Recent screening surveys have shown the presence of unknown source halogenated organic compounds (HOCs) in shale gas wastewater. However, their occurrence, profile, transport in surrounding surface water and environmental risk potentials remain unclear. Here, a method for the extraction and quantitative determination of 13 HOCs in water by solid phase extraction combined with gas chromatography-mass spectrometry (GC-MS) was established. All of the targeted HOCs were detected and peaked at the outfall, while these contaminants were generally not detected in samples upstream of the outfall, suggesting that these contaminants originated from the discharge of shale gas wastewater; this was further supported by the fact that these pollutants were generally detected in downstream samples, with a tendency for pollutant concentrations to decrease progressively with increasing distance from the outfall. However，different HOCs had different transport potential in water. In addition, the toxicological effects of typical HOCs were evaluated using HepG2 as a model cell. The results indicated that diiodoalkanes suppressed HepG2 cell proliferation and induced ROS generation in a concentration-dependent manner. Mechanistic studies showed that diiodoalkanes induced apoptosis in HepG2 cells via the ROS-mediated mitochondrial pathway, decreasing mitochondrial membrane potential and increasing intercellular ATP and Ca2+ levels. On the other hand, RT-qPCR and Western blot assays revealed that the SLC7A11/GPX4 signaling pathway and HO-1 regulation of ferritin autophagy-dependent degradation (HO-1/FTL) pathway were involved in the ferroptosis pathway induced by diiodoalkane in HepG2 cells. Our study not only elucidates the contamination profiles and transport of HOCs in surface water of typical shale gas extraction areas in China, but also reveals the toxicity mechanism of typical diiodoalkane.
Keywords: Diiodoalkane; Ferroptosis; Halogenated organic compounds; Shale gas wastewater.
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