Amphibian declines are a prominent part of the global biodiversity crisis and have received special consideration because they have occurred relatively recently, on a global scale, and in seemingly pristine habitats where no obvious anthropogenic cause is apparent. Although several causes for declines have been implicated, the isolation of a singular cause has proven elusive. Consequently, it has been hypothesized that complex interactions between multiple environmental stressors, particularly those associated with global change, may be responsible. Increasing ultraviolet-B radiation (UV-B) associated with stratospheric ozone depletion is one such stressor that has received considerable attention. UV-B causes enhanced lethal effects when combined with other factors such as aquatic pH, contaminants, temperature and pathogens, but little is known of how UV-B interacts with pervasive biological stressors, such as risk of predation. We exposed Limnodynastes peronii tadpoles to UV-B and predatory chemical cues in a controlled laboratory experiment to determine their independent and interactive effects on survival and morphology. We show that UV-B and risk of predation interact synergistically to enhance mortality above the additive effects of the independent stressors, and that exposure to UV-B affects the ability of tadpoles to morphologically respond to predatory chemical cues (i.e. predator-induced phenotypic plasticity), which has implications for their survival in an environment with predators. This highlights the importance of considering both anthropogenic and naturally occurring stressors when examining the underlying causes of amphibian declines.