Effects of 17α‐ethinylestradiol and bisphenol a on vertebral development in the fathead minnow (Pimephales Promelas)

Growth, reproductive ability, and metabolic functions may be impaired by disruption of early endocrine patterning. Natural and synthetic estrogens detected in surface waters have been linked to reproductive endocrine signaling disruption in several species. The present study characterizes the nonreproductive morphological endpoint of vertebral anomalies in fish exposed to environmental estrogens. Estrogen is a proliferation-inducing compound in osteoblasts, regulating cartilage and bone deposition during development in vertebrates. The hypothesis for the present work is that xenobiotics with estrogenic activity adversely impact vertebral bone formation. Fathead minnows (Pimephales promelas) were exposed to 0.1 to 100 μg/L 17α-ethinylestradiol (EE2) and 0.1 to 1,000 μg/L bisphenol A (BPA) from egg stage (24 h postfertilization) to 25 to 26 d posthatch. Fish were measured for length and analyzed microscopically to determine degree of skeletal development (developmental score) and the occurrence of spinal abnormalities, including vertebral compression, bone fusion, and spinal curvatures. Fish length and developmental score were inversely related to vertebral malformations in exposed fish. Skeletal developmental was affected significantly in EE2-exposed fish: Vertebral malformations were observed in up to 62% of fish in a nonmonotonic dose-response. However, BPA did not significantly impair skeletal development or induce vertebral malformations. The bioassay results suggest vertebral bone development is a potential endpoint of endocrine disruption from potent estrogenic compounds in surface waters.