Effects of In Utero and Childhood Tobacco Smoke Exposure and 2-Adrenergic Receptor Genotype on Childhood Asthma and Wheezing

Department of Preventive Medicine, Keck School of Medicine, University of Southern California, 1540 Alcazar St, CHP 236, Los Angeles, CA 90033, USA.
PEDIATRICS (Impact Factor: 5.47). 08/2008; 122(1):e107-14. DOI: 10.1542/peds.2007-3370
Source: PubMed


Associations between single-nucleotide polymorphisms in the beta2-adrenergic receptor gene and asthma and wheeze have been inconsistent. Recent studies indicated that tobacco smoke affects beta2-adrenergic receptor gene expression and associations of beta2-adrenergic receptor gene variants with asthma in adults. We aimed to investigate the joint effects of in utero and childhood secondhand tobacco smoke exposure and 2 well-characterized functional single-nucleotide polymorphisms (Arg16Gly and Glu27Gln) of beta2-adrenergic receptor gene on asthma and wheezing in 3128 non-Hispanic and Hispanic white children of the Children's Health Study.
We fitted logistic regression models to estimate odds ratios and 95% confidence intervals for the independent and joint effects of these single-nucleotide polymorphisms and in utero and secondhand tobacco smoke exposure on asthma and wheeze outcomes.
Exposures to in utero maternal smoking and secondhand tobacco smoke were associated with wheezing. Children who were homozygous for the Arg16 allele and were exposed to maternal smoking in utero were at a threefold increased risk for lifetime wheeze compared with children who were unexposed and had at least 1 Gly16 allele. We found similar joint effects of secondhand tobacco smoke and Arg16Gly with wheezing. The risk for lifetime, current, and nocturnal wheeze increased with the number of smokers at home among Arg16 homozygous children. The results were consistent in 2 cohorts of children recruited in 1993 and 1996. Diplotype-based analyses were consistent with the single-nucleotide polymorphism-specific results. No associations were found for Glu27Gln.
Both in utero and childhood exposure to tobacco smoke were associated with an increased risk for wheeze in children, and the risks were greater for children with the Arg16Arg genotype or 2 copies of the Arg16-Gln27 diplotype. Exposures to smoking need to be taken into account when evaluating the effects of beta2-adrenergic receptor gene variants on respiratory health outcomes.

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Available from: Muhammad T Salam, Dec 25, 2013
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    • "Most evidence regarding postnatal effects of intrauterine smoke exposure in humans on subsequent lung function or respiratory morbidity has been derived from epidemiological and physiological studies [Stocks and Dezateux, 2003; Svanes et al. 2004; Moshammer et al. 2006; Palmer et al. 2006; Goksor et al. 2007; Haberg et al. 2007; Wang et al. 2008; Hayatbakhsh et al. 2009; Wenten et al. 2009; Henderson et al. 2010; Hersoug et al. 2010; Schultz et al. 2010; Abbott and Winzer-Serhan, 2012; Neuman et al. 2012]. Prenatal nicotine exposure may predispose to BHR during infancy, especially in those with a maternal history of asthma, with BHR still evident in early adulthood [Goksor et al. 2007]. "
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    Therapeutic Advances in Respiratory Disease 02/2013; 7(3). DOI:10.1177/1753465813479428 · 1.95 Impact Factor
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    • "The influence of the exposure to tobacco smoke on the development of asthma has been investigated at different stages of life and by means of diverse study models. It has been observed that the children who are exposed in utero have a greater risk of presenting wheezing at some time during their lives and in the previous year [32]; in the same way, they also have a greater necessity of medical attention for asthma in the emergency services [33]. When considering the passive exposure to and the prevalence of, asthma, the results have been contradictory, discovering studies with a direct association [9, 33], and others in which, inclusively, a protective effect has been reported [34]. "
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    • "In IgE production and asthma, the maternal influence on gene-environment interaction is more prominent than the paternal influence is. Several studies have supported the gender-dependent gene-environment interactions on asthma development, such as polymorphisms of CTLA-4 [26], GSTM1 [94, 95], GSTP1 [96], IL-13 [97], IL-1Ra [98], βAR [99], TGF-beta1 [100], HLA-G [101, 102], CD14 [103–106], and TLR2 [107], may influence the development of asthma through interactions with other maternal environmental factors, such as maternal tobacco smoke exposure, maternal atopy, or maternal prenatal exposure to a farming environment. Sensitization of the fetus due to interactions between exclusive in utero maternal environmental factors and fetus susceptible genes may be the most important reason why maternal influence is greater than paternal influence during fetal and infancy periods. "
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