Key result
Passive exposure to heat-not-burn cigarettes in children significantly increased oxidative stress, platelet activation, and thrombus formation, and reduced endothelial function compared to controls.
Why the study?
There is limited understanding regarding the impact of passive smoking from heat-not-burn cigarettes on children.
Does passive smoke exposure to heat-not-burn cigarettes increase oxidative stress, endothelial dysfunction, and platelet activation in children compared to unexposed controls or traditional tobacco?
Observational (n=78)
Does passive smoke exposure to heat-not-burn cigarettes increase oxidative stress, endothelial dysfunction, and platelet activation in children compared to unexposed controls or traditional tobacco?
Passive exposure to heat-not-burn cigarettes is associated with similar levels of heightened oxidative stress, endothelial dysfunction, and platelet activation in children as traditional tobacco smoke.
Passive HNBC exposure may alter children's oxidative and endothelial markers; leaves open clinical relevance pending prospective data.
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.
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Loffredo et al. (2024) conducted an observational in Passive smoke exposure (n=78). Heat-not-burn cigarette (HNBC) passive smoking vs. Traditional tobacco (TT) passive smoking and unexposed controls was evaluated on Oxidative stress, endothelial function, and platelet function. Passive exposure to heat-not-burn cigarettes in children significantly increased oxidative stress, platelet activation, and thrombus formation, and reduced endothelial function compared to controls.
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