Bioavailability and fate of sediment-associated trenbolone and estradiol in aquatic systems
Endocrine disrupting effects in aquatic organisms have been observed in systems influenced by steroid hormones. Associating endocrine disruption with aqueous concentrations of steroids alone may overlook the influence of source–sink dynamics in sediments on steroid hormone bioavailability. The objective of this study was to determine the fate of 17β-estradiol and 17β-trenbolone in two field sediments and to evaluate the corresponding bioavailability of the compounds to the fathead minnow (Pimephales promelas). Steroid fate was evaluated using analytical chemistry and verified by assessing the biological activity using yeast based in vitro assays. Effective bioavailability of the steroids was inferred from changes in hepatic vitellogenin expression (increased expression in males exposed to 17β-estradiol, and reduced expression in females exposed to 17β-trenbolone). In experiments conducted with 17β-estradiol, no induction of hepatic vitellogenin mRNA expression was observed in male fish exposed to sediment-associated 17β-estradiol. In contrast, female minnows exposed to sediment-associated 17β-trenbolone experienced significant reductions in hepatic vitellogenin compared to negative controls. In both systems, the parent compounds were shown to degrade rapidly to the more persistent metabolites, estrone and trendione, both of which were found predominantly associated with the sediments. Results from the yeast estrogen screen indicate a reduction in biological activity as biotransformation of 17β-estradiol occurs; results from the yeast anti-estrogen screen were inconclusive and unable to substantiate 17β-trenbolone fate in aquatic systems. Collectively, these data support the contention that steroid hormones associated with the sediment can become bioavailable to fish, and that sediment characteristics influence the observed bioavailability of these compounds.