Effects of gas phase extract of cigarette smokegenerated from heated tobacco and burned cigarette on human vascularendothelial cells

Abstract

The present study established a method to prepare heated tobacco-derivedcigarette smoke extract (hCSE) and burned cigarette-derived CSE (bCSE), andcompared their effects on human umbilical vein endothelial EA.hy926 cells. Threetypes of tobacco heating devices (Ploom S, glo, and IQOS) were used in order togenerate cigarette smoke at different heating temperatures. hCSE and bCSE wereprepared using the puffing regimen parameters of the CORESTA approach (55 mLpuff volume, 3 sec puff duration, and 1 puff every 30 sec). Tar phase (nicotineand tar) of cigarette smoke was removed by passing through a Cambridge glassfiber filter. The rank order of amounts of nicotine and tar trapped on theCambridge filter was Ploom S (6 ± 1 mg/91 puffs) < glo (16 ± 1 mg/91 puffs)< IQOS (56 ± 3 mg/91 puffs) < hi-lite (228 ± 2 mg/91 puffs). Crude hCSEand bCSE caused a decrease in mitochondrial metabolic activity and theexpression level of endothelial nitric oxide synthase, with the rank order ofpotency as follows: Ploom S < glo < IQOS < hi-lite. The reduction inmitochondrial metabolic activity was diminished by removing nicotine and tarfrom cigarette smoke with Cambridge filter. These results indicated that highercytotoxicity of cigarette smoke to vascular endothelial cells were correlatedwith higher heating/burning temperatures [Ploom S (200℃) < glo (240℃) <IQOS (300−350℃) < hi-lite (770−870℃)].