The closure of a human lung airway is modeled as an instability of a two-phase flow in a pipe coated internally with a Newtonian liquid. For a thick enough coating, the Plateau-Rayleigh instability creates a liquid plug which blocks the airway, halting distal gas exchange. Owing to a bi-frontal plug growth, this airway closure flow induces high stress levels on the wall, which is the location of airway epithelial cells. A parametric numerical study is carried out simulating relevant conditions for human lungs, either in ordinary or pathological situations. Our simulations can represent the physical process from pre- to post-coalescence phases. Previous studies have been limited to pre-coalescence only. The topological change during coalescence induces a high level of stress and stress gradients on the epithelial cells, which are large enough to damage them, causing sub-lethal or lethal responses. We find that post-coalescence wall stresses can be in the range of 300% to 600% greater than pre-coalescence values, so introduce a new important source of mechanical perturbation to the cells.