Toxicological and physiological effects of the surfactant dioctyl sodium sulfosuccinate at varying salinities during larval development of the Gulf Killifish (Fundulus grandis)
Abstract
© 2015 by Taylor & Francis Group, LLC. Formulations of Corexit®, a family of oil dispersants used in large-scale oil spills, were the primary emulsification agents utilized to enhance the biodegradation of Macondo-252 oil following the Deepwater Horizon spill (DWH) in the Gulf of Mexico (Deepwater Horizon Unified Command [DHUC] 2011). An estimated 6.9 million liters of the dispersant Corexit 9500A was applied in the northern Gulf of Mexico in response to the DWH, with smaller amounts of Corexit 9527 also applied (www.restorethegulf.gov). Although precise formulations are proprietary, Corexit 9527 consists of approximately 48% nonionic surfactants (ethoxylated sorbitan monooleate, ethoxylated sorbitan trioleate, and sorbitan monooleate), 35% of the anionic surfactant, dioctyl sodium sulfosuccinate (DOSS), and 17% hydrocarbon solvents (Wheelock et al. 2002). Although exact percentages are unknown, the primary components of Corexit 9500A as released by the manufacturer (Nalco) include sorbitan, butanedioic acid, propanol, hydro-treated petroleum distillates, and DOSS. The presence of anionic surfactants, such as DOSS, in these mixtures serves to decrease the surface tension between the water–oil interface, facilitating the formation of small (~100 μm) oil-surfactant micelles (National Research Council [NRC] 2005). The resulting droplets are maintained in the water column due to their greater surface-area-to-volume ratio, which increases physical and microbial degradation. Unfortunately, surfactants are also able to interact with biological membranes, where they can exert toxic effects in aquatic organisms (Abel and Skidmore 1975, Attwood and Florence 1983). Acute exposures of the surfactant, sodium lauryl sulfate (SLS), in rainbow trout (Oncorhynchus mykiss) resulted in damage to the gill epithelial tissue and was characterized by swelling of filament epithelium, increase and subsequent cell death of mitochondrial rich cells (MRC), and sloughing of dead epithelial cell (Abel and Skidmore 1975).