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The evaluation of multigeneration, population-level impacts is particularly important in the risk assessment of endocrinedisrupting compounds, because adverse effects may not be evident during the first generation of exposure. Population models were developed for the sheepshead minnow (Cyprinodon variegatus) exposed to 17b-estradiol (E2) for two complete generations (F1 and F2) to determine population-level effects of multigenerational exposure to a model estrogen. Stage-structured matrix models were used to determine interactions between treatment and the number of generations exposed. Reproduction was significantly reduced in both the 0.08 and 0.2 μg E2/L treatments in both generations, and embryo and larval stages experienced reduced survival at 0.2 μg/L in the second generation only. However, increased female to male sex ratio in these treatments compensated for the loss in reproductive output, and significant population-level effects only occurred in the 0.2 μg E2/L treatment of the F2 population. The F2 population in the 0.2 μg E2/L treatment also had an altered, stable stage distribution relative to the control population of both generations and the F1 population in the 0.2 μg E2/L treatment, resulting in additional population-level effects. These results demonstrate that continued exposure to E2 had compounding effects on sheepshead minnow populations and that long-term exposures may be necessary to understand the risk that exposures to environmental estrogens pose to native populations. Although population-level effects did not occur in the F1 generation, a risk decision based on F1 organism-level effects would be protective of the population exposed for two generations. [ABSTRACT FROM AUTHOR]

A 280-d study examined the effects of 17β-estradiol (E2) on reproduction and development of the sheepshead minnow (Cyprinodon variegatus) exposed from the parental (F0) through three subsequent (F1, F2, and F3) generations and evaluated the need for multigenerational assessments of the risks of endocrine-disrupting chemicals. This first three-generation study exposed adult F0 and F1 fish to measured concentrations of 0.01, 0.04, 0.08, 0.2, and 0.3 μg E2/L; the F2 and F3 generations were exposed to 0.2 μg E2/L or less. The cumulative 21-d production of normal embryos was significantly reduced in the F0 generation at 0.3 μg E2/L and in the F1 and F2 generations at 0.08 μg E2/L or more. The daily reproductive rate was significantly reduced in all three generations at 0.08 μg E2/L or more during spawning days 8 to 14 and 15 to 21. The proportion of infertile eggs from F1 fish was significantly increased above that of the solvent controls at 0.04 and 0.2 μg E2/L and from F2 fish at 0.04 μg E2/L or more. Changes in liver, kidney, and gonadal tissues were seen in the F0 and F1 generations exposed to 0.2 μg E2/L or more. The female gonadosomatic index was significantly decreased at 0.3 μg E2/L in the F0 and F1 generations. Estradiol affected the hepatosomatic index only in female F1 fish, but not in a dose-dependent manner. All F1 fish in 0.3 μg E2/L appeared to be phenotypically female. Our results indicate that life-cycle exposure to E2 significantly decreased embryo production by F1 and F2 fish at concentrations lower than those affecting the F0 generation, and they emphasize the importance of evaluating the impact of an estrogenic chemical on reproduction through a minimum of two (F0 and F1) generations.