Bad New Benzos: Anti-Anxiety Drugs Increase Fish Survival . . . Why is This a Problem?
This question seems unnecessary, but let's ask it anyway: Why do we care about water pollution? There are myriad reasons, of course, but a common answer is that we are concerned about poisoning wildlife. Chemicals in both industrial and residential wastewater are potentially toxic to an array of species and can alter the functionality of entire food webs. We should not toxify nature.
Of course poisoning wildlife is bad. We are (rightfully) so concerned about how many animals die as a result of human activities, however, that we sometimes forget just how high natural mortality rates can be. Nature is not a forgiving place. Human activities often amplify naturally high mortality rates--a double-whammy that throws populations into a tailspin of decline. This is an all-too common problem at the crux of many conservation issues. On the other hand, reducing a population's natural mortality rate is not necessarily a good thing either. Adjusting the natural rhythms of the food web in either direction can have severe implications for stability and functionality of entire ecological communities.
This leads us to an interesting ecotoxicology question . . . what happens when pollutants have beneficial effects on wild organisms? We know that various nutrients can stimulate microbe proliferation, such as algal blooms that occur in response to agricultural runoff. What happens when pollutants prove to be a boosters to other organisms, or even large consumers?
A study recently published in the journal Environmental Research Letters cleverly tackles questions about the potential benefits of chemicals on wildlife, and the results can open us up to discussion about why such effects might not yield positive outcomes. A group of researchers from Sweden’s Umeå University, led by Jonatan Klaminder, showed that fish living in water contaminated by a common pharmaceutical actually had lower mortality rates than their counterparts living in clean water.
What kind of chemical actually increases fish survival? In this case, it was an anti-anxiety medication, Oxazepam. This drug is one of the benzodiazepines (other familiar brands are Xanax and Ativan) commonly prescribed for anxiety, insomnia, irritable bowel syndrome, and the effects of alcohol withdrawal. "Benzos" are among the most commonly prescribed drugs in the U.S., and they are now showing up in waterways in many developed countries (we excrete many of the drugs and vitamins that we put into our bodies, and they are carried into the environment with wastewater).
Oxazepam and similar drugs help alleviate anxiety by binding with the GABA-A receptors in the central nervous system (CNS). The CNS is an extremely ancient, conserved part of our neural network that is shared by all vertebrates. Therefore, fish have GABA-A receptors just like we do. When fish have to live in water contaminated with Oxazepam, the drug binds to their receptors just as it does to ours. No one has asked fish if the drug makes them feel less anxious, but a previous study (Brodin et al. 2013) showed that it does indeed make them bolder and more active.* Bolder, more active fish turn out to be more efficient foragers, which leads us to the next part of the story.
Effective foraging is the key to life for wild animals. Thus, Klaminder and colleagues decided to investigate whether Oxazepam affected the survival rates of wild-caught Eurasian perch (Perca fluviatilis). They tested both adult fish and eggs (roe) in three different water conditions: control (no Oxazepam), low Oxazepam (1 µg1-1) and high Oxazepam (1000 µg1-1). The researchers then compared the activity levels and survival rates of both adult and young fish from the different treatments. The young fish were assessed 30 days after hatching from the eggs that went through the experiment. The researchers also measured the concentration of Oxazepam in the body tissues of the fish.
Both activity levels and survival rates were higher in Oxazepam-exposed adults and youngsters. Specifically, the young fish in the high concentration treatment experienced significantly lower mortality than those in the control and low concentration treatment, and adult fish in both the low and high concentration treatments experienced significantly lower mortality than those in the control treatment (see figure above, click to embiggen).
It should be noted that the "low” concentration is much, much lower than concentrations recorded in some waterways (up to 1.9 µg1-1; Loos et al. 2013), and that the fish from the “low” treatment had concentrations of up to 7 µg kg-1 in their actual tissues.
So, Oxazepam is beneficial for fish! Our inadvertent drugging of wildlife finally did some good, right?
Eurasian perch, and many fish like them, have extremely high natural mortality rates—up to 92% will die within one week of hatching (Viljanen & Holopainen 1982). Other organisms that interact with the perch are adapted to conditions in which a very tiny portion of these fish will reach adulthood. For example, Eurasian perch eat a variety of invertebrates and smaller fish, all of which would face a sudden spike in predation pressure if populations of the perch were to boom. If humans start putting substances into the water that allow more of these fish to survive, lower perch mortality rates could have significant impacts on the species that they eat, and the species that those organisms eat, and the other species that depend on any of the above prey species, and the plants and algae eaten by those prey species, and any other animals that also eat those plants and algae . . . the cascading effects could be far-reaching indeed. These effects are beyond the scope of the experiments presented in Klaminder et al. (2014), but it will be fascinating to follow future research that explores the cascading effects of reduced predator mortality in contaminated waterways.
Even when humans "help" a species out by accident, it is not necessarily a good thing. Our ultimate goal should not be to simply minimize wildlife mortalities, but to avoid disrupting vital rates for as many species as possible. No species exists in isolation, and any effects we have on one organism will inevitably affect others, in one way or another. This study by Klaminder and colleagues is an extremely useful and neat example of these effects, and the implications of the findings are critical for future management efforts involving pharmaceutical contamination.
Brodin, T., J. Fick, M. Johnson & J. Klaminder. 2013. Dilute concentrations of a psychiatric drug alter behavior of fish from natural populations. Science 15:814-815.
J. Klaminder, M. Jonsoon, J. Fick, A. Sundelin, & T. Brodin (2014). The conceptual imperfection of aquatic risk assessment tests: highlighting the need for tests designed to detect therapeutic effects of pharmaceutical contaminants Environmental Research Letters, 9 : doi:http://10.1088/1748-9326/9/8/084003
Loos, R. et al. 2013. EU-wide monitoring survey on waste water treatment plant effluents. Water Research 47:6475-87.
Viljanen, M. & I. J. Holopainen. 1982. Population-density of perch (Perca fluviatilis 1) at egg, larval, and adult stages in the dysoligotrophic lake suomunjarvi, Finaland. Ann. Zool. Fennici. 19 39-46:
*The fact that Oxazepam makes fish bolder and more active is somewhat confusing, because the drug is primarily used for its sedative effects in humans. More research is needed, but studies have shown that a related drug, Diazepam, makes young children hyperactive (Oxezepam is also a metabolite of Diazepam).