Using the Tea Bag Index to determine how two human pharmaceuticals affect litter decomposition by aquatic microorganisms.

This study demonstrates that independent additive effects of two human pharmaceuticals, the antibiotic trimethoprim and the artificial estrogen 17a-Ethinylestradiol (EE2), inhibit plant litter decomposition by aquatic microorganisms. The constant release of pharmaceuticals, such as these, has the potential to affect aquatic microbial metabolism and alter biogeochemical cycling of carbon and nutrients. Here we advance the Tea Bag Index (TBI) for decomposition by using it in a series of contaminant exposure experiments testing how interactions between trimethoprim and EE2 affect aquatic microbial activity. The TBI is a citizen science tool used to test microbial activity by measuring the differential degradation of green and rooibos tea as proxies for respectively labile and recalcitrant litter decomposition. Exposure to either trimethoprim or EE2 decreased decomposition of green tea, suggesting additive effects upon microbial activity. Exposure to EE2 alone decreased rooibos tea decomposition. Consequently, trimethoprim and EE2 stabilized labile organic matter against microbial degradation and restricted decomposition. We propose that the method outlined could provide a powerful tool for testing the impacts of multiple interacting pollutants upon microbial activity, at a range of scales, across aquatic systems and over ecologically relevant time scales.

17α-ethynylestradiol (EE2) limits the impact of ibuprofen upon respiration by streambed biofilms in a sub-urban stream.

Pharmaceutical compounds such as the non-steroidal anti-inflammatory drug ibuprofen and the artificial estrogen 17α-ethynylestradiol (EE2) are contaminants of emerging concern in freshwater systems. Globally, human pharmaceutical use is growing by around ~ 3% per year; yet, we know little about how interactions between different pharmaceuticals may affect aquatic ecosystems. Here, we test how interactions between ibuprofen and EE2 affect the growth and respiration of streambed biofilms. We used contaminant exposure experiments to quantify how these compounds affected biofilm growth (biomass), respiration, net primary production (NPP) and gross primary production (GPP), both individually and in combination. We found no effects of either ibuprofen or EE2 on biofilm biomass (using ash-free dry mass as a proxy) or gross primary production. Ibuprofen significantly reduced biofilm respiration and altered NPP. Concomitant exposure to EE2, however, counteracted the inhibitory effects of ibuprofen upon biofilm respiration. Our study, thus, demonstrates that interactions between pharmaceuticals in the environment may have complex effects upon microbial contributions to aquatic ecosystem functioning.