Polychlorinated naphthalenes (PCNs) are widely distributed in the aquatic environment and can be transmitted through the food chain, which can amplify their toxic effects on human. To inhibit their transmission in the trophic level, this study aimed to predict the joint toxicity mechanism of polychlorinated naphthalenes (PCNs) to the key organisms and control scheme of its toxicity in the aquatic food chain (green algae-Daphnia magna-fish). The toxic effect grade and mode of action (MoA) of PCNs on the food chain were first predicted to guide the establishment of toxic mechanism model. QSAR models were constructed to quantify the mechanism of aquatic toxicity due to PCNs. The results showed the PCN compounds studied were highly toxic at all the trophic levels of the aquatic food chain. The binding ability of PCNs to the aquatic organisms was the main factor causing the toxicity of PCNs in the food chain, followed by electronic parameters E_HOMO and E_LUMO. Moreover, the binding ability between PCNs and food chain receptors was related to the molecular hydrophobicity, the hydrophobicity can be changed by adjusting the ability of PCNs to be adsorbed by sediment and their chlorine substituents, while the effect of PCNs electronic parameters (E_HOMO and E_LUMO) can be adjusted by their solvation effect. In addition, the macro-control scheme of PCN-based aquatic toxicity mechanism was established, and the molecular dynamics (MD) simulation confirmed its effectiveness and accessibility. The MD simulation showed the inhibition effect of nutrition-grade toxicity in the food chain was significant when the external stimulation conditions of solvation, anaerobic dechlorination and molecular adsorption were improved, with the decrease range of 66.26–263.16%, 198.93–323.98% and 189.24–549.48%, respectively. This work reveals new insights into the mechanism of PCNs joint toxicity to aquatic ecosystem food chain and develop appropriate strategies for its ecological risk management.

多氯萘（PCN）在水生环境中广泛分布，并可以通过食物链传播，从而放大了它们对人体的毒性作用。为了抑制它们在营养水平上的传播，本研究旨在预测多氯萘（PCNs）对关键生物的联合毒性机制及其在水生食物链（绿藻-大水蚤）中的毒性控制方案。-鱼）。首先预测了PCNs在食物链上的毒性作用等级和作用方式（MoA），以指导毒性机制模型的建立。构建了QSAR模型以量化PCN引起的水生毒性机理。结果表明，所研究的PCN化合物在水生食物链的所有营养水平上均具有剧毒。PCN与水生生物的结合能力是引起PCN在食物链中毒性的主要因素，其次是电子参数E _HOMO和E _LUMO。此外，PCNs与食物链受体之间的结合能力与分子疏水性有关，可以通过调节PCNs被沉积物及其氯取代基吸附的能力来改变疏水性，而PCNs的电子参数（E _HOMO和Ë _LUMO）可以通过其溶剂化效果进行调整。此外，建立了基于PCN的水生毒性机理的宏观调控方案，并通过分子动力学（MD）仿真验证了其有效性和可及性。分子动力学模拟表明，改善溶剂化，厌氧脱氯和分子吸附等外部刺激条件，对食物链营养级毒性的抑制作用显着，下降幅度分别为66.26-263.16％，198.93-323.98％和189.24。分别为–549.48％。这项工作揭示了PCNs对水生生态系统食物链的联合毒性机理的新见解，并为其生态风险管理制定了适当的策略。