Calcium complexation

Inhibition by calcium complexation relies largely on the requirement that small calcium oxide/hydroxide templates must form in the pore water of cement pastes before silicate tetrahedra can condense into dimeric and oligomeric silicates to form C–S–H. Calcium complexation involves either removing calcium from solution by forming insoluble salts, or chelating calcium in solution. Calcium complexation lowers the amount of calcium effectively in solution, delaying the time to Ca(OH)₂ super-saturation and preventing precipitation of the necessary templates. Simple calcium complexation should dramatically increase the amount of Si(OH)₄ tetrahedra in solution, and indeed this is observed with most retarders. However, if the retarder were acting solely by calcium complexation, then one molecule of retarder would be required per calcium ion in solution, and good inhibitors are used in much smaller quantities, on the order of 0.1-2% by weight of cement. In addition, there is no simple correlation between either calcium binding strength or calcium salt solubility and retarding ability. Yet it has been shown that in pure systems, i.e., of C3S and C2S, that the lime concentration in solutions is the most important factor in determining the precipitation of C–S–H. Therefore, although calcium complexation must play some role in inhibition, other mechanisms of inhibition must be at work as well. An example of a retarder that operates primarily through calcium complexation is tartaric acid, however, the formation of insoluble calcium tartrate on cement grains suggest that dissolution/precipitation occurs in addition (Figure 2).

Figure 2: Schematic representation of cement hydration in the presence of tartaric acid. The aluminate (and aluminate ferrate) phases (shown in purple) surround the silicate phases (C3S and C2S). Tartaric acid adsorbs onto the aluminum surfaces and reacts with calcium ions from gypsum to deposit a thick calcium tartrate coating on the cement grain. Adapted from M. Bishop, PhD Thesis, Rice University, 2001.

Nucleation poisoning

As with calcium complexation, nucleation poisoning must rely on the formation of small calcium oxide/hydroxide templates in the pore water of cement pastes before silicate tetrahedra can condense into dimeric and oligomeric silicates to form C–S–H. Inhibition by nucleation poisoning is where the retarder blocks the growth of C–S–H or Ca(OH)₂ crystals through inhibiting agglomerates of calcium ions from forming the necessary hexagonal pattern. Nucleation inhibitors act on the surface of small clusters, therefore, less than one molecule of retarder per calcium ion is required to produce dramatic results. This type of inhibition also results in an increase in the amount of silicate ions in solution, as condensation of silicate chains onto calcium oxide templates to form the C–S–H is inhibited. As a retarder sucrose acts via nucleation poisoning/surface adsorption.

Surface adsorption

Surface adsorption of inhibitors directly onto the surface of either the anhydrous or (more likely) the partially hydrated mineral surfaces blocks future reactions with water. In addition, if such inhibitors are large and anionic, then they produce a negative charge at the surface of the cement grains, causing the grains to repel each other thereby reducing inter-particle interactions. Lignosulfonates are typical of retarders that act via surface adsorption.

Protective coating/osmotic bursting

The formation of a protective coating with its subsequent bursting due to the build up of osmotic pressure was originally posited to explain the existence of the induction period in C3S and cement hydration, however it may be applied to inhibition in general. In this mechanism, a semi-permeable layer at the surface of the cement grain forms and slows down the migration of water and lengthens the induction period. Osmosis will drive water through the semi-permeable membrane towards the unhydrated mineral, and eventually the flow of water creates higher pressure inside the protective coating and the layer bursts. Hydration is then allowed to continue at a normal rate.

Dissolution-precipitation

A detailed study of several retarders (in particular the organic phophonates) has shown that the actually accelerate certain stages of the hydration process. This is unexpected since the phosphonates have been termed “super retarders,” due to their increased effect on cement hydration relative to the effect of conventional retarders. So how is it that a retarder can be so efficient at hydration inhibition at the same time as accelerating the process? The ability of phosphonates to retard cement setting is due to the lengthening the induction period, without slowing down the time it takes for setting to occur (once the acceleratory period has begun).

Phosphonates are known to complex calcium and other M²⁺ cations, poison the nucleation and growth of barium sulfate crystals, and inhibit the hydration of Fe₂O₃ and Al₂O₃ surfaces via direct surface adsorption, thus it was assumed that with regard to cement hydration inhibition occurred by one of these mechanism. However, the mechanism by which phosphonates inhibit cement hydration consists of two steps. First dissolution, whereby calcium is extracted from the surface of the cement grains (Figure 3a) exposing the aluminum rich surface to enhanced (catalyzes) hydration and ettringite formation (Figure 3b). Second precipitation, whereby the soluble calcium-phosphonate oligomerizes either in solution or on the hydrate surface to form an insoluble polymeric Ca-phosphonate (Figure 3c). The Ca-phosphonate material binds to the surface of the cement grains inhibiting further hydration by acting as a diffusion barrier to water as well as a nucleation inhibitor.

Figure 3: Schematic representation of the H₆ntmp inhibition of cement showing (a) the phosphonic acid promoting calcium dissolution, allowing water and gypsum to react with the aluminum phases at the surface of the cement grain, (b) the formation of a meta-stable calcium phosphonate, which precipitates onto the hydrating aluminate surfaces (c), forming a barrier to water and sulfate diffusion. Adapted from M. Bishop, PhD Thesis, Rice University, 2001.