Due to continuous pharmaceutical contamination of the aquatic ecosystem, there has been growing evidence that pollutants such as the antidepressant fluoxetine can increase fish offspring production. However, such an increase may happen at a hidden cost, for instance, if pharmaceuticals also disrupt key reproductive behaviours, like where and how fish choose to spawn, that can determine whether those offspring will ultimately survive. To assess this possibility, we exposed turquoise killifish (Nothobranchius furzeri) to a field-realistic concentration of fluoxetine (317 ng/L) in a controlled laboratory experiment. Fish were given a choice of white, orange, or black sand as a spawning substrate, both in single pairs and in groups. The fluoxetine-exposed group produced about 50% more eggs in single pairs, but this effect was not observed in groups. Despite the social context, fish deposited roughly four times more eggs on black sand than on orange or white sand, and fluoxetine did not alter this habitat preference. These results show that environmentally relevant fluoxetine concentrations can boost reproductive output without necessarily affecting spawning-site selection. The broader ecological implications of such changes will depend on how pharmaceutical-induced shifts in reproduction interact with natural social and habitat dynamics in the wild.