Gene-gene-environment interactions of prenatal exposed to environmental tobacco smoke, CYP1A1 and GSTs polymorphisms on full-term low birth weight: relationship of maternal passive smoking, gene polymorphisms, and FT-LBW

J Matern Fetal Neonatal Med. 2019 Jul;32(13):2200-2208. doi: 10.1080/14767058.2018.1429394. Epub 2018 Jan 30.

Abstract

Objective: To examine the interaction effects of prenatal exposed to environmental tobacco smoke (ETS) and genotypes of cytochrome P4501A1 (CYP1A1), glutathione S-transferases (GSTs) on the risk of full-term low birth weight (FT-LBW).

Study design: We conducted a case-control study among pregnant women at two Women and Children's Hospitals in Guangdong, China (n = 910). Information was collected through interview, medical records review, and blood lab tests. Maternal selfreport and serum cotinine concentration were combined to define prenatal exposed to ETS. Logistic regression approach was applied for statistical analysis.

Results: Our results showed that regardless of genotypes, prenatal exposed to ETS significantly increased the risk of FT-LBW. Then, two-way interactions showed increased prevalence of FT-LBW in prenatal exposed to ETS mothers with the CYP1A1 variant genotype (MspI "CC"), or with GSTT1-null genotype. Furthermore, three-way interactions showed that women with CYP1A1 variant (MspI "TC" or BsrDI "AG") genotypes and GSTT1 "null" genotype had higher risk to give birth of FT-LBW. Additionally, among nonexposed ETS mothers, genotype did not independently confer adverse effects on FT-LBW.

Conclusions: Our results revealed that prenatal exposed to ETS is independently associated with FT-LBW while gene polymorphisms of CYP1A1 and GSTs merely play modified roles in this process. This study extends understanding of three-way interaction, and stresses the need to tobacco control toward pregnant women for better pregnant outcomes.

Keywords: Gene polymorphisms; environmental exposure; full-term low birth weight; interaction; smoke; tobacco.

Publication types

  • Multicenter Study

MeSH terms

  • Adult
  • Case-Control Studies
  • Cytochrome P-450 CYP1A1 / metabolism*
  • Female
  • Glutathione Transferase / metabolism*
  • Humans
  • Infant, Newborn
  • Infant, Small for Gestational Age
  • Logistic Models
  • Polymorphism, Genetic
  • Pregnancy
  • Prenatal Exposure Delayed Effects / epidemiology
  • Prenatal Exposure Delayed Effects / metabolism*
  • Self Report
  • Tobacco Smoke Pollution / adverse effects*

Substances

  • Tobacco Smoke Pollution
  • CYP1A1 protein, human
  • Cytochrome P-450 CYP1A1
  • glutathione S-transferase T1
  • Glutathione Transferase