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

We have studied mortality patterns in a large cohort of rubber workers. We have examined workers exposed to curing fumes, processing dusts, and industrial talc and have begun to evaluate exposures of these workers in detail. Gastrointestinal (especially stomach) cancer appears in excess in processing workers. Lung cancer is excessive in curing workers. Leukemia is increased generally. All three groups studied for respiratory disease have an increase in disease prevalence which is related to intensity and duration of exposure. Since both an increase in stomach cancer and respiratory disease is seen in processing workers, exposures in this area must be controlled. Since both lung cancer and chronic respiratory disease is excessive in curing rooms, this exposure must be controlled. The leukemia risk is probably related to solvents. Whether this is all explainable by past benzene exposure is unknown. Further studies are planned to refine our knowledge concerning these risks so that occupational disease in the rubber industry can be prevented.
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PMID:Occupational disease in the rubber industry. 102 15

The first group of non-bred rats was injected intrapleurally 20 mg of benzene extracted chrysotil-asbestos dust in saline; the second group of rats was injected 20 mg of the same dust but with benz(a)pyrene absorbed on it (0.4 mg). Pleural mesotheliomas were observed in 48.57% of cases in the first group and in 41.37% of cases in the second one. The difference was not significant. There was no difference in the percentage of premesotheliomatous lesions. But, in the second group tumors of other organs were found. The role of asbestos pollution by carcinogenic hydrocarbons in the genesis of lung cancer and pleural mesothelioma is discussed.
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PMID:[Mechanism of the induction of asbestos mesotheliomas in the pleura of rats]. 127 66

Human cytochrome P450IIE1 (CYP2E) is involved in the metabolic activation of procarcinogens such as N-nitrosodimethylamine, benzene and ethyl carbamate. We screened DNA from 28 individuals for restriction fragment length polymorphisms (RFLPs) is the human P450IIE1 gene and detected an RFLP for the restriction endonuclease DraI. The distribution of the genotypes of this polymorphisms among lung cancer patients (n = 74) differed from that among controls (n = 73) with statistical significance of p < 0.05. In addition, the distribution among patients with cancers of the digestive system (n = 38) was also different from that among controls. Our findings indicate an association between the DraI polymorphism of the IIE1 gene and susceptibility to cancers of the lung and the digestive system.
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PMID:Human cytochrome P450IIE1 gene: DraI polymorphism and susceptibility to cancer. 136 74

Cytochrome P450IIE1 is responsible for the activation of carcinogenic N-nitrosamines, benzene, urethane, and other low-molecular-weight compounds. Restriction fragment length polymorphisms (PstI and RsaI restriction enzymes) have been identified in the cytochrome P450IIE1 transcription regulatory region that may affect expression. This study describes the PstI and RsaI polymorphisms in different racial populations and in a case-control study of lung cancer. The allelic frequencies were markedly different in Japanese, African-Americans, and Caucasians: the PstI rare allele was present at a frequency of 2% in Caucasians, 5% in African-Americans, and 24% in Japanese (P < 0.05). For the RsaI rare allele, frequencies were 2% in Caucasians, 2% in African-Americans, and 27% in Japanese (P < 0.05). The assay was also applied to 128 individuals enrolled in a case-control study of lung cancer. Although limited in statistical power, the data indicate no evidence for an association in the aggregate of cytochrome P450IIE1 PstI [for which the odds ratio was 0.7 (95% confidence interval (C.I.) = 0.2-2.8)] or RsaI [for which the odds ratio was 0.9 (95% C.I. = 0.2-5.4)] restriction fragment length polymorphisms with lung cancer in this U.S. population. When analyzed by race, the lung cancer odds ratio for the PstI mutant allele in African-Americans was 0.19 (95% C.I. = 0.03-1.38), and in Caucasians it was 4.13 (95% C.I. = 0.34-48.8). For the RsaI mutant allele, the odds ratios were 0.20 (95% C.I. = 0.02-2.43) and 4.28 (95% C.I. = 0.35-50.6), respectively. The ethnic differences of these restriction fragment length polymorphisms might be related to genetic susceptibilities for lung cancer among Caucasians and for gastric or esophageal cancer among Japanese.
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PMID:Cytochrome P450IIE1 genetic polymorphisms, racial variation, and lung cancer risk. 142 19

