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

One of the most widely studied carcinogenic agents in the environment is the polycyclic hydrocarbon, benzo(a) pyrene. As a component of soot from the inefficient combustion of coal, its association with cancer can be traced back 200 years, but its possible relevance to lung cancer as a widely distributed air relevance to lung cancer as a widely distributed air pollutant has been investigated only during the past 25 years. Domestic coal fires have been shown to be important sources, and smaller amounts come from industrial sources and from motor vehicles. There is evidence now that the concentration of benzo (a) pyrene in large towns in Britain has decreased by a factor of about ten during the last few decades, as a result of changing heating methods and smoke control. In view of the overwhelming effect of cigarette smoking, it is difficult to determine whether the benzo(a)pyrene content of the air has had any importnat effect on the development of lung cancer, but careful analysis of trends in mortality may now throw some light on this. Among other materials with carcinogenic properties that may be dispersed into the general air, asbestos is the one that has been investigated most thoroughly. The association between exposure to asbestos and the development of lung cancer and mesothelioma of the pleura has been clearly demonstrated among people occupationally exposed to the dust, but as far as the general public is concerned, any risk may be limited to the immediate vicinity of major sources. These and other hazards demonstrated among occupational gropus serve as a warning however to maintain careful scutiny of urban air pollutants in relation to the acetiology of cancer.
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PMID:Coal fires, industrial emissions and motor vehicles as sources of environmental carcinogens. 6 45

Cultured human diploid skin fibroblasts incubated with [G-3H]benzo(a)pyrene yielded about 10 times more H2O-=soluble benzo(a)pyrene metabolites and DNA adducts of stationary growth phase than did proliferating cultures. This increased formation could be blocked by alpha-naphthoflavone. Trichloropropenoxide and cyclohexenoxide, inhibitors of the epoxide hydratase, inhibited predominantly the formation of DNA adducts. Cultures from older individuals formed significantly more benzo(a)pyrene metabolites and DNA adducts, but control cultures from patients with either lung cancer or melanoma did not. The age influence was not apparent when the ratio of DNA adducts to H2O-soluble metabolites was determined for each individual cell line. However, the proportion of DNA-bound material in the cells from patients with lung cancer was significantly increased compared to cells from melanoma patients or healthy individuals.
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PMID:Metabolism and formation of DNA adducts of benzo(a)pyrene in human diploid fibroblasts. 42 49

Administration of oil-attached Nocardia rubra cell-wall skeleton (N. rubra-CWS) was evaluated for the effect of the induction of lung cancers in ACI/N rats. Lung cancers were induced by 15 weekly intratracheal instillations of 3 mg benzo[a]-pyrene with 3 mg ferric oxide. After the 10th instillation of the carcinogen, rats received seven subcutaneous injections of 100 microgram of N. rubra-CWS at 2-week intervals. In the observation period of 56 weeks, the cumulative incidence of lung cancer was 71.4% in the control group and 48.0% in the N. rubra-CWS treated group. The latent period of tumor induction was prolonged in the group treated with N. rubra-CWS.
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PMID:Effect of Nocardia rubra cell-wall skeleton on the induction of lung cancer in ACI/N rats. 44 76

A very large variation (44-fold) was observed in the ability of short-term organ cultures of peripheral lung tissue from lung-cancer patients to metabolize the environmental carcinogen benzo(alpha)pyrene to organic solvent-soluble metabolites. The amounts of benzo(alpha)pyrene (2 microM) metabolized ranged from little (1%) to almost total (96.2%) metabolism within 24 h of culture. Previous work by Kellerman et al. (1973) has suggested a relationship between susceptibility to lung cancer and the indicibility of aryl hydrocarbon hydroxylase activity in cultured human lymphocytes. The metabolic fate of carcinogenic polycyclic aromatic hydrocarbons in the respiratory tract in vivo is undoubtedly more closely mimicked by short-term organ culture of human lung than by cultured lymphocytes. Thus the very wide interindividual variation observed in pulmonary metabolism of benzo(alpha)pyrene in this study and the large variations in covalent binding to human bronchial DNA observed by Harris et al. (1976) strongly suggest that there may be little basis for screening humans for variations in lymphocyte aryl hydrocarbon hydroxylase activity as a means of assessing their susceptibility to lung cancer.
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PMID:Large interindividual variations in metabolism of benzo(alpha)pyrene by peripheral lung tissue from lung cancer patients. 48 61

