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Keywords:

  • 17β-estradiol;
  • Methane;
  • Carbon dioxide;
  • Methane-oxidizing bacteria;
  • Methane oxidation function

Abstract

17β-estradiol (17β-E2), a widespread and natural estrogen in the environment, has imposed a serious threat to the safety and function of aquatic ecosystems because of worsening pollution and high potential toxicity. In the present study, the authors focus on the impact of 17β-E2 pollution on water microbial methane oxidation function. The authors investigated the mechanism of its influence on water microbial activity and discuss the growth rate of methane-oxidizing bacteria. The results showed that 17β-E2 could significantly inhibit the function of water microbial methane oxidation. When 17β-E2 concentration was ≥5 ng L−1, the methane oxidation rate increased with increasing 17β-E2 and finally settled to a constant value. Furthermore, the authors found no significant linear correlation between 17β-E2 concentrations and its methane oxidation rate. However, increasing 17β-E2 dramatically improved water microbial community activity, because a significant or highly significant promotion in the generation rate of CO2 was measured. Moreover, within a certain period of time and at certain concentrations, positive linear correlation existed between water CO2 generation rate and 17β-E2 concentrations. In addition, the growth rate of culturable methane-oxidizing bacteria was promoted when 17β-E2 pollution concentration from 2 ng L−1 to 20 ng L−1. Therefore, 17β-E2 pollution can inhibit microbial methane oxidation function in water, which indirectly promotes the release of water methane and directly contributes to the rate of water-generated and released CO2. Specifically, 17β-E2 pollution can promote water emissions of greenhouse gases. Environ Toxicol Chem 2014;33:768–775. © 2014 SETAC