Lifestyle and Environment · Environmental Exposures
RRM Academy Synopsis
Early BPA or EE2 exposure cut medaka fertilization two generations on
A lab experiment found that brief embryonic exposure to BPA or EE2 lowered fertilization among medaka fish two generations later. BPA is a plastics chemical and EE2 is a synthetic estrogen. The exposed fish and their first offspring showed no apparent abnormalities, apart from two sex-reversed EE2 fish. Both exposed lineages had lower embryo survival later.
Key Findings
- Embryos exposed to BPA or EE2 for the first 7 days of development showed no apparent phenotypic abnormalities in F0 or F1, apart from two EE2-treated F0 fish with sex reversal.
- Both the BPA and EE2 lineages had significantly reduced fertilization in the F2 generation. The authors describe the drop as approximately 30%.
- Embryo survival in the F3 generation was significantly lower in both lineages than in controls. The authors report an approximate 20% reduction in F3 survival rates.
- Compared with controls, the BPA lineage had significantly reduced F3 fertilization (p < 0.05), and both lineages had lower F4 embryo survival (p < 0.05).
- Fertilization in F0 and F1 adults, and embryo survival in F0, F1 and F2, showed no significant difference from controls.
Interpretation
The authors ran a controlled laboratory experiment in medaka, a small fish used as a model for how early exposures reach later generations. Each treatment group had three replicate dishes of fertilized eggs, and six breeding pairs from the same group produced each later generation. Embryos got one seven-day exposure and nothing afterward. Only the germ cells of F1 fish were exposed, inside the F0 fish, so the authors treat F2 as the first transgenerational generation. They state that the mechanism is unknown and call for studies in wild fish.
RRM Context
Restorative reproductive medicine seeks the causes of low fertility. Chemical exposure is one possible cause. The authors cite rat studies where plastics, herbicides and pesticides led to disease in later generations. They add that EE2 is in combination oral contraceptives. It also turns up in water downstream of wastewater treatment plants.
Abstract
The transgenerational consequences of environmental contaminant exposures of aquatic vertebrates have the potential for broad ecological impacts, yet are largely uninvestigated. Bisphenol A (BPA) and 17α-ethinylestradiol (EE2) are two ubiquitous estrogenic chemicals present in aquatic environments throughout the United States and many other countries. Aquatic organisms, including fish, are exposed to varying concentrations of these chemicals at various stages of their life history. Here, we tested the ability of embryonic exposure to BPA or EE2 to cause adverse health outcomes at later life stages and transgenerational abnormalities in medaka fish. Exposures of F0 medaka to either BPA (100 μg/L) or EE2 (0.05 μg/L) during the first 7 days of embryonic development, when germ cells are differentiating, did not cause any apparent phenotypic abnormalities in F0 or F1 generations, but led to a significant reduction in the fertilization rate in offspring two generations later (F2) as well as a reduction of embryo survival in offspring three generations later (F3). Our present observations suggest that BPA or EE2 exposure during development induces transgenerational phenotypes of reproductive impairment and compromised embryonic survival in fish of subsequent generations. These adverse outcomes may have negative impacts on populations of fish inhabiting contaminated aquatic environments.
