Abstract
Phthalate esters (PAEs), ubiquitous plastic additives, have emerged as persistent contaminants in aquatic ecosystems, yet their propagation from molecular initiating events to ecosystem-level collapse remains poorly integrated. This review synthesizes current knowledge on the source-to-sink dynamics of PAEs, revealing a critical paradox in their bioaccumulation patterns: unlike classical persistent organic pollutants, high molecular weight PAEs exhibit distinct trophic dilution rather than biomagnification along food webs, driven by metabolic biotransformation in higher trophic organisms. Despite this dilution, PAEs trigger a bottom-up toxicity cascade. Driven by molecular initiating events, PAEs induce a range of adverse effects at the individual level, including immunotoxicity, neurotoxicity, endocrine disruption, metabolic dysfunction, and trans-trophic oxidative stress. Crucially, prolonged exposure drives epigenetic reprogramming, which reduces reproductive output, thereby threatening long-term population recruitment. These individual and population deficits could escalate into higher ecological consequences, specifically by diminishing benthic biological control over phytoplankton, dampening energy transfer efficiency, and simplifying community structure, thereby posing a potential threat to primary productivity and aquatic ecosystem sustainability. Despite recent advances, critical knowledge gaps remain, particularly regarding their cascading impacts on ecosystem services, as well as synergistic interactions between PAEs and other contaminants. In order to validate laboratory results with actual ecological risk assessments, future research should incorporate multi-scale models and quantitative adverse outcome Pathways as well as their synergistic interactions between PAEs and other contaminants, and advanced in vitro systems such as organoids. Resolving these issues is essential to reducing the risks that PAEs pose to aquatic environments.