Polycyclic aromatic hydrocarbons (PAHs), as persistent
environmental
pollutants, often reside in nonaqueous-phase liquids (NAPLs). Mycobacterium sp. WY10, boasting highly hydrophobic surfaces,
can adsorb to the oil–water interface, stabilizing the Pickering
emulsion and directly accessing PAHs for biodegradation. We investigated
the impact of Triton X-100 (TX100) on this interfacial uptake of phenanthrene
(PHE) by Mycobacteria, using n-tetradecane (TET) and bis-(2-ethylhexyl) phthalate (DEHP) as NAPLs. Interfacial tension, phase
behavior, and emulsion stability studies, alongside confocal laser
scanning microscopy and electron microscope observations, unveiled
the intricate interplay. In surfactant-free systems, Mycobacteria
formed stable W/O Pickering emulsions, directly degrading PHE within
the NAPLs because of their intimate contact. Introducing low-dose
TX100 disrupted this relationship. Preferentially binding to the cells,
the surfactant drastically increased the cell hydrophobicity, triggering
desorption from the interface and phase separation. Consequently,
PAH degradation plummeted due to hindered NAPL access. Higher TX100
concentrations flipped the script, creating surfactant-stabilized
O/W emulsions devoid of interfacial cells. Surprisingly, PAH degradation
remained efficient. This paradox can be attributed to NAPL emulsification,
driven by the surfactant, which enhanced mass transfer and brought
the substrate closer to the cells, despite their absence at the interface.
This study sheds light on the complex effect of surfactants on Mycobacteria
and PAH uptake, revealing an antagonistic effect at low concentrations
that ultimately leads to enhanced degradation through emulsification
at higher doses. These findings offer valuable insights into optimizing
bioremediation strategies in PAH-contaminated environments.