Genotoxic and teratogenic effect of freshwater sediment samples from the Rhine and Elbe River (Germany) in zebrafish embryo using a multi-endpoint testing strategy.

The embryotoxic potential of three model sediment samples with a distinct and well-characterized pollutant burden from the main German river basins Rhine and Elbe was investigated. The Fish Embryo Contact Test (FECT) in zebrafish (Danio rerio) was applied and submitted to further development to allow for a comprehensive risk assessment of such complex environmental samples. As particulate pollutants are constructive constituents of sediments, they underlay episodic source-sink dynamics, becoming available to benthic organisms. As bioavailability of xenobiotics is a crucial factor for ecotoxicological hazard, we focused on the direct particle-exposure pathway, evaluating throughput-capable endpoints and considering toxicokinetics. Fish embryo and larvae were exposed toward reconstituted (freeze-dried) sediment samples on a microcosm-scale experimental approach. A range of different developmental embryonic stages were considered to gain knowledge of potential correlations with metabolic competence during the early embryogenesis. Morphological, physiological, and molecular endpoints were investigated to elucidate induced adverse effects, placing particular emphasis on genomic instability, assessed by the in vivo comet assay. Flow cytometry was used to investigate the extent of induced cell death, since cytotoxicity can lead to confounding effects. The implementation of relative toxicity indices further provides inter-comparability between samples and related studies. All of the investigated sediments represent a significant ecotoxicological hazard by disrupting embryogenesis in zebrafish. Beside the induction of acute toxicity, morphological and physiological embryotoxic effects could be identified in a concentration-response manner. Increased DNA strand break frequency was detected after sediment contact in characteristic non-monotonic dose-response behavior due to overlapping cytotoxic effects. The embryonic zebrafish toxicity model along with the in vivo comet assay and molecular biomarker analysis should prospectively be considered to assess the ecotoxicological potential of sediments allowing for a comprehensive hazard ranking. In order to elucidate mode of action, novel techniques such as flow cytometry have been adopted and proved to be valuable tools for advanced risk assessment and management.

Primary DNA damage but not mutagenicity correlates with ciprofloxacin concentrations in German hospital wastewaters.

Recently, we showed for the wastewater of a large Swiss university hospital that primary DNA damage, assessed by a bacterial SOS repair assay (umuC test), could be largely assigned to a specific class of antibiotics, the fluoroquinolones (FQs) (Hartmann et al. [1998] Environ Toxicol Chem 17:377-382). In an attempt to confirm the significance of FQs for the bacterial DNA damaging effects in native hospital wastewaters, 25 samples from five German clinics were screened in this study by the umuC test. The results were compared to HPLC-derived concentrations of ciprofloxacin, an important member of the FQs. Ten samples (40%) were umuC-positive and ciprofloxacin concentrations ranged from 0.7 to 124.5 microg/L (n = 24). Primary DNA damage, as indicated by the umuC test, correlated strongly with ciprofloxacin concentrations in a logistic, dose-dependent manner (r2 = 0.896), almost irrespective of the use of S9 metabolic activation. The lowest observed effect concentration (LOEC) for ciprofloxacin was 5.2 microg/L (+S9) and 5.9 microg/L (-S9). Similar to our previous findings, these results indicate that positive umuC results in hospital wastewater are strongly dependent on the presence of fluoroquinolone antibiotics. In a second part of the study, previously generated Ames and V79 chromosomal aberration data of the same samples (Gartiser and Brinker [1995] in Umweltbundesamt Texte 74/95) were compared with the newly generated results. Neither the mutagenic effects detected by the Ames assay (8%, n = 25) nor the positive V79 results (46% n = 13) seemed to be caused by ciprofloxacin. Therefore, the Ames and V79 results suggest the presence of additional mutagens that are yet to be identified.

[Roentgen contrast media, source for AOX-contamination of waste water by hospitals]. / Röntgenkontrastmittel, Quelle für die AOX-Belastung des Abwassers durch Krankenhäuser.

PURPOSE: To identify the sources for the exceeding of the upper limit of the AOX (adsorbable organic halogen, X = Cl, Br, I) in hospital waste-water and to estimate the contribution of hospital waste-water to the AOX of municipal waste-water. METHODS: For several hospitals with different medical directions, the expected AOX-concentration, as far as it is caused by iodine contrast media, was ascertained by the contrast media consumption and the water consumption. The results were compared with the measured AOX concentrations. RESULTS: The AOX-concentration of hospital waste-water varies between 0.41 mg/l and 0.94 mg/l. CONCLUSION: As a source of AOX iodine contrast media have been identified and may contribute considerably to the AOX. Hospitals with a radiological department may exceed the upper limit of the AOX which has to be observed in German municipal waste-water.

AOX-emissions from hospitals into municipal waste water.

Adsorbable organically bound halogens (AOX) are mostly persistent in the environment, and accumulate in the food web. Some of them are toxic to humans and other organisms. AOX were measured in the effluents from six German hospitals of different size and departments like internal medicine and ear-nose and throat (ENT) as well as from laundry, kitchen and laboratory. The concentrations in the day time mixed samples of the total effluent were 0.13 mg l(-1)-0.94 mg l-1 (phi = 0.43 mg l-1). For the separately investigated departments the lowest concentrations were found in the effluent from laundry and kitchen (0.015 mg l-1), and the highest ones in the effluents from the medical departments (0.12-1.71 mg l-1, phi 0.95 mg l-1 during the week and 0.06-0.10 mg l-1 at the week-end) and the laboratories (0.05-14.2 mg l-1, phi 2.73 mg l-1). The AOX concentration in night time mixed samples were 0.07-0.41 mg l-1 (phi = 0.41 mg l-1) for the total effluents and 0.25-2.64 mg l-1 (phi = 1.11 mg l-1) for medical departments. Concentrations expected by computing the input of AOX attributable to pharmaceuticals were between 11% and 16% for two hospitals and 7.7% for an ENT department. One additional important source of AOX in hospital effluents may be x-ray contrast media containing a iodine carbon bond.