Detection of the Destruction Mechanism of Perfluorinated Elastomer (FFKM) Network under Thermo-oxidative Aging Conditions

The changes of crosslinking network of perfluorinated elastomer (FFKM) cured by TAIC and DBPH under thermo-oxidative aging conditions were investigated. Two competitive processes including post-curing and network destruction occur simultaneously, which directly affect the storage modulus and crosslinking density. With the increase of aging temperature, the network destruction becomes dominant. FTIR and XPS characterizations further reveal that the network destruction happens preferentially on the crosslink points of TAIC structure, and the post-curing is mainly caused by the decomposition of residual curing agent DBPH. Unlike the easier breaking of TAIC structure in the crosslinking network, both the backbone and the pendent groups of FFKM itself are much more stable. To further figure out the destruction mechanism, TGA-FTIR-GC-MS test was also conducted and a schematic degradation process of TAIC structure was proposed. It is found that the destruction of TAIC crosslinking points happens first on the unstable exocyclic C-N bonds and the intermediate ring radicals could eventually decompose into volatile hydrogen isocyanate (HCNO) under extreme condition.

Automated summary

The changes in the crosslinking network of perfluorinated elastomer (FFKM) cured by TAIC and DBPH under thermo-oxidative aging conditions were studied. The network destruction becomes dominant with increasing aging temperature, mainly occurring on the crosslink points of TAIC structure. The post-curing is mainly caused by the decomposition of residual curing agent DBPH. TGA-FTIR-GC-MS test reveals that the destruction of TAIC crosslinking points occurs first on the unstable exocyclic C-N bonds. A schematic degradation process of TAIC structure was proposed.