Abstract

Children are commonly exposed to second-hand smoke (SHS) in the domestic environment or inside vehicles of smokers. Unfortunately, prenatal tobacco smoke (PTS) exposure is still common, too. SHS is hazardous to the health of smokers and non-smokers, but especially to that of children. SHS and PTS increase the risk for children to develop cancers and can trigger or worsen asthma and allergies, modulate the immune status, and is harmful to lung, heart and blood vessels. Smoking during pregnancy can cause pregnancy complications and poor birth outcomes as well as changes in the development of the foetus. Lately, some of the molecular and genetic mechanisms that cause adverse health effects in children have been identified. In this review, some of the current insights are discussed. In this regard, it has been found in children that SHS and PTS exposure is associated with changes in levels of enzymes, hormones, and expression of genes, micro RNAs, and proteins. PTS and SHS exposure are major elicitors of mechanisms of oxidative stress. Genetic predisposition can compound the health effects of PTS and SHS exposure. Epigenetic effects might influence in utero gene expression and disease susceptibility. Hence, the limitation of domestic and public exposure to SHS as well as PTS exposure has to be in the focus of policymakers and the public in order to save the health of children at an early age. Global substantial smoke-free policies, health communication campaigns, and behavioural interventions are useful and should be mandatory.

Highlights

  • Second-hand smoke (SHS) consists of mainstream smoke exhaled by a smoker and side-stream smoke from the smouldering tobacco product [1]

  • The authors found that matrix metalloproteinase-9 (MMP-9) concentrations and activity were significantly higher in the probed nasal secretions of children exposed to SHS

  • These study results report that prenatal tobacco smoke (PTS) and SHS exposure has a negative influence on the lipid profile in children up to adulthood accompanied by associated health effects

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Summary

Introduction

Second-hand smoke (SHS) consists of mainstream smoke exhaled by a smoker and side-stream smoke from the smouldering tobacco product [1]. Prenatal tobacco smoke (PTS) exposure can cause poor birth outcomes and pregnancy complications. PTS is linked with biochemical changes in the placenta, leading to alterations to the antioxidant system of the foetus, associated with several adverse health effects both prenatal and postnatal. PTS exposure can lead to pulmonary diseases, e.g., COPD, wheezing, asthma, kidney diseases as well as cardiovascular diseases in later life. The early events during pregnancy and childhood play a key role in the development of the human body In this vulnerable phase, exposure to tobacco smoke have been shown to have deleterious effects on the development process and may result in permanent damage [15]. The genetic predisposition can lead to substantially aggravated risk for diseases of children exposed to SHS [16,17,18,19]. According to the World Health Organization (WHO), data from 2004 from 192 countries showed

Biomarkers that
Matrix
Matrix Metalloproteinase-9
Immune-Regulatory Cytokines
Cysteinyl Leukotrienes and Urinary Leukotriene E4
Estimated Glomerular Filtration Rate and Kidney Function
Cardiovascular Status
C-Reactive Protein
Immune Status
Lipid Profile
Oxidative Stress
Hormone Status
Genetic Predisposition
Anti-Inflammatory Cytokine Genes
CD14 Gene
Variants at Chromosome 17 Region q21
ATPase-Related Genes and Bronchial Hyper-Responsiveness
MSX1 Gene
Protein Expression in Foetal Liver
Dysregulation of Diverse MicroRNAs
10. Leukocyte Telomere Length
11. DNA Methylation
Findings
12. Conclusions
Full Text
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