Chemical efflux of environmental estrogens

Arizona State University, Scottsdale AZ

Investigators

Abstract

Wastewater treatment employs biological processes to reduce contaminants prior to discharge into the environment. Among the suite of chemicals that must be treated are emerging contaminants, which include endocrine disruptors, antibiotics, and illicit drugs, among others. Such pollutants, specifically estrogen mimics, survive wastewater treatment and have been shown to contribute to endocrine disruption in aquatic animals. The extent of wastewater-derived contaminants is well-studied in public surface water, reclaimed water, and reused water in the US; however, little is known about the extent of emerging contaminants on Tribal lands. The broader scope of emerging contaminant attenuation is being explored in Tribal communities through a joint partnership with the Inter-Tribal Council of Arizona, in which modules are being developed for the training of water professionals in emerging areas of wastewater treatment, pollution, and reuse. The overall objective of this project is to determine if multi-drug efflux mechanisms or chemical efflux in wastewater bacteria contributes to estrogen attenuation during secondary treatment. Preliminary studies show that estrogens such as 17b-estradiol, nonylphenol, and bisphenol-A induce genes encoding multi-drug efflux proteins and are substrates of efflux pumps. These pumps may play a significant role in the cycling of emerging contaminants in wastewater. The membrane-bound proteins are expressed in response to toxic chemical accumulation and convey one form of multi-drug resistance in bacteria. A key hypothesis is that efflux pumps export endocrine disrupting chemicals from the bacterium prior to biodegradation, leading to attenuation during wastewater treatment. The primary goals are to (1) quantify multi-drug efflux genes and proteins in wastewater bacteria, (2) identify wastewater substrates of efflux pumps, and (3) evaluate if efflux of estrogens from bacteria is a major transport mechanism that contributes to attenuation. The novel concept of estrogen-induced antibiotic resistance may contribute to estrogen mimic attenuation and will be tested in this project.