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Tytuł oryginału: Biomarkers of genotoxicity of urban air pollution: achievements, problems, prospects.
Autorzy: Kyrtopoulos Soterios A., Georgiadis Panagiotis
Źródło: Prz. Epidemiol. 2002: 56 supl.: Conference on molecular epidemiology in preventive medicine - achievements and new challenges s.215-228, il., tab., bibliogr. 31 poz. - Konferencja pt. Molekularna epidemiologia w medycynie prewencyjnej - osiągnięcia i nowe wyzwania Kraków 20-22.06. 2002
Sygnatura GBL: 301,250

Hasła klasyfikacyjne GBL:
  • toksykologia
  • ochrona środowiska

    Typ dokumentu:
  • praca związana ze zjazdem

    Streszczenie angielskie: Recent evidence suggests that exposure to urban air pollution may result in increased risk of lung cancer. Extrapolation from occupational exposure and risk data suggests that, among potential carcinogens present in polluted urban air, polycyclic aromatic hydrocarbons (PAH's) may make a major contribution to such an effect. The use of biomarkers of genotoxicity in population studies may help to reduce uncertainty involved in the risk of cancer associated with relatively low air pollution levels. While increases in biomarkers of exposure to urban air PAH's, as well as biomarkers of early genetic effects, have been detected in subject exposed to relatively high levels of air pollution, biomarker studies in populations exposed to ambient PAH concentrations below approx. 20 ng/m**3have not demonstrated clear effect, possibly because of the existence of multiple sources and routes of human exposure. Results from a recent molecular epidemiology study designed to investigate biomarker variation in subjects exposed to low to moderate levels of urban air pollution (the AULIS project) have also failed to show any consistent effects of ambient air PAHs. The most important parameter found in this study to influence the levels of bulky DNA adducts in blood lymphocytes was exposure to environmental tobacco smoke (ETS), wwhile at very low levels of ETS exposure an effect of consumption of roasted meat could be detected. Strong interactions between these exposures and genetic variation in phase I and phase II xenobiotic metabolism ...

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