Biofilm-constrained sulfidogenesis: mechanisms, inhibition strategies, and a framework for sustainable control.

Sulfidogenesis by sulfate-reducing bacteria (SRB) causes odor emissions, microbiologically influenced corrosion, and operational failures in wastewater, petroleum, and other anaerobic engineered systems. Although numerous chemical and biological strategies have been developed to suppress sulfide production, their effectiveness in field applications often remains inconsistent. This review argues that the long-recognized discrepancy between laboratory inhibition and field-scale control originates fundamentally from biofilm-imposed transport limitation, metabolic stratification, and ecological resilience rather than insufficient inhibitor potency alone. We first summarize how biofilm architecture reshapes the metabolic vulnerability of sulfate reduction by regulating sulfate accessibility, electron transfer, metabolic stratification, and microbial interactions. Existing inhibition strategies are subsequently reorganized into four complementary control layers comprising metabolic inhibition, redox-mediated competition, biocidal disruption of cellular integrity, and physicochemical stress induced by pH shock. The limitations of these strategies are further discussed in the context of mature biofilms, where transport resistance, extracellular polymeric substances, physiological heterogeneity, and ecological resilience collectively limit inhibitor accessibility and reduce long-term inhibition efficiency. Based on this synthesis, a biofilm-integrated framework is proposed that combines biofilm destabilization, multi-node metabolic inhibition, and ecological restructuring to achieve sustainable sulfidogenesis control. Future research priorities include identifying new metabolic vulnerability nodes, quantifying reactive transport within biofilms, understanding microbial resilience and recovery, and developing predictive biofilm management strategies. This review provides a conceptual foundation for translating laboratory inhibition into durable field-scale sulfidogenesis control.