Developmental disturbances and deformities in 4th-instar larvae and emerging adults induced by chronic 6 PPD-quinone exposure in the aquatic midge Chironomus riparius

N-(1,3-dimethylbutyl)-N′-phenyl- p -phenylenediamine-quinone(6PPD-Q), a ubiquitous aquatic contaminant formed through oxidative transformation of the tire rubber additive N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine (6PPD), is toxic to aquatic organisms. Despite its environmental prevalence, its chronic toxicity to freshwater invertebrates largely unknown. We examined the acute and chronic toxicological effects of 6PPD-Q on the freshwater midge Chironomus riparius across multiple biological, biochemical, and molecular endpoints. Acute toxicity assays yielded 24-h and 48-h LC 50 values exceeding 1,000 μg L -1 , demonstrating low acute hazard. Conversely, chronic exposure reduced survival, delayed developmental, decreased emergence rate. Exposure to 300 μg L -1 6PPD-Q significantly reduced emergence rate ( p < 0.05), whereas 30 and 300 μg L -1 delayed adult emergence by 4–5 days. Pupal survival declined dose-dependently and significantly at 300 μg L -1 ( p < 0.05). Morphological abnormalities including wing and leg deformities were evident in emerged adults. 6PPD-Q significantly elevated superoxide dismutase (SOD) activity across all treatment concentrations ( p < 0.01), whereas catalase (CAT) activity was significantly increased only at 300 μg L -1 ( p < 0.05). Exposure to 6PPD-Q significantly downregulated expression of the ecdysteroid receptor gene ultraspiracle protein ( USP ) at 30 and 300 μg L -1 ( p < 0.01). These findings indicate that 6PPD-Q may interfere with antioxidant defense and USP-associated molting regulation. Further mechanistic studies and risk management strategies are warranted.