Reactions of sulfoxides with reactive oxygen species to reveal the radical chemistry of pollution-derived particulate matter.

The radical reactions of dimethylsulfoxide (DMSO) and tetrahydrothiophene-1-oxide (THTO) with reactive oxygen species (ROS) in the presence of a nitroxide radical scavenger have been evaluated both synthetically and in analytical practice. Fenton-mediated generation of oxygen-centred radicals produced several unusual products that reflect the fragmentation and ring-opening radical mechanisms of DMSO and THTO respectively. Addition of pollution-derived ROS to DMSO/THTO nitroxide solutions produced LC-MS detectable amounts of the same products isolated from the larger-scaled Fenton reactions. For air pollution analysis, these results highlight the complexity surrounding DMSO reactivity and fragmentation, and indicate that THTO produces simpler outcomes that should facilitate analysis of the processes involved.

E-cigarettes induce toxicity comparable to tobacco cigarettes in airway epithelium from patients with COPD.

BACKGROUND: The health effects of e-cigarettes in patients with pre-existing lung disease are unknown. The aim of this study was to investigate whether aerosols from a fourth-generation e-cigarette produces similar in-vitro cytotoxic, DNA damage and inflammatory effects on bronchial epithelial cells (BECs) from patients with COPD, as cigarette smoke. METHODS: BECs from patients with COPD who underwent surgery for lung cancer and comparator (immortalised 16HBE) cells were grown at air liquid interface (ALI). BECs were exposed to aerosols from a JUUL® e-cigarette (Virginia Tobacco and Menthol pods at 5% nicotine strength) or reference 3R4F cigarette for 30 min at ALI. Cell cytotoxicity, DNA damage and inflammation were measured. RESULTS: In response to the Virginia Tobacco and Menthol flavoured e-cigarette aerosols, COPD BECs showed comparable LDH release (cell cytotoxicity, p = 0.59, p = 0.67 respectively), DNA damage (p = 0.41, p = 0.51) and inflammation (IL-8, p = 0.20, p = 0.89 and IL-6, p = 0.24, p = 0.93), to cigarette smoke. 16HBE cells also showed comparable cellular responses to cigarette smoke. CONCLUSION: In airway cells from patients with COPD, aerosols from a fourth-generation e-cigarette were associated with similar toxicity to cigarette smoke. These results have potential implications for the safety of e-cigarette use in patients with lung disease.