High-strength, low-alloy, martensitic steels are known to be subject to hydrogen embrittlement. This was demonstrated by measurements of crack-tip pH and localized hydrogen content at the fracture surface, and also by observation of electrochemical behavior of simulated “crevices.” The effect of certain oxidizing inhibitors was used to elucidate the mechanisms of stress-corrosion cracking (SCC) and to retard crack growth.

Hydrazine additions reduced the crack growth rate by an order of magnitude for D6AC in aqueous solutions. A 2 percent addition of hyrazine to solutions either with or without chlorides increased K_Iscc from 12 (without inhibitor) to 25 ksi∓in. (with inhibitor). The critical flaw size varies as the square of K_Iscc, so doubling K_Iscc is the equivalent of increasing the size of a critical flaw fourfold, which in turn makes more likely its detection non-destructively. Localized hydrogen analyses at various locations on the fracture surface of a D6AC specimen pulled to failure after exposure in hydrazine-inhibited solution (with or without chlorides) showed no hydrogen enrichment of the fracture surface (as compared to the bulk specimen remote from the fracture), hence no hydrogen embrittlement.

While sodium dichromate additions also increased K_Iscc and reduced the crack-growth rate in chloride-free solutions, they were not effective in 0.1 N sodium chloride solutions.

Special electrochemical measurements (with and without chlorides) showed that in the presence of the hydrazine inhibitor, the electrode potential of D6AC at the tip of an advancing corrosion fatigue crack was above (more noble than) the potential of the equilibrium hydrogen electrode. By contrast, the electrode potential at the apex of an advancing corrosion fatigue crack in D6AC exposed in dichromate-inhibited, chloride-containing solution was below (more active than) the potential of the equilibrium hydrogen electrode. Thus dichromate additions did not prevent hydrogen entry into D6AC in chloride solutions.