title: Cigarette smoke but not electronic cigarette aerosol activates a stress response in human coronary artery endothelial cells in culture.
abstract: It is generally acknowledged that e-cigarettes are unlikely to be as harmful as conventional cigarettes, but there is little data that quantifies their relative harms. We investigated the biological response to e-cigarette aerosol exposure (versus conventional cigarette smoke exposure) at the cellular level, by exposing human coronary artery endothelial cells (HCAEC) to aqueous filtered extracts of e-cigarette aerosol or cigarette smoke and looking at gene expression changes consistent with a stress response. This included genes controlled by the oxidant-stress sensing transcription factor NFR2 (NFE2L2), and cytochrome P450 family members.
  
  
  
  Cigarette smoke extract (CSE) was created using mainstream smoke from a single cigarette drawn through 10ml of endothelial cell growth media MV2. Electronic cigarette aerosol extract (eCAE) was created using the same apparatus, using a constant power output of 10.8w (4.2V) and 18mg/ml nicotine solution. eCAE was generated using 5 cycles of 5s heat with at least 10s in between each puff to allow the coil to cool, air being drawn through the device at 70ml/minute.
  
  
  
  HCAEC responded to the noxious components in CSE, resulting in activation of NRF2 and upregulation of cytochrome p450. However, eCAE did not induce NRF2 nuclear localisation, upregulation of NRF2-activated genes, or the upregulation of cytochrome p450.
  
  
  
  The use of e-cigarettes as a substitute for conventional cigarettes is likely to reduce immediate tobacco-related harm, at least with respect to cardiovascular harms.
authors.affiliation: School of Clinical Sciences, University of Bristol, Bristol, UK.
authors.forename: Jack E
authors.initials: JE
authors.lastname: Teasdale
authors.affiliation: School of Clinical Sciences, University of Bristol, Bristol, UK.
authors.forename: Andrew C
authors.initials: AC
authors.lastname: Newby
authors.affiliation: MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK; School of Social and Community Medicine, University of Bristol, Bristol, UK.
authors.forename: Nicholas J
authors.initials: NJ
authors.lastname: Timpson
authors.affiliation: MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK; UK Centre for Tobacco and Alcohol Studies, School of Experimental Psychology, University of Bristol, Bristol, UK. Electronic address: marcus.munafo@bristol.ac.uk.
authors.forename: Marcus R
authors.initials: MR
authors.lastname: Munafò
authors.affiliation: School of Clinical Sciences, University of Bristol, Bristol, UK.
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: White
mesh_terms: D000336:Aerosols / Q000009:adverse effects*; D002478:Cells, Cultured; D003331:Coronary Vessels / Q000187:drug effects* / Q000378:metabolism; D066300:Electronic Nicotine Delivery Systems / Q000009:adverse effects*; D042783:Endothelial Cells / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D012906:Smoke / Q000009:adverse effects*; D012907:Smoking / Q000009:adverse effects; D062789:Tobacco Products
chemical_list: D000336:Aerosols; D012906:Smoke
keywords: Cigarettes; E-cigarettes; Human coronary artery cells; Stress response