Impact of heat-not-burn cigarette passive smoking on children's oxidative stress, endothelial and platelet function

• Published in: Environmental pollution (1987) Vol. 345; p. 123304
• Main Authors: Loffredo, Lorenzo, Carnevale, Roberto, Pannunzio, Arianna, Cinicola, Bianca Laura, Palumbo, Ilaria Maria, Bartimoccia, Simona, Nocella, Cristina, Cammisotto, Vittoria, Violi, Francesco, Biondi-Zoccai, Giuseppe, Frati, Giacomo, Zicari, Anna Maria, Magna, Arianna, Izzo, Raffaella, Capponi, Martina, Brindisi, Giulia, Salvatori, Francesca, Castellani, Valentina, Amico, Alessandra D’, Trivigno, Chiara, Totè, Chiara, Maggio, Enrico, Miraldi, Fabio, Duse, Marzia, Pignatelli, Pasquale, Spalice, Alberto, Antonucci, Flavia
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 15.03.2024
• Subjects: bioavailability; blood serum; Child; childhood; Children; cigarettes; cotinine; Endothelial function; Flow-mediated dilation; Heat-not-burn cigarettes; Heated tobacco products; Hot Temperature; Humans; hydrogen; Hydrogen Peroxide; Isoprostanes; ligands; NADPH oxidase; Oxidative stress; Oxidative Stress - physiology; Passive smoking; peptides; platelet activation; pollution; smoke; Thrombosis; Tobacco Products; Tobacco Smoke Pollution - adverse effects; Oxidative stress; Flow-mediated dilation; Heat-not-burn cigarettes; NADPH oxidase; Passive smoking; Children; Endothelial function; Heated tobacco products
• ISSN: 0269-7491; 1873-6424; 1873-6424
• DOI: 10.1016/j.envpol.2024.123304

Growing global use of heat-not-burn cigarettes (HNBC) prompts investigation. Prior studies assessed HNBC's effects on cardiovascular health, revealing heightened oxidative stress, platelet activation, and endothelial dysfunction. However, limited understanding exists regarding passive smoking's impact on children exposed to HNBC. This study aims to assess levels of oxidative stress, endothelial and platelet function among children exposed to passive smoke from HNBC, traditional tobacco (TT) cigarettes and unexposed subjects. Seventy-eight children (2–18 years) were divided into three groups: HNBC passive smokers (n = 26), TT cigarette exposed (n = 26), and control (CNT) group (n = 26, unexposed). Oxidative stress was evaluated by serum NADPH oxidase-2 (NOX2) activity, assessed by soluble Nox2-derived peptide (sNOX2-dp), isoprostanes, hydrogen peroxide (H2O2) production, hydrogen break-down activity (HBA) and NO bioavailability. Endothelial function was assessed by brachial flow-mediated dilation (FMD). Platelet function was evaluated by soluble CD40 ligand (sCD40L), soluble P-selectin (sP-selectin) and thrombus formation by T-TAS analysis. Passive smoking-exposed children (both HNBC and TT) exhibited significantly increased serum sNOX2-dp, isoprostanes, H2O2, sCD40L sP-selectin and thrombus formation versus controls. Conversely, exposed children displayed reduced brachial FMD and serum NO bioavailability. No significant differences were found between children exposed to passive smoking of HNBC vs TT. Multivariable regression linked sNOX2 (standardized coefficient β: 0.284; SE: 0.040; p = 0.01) and H2O2 (standardized coefficient β: 0.243; SE: 0.0; p = 0.02) as independent predictors of FMD, and isoprostanes (standardized coefficient β:0.388; SE: 0.022; p < 0.001) and serum cotinine (standardized coefficient β:0.270; SE: 0.048; p = 0.01) with sNOX2-dp levels. Exposure to HNBC smoke heightened oxidative stress, endothelial dysfunction, platelet activation, and thrombus formation in children. Findings suggest avenues for interventions to curb childhood passive smoking exposure. [Display omitted] •Children exposed to passive smoke from HNBC and TTC exhibit elevated oxidative stress.•Children exposed to passive smoke from HNBC and TTC have endothelial dysfunction.•Children exposed to passive smoke from HNBC and TTC show increased platelet activation.•These elevations could potentially raise the cardiovascular risk in children.