Advanced in vitro exposure systems.

Exposure to aerosols from electronic cigarettes using the MESH™ technology has a reduced biological impact on bronchial epithelial cell cultures compared with exposure to cigarette smoke

11. Aug. 2019

Gordon Research Conference, Integration of Emerging Technologies in Mechanistic and Translational Toxicology,Andover, August 11–16, 2019

Albert Giralt, Florian Martin, Anita R. Iskandar, Alain Sewer, Laura Ortega Torres, AthanasiosKondylis, Patrice Leroy, Celine Merg, ShoaibMajeed, Emmanuel Guedj, Thomas Schneider, KeyurTrivedi, Stefan Frentzel, Nikolai V. Ivanov, Manuel C. Peitsch, Julia Hoeng


PMI R&D, Philip Morris Products S.A., Quai Jeanrenaud5, CH-2000 Neuchâtel, Switzerland
 

In contrast to 3R4F CS exposure, exposure to IQOS MESH™ Classic Tobacco aerosols did not cause tissue damage or have an impact on ciliary beating functionality in bronchial epithelial cell cultures despite resulting in greater concentrations of deposited nicotine. Cultures exposed to IQOS MESH™ Classic Tobacco aerosols showed fewer changes in proteins involved in xenobiotic metabolism than those exposed to CS.

 

Introduction and objectives
The harmful effects of cigarette smoke (CS) exposure on the respiratory tract are widely known. Electronic cigarette (EC) exposure has been suggested to result in less harm than CS exposure. Many studies have assessed the potential toxicity  of  EC sinvitro. However, most studies have tested the effects of liquid formulations applied directly to cell cultures but not those of formulations applied as vapor/aerosols. In this study, we examined the effects of acute exposure of human bronchial organotypic epithelial cell cultures to whole aerosols generated by a novel EC device that uses MESH™ technology and to diluted CS from the 3R4F reference cigarette (RC). Six independent exposure experiments were conducted in VITROCELL® exposure systems. In each experiment, cell cultures were exposed at the air–liquid interface to undiluted “ClassicTobacco” aerosols generated from the EC for 28 or 112 puffs or to diluted CS for 112 puffs. Deposited nicotine concentrations in the exposure chamber were measured as an exposuremarker. Using a systems toxicology approach, we complemented our histological and functional findings with the results of quantitative analysis of molecular changes within a 48-hour recovery period following exposure (global mRNA expression profiles and targeted protein profiles, including those of secretory proteins).

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