Failure mechanism of zinc adipate as a β-nucleating agent for polypropylene in the presence of calcium stearate

Although zinc dicarboxylic acids are highly effective beta-nucleating agents (beta-NAs), they lose their beta-nucleating ability in isotactic polypropylene (iPP) upon the addition of calcium stearate (CaStr(2)). In this study, we investigated the failure mechanism of these p-NAs in terms of the chemical and physical interactions of zinc adipate (ZnAA) with CaStr(2). No chemical reaction occurs between CaStr(2) and ZnAA; rather, it is the physical interactions between this beta-NA and CaStr(2) that are responsible for the loss of beta-nucleating ability. Based on the experimental findings and molecular dynamics (MD) simulations, we suggest a blocking effect of CaStr(2) on nucleation as a possible failure mechanism. MD simulations confirmed that the aggregation of CaStr(2) on the beta-NA surface, observed experimentally using polarized optical microscopy and scanning electron microscopy, resulted from the binding energy for the interaction between ZnAA and CaStr(2) being higher than that for iPP/CaStr(2). Because the active nucleation sites on the surface of the beta-NA were covered, lattice matching between ZnAA and the iPP chains was hindered. Therefore, the addition of CaStr(2) weakens the beta-nucleating ability of ZnAA, leading to inhibition of the epitaxial crystallization process, thereby decreasing the degree of beta-crystal formation and, consequently, lowering the toughness of the resulting iPP.

Automated summary

The physical interactions between zinc adipate and calcium stearate result in the loss of beta-nucleating ability, blocking the nucleation sites and hindering lattice matching in isotactic polypropylene. This leads to inhibition of the epitaxial crystallization process, decreasing the degree of beta-crystal formation and lowering the toughness of the resulting iPP.