Environmental co-exposure to microplastics and phenol may influence redox signaling and tumor microenvironment dynamics.

Environmental exposure patterns have shifted from single-compound exposure to complex co-exposure scenarios. Among widespread pollutants, microplastics (MPs) and phenol may interact biologically despite their distinct physicochemical properties. Phenol is associated with oxidative stress-related toxicity, whereas MPs may serve as potential carriers and redox-active modifiers. This review proposes that MP-induced oxidative stress and phenol-mediated antioxidant disruption may jointly reshape redox-sensitive intracellular signaling under MPs-phenol co-exposure conditions, with mitogen-activated protein kinase (MAPK) pathways proposed as potential convergence nodes. Within this framework, MAPK signaling may link oxidative stress to hypoxia-inducible factor 1α (HIF-1α) stabilization, angiogenic responses, and tumor-associated processes, and may also facilitate NF-κB/STAT3-mediated inflammatory signaling and PD-L1 regulation. Because direct experimental evidence for these integrated mechanisms remains limited, this framework should be regarded as a biologically plausible and testable model rather than a confirmed causal pathway. This review highlights key knowledge gaps and future priorities for evaluating how complex environmental co-exposures may influence cancer progression and immune regulation.