17\u03b1-ethynylestradiol (EE2) limits the impact of ibuprofen upon respiration by streambed biofilms in a sub-urban stream

Peter Mcclean,William Ross Hunter

doi:10.1007/s11356-020-10096-5

Abstract

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.

Highlights

Human pharmaceuticals and personal care products (PPCPS) are contaminants of emerging concern within the environment (Rosi-Marshall and Royer 2012; Gaston et al 2019)
Biofilm net primary production (NPP) was negative in all treatments, with ibuprofen exposure resulting in a significant decrease in oxygen consumption (p = 0.009; df = 1; F = 7.483), reflecting the effect on biofilm respiration (Fig. 1C; Table 1c)
Our study demonstrates that interactions between the non-steroidal anti-inflammatory drugs (NSAIDs) ibuprofen and the artificial estrogen EE2 have a significant effect upon the streambed biofilm respiration

Summary

Introduction

Human pharmaceuticals and personal care products (PPCPS) are contaminants of emerging concern within the environment (Rosi-Marshall and Royer 2012; Gaston et al 2019). Triclosan and trimethoprim) and artificial estrogens (e.g. 17α-ethynylestradiol) into the aquatic environment (Gros et al 2007; Álvarez-Muñoz et al 2015; Archer et al 2017) This is potentially problematic because these compounds are designed to produce physiological effects within an organism, at ultra-low (nano-molar) concentrations (Rosi-Marshall and Royer 2012; Van Boeckel et al 2014; Álvarez-Muñoz et al 2015). Eco-toxicological studies reveal that PPCPs at environmental concentrations can have significant physiological effects on both aquatic fauna and microorganisms, with the potential to disrupt aquatic ecosystem functioning altering carbon and nutrient cycling, and negatively affect water quality (Jobling et al 2003; Hernando et al 2006; Rosi-Marshall et al 2013; Drury et al 2013; Żur et al 2018; Gallagher and Reisinger 2020). A mechanistic understanding of the interactions between different PPCPs is needed if we are to fully understand their environmental impacts

Methods

Results

Conclusion