This study investigated the degradation characteristics and conducted a risk assessment of four pesticides (Diniconazole, Dinotefuran, Metconazole, and Tebuconazole) in the leaves and roots of radish. Radish was cultivated in two greenhouse fields, and samples were collected at 0, 1, 2, 3, 5, 7, and 10 days after pesticide application. Sample analysis was performed using LC-MS/MS, and the recovery rates ranged from 70.1% to 118.6%. The biological half-life of Diniconazole was found to be 6.2 days (leaf and root), Dinotefuran was 5.3 days (leaf) and 4.6 days (root), Metconazole was 9.3 days (leaf) and 3.2 days (root), and Tebuconazole was 8.0 days (leaf) and 5.1 days (root). After comparing the maximum residue limits (MRL) of each pesticide in Korea with the residues during the pre-harvest interval (PHI), Diniconazole showed a Hazard quotient (HQ) exceeding 1, indicating potential risks for true consumers. Furthermore, Tebuconazole showed an HQ of 0.3 or higher, indicating a significant level of risk.

The widespread application of pesticides in agriculture has raised increasing concerns regarding their ecological impact, particularly in aquatic environments. Among these, α-cypermethrin, a highly active isomeric form of cypermethrin, has been extensively used due to its potent insecticidal efficacy and low mammalian toxicity. However, its toxicity to non-target aquatic organisms remains insufficiently understood at the metabolic level. In this study, a targeted metabolomics approach was employed to investigate the biochemical effects of α-cypermethrin in adult zebrafish. Acute toxicity was first determined to establish sublethal exposure concentrations (0.15 µg/L and 1.5 µg/L), followed by a 48 h exposure under a controlled flow-through system. GC-MS/MS-based analysis quantified 395 metabolites, and multivariate statistical models (principal component analysis (PCA) and partial least square-discriminant analysis (PLS-DA)) revealed clear dose-dependent metabolic alterations at two time points. Pathway analysis identified disruptions in glycolysis, glycerolipid metabolism, amino acid turnover, and glutathione pathways. Notably, glutamate depletion and associated reductions in GABA (4-Aminobutanoate) and TCA (Tricarboxylic acid) cycle intermediates suggest oxidative stress-induced metabolic bottlenecks. These results provide mechanistic insights into α-cypermethrin-induced toxicity and demonstrate the utility of metabolite-level biomarkers for environmental monitoring. This study contributes to a systems-level understanding of how sublethal pesticide exposure affects vertebrate metabolism, offering a basis for improved ecological risk assessment and pesticide regulation.