Acute toxicity and health effect of perfluoroisobutyronitrile on mice: a promising substitute gas-insulating medium to SF6.

Perfluoroisobutyronitrile (C4F7N) is a new eco-friendly gas insulation medium that has potential to replace the most greenhouse gas sulfur hexafluoride (SF6) used in power industry. In order to ensure the engineering application safety, an in-depth assessment of the acute inhalation toxicity of C4F7N gas mixture is required. This article revealed gender differences in male and female mice after exposure to C4F7N and the physiological recovery characteristics of surviving mice by means of 4 h acute inhalation toxicity tests, hematological determinations and histopathological examination. Comparative analysis on the toxicity of C4F7N on mice and rats is also evaluated. We find that the LC50 of C4F7N for male and female mice is 1175 ppm (4 h), 1380 ppm (4 h) and female ones are more tolerant to C4F7N. Mice that exposed to 1000 ppm C4F7N for 4 h could survive and return to their normal state after the 14-day observation period without irreversible damage. The toxic effect duration of C4F7N on rats is longer than that of mice. Relevant results revealed the acute inhalation toxicity of C4F7N systematically and provided fundamental reference for inhalation safety protection and engineering application.

Mechanistic study of C5F10O-induced lung toxicity in rats: An eco-friendly insulating gas alternative to SF6.

The global warming and other environmental problems caused by SF6 emissions can be reduced due to the widespread use of eco-friendly insulating gas, perfluoropentanone (C5F10O). However, there is an exposure risk to populations in areas near C5F10O equipment, so it is important to clarify its biosafety and pathogenesis before large-scale application. In this paper, histopathology, transcriptomics, 4D-DIA proteomics, and LC-MS metabolomics of rats exposed to 2000 ppm and 6000 ppm C5F10O are analyzed to reveal the mechanisms of toxicity and health risks. Histopathological shows that inflammatory cell infiltration, epithelial cell hyperplasia, and alveolar atrophy accompanied by alveolar wall thickening are present in both low-dose and high-dose groups. Analysis of transcriptomic and 4D-DIA proteomic show that Cell cycle and DNA replication can be activated by both 2000 ppm and 6000 ppm C5F10O to induce cell proliferation. In addition, it also leads to the activation of pathways such as Antigen processing and presentation, Cell adhesion molecules and Complement and coagulation cascades, T cell receptor signal path, Th1 and T cell receptor signal path, Th1 and Th2 cell differentiation, complement and coagulation cascades. Finally, LC-MS metabolomics analysis confirms that the metabolic pathways associated with glycerophospholipids, arachidonic acid, and linoleic acid are disrupted and become more severe with increasing doses. The mechanism of lung toxicity caused by C5F10O is systematically expounded based on the multi-omics analysis and provided biosafety references for further promotion and application of C5F10O.