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Effects of the antimicrobial contaminant triclocarban and co-exposure with the androgen 17â-trenbolone, on reproductive function and ovarian transcriptome of the fathead minnow (Pimephales promelas)
Citation:
Villeneuve, Dan, K. Jensen, J. Cavallin, E. Durhan, N. Garcia-Reyero, M. Kahl, R. Leino, E. Makynen, L. Wehmas, E. Perkins, AND G. Ankley. Effects of the antimicrobial contaminant triclocarban and co-exposure with the androgen 17â-trenbolone, on reproductive function and ovarian transcriptome of the fathead minnow (Pimephales promelas). ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY. Society of Environmental Toxicology and Chemistry, Pensacola, FL, 36(1)::231-242, (2017).
Impact/Purpose:
Triclocarban (TCC) is a chlorinated biphenyl ether that has been used for more than 50 years as an antimicrobial agent in consumer products such as soaps, deodorants, skin creams and toothpaste. Almost 500,000 kg of TCC are used on an annual basis in the USA, and it is one of the most frequently detected personal care products in the environment, found in a variety of matrices, including waste water treatment plant (WWTP) effluents and biosolids, surface waters and sediments. Recent research has suggested that TCC has the potential to cause toxicity through interactions with vertebrate endocrine systems. Specifically, it has been postulated that TCC may exhibit a new mode of endocrine disruption, augmentation of endogenous hormonal activities. Additionally, despite its widespread use and broad distribution in aquatic environments, TCC’s potency as a reproductive toxicant in fish has not been well characterized. The current investigation provides novel data on this ubiquitous environmental contaminant which suggests that TCC is reproductively toxic to fish at concentrations just slightly below those commonly detected in the environment (margin of safety <50). Based on evaluation of both ovarian transcriptomics and a variety of targeted endpoints anchored to an established adverse outcome pathway for androgen receptor agonism leading to reproductive dysfunction, our data provide no support for the hypothesis that TCC specifically modulates the endocrine system to cause reproductive toxicity. Rather, reproductive impacts were observed at a concentration just 2-fold below that which caused overt toxicity in males. We conclude that there is little need to view TCC as a new type of endocrine active chemical, but that its effect concentrations as chronic toxicant are quite close to environmentally relevant exposure concentrations and likely pose a significant risk to aquatic organisms, particularly in areas near known TCC sources, such as waste water treatment plant discharges. Results of this research may be of direct interest to OCSPP/OPPT.
Description:
Triclocarban (TCC) is a widely used antimicrobial agent that is routinely detected in surface waters. The present study was designed to examine TCC’s efficacy and mode of action as a reproductive toxicant in fish. Reproductively mature Pimephales promelas were continuously exposed to either 1 or 5 ìg TCC/L, 0.5 ìg 17â-trenbolone (TRB)/L or a mixture (MIX) of 5 ìg TCC and 0.5 ìg TRB/L for 22 d and a variety of reproductive and endocrine-related endpoints were examined. Cumulative fecundity was significantly reduced in fathead minnows exposed to TRB, MIX or 5 ìg TCC/L. Exposure to 1 ìg TCC/L had no effect on reproduction. In general both TRB and MIX treatments caused similar physiological effects, evoking significant reductions in female plasma vitellogenin, estradiol, and testosterone, and significant increases in male plasma estradiol. However, effects of the MIX treatment on the ovarian transcriptome had little resemblance to those elicited by either TRB or TCC (5 ìg/L) only. Overall, TCC was reproductively toxic to fish at concentrations at or near those that have been measured in surface water. There was little evidence that TCC elicits reproductive toxicity through a specific mode of endocrine or reproductive action, nor that it could augment the androgenic effects of TRB. Nonetheless, transcriptomic results pointed toward modulation of certain signaling pathways known to cross-talk with steroid hormone signaling.
