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Primary DNA Damage But Not Mutagenicity Correlates with Ciprofloxacin Concentrations in German Hospital Wastewaters

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Abstract.

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 μg/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 μg/L (+S9) and 5.9 μg/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.

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Received: 8 March 1998/Accepted: 27 August 1998

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Hartmann, A., Golet, E., Gartiser, S. et al. Primary DNA Damage But Not Mutagenicity Correlates with Ciprofloxacin Concentrations in German Hospital Wastewaters. Arch. Environ. Contam. Toxicol. 36, 115–119 (1999). https://doi.org/10.1007/s002449900449

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  • DOI: https://doi.org/10.1007/s002449900449

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