Causes of endocrine disrupting potencies in surface water in East China.
Surface water is essential for human health and ecological diversity, but some endocrine disrupting chemicals are detectable. Both thyroid receptor (TR) and androgen receptor (AR) agonistic/antagonistic potencies in grade II surface water in East China were investigated using reporter gene assays. While none of the water exhibited agonistic potency, significant AR and TR antagonistic potencies were detectable. TR antagonistic equivalents (TR-AntEQ) and AR antagonistic equivalents (AR-AntEQ) ranged from 3.6 to 76.1 μg dibutyl phthalate/L and from 2.3 to 242.6 μg flutamide/L, respectively. The TR and AR antagonistic potencies in the Yangtze River watershed were highlighted, with equivalents greater than the lowest observable effect concentration (LOEC) of dibutyl phthalate and flutamide, respectively. Phthalate esters (PAEs) being the most abundant explained most of the TR antagonistic potency, contributing more than 65% of the TR-AntEQ and diisobutyl phthalate (DiBP) was the major contributor. In most surface waters studied, PAEs contributed little of the AR-AntEQ, but the frequently detected octylphenol, nonylphenol and benzo[a]pyrene might be responsible.
State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, PR China.
Wei
W
Shi
State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, PR China; South China Institute of Environmental Science, Ministry of Environmental Protection (MEP), Guangzhou, PR China.
Dongyang
D
Deng
State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, PR China.
Yuting
Y
Wang
State Environmental Protection Key Laboratory of Monitoring and Analysis for Organic Pollutants in Surface Water, Jiangsu Provincial Environmental Monitoring Center, Nanjing, PR China.
Guanjiu
G
Hu
State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, PR China.
Jing
J
Guo
State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, PR China.
Xiaowei
X
Zhang
Key Laboratory of Reproductive Medicine & Institute of Toxicology, Nanjing Medical University, Nanjing, PR China.
Xinru
X
Wang
State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, PR China; Department of Veterinary Biomedical Sciences and Toxicology Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada; Department of Zoology, and Center for Integrative Toxicology, Michigan State University, East Lansing, MI, USA; School of Biological Sciences, University of Hong Kong, Hong Kong Special Administrative Region; Department of Biology and Chemistry and State Key Laboratory for Marine Pollution, City University of Hong Kong, Hong Kong Special Administrative Region.
John P
JP
Giesy
State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, PR China. Electronic address: yuhx@nju.edu.cn.
Hongxia
H
Yu
State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University, Nanjing, PR China.
Ziheng
Z
Wang
D059002:Androgen Receptor Antagonists / Q000378:metabolism*; D000728:Androgens / Q000378:metabolism*; D000818:Animals; D002460:Cell Line; D002681:China; D002522:Chlorocebus aethiops; D052244:Endocrine Disruptors / Q000633:toxicity*; D017930:Genes, Reporter / Q000187:drug effects; D051379:Mice; D011988:Receptors, Thyroid Hormone / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015534:Trans-Activators / Q000378:metabolism; D062065:Wastewater / Q000633:toxicity; D014874:Water Pollutants, Chemical / Q000633:toxicity*
D059002:Androgen Receptor Antagonists; D000728:Androgens; D052244:Endocrine Disruptors; D011988:Receptors, Thyroid Hormone; D015534:Trans-Activators; D062065:Wastewater; D014874:Water Pollutants, Chemical
Agonist equivalents; Androgen receptor; Antagonist equivalents; Bioassay; Reporter gene assay; Thyroid receptor