Impacts of ash-induced environmental alkalinization on fish physiology, and their implications to wildfire-scarred watersheds.

Changes in land use, a warming climate and increased drought have amplified wildfire frequency and magnitude globally. Subsequent rainfall in wildfire-scarred watersheds washes ash into aquatic systems, increasing water pH and exposing organisms to environmental alkalinization. In this study, 15 or 20 °C-acclimated Chinook salmon (Oncorhynchus tshawytscha) yearlings were exposed to an environmentally-relevant ash concentration (0.25 % w/v), increasing water pH from ∼8.1 to ∼9.2. Salmon experienced significant disturbance to blood plasma pH (pHe) and red blood cell intracellular pH (RBC pHi) within 1 h, but recovered within 24 h. Impacts on plasma ion concentrations were relatively mild, and plasma glucose increased by 2- to 4-fold at both temperatures. Temperature-specific differences were observed: 20 °C salmon recovered their pHe more rapidly, perhaps facilitated by higher basal metabolism and anaerobic metabolic H+ production. Additionally, 20 °C salmon experienced dramatically greater spikes in plasma total ammonia, [NH3] and [NH4+] after 1 h of exposure that decreased over time, whereas 15 °C salmon experienced a gradual nitrogenous waste accumulation. Despite pHe and RBC pHi recovery and non-lethal nitrogenous waste levels, we observed 20 % and 33 % mortality in 15 and 20 °C treatments within 12 h of exposure, respectively. The mortalities cannot be explained by high water pH alone, nor was it likely to be singularly attributable to a heavy metal or organic compound released from ash input. This demonstrates post-wildfire ash input can induce lethal yet previously unexplored physiological disturbances in fish, and further highlights the complex interaction with warmer temperatures typical of wildfire-scarred landscapes.