Constructing Lattice Disorder-Induced Cascade Sites for Carbon Dioxide Photohydrogenation

Efficient photocatalytic CO 2 reduction (CO 2 RR) requires multifunctional catalysts with cascading active sites to manage complex reaction pathways. Bi 2 Sn 2 O 7 (BSO) catalysts are promising for CO 2 RR, yet the specific roles of Bi and Sn sites, particularly regarding cascade mechanisms, remain unclear. Traditional synthesis methods yield highly ordered lattices, often neglecting the role of Sn sites, with BSO typically utilized as a single-site catalyst. Herein, a BSO catalyst with a disordered surface ( d -BSO) was synthesized via lattice disorder engineering, and the functional division of Bi and Sn sites in establishing cascade active sites was systematically investigated. The results suggest that Bi–oxygen vacancy (OV) sites function as dual-purpose active sites for H 2 O dissociation and CO 2 activation, while symmetric Sn sites (Sn1–OV–Sn2) released by lattice disorder serve as the single functional site for CO 2 adsorption and activation during CO 2 RR. These symmetrical Sn sites create a distinct Sn1–O–C–Sn2 structure, where the overlap of Sn 5 s /5 p and CO 2 empty orbitals in various spatial directions boosts electron supply and CO 2 activation. The distinct roles of Sn sites used for CO 2 activation and Bi sites used for H 2 O dissociation align with the catalytic cascade mechanism, supporting the potential of lattice disorder engineering for constructing cascade catalysts. Lattice disorder-induced Bi/Sn cascade sites and the built-in electric field boost CO production to 50.36 μmol g –1 h –1 with 100% selectivity, a 37.8-fold increase over pristine BSO (1.34 μmol g –1 h –1, 70.89%) under 2 h gas−solid water vapor (GSV) conditions. Under gas−solid liquid conditions, the catalyst shows highly stability maintaining 21.70 μmol g –1 h –1 for 5 h unlike its deactivation under the GSV conditions. This work elucidates the cascade mechanism in pyrochlores and demonstrates lattice disorder engineering as a potent strategy for activating multifunctional sites.