Anita R. Iskandar, Filippo Zanetti, Athanasios Kondylis, Florian Martin, Alain Sewer, Laura Ortega Torres, Shoaib Majeed, Sandro Steiner, Emmanuel Guedj, Celine Merg, Thomas Schneider, Keyur Trivedi, Stefan Frentzel, Nikolai V. Ivanov, Manuel C. Peitsch, Julia Hoeng
PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud 5, CH-2000 Neuchâtel, Switzerland
The impacts of an acute exposure to cigarette smoke (CS) and to aerosol from a novel electronic cigarette (EC) device using MESH™ technology were assessed using human organotypic buccal epithelial cultures and small airway epithelial cultures. A paired design was implemented: in parallel to the exposure to CS or EC aerosol, cultures were also exposed to air in the same exposure module. Tissue damage was not seen in cultures exposed to the IQOS MESH™ Classic Tobacco aerosol despite resulting in greater concentrations of deposited nicotine. In buccal cultures, CS and IQOS MESH™ Classic Tobacco aerosol elicited different infammatory response.
Introduction and Objectives
The harm of cigarette smoke (CS) exposure to both the lower and upper respiratory tracts is widely known. Electronic cigarette (EC) exposure has been suggested to exert less harm compared with CS exposure. Many studies have assessed the potential toxicity of ECs in vitro. However, most studies tested the effects of the liquid formulations applied directly on cell cultures but not the effects of the formulations applied as a vapor/aerosol. In this study, using human organotypic buccal and small airway epithelial cultures, we examined the effects of an acute exposure to whole aerosol generated by a novel EC device, using MESH™ technology, and to whole mainstream CS. Nine independent exposure experiments were conducted. In each experiment, cultures were exposed at the air-liquid interface to undiluted aerosol of “Classic Tobacco” favor generated from the novel EC for 112 puffs or to diluted CS for the same puff number in Vitrocell® exposure systems. Deposited nicotine concentrations in the exposure chamber were measured as an exposure marker. Using systems toxicology, we complemented histological analysis with quantitative analysis of molecular changes within 48 hours following exposure (global expression proles of both mRNA and miRNA and targeted protein proles, including secretory proteins).