Tailoring the release of encapsulated corrosion inhibitors from damaged coatings: Controlled release kinetics by overlapping diffusion fronts

The goal of this work is to model the release of corrosion inhibitors from damaged organic coatings. In the present study, the healing response (i.e. the active corrosion protection) is triggered by the ingress of moisture in the coating through the walls of a damaged site, followed by the transport of the corrosion inhibitors to the exposed metal substrate by diffusion through the moisture present in the polymeric coating. We propose a mathematical–analytical model for each step of the healing response in order to determine, through computer simulation, the particle configurations that lead to desired regimes of inhibitors release into the damaged site. The used methodology is based on overlapping Fickian leaching kinetics of the individual corrosion inhibitor particles present in the coating. With the proposed model we analyze different release behaviors proportional to tα with 0.25 < α ≤ 1 reported in the literature. We study in detail the conditions yielding a linear release of corrosion inhibitors and determine the range of release rates that can be achieved as a function of the particle size distribution within the coating, the moisture diffusion through the coating and the capsule dissolution kinetics. In particular, we clearly demarcate the systems in which the linear release behavior cannot be obtained. Furthermore, we find that our model cannot predict the experimentally observed t0.25 kinetics for any configuration and condition considered, which indicates that the release of inhibitor compounds from particle dissolution in these systems may not follow a Fickian behavior.

► A model to analyze the wide range of different leaching kinetics observed experimentally is given.
► The model allows identifying the release kinetics for each inhibitor-coating system.
► The model serves to obtain the particle density function for a prescribed leaching kinetics.
► The model rejects diffusive inhibitor transport mechanisms to explain t0.25 leaching kinetics.
► The model confirms such transport mechanism to explain the tα with 0.5 < = α < = 1 leaching kinetics.