Key result
Parental cigarette smoking may substantially contribute to the etiology of congenital heart defects through induction of germ-cell mutation or interference with epigenetic pathways.
Why the study?
Does parental cigarette smoking increase the risk of congenital heart defects in offspring?
Does parental cigarette smoking increase the risk of congenital heart defects in offspring?
This review highlights the biological plausibility of parental smoking as a teratogen for congenital heart defects, emphasizing the need for further epidemiological and gene-environment interaction studies.
Answers are grounded in this paper and cite their sources.
Supports preconception smoking cessation counseling; leaves open causal confirmation in congenital heart defects pending prospective studies.
Cigarette smoking is a powerful human germ cell mutagen and teratogen. Congenital heart defects (CHD) is the most prevalent of all birth defects and leading cause of death in the first year of life. The purpose of this article is to review the epidemiology of the impact of cigarette smoking on CHD risk as well as to discuss the potential biological mechanisms of smoking-mediated abnormal cardiac development. Although epidemiological studies of association between parental smoking and CHD are limited, biological evidence support the concept that cigarette smoking may substantially contribute to the aetiology of CHD through induction of either male and female germ-cell mutation or interference with epigenetic pathways. Further research is needed to better define the relationship between parental smoking and the risk of heart defects as well as to assess parental-fetal gene-smoking interactions.
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Gianicolo et al. (2010) conducted a review in Congenital heart defects (CHD). Parental cigarette smoking was evaluated on Congenital heart defects (CHD) risk. Parental cigarette smoking may substantially contribute to the etiology of congenital heart defects through induction of germ-cell mutation or interference with epigenetic pathways.
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