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Zhao, Wenjun, Zhisheng Xu, and Long Yan. Surfaces and Interfaces (2025): 107125.
N,N-Dimethyldodecylamine-N-oxide (OB-2) plays a critical role as a co-surfactant in the development of environmentally benign aqueous film-forming foams (AFFF). When combined with the zwitterionic short-chain fluorocarbon surfactant PFH-BZ at a 1:2 molar ratio, OB-2 significantly enhances surface activity, micellization behavior, and overall foam performance. The PFH-BZ/OB-2 blend exhibits a remarkably low surface tension of 22.13 mN/m and high foam height and stability, highlighting strong synergistic interactions between the hydrophobic fluorinated framework of PFH-BZ and the amphiphilic structure of OB-2.
Electrostatic shielding introduced by inorganic salts further modulates OB-2-containing formulations. Increased ionic strength reduces intermolecular repulsion and promotes tighter surfactant packing at the interface, resulting in improved spreading behavior, micelle formation, and viscosity. At optimal conditions-specifically 0.05 mol/L NaCl-the PFH-BZ/OB-2 system demonstrates superior performance, with enhanced bubble evolution and delayed drainage (time to 25% mass loss: 48.35 s), attributed to stabilized interfacial films and controlled micellar aggregation.
Importantly, OB-2 contributes to mitigating the limitations of short-chain fluorocarbon surfactants by facilitating cooperative assembly and improving foam resilience without compromising biodegradability. These findings position N,N-dimethyldodecylamine-N-oxide as a key formulation component in next-generation, environmentally compliant fire-fighting foams, while providing mechanistic insights into salt-surfactant interactions and interfacial stabilization strategies.
Park, Eun-Jung, et al. Toxicology in Vitro (2025): 106102.
This case study highlights the mechanistic toxicology of dodecyldimethylamine oxide (DDAO), a widely used surfactant in household spray formulations, with emphasis on its cellular impacts in human bronchial epithelial cells. Experimental evidence demonstrates that short-term exposure (6 h) to DDAO induces non-apoptotic cell death characterized by rapid reductions in cellular impedance and the formation of numerous cytoplasmic microvacuoles. Mitochondrial ultrastructure was significantly compromised, including inner membrane condensation, elevated cytochrome C release, suppressed ATP production, and decreased mitochondrial volume-events that collectively disrupt second messenger homeostasis.
DDAO exposure also impaired intracellular organelles such as lamellar bodies, which appeared within mitochondria or vacuolation structures, indicating profound disturbance in membrane-bound compartments. Cytokine profiling revealed a selective immunological shift: while chemotactic cytokines diminished, pro-inflammatory mediators including IL-6, IL-11, MMP-1, and MMP-3 were upregulated. Notably, DDAO markedly enhanced LAMP-2 expression and expanded acidic lysosomal compartments, suggesting activation of a lysosomal stress response.
Gene expression analysis identified lipid metabolism pathways as the most strongly affected, and the rapid collapse of acidic compartments at concentrations ≥40 μg/mL supports a mechanism of lysosomal-associated cell death potentially driven by lipotoxicity. Overall, this study indicates that DDAO compromises mitochondrial and lysosomal integrity, with lysosomal membrane proteins potentially mitigating cellular damage, offering critical mechanistic insight for evaluating the safety of DDAO-containing consumer products.
