By H.-W. Schlipköter (auth.), Prof. Dr. Norbert H. Seemayer, Dipl.-Biologe Wolfgang Hadnagy (eds.)
Environmental Hygiene II offers with the review of environmental pollution and their relevance to human wellbeing and fitness. major themes comprise mutagenic and carcinogenic task of environmental chemical substances, particular results of heavy metals, detailed organic symptoms for screening environmental contaminants and tracking of indoor/outdoor air pollution. additionally, overview of publicity to environmental and occupational chemical compounds in guy are awarded in addition to epidemiological experiences at the well-being results via environmental toxins, experiences of inhalation toxicology and techniques and coverage of environmental control.
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Extra resources for Environmental Hygiene II
Genotoxic = C- T > 19% We were not able to examine lung cells since their lower DNA-content and thermolability made them unsuitable for the alkaline elution method performed in vitro (Brendler 1989). These results, however, show that NDMA is well activated by the major target organ liver, but not by a second target organ kidney. This may be a reflection of the lower activating capability of this organ. Funher studies were carried out in vivo to assess the role of pharamcokinetics on organ specifity.
Chemical Carcinogens", Kap. 12,2. , 643-828. Romruen, K. L (1984) Metabolic activation capabilities of S9 and hepatocytes from uninduced rats to convert carcinogenic N -nitrosamines to mutagens. Mutation Res. 140, 147-153. ; Schmahl, D. L (1989) In vitro effects of hepatic and extrahepatic N - nitrosamine carcinogens in primary hepatocytes isolated from rat, hamster and porcine liver. , submitted. Tompa, A. and Langenbach, R. (1979) Culture of adult lung cells: Benzo(a)pyrene metabolism and mutagenesis.
Twenty-four hours after plating the culutres are exposed to the test chemical. Toxicity is determined in a day-7 colony forming assay (right side of Figure 1). To measure transformation (left side of diagram), selection for carcinogen induced enhanced growth variants (EGV) is begun 4 days after carcinogen exposure by selective removal of the 3T3 fibroblasts or, in the case of the defined media system, by switching to growth factor free media containing serum. This induces terminal differentiation in the normal tracheobronchial cells (Terzaghi, 1989) but not in the "initiated" cells.