Fish population failure caused by an environmental estrogen is long-lasting and regulated by direct and parental effects on survival and fecundity

Despite significant research demonstrating effects of estrogens such as 17α - ethinylestradiol (EE2) on fish, the underlying mechanisms regulating population failure are unknown. Projected water shortages could leave waterways increasingly dominated by wastewater effluent and understanding mechanisms is necessary for conservation and management. Here we identify mechanisms of population failure in three generations of fathead minnows including direct and parental effects on survival and fecundity. EE2 concentrations, as low as 3.2 ng/L, reduced F0 male survival to 17% and juvenile production by 40%. F1 offspring continuously exposed to EE2 failed to reproduce and offspring transferred to clean water reproduced 70 - 99% less than controls. Furthermore, survival of F2s was reduced 51% - 97% compared to controls, despite the absence of direct embryonic exposure. The indirect effect on F2 survival suggests the possibility of transgenerational effects of EE2. Our results suggest that chronically exposed populations may not be able to recover in the absence of immigration.