Lake water chemistry and local adaptation shape NaCl toxicity in .

The increasing application of road deicing agents (e.g., NaCl) has caused widespread salinization of freshwater environments. Chronic exposure to toxic NaCl levels can impact freshwater biota at genome to ecosystem scales, yet the degree of harm caused by road salt pollution is likely to vary among habitats and populations. The background ion chemistry of freshwater environments may strongly impact NaCl toxicity, with greater harm occurring in ion-poor, soft water conditions. In addition, populations exposed to salinization may evolve increased NaCl tolerance. Notably, if organisms are adapted to the water chemistry of their natal environment, toxicity responses may also vary among populations in a given test medium. We examined the potential for this evolutionary and environmental context to interact in shaping NaCl toxicity with a pair of laboratory reciprocal transplant toxicity experiments, using natural populations of the water flea collected from three lakes that vary in ion availability and composition. We observed a strong effect of the lake water environment on NaCl toxicity in both trials. NaCl caused a much greater decline in reproduction and in lake water from a low-ion/calcium-poor environment (20 μS/cm specific conductance; 1.7 mg/L Ca) compared with water from both a Ca-rich lake (55 μS/cm; 7.2 mg/L Ca) and an ion-rich coastal lake (420 μS/cm; 3.4 mg/L Ca). from this coastal lake were most robust to the effects of NaCl on reproduction and . A significant interaction between the population and lake water environment shaped survival in both trials, suggesting that local adaptation to the test waters used may have contributed to toxicity responses. Our findings that the lake water environment, adaptation to that environment, and adaptation to a contaminant of interest may shape toxicity demonstrate the importance of considering environmental and biological complexity in mitigating pollution impacts.