Mechanistic-based constitutive modeling of oxidative aging in aging-susceptible materials and its effect on the damage potential of asphalt concrete

Abstract Oxidative aging is one of the most important factors in reducing the fatigue damage resistance of aging-susceptible materials such as bituminous materials and asphalt concrete. This study proposes a mechanistic-based phenomenological oxidative aging (or oxidative hardening) model by introducing a physically-based oxidative aging internal state variable which captures the effect of aging on the viscoelastic, viscoplastic, and viscodamage responses of aging-susceptible materials, especially bituminous materials. The proposed aging model is formulated as a function of the diffused oxygen content and temperature evolution which ties the mechanical response of aged material to the underlying physics happening during the oxidative aging of asphalt concrete. Phenomenologically, the evolution of the aging internal state variable in asphalt concrete is related to the rate of carbonyl formation during the aging process of the asphalt binder. It is argued that oxidative aging mostly affects the viscous behavior of the aged material, such that the viscosity model parameters in the coupled nonlinear-viscoelastic, viscoplastic, and viscodamage constitutive models are defined as a function of the aging state variable. The qualitative capabilities of the model in capturing the effect of aging on mechanical response of asphalt concrete are verified against a wide range of simulations that include single creep, creep-recovery, repeated creep-recovery, monotonic tension and compression, uniaxial tensile and compressive loading–unloading, and relaxation tests as well as against the rutting performance simulations of an asphalt layer. It is shown that the proposed aging model predicts proper trends for the effect of oxidative hardening on the various mechanical properties of the asphalt concrete, such as the increase in the stiffness and strength, the decrease in ductility, and early initiation and rapid evolution of damage with aging.

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