ArticleInternational journal of legal medicine2010
A common FMO3 polymorphism may amplify the effect of nicotine exposure in sudden infant death syndrome (SIDS).
Article in International journal of legal medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 28 citations in OpenAlex.
- Nicotine Exposure During Gestation: From Placental Dysfunction to Long-Term Neurobehavioral Outcomes.Birth defects research · 2026Review
- Sudden infant death syndrome: deletions of glutathione-S-transferase genes M1 and T1 and tobacco smoke exposure.International journal of legal medicine · 2021Article
- Pharmacogenetics factors influencing smoking cessation success; the importance of nicotine metabolism.Expert opinion on drug metabolism & toxicology · 2021Review
- Article
- Influence of Second-Hand Smoke and Prenatal Tobacco Smoke Exposure on Biomarkers, Genetics and Physiological Processes in Children-An Overview in Research Insights of the Last Few Years.International journal of environmental research and public health · 2020Review
- Genetic and Nongenetic Factors Associated with Protein Abundance of Flavin-Containing Monooxygenase 3 in Human Liver.The Journal of pharmacology and experimental therapeutics · 2017Article
- Microbiome-Gut-Brain Axis: A Pathway for Improving Brainstem Serotonin Homeostasis and Successful Autoresuscitation in SIDS-A Novel Hypothesis.Frontiers in pediatrics · 2016Article
- Assigning cause for sudden unexpected infant death.Forensic science, medicine, and pathology · 2015Article
- Review
- Gene variants predisposing to SIDS: current knowledge.Forensic science, medicine, and pathology · 2011Review
- Genomic risk factors in sudden infant death syndrome.Genome medicine · 2010Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smoking during pregnancy has been identified as one of the major modifiable risk factors of sudden infant death syndrome (SIDS). It has been demonstrated that the risk of SIDS increases with increasing cigarette consumption. A variety of hypotheses have been proposed for explanation, including a genetic predisposition. The flavin-monooxygenase 3 (FMO3) is one of the enzymes metabolising nicotine, and several polymorphisms have already been described in this gene. Here, we studied variations in the exons and introns of the FMO3 gene by direct sequencing analysis and minisequencing in 159 SIDS cases and 170 controls. The three common variants G472A (E158K), G769A (V257M) and A923G (E308G) in the exons of the FMO3 gene were identified. The homozygote 472AA genotype occurred more frequently in SIDS cases than in controls (p = 0.0054) and was more frequent in those SIDS cases for which the mothers reported heavy smoking (p = 0.0084). This study is the first to demonstrate a gene-environment interaction in SIDS. The findings suggest that the common polymorphism G472A of FMO3 could act as an additional genetic SIDS risk factor in children whose mothers smoke. Parents who could pass on the 472A allele should be informed of the increased risk associated with smoking. Smoking mothers should be strongly advised to give up smoking during pregnancy and for at least the first year of the child's life.
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