[New data on syncarcinogenesis in tumors of exogenous origin]

Little is known about syncarcinogenic effects of occupational and environmental substances although it is supposed that different exogenous factors may play critical roles in the development of many human tumors. Epidemiologic results prove syncarcinogenesis for asbestos exposure and smoking (lung cancer), radon exposure and smoking (lung cancer), exposure to aromatic amines and smoking (bladder cancer) and alcohol abuse and smoking (oral, larynx and oesophagus cancer). Animal experiments point to additive effects in carcinogenesis for different nitrosamines and substances like benzo(a)pyrene, carbon tetrachloride, ethanol, vinyl chloride and ionising radiation. It can be concluded from modern concepts of carcinogenesis that syncarcinogenic mechanisms may not only result from genotoxicity but also from influences on cell proliferation and mitogenesis as well as toxicokinetics, DNA repair, intercellular communication, immune system and hormonal effects. New methods of molecular epidemiology seem very promising to study syncarcinogenic effects in animals and humans.