Recently, a mechanism has been proposed to describe how salts do (not) contribute to bubble coalescence inhibition. This is done by considering how ions (re)distribute themselves along the G/L-interface, expressing this as a Gibbs-Marangoni pressure. The thesis’ goal is to investigate the potential and applicability of this mechanism to predict bubble coalescence inhibition for salts in biotechnological processes, specifically bubble columns. This goal is achieved by recreating the mechanism and evaluating whether the Gibbs- Marangoni pressure is a better predictor than the ionic strength. To make this comparison, experiments are performed to study which ionic strengths/concentrations induce bubble coalescence inhibition. These numbers are then modelled in terms of Gibbs-Marangoni pressures, from where it is assessed which of the two better predicts this inhibition. More- over, additional experimental results from the literature have been tested on the model to support this assessment. The outcome of this thesis is a combination of multiple interesting insights. First, the above mechanism is successfully reproduced into a model. This statement is supported by com- paring the model’s results with previous literature applying this mechanism, showing that results deviate less than 10% from each other. Secondly, from the performed experiments, bubble coalescence inhibition by salts is observable at an average ionic strength of 47.82 mM. Using these results in the model shows that this inhibition happens at an average Gibbs-Marangoni pressure of 1312.91 Pa. How- ever, the inhibiting salt concentrations from the experiments deviate by more than 168% compared to the literature. This difference can be caused by many factors, such as dissimilarities in the experimental setups used. It shows that the critical Gibbs-Marangoni pressure is dependent on these factors and therefore not entirely generalizable for all scenarios. Finally, the model’s results are validated by comparing whether the additionally calculated surface tensions deviate less than 10% from the literature. This showed resulting Gibbs- Marangoni pressures are valid for pure salts at concentrations from 0.02-1.50 M. However, the validity of the model for salt mixtures is questionable. To conclude, the proposed mechanism can describe bubble coalescence inhibition for salts in bubble columns. However, its accuracy is debatable as the model’s results cannot be validated for mixtures. This may require the inclusion of other ion contributions into the model, such as ion polarizability, solvation energy and ion-charge density. Hopefully, this brings us closer to better modelling the effect of salts, and other compounds, on bubble coalescence inhibition.