Di-(2-ethylhexyl) phthalate (DEHP), a widely utilized plasticizer, has been increasingly associated with cardiovascular risks. However, the involvement of DEHP in abdominal aortic aneurysm (AAA) remains unclear. To address this gap, C57BL/6 J mice were intragastrically administered with DEHP for 4 weeks in a CaCl₂-induced AAA model. We found that DEHP exacerbated AAA progression, as evidenced by a notable enlargement in the maximal diameter of the abdominal aorta, enhanced vascular inflammation, and accelerated elastin degradation. In vitro experiments confirmed that DEHP, along with its primary metabolite mono-(2-ethylhexyl) phthalate (MEHP), induced M1 macrophage polarization, leading to increased secretion of inducible nitric oxide synthase (iNOS), matrix metalloproteinase-9 (MMP9), and pro-inflammatory factors, including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). Mechanistically, we demonstrated that DEHP and MEHP triggered the activation of the nuclear factor-kappa B (NF-κB) pathway by upregulating phosphorylated p65 and inducing p65 nuclear translocation, which drove M1 macrophage polarization. These findings were further confirmed using a mouse AAA model in vivo. Additionally, DEHP and MEHP promoted the proliferation and migration of primary human aortic vascular smooth muscle cells (VSMCs). Phenotypic switching of VSMCs was markedly accelerated following DEHP and MEHP treatment, potentially through the PI3K-AKT pathway, as characterized by reducing contractile markers (ACTA2 and CNN1) and enhancing proliferative markers (PCNA and SPP1). Overall, our study underscores the pivotal role that DEHP plays in exacerbating AAA by promoting M1 macrophage polarization and VSMCs phenotypic switching, which provides new insights into the adverse health effects of environmental pollution-relevant cardiovascular disease progression.