p-Phenylenediamines (PPDs) have been extensively used in the rubber industry and found to be pervasive in various environmental compartments for decades, while their transformation products and associated ecological and human health risks remain largely unknown. Herein, we developed and implemented a mass spectrometry-based platform combined with self-synthesized standards for the investigation of rubber-derived quinones formed from PPD antioxidants. Our results demonstrated that five quinones are ubiquitously present in urban runoff, roadside soils, and air particles. All of the identified sources are closely related to mankind’s activities. Among the identified quinones, N-(1,3-dimethylbutyl)-N′-phenyl-p-phenylenediamine quinone has been recently found to be highly toxic, causing acute mortality of coho salmon in the Pacific Northwest. Ultrahigh-performance liquid chromatography coupled with triple quadrupole mass spectrometry was then applied for quantification of the five quinones and their corresponding PPD antioxidants. The results revealed interesting distinct distribution and concentration patterns of PPD-derived quinones in different environmental matrices. Daily intake rates of these quinones in a compact city of Hong Kong were estimated to be varied from 1.08 ng/(kg·day) for adults to 7.30 ng/(kg·day) for children, which were higher than the exposure levels of their parent compounds. Considering the prevalence of the use of rubber products, the outcome of this study strongly suggests for additional toxicological studies to investigate potential ecological and human health risks of the newly discovered quinones.

Plastic debris in the global biosphere is an increasing concern, and nanoplastic (NPs) toxicity in humans is far from being understood. Studies have indicated that NPs can affect mitochondria, but the underlying mechanisms remain unclear. The liver and lungs have important metabolic functions and are vulnerable to NP exposure. In this study, we investigated the effects of 80 nm NPs on mitochondrial functions and metabolic pathways in normal human hepatic (L02) cells and lung (BEAS-2B) cells. NP exposure did not induce mass cell death; however, transmission electron microscopy analysis showed that the NPs could enter the cells and cause mitochondrial damage, as evidenced by overproduction of mitochondrial reactive oxygen species, alterations in the mitochondrial membrane potential, and suppression of mitochondrial respiration. These alterations were observed at NP concentrations as low as 0.0125 mg/mL, which might be comparable to the environmental levels. Nontarget metabolomics confirmed that the most significantly impacted processes were mitochondrial-related. The metabolic function of L02 cells was more vulnerable to NP exposure than that of BEAS-2B cells, especially at low NP concentrations. This study identifies NP-induced mitochondrial dysfunction and metabolic toxicity pathways in target human cells, providing insight into the possibility of adverse outcomes in human health.