Spawning Trouble: Synthetic estrogen hampers trout fertility

When women take birth control pills, some of the hormones in the pills ends up in sewage effluent and waterways where it may be harming trout populations. Researchers now say that even short-term, low-level exposures to one such hormone, ethynylestradiol (EE2), can reduce a male trout’s fertility by half.

Toxicologist Irv Schultz and his colleagues at the Battelle Marine Sciences Laboratory in Sequim, Wash., exposed three groups of adult male trout in tanks to different concentrations of ethynylestradiol for 2 months. All the trout exposed to 1,000 parts per trillion (ppt) of EE2 died of liver and kidney hemorrhages before the experiment’s end. The two groups that were exposed to lower concentrations of the estrogen–10 and 100 ppt–appeared to remain healthy. However, further work showed EE2’s effect on reproduction.

To measure fertilization rates, Schultz’s team checked how many embryos were present 28 days after sperm were introduced to eggs from unexposed females. At this time, a trout embryo’s eyes are visible, and the embryo is about to hatch. The scientists found that the sperm from unexposed males fertilized 45 percent of the eggs, while sperm from trout exposed to a mere 10 ppt of EE2 fertilized only 22 percent of the eggs. Ten ppt is at the upper end of the range of EE2 concentrations normally found in the wild.

“I was surprised that such an incredibly low dose had a real effect on these animals–to the point where long-term population problems might exist,” says Lou Guillette, a zoologist at the University of Florida in Gainesville.

In the June Environmental Toxicology and Chemistry, Schultz and his team say the lower fertility rates for the exposed trout seem paradoxical. These fishes’ sperm were just as mobile as those of their unexposed counterparts, and the exposed trouts’ sperm counts were higher.

“If you stopped at sperm counts, you’d conclude from this study that estrogens must be good for male fish,” Guillette says. But the fertilization rates indicate that the opposite is true.

Guillette says this focus on fertility sets Schultz’s study apart from previous EE2 studies with zebra fish and medaka. In those investigations, researchers used sperm count, gonad development, and liver size to measure EE2’s effects. Schultz says that he did a fertility trial because he wanted “a more reproductively relevant” benchmark.

Still, Schultz says, these laboratory tests only hint at the complexity of what happens in the wild. EE2 is just one of an array of contaminants entering waterways from sewage systems (SN: 3/23/02, p. 181: Available to subscribers at A Confluence of Contaminants: Streams’ organic mix may pose environmental risk). Guillette speculates that the effect of EE2 on wild trout may be amplified, blocked, or otherwise altered when the hormone is accompanied by other compounds. “At this point, we don’t know,” he says.

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