Although the occurrence, the fate and the toxicology of emerging pollutants in the aquatic environment have been widely studied, there is still a lack in the correlation of the levels of pollutants with the possible adverse effects in wildlife. The short comings of traditional methods for risk assessment have been observed, and the contributions of the identified compounds to the observed risks are rarely confirmed. Therefore, the main purpose of this thesis was to develop reasonable methods for risk identification of single compounds and mixtures, and to identify and confirm environmental risks caused by non-specific and mechanism-specific toxicity in aquatic systems. In this thesis, optimized methods for risk identification of single compounds and mixtures were developed. For screening-level risk assessment of single compounds, an optimized risk quotient that considers not only toxicological data but also the frequency with which the detected concentrations exceeded predicted no-effect concentrations was used to screen candidate priority pollutants in European surface waters. Results showed that 45 of the 477 analyzed compounds indicated potential risks for European surface waters. For risk assessment of environmental samples, a risk quotient that considers the ratio of the BEQ to the environmental quality standard (EQS) and the frequency of BEQ exceeding EQS was recommended. Results showed that the highest risk of the anti-androgenic activities was presented at the site directly influenced by the effluents of wastewater treatment plants. To confirm the risk of selected pharmaceuticals, the three antimicrobials clarithromycin, triclosan and sulfamethoxazole, the two anti-inflammatories ibuprofen and diclofenac, the anticonvulsant carbamazepine, the lipid-lowering agent bezafibrate, and the stimulant caffeine were used to study their delayed toxicity using the zebrafish larvae behavioral test. Delayed hatch was observed for exposure to triclosan (1 μg/l) and ibuprofen (100 μg/l) in the early stages of development. In the early stages of development after hatching, the larval locomotor behavior following embryonic exposure to 0.1 μg/l triclosan and 1 μg/l caffeine was altered. Furthermore, for a mixture of the respective highest environmental concentrations of the 8 pharmaceuticals changes in larval behavior were observed. Mechanism-specific bioassays and chemical analyses were performed to identify and confirm endocrine disturbance activities (e.g., anti-androgenic activity) in surface waters and aryl hydrocarbon receptor (AhR)-mediated activities in sediments. Spatial and temporal variations of anti-androgenic activities and environmental risks were observed. High cytotoxicity and anti-androgenic activities were observed in surface waters that were directly influenced by the effluents of wastewater treatment plants. Although sediment samples from the upper Danube River were considered less contaminated, high AhR-mediated activities were observed. Furthermore, by combining bioassays, fractionation, chemical analysis and confirmation to an effect-directed analysis (EDA), fractions with adverse effects were screened and effects further associated to specific pollutants and mixtures. The comparison between measured bioanalytical equivalents (BEQs) of sediment samples and BEQs of synthetic mixtures revealed that the US EPA priority PAHs seem to account only to a minor extent for the AhR-mediated activities of the sediment samples, while non-priority substances in medium-polar and polar fractions were high inducers. In this thesis, induced EROD and endocrine disturbance activities were expressed as BEQs of the respective reference standards. In order to properly use the BEQs and confirm the contributions of chemically an alyzed compounds to bioassay-derived BEQs, the factors causing the variations of BEQs and relative potencies (REPs) were mathematically analyzed. The effects of the effect levels, slopes and the maximum response of the concentration-response curves of the samples and reference compounds on REP and BEQ variations were confirmed. Although bioassay-derived BEQs(Bio-BEQs) and chemically estimated BEQs (Chem-BEQs) vary with the selected effect level, the explanation of Bio-BEQs by Chem-BEQs of certain compounds at the same effect level will be theoretically stable
