TY - JOUR
T1 - Electronic Nicotine Delivery Systems Exhibit LowerToxicity Compared to Cigarettes
T2 - "The Replica Study Experience"
AU - Distefano, Alfio
AU - Caruso, Massimo
AU - Emma, Rosalia
AU - Rust, Sonja
AU - Poulas, Konstantinos
AU - Zadjali, Fahad
AU - Boffo, Silvia
AU - Volarevic, Vladislav
AU - Mesiakaris, Konstantinos
AU - Karanasios, Georgios
AU - Al Tobi, Mohammed
AU - Albalushi, Najwa
AU - Giordano, Antonio
AU - Canciello, Angelo
AU - Arsenijevic, Aleksandar
AU - Ilic, Aleksandar
AU - Caruso, Tancredi
AU - Carota, Giuseppe
AU - Spampinato, Maria R.
AU - Zuccarello, Pietro
AU - Ferrante, Margherita
AU - Polosa, Riccardo
AU - Li Volti, Giovanni
N1 - Publisher Copyright:
© FASEB.
PY - 2022/5/1
Y1 - 2022/5/1
N2 - Electronic nicotine delivery systems (ENDS) can reduce the health risks associated with chronic smoke exposure, and their potential benefits are the subject of intense scientific debate. The international "Replica Study Group" replicated independently three relevant studies from the tobacco industry on the cytotoxic and inflammatory effects of cigarette smoke and ENDS aerosol. Our primary goal was to establish the reliability of the results and the robustness of the conclusions. In order to assess cytotoxicity of smoke and aerosol, we exposed human bronchial epithelial cell (H292) to cigarette smoke and to ENDS aerosol at air-liquid interface (ALI). Moreover, we aimed to assess different inflammatory and remodeling mediators release (IL-6, IL-8 and MMP-1) from cells exposed to whole smoke (WS) and to smoke deprived of total particulate matter (vapor phase; VP). We were able to replicate the results obtained in the original studies on cytotoxicity confirming that almost 80% of the cytotoxic effect of smoke is due to the vapor phase of smoke. Moreover, our results substantiated the significantly reduced cytotoxic effects of ENDS aerosol vs. cigarette smoke. However, our data were notably different in terms of inflammatory and remodeling activity triggered by smoke. Altogether, the data obtained independently in different laboratories clearly confirm the reduced toxicity of ENDS products compared to smoke, thus providing a valuable tool to the harm reduction strategies in smokers. Otherwise, we were not able to replicate the results on inflammatory and remodeling mediators released from smoke exposed cells. This could be due to the lack of normalization of the quantity of cytokines released, with the number of viable cells, in the original paper, since the production of cytokines itself requires the metabolic capability of cells.
AB - Electronic nicotine delivery systems (ENDS) can reduce the health risks associated with chronic smoke exposure, and their potential benefits are the subject of intense scientific debate. The international "Replica Study Group" replicated independently three relevant studies from the tobacco industry on the cytotoxic and inflammatory effects of cigarette smoke and ENDS aerosol. Our primary goal was to establish the reliability of the results and the robustness of the conclusions. In order to assess cytotoxicity of smoke and aerosol, we exposed human bronchial epithelial cell (H292) to cigarette smoke and to ENDS aerosol at air-liquid interface (ALI). Moreover, we aimed to assess different inflammatory and remodeling mediators release (IL-6, IL-8 and MMP-1) from cells exposed to whole smoke (WS) and to smoke deprived of total particulate matter (vapor phase; VP). We were able to replicate the results obtained in the original studies on cytotoxicity confirming that almost 80% of the cytotoxic effect of smoke is due to the vapor phase of smoke. Moreover, our results substantiated the significantly reduced cytotoxic effects of ENDS aerosol vs. cigarette smoke. However, our data were notably different in terms of inflammatory and remodeling activity triggered by smoke. Altogether, the data obtained independently in different laboratories clearly confirm the reduced toxicity of ENDS products compared to smoke, thus providing a valuable tool to the harm reduction strategies in smokers. Otherwise, we were not able to replicate the results on inflammatory and remodeling mediators released from smoke exposed cells. This could be due to the lack of normalization of the quantity of cytokines released, with the number of viable cells, in the original paper, since the production of cytokines itself requires the metabolic capability of cells.
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UR - http://www.scopus.com/inward/citedby.url?scp=85130019093&partnerID=8YFLogxK
UR - https://www.mendeley.com/catalogue/4838497c-efd8-3b6e-bbc8-f7b67dd73e8d/
U2 - 10.1096/fasebj.2022.36.s1.r3389
DO - 10.1096/fasebj.2022.36.s1.r3389
M3 - Article
C2 - 35560781
AN - SCOPUS:85130019093
SN - 0892-6638
VL - 36
JO - FASEB Journal
JF - FASEB Journal
IS - S1
ER -