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Epoxy coatings are currently the most popular corrosion protection mechanism for steel reinforcement in structural concrete in North America. However, these coatings are easily damaged on worksites, negating their intended purpose. This study investigated self-healing coatings for steel reinforcement to introduce an autonomous healing mechanism for damaged coatings. Coatings were applied to steel coupons and rebar, intentionally damaged, and introduced to a corrosive environment via salt-water aeration tanks and accelerated corrosion testing. Performance of the experimental coatings was evaluated qualitatively and quantitatively. Adhesion strength and effects of coating thickness were also studied. Results from pre-corroded coated steel coupons submerged in salt-water aeration tanks exhibited improved corrosion resistance performance with self-healing coatings, although self-healing and conventional coatings performed similarly under other conditions. Steel reinforcement with a self-healing coating embedded in concrete and subjected to accelerated corrosion testing lasted longer than the conventionally coated counterparts. Self-healing coatings had comparable adhesion to the substrate as do conventional coatings. With numerous avenues for future research towards the adoption of self-healing coatings for steel reinforcement, this paper shows preliminary results demonstrating the potential benefits of their use.

Intratracheal injection of MnSOD-PL has been shown to protect the murine lung from irradiation-induced damage. To translate this modality to fractionated radiotherapy in the clinic, an inhalation model for the delivery of MnSOD-PL was developed. To demonstrate that MnSOD-PL can be delivered to the lungs, an ultrasonic nebulizer was used to deliver either 1 mg of alkaline phosphatase-PL (Alk-PL) complex or hemagglutinin epitope-tagged MnSOD (HA-MnSOD) to C57BL/6J mice. Other mice were intratracheally-injected with Alk-PL or HA-MnSOD-PL (500 μg plasmid DNA). All mice were sacrificed 24 hours after MnSOD-PL administration with the lungs assayed for increased MnSOD biochemical activity or DNA expression. An increase was observed in MnSOD biochemical activity from levels of 2.23 ± 0.15 U/mg protein in control mice to 5.0 ± 0.21 U/mg protein in mice that inhaled MnSOD-PL (p= 0.024). Real time PCR (RT-PCR) using primers specific for the human MnSOD gene detected a significant increase in MnSOD mRNA expression in mice that inhaled MnSOD-PL compared to control, C57BL/6J mice. In a second experiment, subgroups of mice inhaled 0, 250, 500, 1000, or 2000 μg of HA-MnSOD plasmid DNA over 5 minutes. MnSOD biochemical activity was significantly increased with maximal activity of 5.0 ± 0.4 U/mg protein at 500 μg plasmid DNA compared to 2.3 ± 0.1 in control, non-treated lungs (p= 0.0241). To demonstrate that inhalation of MnSOD-PL protected against irradiation-induced lung damage, C57BL/6J mice inhaled 1.0 mg of MnSOD-PL over 10 minutes or were intratracheally-injected with 0.5 mg of MnSOD-PL. Twenty-four hours later, control mice as well as MnSOD-PL-treated mice were irradiated to 20 Gy and followed for development of organizing alveolitis. Mice inhaling MnSOD or injected intratracheally with MnSOD-PL had significantly increased survival (p