First-principles study of chemical species adsorption and solid electrolyte interphase formation on defective sodium metal anodes

The solid electrolyte interphase (SEI) on sodium metal anodes governs passivation and ion transport, but its early formation, controlled by chemical species–defect interactions, remains insufficiently understood at the atomic scale. Using density functional theory calculations, we investigate the adsorption of 22 chemical species that include electrolyte solvents, salts, and decomposed species on the defective substrate, which contains terraces, clusters of adatoms, and multi-atom vacancies. Analysis of optimized structures and charge transfer shows that undercoordinated defect sites, such as pyramidal adatom clusters and vacancy rims, constitute highly reactive regions that strongly polarize adsorbed species, induce significant surface reconstruction, and promote charge transfer-assisted activation of electrolyte molecules. This activation fragments salt-anion intermediates and yields compact inorganic phases that form ionic bonds with undercoordinated Na sites in defects, accounting for the preferential formation of an inorganic-rich SEI at the most reactive surface regions. In contrast, carbonate solvents exhibit minimal charge transfer, negligible molecular distortion, and moderate adsorption energies, indicating that they remain largely intact upon contact and affect the interface mainly through polarization and the Pauli-repulsion effect. Organic SEI fragments bind with intermediate strength through localized coordination while their alkyl groups remain electronically passive, consistent with their prevalence in the more dynamic and solvent-accessible outer SEI region. Small volatile decomposition products show weak physisorption and preferentially desorb rather than incorporate into the interphase. These results relate morphological heterogeneity to site-specific reactivity and support electrolyte selection criteria that favor compact inorganic nucleation at undercoordinated defects while limiting pathways associated with dendrite-promoting protrusion growth and parasitic side reactions.