of the different nickel species in reaching regulatory decisions and the fact that different risk assessment considerations may apply for compounds that appear to produce immortality and cancer by genetic/epigenetic mechanisms (like nickel subsulfide), compounds that may present a threshold for the induction of tumors in rats (like high-temperature nickel oxide), or compounds that may only have an enhancing effect on carcinogenicity (like nickel sulfate).
 ...
PMID:Carcinogenicity assessment of selected nickel compounds. 907 3

Rats and other rodents are exposed by inhalation to identify agents that might present hazards for lung cancer in humans exposed by inhalation. In some cases, the results are used in attempts to develop quantitative estimates of human lung cancer risk. This report reviews evidence for the usefulness of the rat for evaluation of lung cancer hazards from inhaled particles. With the exception of nickel sulfate, particulate agents thought to be human lung carcinogens cause lung tumors in rats exposed by inhalation. The rat is more sensitive to carcinogenesis from nonfibrous particles than mice or Syrian hamsters, which have both produced false negatives. However, rats differ from mice and nonhuman primates in both the pattern of particle retention in the lung and alveolar epithelial hyperplastic responses to chronic particle exposure. Present evidence warrants caution in extrapolation from the lung tumor response of rats to inhaled particles to human lung cancer hazard, and there is considerable uncertainty in estimating unit risks for humans from rat data. It seems appropriate to continue using rats in inhalation carcinogenesis assays of inhaled particles, but the upper limit of exposure concentrations must be set carefully to avoid false-positive results. A positive finding in both rats and mice would give greater confidence that an agent presents a carcinogenic hazard to man, and both rats and mice should be used if the agent is a gas or vapor. There is little justification for including Syrian hamsters in assays of the intrapulmonary carcinogenicity of inhaled agents.
 ...
PMID:Relevance of particle-induced rat lung tumors for assessing lung carcinogenic hazard and human lung cancer risk. 940 Jul 48

Epidemiologic evidence on the relation between exposure to metals and cancer is reviewed. Human exposure to metals is common, with wide use in industry and long-term environmental persistence. Historically, the heaviest metal exposures occurred in the workplace or in environmental settings in close proximity to industrial sources. Among the general population, exposure to a number of metals is widespread but generally at substantially lower levels than have been found in industry. The carcinogenicity of arsenic, chromium, and nickel has been established. Occupational and environmental arsenic exposure is linked to increased lung cancer risk in humans, although experimental studies remain inconclusive. Experimental studies clearly demonstrate the malignant potential of hexavalent(VI) chromium compounds, with solubility being an important determining factor. Epidemiologic studies of workers in chromium chemical production and use link exposure to lung and nasal cancer. Experimental and epidemiologic data show that sparingly-soluble nickel compounds and possibly also the soluble compounds are carcinogens linked to lung and nasal cancer in humans. Some experimental and epidemiologic studies suggest that lead may be a human carcinogen, but the evidence is inconclusive. Although epidemiologic data are less extensive for beryllium and cadmium, the findings in humans of excess cancer risk are supported by the clear demonstration of carcinogenicity in experimental studies. Other metals, including antimony and cobalt, may be human carcinogens, but the experimental and epidemiologic data are limited.
 ...
PMID:The carcinogenicity of metals in humans. 949

The focus of this article is to examine how the choice of comparison group affects the identification and interpretation of cause-specific health risks in occupational cohorts when different external control populations are used. The mortality experience of approximately 31,000 high nickel alloys workers is compared with the total US population and to local populations in geographic proximity to the plants. Generally, the patterns of relative risks derived for the total cohort and various subgroups are similar across the different comparison populations. Estimated elevated risks are usually lower when cohort mortality is compared with that of local populations. An overall significant 13% risk for lung cancer is noted when compared with that of the total US population. However, no significant excess is identified when local populations are used. Subset analysis identified significant excesses of colon cancer among nonwhite males (50%-150%) and kidney cancer among white male workers employed in melting (approximately 100%), irrespective of the comparison population.
 ...
PMID:Using alternative comparison populations to assess occupation-related mortality risk. Results for the high nickel alloys workers cohort. 980 Jan 77


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>