Biological monitoring is an efficient tool in the evaluation of exposure to chemical agents. However, the dose-response of adverse health effects using biological exposure indices and biological limit values are rarely available. This paper presents an estimation of the occupational exposure limit value of 1-hydroxypyrene in urine, a biological exposure indicator of polycyclic aromatic hydrocarbons (PAH). A large-scale study of the exposure of cokeoven workers to PAH, in which both air sampling (benzene soluble matter and individual PAH including benzo(a)pyrene) and biological monitoring (1-hydroxypyrene in urine) were applied, made it possible to establish an empirical mathematical relationship between the air sampling data and biological monitoring data. It was calculated that cokeoven workers with a urinary concentration of 1-hydroxypyrene of 2.3 mumol/mol creatinine after a 3-day working period equals the airborne threshold limit value (TLV) of coal tar pitch volatiles (CTPV). Epidemiological studies have quantified the relative risk of lung cancer for topside and non-topside cokeoven workers. The published environmental exposure data of topside and non-topside cokeoven workers were used to determine the time-average exposure. The data of 1-hydroxypyrene in the urine of cokeoven workers and data of epidemiological studies from different coke plants were combined according to the concentrations of PAH in the air. Thus, it was possible to establish an indirect relationship between lung cancer mortality risk and the biological exposure indicator for cokeoven workers. Exposure at the level of the suggested tentative biological exposure limit (BEL) of 2.3 mumol/mol creatinine is estimated to be equal to a relative risk of lung cancer of approximately 1.3.
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PMID:Biological exposure limit for occupational exposure to coal tar pitch volatiles at cokeovens. 158 24

The findings of the studies summarized in this report provide some understanding of the possible role of dosimetry in the different response of the rats and mice to benzene in the long-term bioassay studies. The more sensitive species, the mice, definitely has a higher capacity to metabolize benzene and to metabolize it to more of the putative toxic metabolites than do rats. A major finding of these studies is that in three different animal species, from mice to monkeys, the metabolic pathways leading to production of the putative toxic metabolites appear to be low-capacity, high-affinity pathways that are saturated at relatively low-exposure concentrations. This does not prove, but suggests, that the same may be true in humans. If the total formation of the putative toxic metabolites is predictive of the toxicity of benzene, then the animal studies suggest that calculations of the risk associated with low dose exposures based on the results of animal studies conducted at high doses would underestimate the toxicity of benzene. The current report concerns only dosimetry. Another problem in assessing the risk to humans from benzene exposure is the fact that the animal models do not respond to benzene in the same way as humans. The major concern for humans exposed to benzene, based on epidemiology studies, is the risk of developing acute myelogenous leukemia (Rinksy, 1987). The cancers developed by the rodents on the long-term bioassay studies were at other sites (liver, lung, Zymbal's gland, lymph tissue, ovaries, and mammary gland). There is as yet no good animal model for benzene-induced leukemia. However, it has been suggested that benzene may also increase the incidence of Hodgkin's disease, malignant lymphoma, multiple myeloma and lung cancer in humans, although a statistical basis for this is lacking (Askoy, 1985). It is not unreasonable to assume that whatever form of cancer is induced, the induction is most likely through the reactive metabolites produced from benzene. Therefore, the dosimetry of these metabolites is pertinent. Our studies indicate that benzene metabolite dosimetry data obtained in animals provides data relevant to the estimation of human risks.
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PMID:Benzene dosimetry in experimental animals: relevance for risk assessment. 162 Jul 20

Cytochrome P450IIE1 (P450IIE1) is involved in metabolic activation of carcinogenic nitrosamines, aniline and benzene. We detected a restriction fragment length polymorphism of the human P450IIE1 gene with the restriction endonuclease DraI. The population was thus divided into three genotypes, namely, heterozygotes (CD) and two forms of homozygotes (CC and DD). The distribution of these genotypes among lung cancer patients differed from that among controls with statistical significance of P less than 0.05 (chi 2 = 7.01 with 2 degrees of freedom). This result strongly suggests that host susceptibility to lung cancer is associated with the DraI polymorphism of the P450IIE1 gene.
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PMID:Association between restriction fragment length polymorphism of the human cytochrome P450IIE1 gene and susceptibility to lung cancer. 167 75

