The development of copper-based materials with a high efficiency and low cost is desirable for use in iodine (I₂) remediation. Herein, Cu⁰-nanoparticles-functionalized, ZIF-8 (Zeolite Imidazole Framework-8)-derived, nitrogen-doped carbon composites (Cu@Zn-NC) were synthesized by ball milling and pyrolysis processes. The as-prepared composites were characterized using SEM, BET, XRD, XPS, and FT-IR analyses. The results showed that the morphology of ZIF-8 changed from a leaf-like structure into an irregular structure after the introduction of a copper salt and carbonization. The copper in the pyrolysis samples was mainly in the form of Cu⁰ particles. The presence of an appropriate amount of Cu⁰ particles could increase the specific surface area of Cu@Zn-NC. The subsequent batch adsorption results demonstrated that the as-fabricated composites showed high I₂ adsorption amounts (1204.9 mg/g) and relatively fast dynamics in an iodine–cyclohexane solution when the Cu content was 30% and the pyrolysis temperature was 600 °C, outperforming the other Cu-based materials. The isothermal adsorption followed both Langmuir and Dubinin–Radushkevich isotherm models, while the kinetics of I₂ adsorption followed a pseudo-second-order kinetic model. The activation energy (E_α) of the adsorbent was determined to be 47.2 kJ/mol, according to the Arrhenius equation. According to the experimental and DFT analyses, I₂-Zn interactions and I₂-Cu⁰ chemisorption jointly promoted the elimination of iodine. In general, this study provided an operative adsorbent for the highly effective capture of iodine in solution, which might be worth applying on a large scale.

Chlorophenylacetonitriles are known as one of the emerging nitrogenous disinfection byproducts (N-DBPs) in chlorinated drinking water due to their concerned cytotoxicity and genotoxicity compared to regulated carbonaceous DBPs. However, under low-dose exposure, the in vivo pathological consequences of chlorophenylacetonitriles remain largely unresolved. Here, C57BL/6J mice were exposed to 2-chlorophenylacetonitrile (2-CPAN) via drinking water (100 ug/L) for six months, and an integrated histopathological and genome-wide transcriptomic approach was employed to mechanistically characterize its multi-organ toxicological consequences. 2-CPAN ingestion significantly suppressed body weight (35.9 ± 2.0 g vs. 47.6 ± 11.6 g, p < 0.05) and induced severe gastroenteropathy—including gastric lamina propria inflammatory infiltration, intestinal villous blunting, crypt disorganization, transmural mononuclear infiltration, and abrogating epithelial barrier integrity. Intestinal barrier failure drove portal translocation of luminal PAMPs, potentially triggering splenic white pulp atrophy, red/white pulp boundary dissolution, and parenchymal changes consistent with fibrotic remodeling. Splenic RNA sequencing revealed a bipartite transcriptomic reprogramming: upregulated pathways were enriched in the ribosome, MAPK signaling, cytokine–cytokine receptor interaction, and chemokine signaling pathways. A proteotoxic stress module (Hspa1a, 9.4-fold; Hspa1b, 10.2-fold) and a chemokine effector hub (Ccl2, 3.43-fold; Ccl5, 2.9-fold; Ccl19, 2.58-fold; Ccl21a, 2.15-fold) were identified by the STRING network. Downregulated pathways converged on cell cycle suppression, with concurrent loss of Ccne1/Ccne2 and Cdc6 (G1/S block), Ccnb1 and Plk1 (G2/M arrest), and Rrm2/Tars3/TrnM (dNTP and aminoacyl-tRNA starvation), collectively forcing splenic lymphocytes into irreversible proliferative failure. These findings provide the first mechanistically resolved in vivo evidence that chronic 2-CPAN exposure drives a potential gut–spleen toxicological axis, underscoring the urgent need to incorporate organ endpoints by long-term exposure into N-DBP risk assessment.