Abstract

Smoking is a major global public health problem, a trigger for chronic diseases and a significant preventable risk factor of global death. Smoking represents a major cardiovascular risk factor for adults, but the effect of passive smoking in children is not well established. The study evaluated the relationship between serum biomarkers such as lipids, cholesterol, triglycerides and passive smoking in children. We noticed that passive smoking creates alterations in HDL-cholesterol which decreased significantly in the presence of passive smoking.

Highlights

  • With the growing exposure to smoking in children was reported worldwide, in 2016, an estimated one-third of females, one-fifth of males globally and approximately 66% of children aged 3-11 years were exposed to second-hand smoke (SHS)

  • The aim of study was to assess the levels of lipid biomarkers used for cardiovascular risk like total cholesterol, HDL-cholesterol, LDL-cholesterol, total lipid and triglycerides (TG) in relation to smoking exposure in children

  • The serum levels of lipid biomarkers were dosed and the results showed the mean values, as follow: 4.12 g/l for lipids, 162.61 for total cholesterol, a slightly increase median value considering the lower values reported by age [3]

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Summary

Introduction

With the growing exposure to smoking in children was reported worldwide, in 2016, an estimated one-third of females, one-fifth of males globally and approximately 66% of children aged 3-11 years were exposed to second-hand smoke (SHS). While the pulmonary consequences of SHS exposure are clinically apparent in childhood, the cardiovascular effects of SHS exposure are occult but substantial [2] It appears that SHS exposure in early childhood, even in utero, can cause persistent lipoprotein changes later in life [3], increased incidence of obesity [4], lower high-density lipoprotein cholesterol (HDL C) levels in children [5]. The nicotine induces lipolysis via catecholamine action at β-adrenoreceptors, increasing plasma free fatty acid concentrations, which could result in enhanced synthesis of LDL and lowering of HDL cholesterol. May enhance insulin resistance via increased levels of insulin-antagonistic hormones (cortisol, catecholamine, and growth hormone) and directly activating AMP-activated protein kinase in adipose tissue mediating the effect of nicotine [11] on insulin sensitivity [12]

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