This study was set up to investigate whether work as a stoker is associated with an increased risk of specific malignant neoplasms. For this purpose, a cohort of 2777 male stokers was followed up through a 10 year period with regard to cause specific mortality. Comparisons were made with another cohort of unskilled male workers in physically demanding jobs. The mortality of the stokers was significantly increased for lung cancer (standardised mortality ratio (SMR) 145, 95% confidence interval (95% CI) 110-186) and for multiple myeloma (SMR 388, 95% CI 106-994). Also, increases were seen for cancer of the urinary organs and cancer of the mouth and throat. The combustion products to which the stokers have been exposed comprise several carcinogenic agents including polycyclic aromatic hydrocarbons, benzene, arsenic, and radionuclides. It seems likely that the occupational exposure of stokers has contributed to their excess cancer mortality.
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PMID:A mortality study of Danish stokers. 173 55

Risk assessment methodologies have been successfully applied to control societal risk from outdoor air pollutants. They are now being applied to indoor air pollutants such as environmental tobacco smoke (ETS) and radon. Nonsmokers' exposures to ETS have been assessed based on dosimetry of nicotine, its metabolite, continine, and on exposure to the particulate phase of ETS. Lung cancer responses have been based on both the epidemiology of active and of passive smoking. Nine risk assessments of nonsmokers' lung cancer risk from exposure to ETS have been performed. Some have estimated risks for lifelong nonsmokers only; others have included ex-smokers; still others have estimated total deaths from all causes. To facilitate interstudy comparison, in some cases lung cancers had to be interpolated from a total, or the authors' original estimate had to be adjusted to include ex-smokers. Further, all estimates were adjusted to 1988. Excluding one study whose estimate differs from the mean of the others by two orders of magnitude, the remaining risk assessments are in remarkable agreement. The mean estimate is approximately 5000 +/- 2400 nonsmokers' lung cancer deaths (LCDSs) per year. This is a 25% greater risk to nonsmokers than is indoor radon, and is about 57 times greater than the combined estimated cancer risk from all the hazardous outdoor air pollutants currently regulated by the Environmental Protection Agency: airborne radionuclides, asbestos, arsenic, benzene, coke oven emissions, and vinyl chloride.
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PMID:Risk assessment methodologies for passive smoking-induced lung cancer. 218 73

Epidemiological studies-especially data from smog episodes-indicate that antropogenous outdoor air pollution exercises a deleterious effect on health and particularly on the respiratory organs. Controlled exposure test in animals and man confirm this. The main pollutants are SO2, suspended dust particles (dust aerosols or solid atmospheric condensation nuclei) as well as NO2 (NOx) and O3. The adverse influence of quite a number of meteorological factors such as low temperature and inversion cannot be denied. During smog conditions in January 1985 in the Federal Republic of Germany there was a highly significant negative correlation between atmospheric temperature and the rate of exacerbations of bronchitis. Indoor air pollution is gaining in importance. Airtight sealing of buildings associated with reduced indoor ventilation results in novel health upsets ("sick building syndrome"). Interiors are characterised by an accumulation of CO2, CO, NO2, dust aerosols and various organic substances such as benzene, benzypyrene, formaldehyde, nitrosamines etc. Cigarette smoke is a frequent cause of indoor air pollution. The possible unhealthy effects of passive smoking (mainly the inhalation of sidestream smoke) have been frequently studied. Infants of smoking parents are more often affected by respiratory diseases than non-exposed children. The same applies to schoolchildren: the incidence of bronchial signs and symptoms increases with increasing smoke consumptions of the parents. However, no definitely established effect on lung function has been seen in children, adults and asthmatics. The important question as to whether passive smoking increases lung cancer risk is still a subject of controversial discussion among experts.
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PMID:[General environmental pollutants and passive smoking]. 219 21


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