Cigarette smoking still represents an important cause of cardiovascular and neoplastic diseases. The damage created by cigarette smoke does not only occur through direct inhalation of toxic substances but it also involves passively exposed people who inhale combustion elements emitted by the cigarette (second-hand smoke). This also occurs through inhalation, ingestion or transdermal contact of toxic substances deposited on the surfaces of closed environments such as apartments and vehicles (third-hand smoke).
Increased oxidative stress due to passive smoke can result in cardiovascular damage through the onset of endothelial dysfunction, increase in intimal-media thickening and platelet activation. NADPH oxidase activation has been recognized as the major reactive oxygen species source. NADPH oxidase plays a pivotal role in modulating arterial tone and in inducing platelet activation in humans. Passive smoke increases cardiovascular risk and atherosclerosis by endothelial dysfunction and platelet activation. Children are a frail population that is prevalently exposed to the damages derived from passive smoking. Experimental studies showed that passive smoking provokes endothelial dysfunction and atherosclerosis by NADPH oxidase activation. However, until now, there aren't studies in humans that have explored the role of NADPH oxidase in children exposed to passive smoking.
The aim of this research project will be to assess NADPH oxidase activation on endothelial function and platelet activation in 200 children exposed or not to passive smoke.
Flow mediated dilation and intima-media thickness assessment will be used as surrogate markers of atherosclerosis. Platelet activation will be assessed by markers of platelet activation such as p-selectin; furthermore the components of NETs (i.e. chromatin, histones and granular enzymes), that promote coagulation and platelet activation thereby increasing the risk of thrombosis and cardiovascular disease, will be evaluated.
