13, 14 In addition to indirect maternal exposure, children can also be exposed to secondhand tobacco smoke or thirdhand tobacco smoke during postnatal life. 11, 12 Nicotine has also been shown to be concentrated in the breast milk of mothers who smoke. 4, 10 Nicotine, the primary addictive substance in tobacco smoke, has been shown to cross the placenta in utero as evidenced by high levels of cotinine, a nicotine metabolite, in the amniotic fluid of pregnant smokers and in blood spots from neonates exposed in utero. 9 In particular, exposures to nicotine carbon monoxide acrolein and carcinogens, including polycyclic aromatic hydrocarbons, aromatic amines, and tobacco-specific N-nitrosamines, can be detrimental, especially during fetal life and periods of rapid postnatal organ growth, including the lungs and brain. Tobacco smoke contains more than 4,000 chemicals, many of which have been associated with deleterious health consequences. 4, 5, 6, 7, 8 The goals of this review are to examine the effects of tobacco smoke and nicotine exposure on prenatal and postnatal lung development, assess the relationship between tobacco smoke and nicotine exposure and respiratory morbidities in children, and evaluate the role of genetics and epigenetics on the respiratory phenotypes of children exposed to tobacco smoke and nicotine. 3 Exposure to tobacco smoke and nicotine during in utero and postnatal life has been shown to disturb lung development, increase susceptibility to lower respiratory tract infections, increase prevalence of wheezing, and exacerbate respiratory symptoms in children with chronic lung diseases. 1, 2 Although the majority of postnatal lung growth occurs within the first 2 years of life, modest alveolar growth continues through the first 15 years of life. Lung development begins during early embryogenesis and extends into late childhood. Finally, this review outlines the respiratory morbidities associated with childhood secondhand smoke and nicotine exposure and examines genetic and epigenetic modifiers that may influence respiratory health in infants and children exposed to in utero or postnatal tobacco smoke. In addition, this review examines the role of prenatal and postnatal tobacco smoke and nicotine exposure and its association with augmenting infection risk, skewing the immune response toward a T-helper type 2 bias and increasing risk for developing an allergic phenotype and asthmalike symptoms during childhood. This review examines the impact of prenatal tobacco and nicotine exposure on lung development with a particular focus on nicotinic acetylcholine receptors. Recently, genomic and epigenetic risk factors, such as alterations in DNA methylation, have been identified that may influence the risk for long-term disease. Exposed neonates are at increased risk for diminished lung function, altered central and peripheral respiratory chemoreception, and increased asthma symptoms throughout childhood. In utero tobacco and nicotine exposure remains common, occurring in approximately 10% of pregnancies within the United States. The following review examines recent discoveries in the fields of lung development and tobacco and nicotine exposure, emphasizing studies published within the last 5 years. Tobacco smoke and nicotine exposure during prenatal and postnatal life can impair lung development, alter the immune response to viral infections, and increase the prevalence of wheezing during childhood.
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