Exposure to whole cigarette smoke from reference cigarettes results in the prompt (peak activity is 6 hrs), but fairly weak (similar to 2 fold), induction of murine pulmonary microsomal monooxygenase activity. This activity can be detected by using as substrates either benzo(a)pyrene or ethoxyresorufin, and can be inhibited by treatment with cycloheximide or actinomycin D. Unlike the induction of pulmonary monooxygenases following intratracheal administration of 3-methylcholanthrene, these cigarette smoke-induced increases were not unequivocally linked to the Ah locus. Whole smoke condensate and fractions derived from these condensates can; a) induce pulmonary monooxygenase activity, b) inhibit benzo(a)pyrene metabolism in vitro, c) be metabolized to forms mutagenic to Salmonella typhimurium tester strains TA153, or TA98, d) transform C3H 10T1/2 cells in vitro, and e) enhance the carcinogenicity of benzo(a)pyrene in murine pulmonary tissue. A potentially important observation is that whereas hepatic tissue is capable of activating whole cigarette smoke condensate to mutagenic forms in vitro, murine pulmonary tissue does not seem capable of such activation. Although these pulmonary-derived tissue homogenates have significant AHH activity and can metabolize Aflatoxin B1, 2-aminofluorene and 7, 8-dihydro-7,8-dihydroxybenzo(a)pyrene to mutagenic forms, these homogenates fail to activate both cigarette smoke condensate and the pro-mutagen, 6-aminochrysene. These results are discussed with reference to the concept that whole cigarette smoke may be both a potential "initiator" and "promotor" of lung cancer in mice, and that this latter property may be the most important in determining cancer risk.
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PMID:Biological activity of tobacco smoke and tobacco smoke-related chemicals. 51 Feb 43

Short-term organ cultures of peripheral lung from lung cancer patients metabolise benzo[alpha]pyrene to ethylacetate-soluble metabolites, which covalently bind to tissue macromolecules. The nature and quantities of metabolites formed and the extent of covalent binding are dependent upon the time of incubation, the substrate concentration and interindividual variability in the metabolic activity of the lung. Individuals whose lungs rapidly metabolise the carcinogen exhibit more extensive further metabolism of primary metabolites and higher levels of covalent binding. Certain striking differences in the relative retention in the tissue or release into the extra-cellular medium of different metabolites have been found as illustrated by the observation that the ratio of 7,8-dihydro-7,8-dihydroxybenzo[alpha]-pyrene to 9,10-dihydro-9,10-dihydroxybenzo[alpha]pyrene was always significantly higher in the tissue than in the extracellular medium.
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PMID:Metabolism and covalent binding of benzo[alpha]pyrene in human peripheral lung. 54 46

Data are presented which suggest that cigarette smoking, and to a lesser degree, urban pollution as indexed by benzo[a]pyrene are etiologic factors in the causation of lung cancer. The dose--response relationship to benzo[a]pyrene to lung cancer death rate in the urban community was estimated by using data on lung cancer deaths among coke oven workers. It appears to be an excess of 2--5 mumg/m3 of benzo[a]pyrene per 100,000 population, suggesting that a lifetime community exposure to benzo[a]pyrene on a continuing basis may have a greater impact on lung deaths in the community than that considered by the Royal College of Physicians.
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PMID:The "urban factor" and lung cancer: cigarette smoking or air pollution? 64 86

The substantial reduction in air pollution, and particularly in components such as benzo[a]pyrene in urban areas of the United Kingdom during the past few decades has presented an opportunity to consider further the possible role of carcinogens in the air in relation to lung cancer. While the overall trends in lung cancer mortality have undoubtedly been dominated by changes in smoking, the marked contrasts that at one time existed between these death rates in urban and rural areas have gradually diminished. This may indicate that air pollution contributed appreciably to the urban/rural differences in lung cancer at one time, but it is still difficult to disentangle any effects it may have had from those of changing smoking habits.
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PMID:Trends in urban air pollution in the United Kingdom in relation to lung cancer mortality. 64 92

A component capable of binding benzo(a)pyrene was measured in plasma from cigarette smokers and nonsmokers. This plasma fraction was found to have a high specificity of binding to benzo(a)pyrene, bound benzanthracene competitively with benzo(a)pyrene, and was positively correlated (r = 0.861, p less than 0.001) with the capacity of the individual subject's lymphocytes to be induced for AHH activity in culture. An inverse correlation (r = -0.957, p less than 0.001) between the presence of the plasma component in lung cancer patients and the capacity of lung cancer patients' lymphocytes to be induced in culture is unexplained at this time. A benzo(a)pyrene-binding fraction was not found in induced or uninduced cultured lymphocytes from smokers or nonsmokers, or in homogenates of lung excisional tissue from smokers with or without primary lung cancer.
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PMID:A human plasma component that binds benzo(a)pyrene. 72 71

Planning of coal hydrogenation processes, such as liquifaction and gasification, requires consideration of public health implications. Commercial plants will require coal quantities greater than or equal to 20,000 tons/day and the large size of these plants calls for careful consideration of the potential health hazards from the wastes and products of such processes. Analysis of pollution potential can roughly be divided into three categories: raw material structure and constituents, process design, and mode of plant operation. Identifiable pollutants include hydrogen cyanide, phenols, cresols, carbonyl and hydrogen sulfides, ammonia, mercaptans, thiocyanides, aniline, arsenic, trace metals and various polycyclic hydrocarbons. One study of workers in a hydrogenation process has revealed an incidence of skin cancer 16-37 times that expected in the chemical industry. In addition, a number of high boiling point liquid products were identified as being carcinogenic, and air concentrations of benzo[a]pyrene up to 18,000 mug/1000 m3 were reported. Health statistics on occupational groups in other coal conversion industries have shown significantly higher lung cancer rates, relative to groups without such occupational exposures. These data suggest that coal hydrogenation plants must be carefully planned and controlled to avoid harm to environmentally and occupationally exposed populations.
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PMID:Coal hydrogenation and environmental health. 78 66


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