ArticleScientific reports2022
Association between maternal smoke exposure and congenital heart defects from a case-control study in China.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 28 citations in OpenAlex.
- Deciphering epigenetic regulation in cardiac developmental toxicity: Mechanisms and implications (Review).Molecular medicine reports · 2026Review
- Maternal Immune Activation: Implications for Congenital Heart Defects.Clinical reviews in allergy & immunology · 2025Review
- 2025 Heart Disease and Stroke Statistics: A Report of US and Global Data From the American Heart Association.Circulation · 2025Review
- Trends in cardiovascular and cerebrovascular health scores in the Kailuan population from 2006 to 2011.World journal of cardiology · 2024Article
- Advancements in Cardiovascular Disease Research Affected by Smoking.Reviews in cardiovascular medicine · 2024Review
- Integrated mRNA- and miRNA-sequencing analyses unveil the underlying mechanism of tobacco pollutant-induced developmental toxicity in zebrafish embryos.Journal of translational medicine · 2024Article
- 2024 Heart Disease and Stroke Statistics: A Report of US and Global Data From the American Heart Association.Circulation · 2024Review
- Maternal smoking around birth and its influence on offspring allergic diseases: A mendelian randomization study.The World Allergy Organization journal · 2024Article
- The Impact of Prenatal Environmental Tobacco Smoking (ETS) and Exposure on Chinese Children: A Systematic Review.Children (Basel, Switzerland) · 2023Review
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is a gap in knowledge how maternal exposure to environmental tobacco smoke (ETS) is associated with offspring congenital heart defects (CHDs). In this case-control study, we collected data on 749 fetuses with CHDs and 880 fetuses without any congenital anomalies to examine the association of maternal ETS with fetal CHDs and the potentially moderating effect by maternal hazardous and noxious substances (HNS), periconceptional folate intake and paternal smoking. Maternal exposure to ETS in first trimester was associated with increased risk of CHDs in a dose-response gradient, with the AORs (95% CI) were1.38 (1.00-1.92), 1.60 (1.07-2.41), and 4.94 (2.43-10.05) for ETS < 1 h/day, 1-2 h/day, and ≥ 2 h/day, respectively. With the doubly unexposed group as reference categories, AORs for maternal ETS exposure ≥ 2 h/day in the absence of folate intake, in the presence of HNS exposure or paternal smoking, were 7.21, 11.43, and 8.83, respectively. Significant additive interaction between ETS exposure and maternal folate intake on CHDs was detected. Maternal ETS exposure during first trimester may increase the risk of offspring CHDs in a dose-response shape, and such effect may be modified by maternal folate intake or other potential factors.
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