PMID- 35675978
OWN - NLM
STAT- MEDLINE
DCOM- 20220610
LR  - 20230712
IS  - 1347-4715 (Electronic)
IS  - 1342-078X (Print)
IS  - 1342-078X (Linking)
VI  - 27
DP  - 2022
TI  - Gene-environment interactions related to maternal exposure to environmental and 
      lifestyle-related chemicals during pregnancy and the resulting adverse fetal 
      growth: a review.
PG  - 24
LID - 10.1265/ehpm.21-00033 [doi]
LID - 24
AB  - BACKGROUND: There are only limited numbers of reviews on the association of 
      maternal-child genetic polymorphisms and environmental and lifestyle-related 
      chemical exposure during pregnancy with adverse fetal growth. Thus, this article 
      aims to review: (1) the effect of associations between the above highlighted 
      factors on adverse fetal growth and (2) recent birth cohort studies regarding 
      environmental health risks. METHODS: Based on a search of the PubMed database 
      through August 2021, 68 epidemiological studies on gene-environment interactions, 
      focusing on the association between environmental and lifestyle-related chemical 
      exposure and adverse fetal growth was identified. Moreover, we also reviewed 
      recent worldwide birth cohort studies regarding environmental health risks. 
      RESULTS: Thirty studies examined gene-smoking associations with adverse fetal 
      growth. Sixteen maternal genes significantly modified the association between 
      maternal smoking and adverse fetal growth. Two genes significantly related with 
      this association were detected in infants. Moreover, the maternal genes that 
      significantly interacted with maternal smoking during pregnancy were cytochrome 
      P450 1A1 (CYP1A1), X-ray repair cross-complementing protein 3 (XRCC3), 
      interleukin 6 (IL6), interleukin 1 beta (IL1B), human leukocyte antigen (HLA) DQ 
      alpha 1 (HLA-DQA1), HLA DQ beta 1 (HLA-DQB1), and nicotinic acetylcholine 
      receptor. Fetal genes that had significant interactions with maternal smoking 
      during pregnancy were glutathione S-transferase theta 1 (GSTT1) and fat mass and 
      obesity-associated protein (FTO). Thirty-eight studies examined the association 
      between chemical exposures and adverse fetal growth. In 62 of the 68 
      epidemiological studies (91.2%), a significant association was found with adverse 
      fetal growth. Across the studies, there was a wide variation in the analytical 
      methods used, especially with respect to the genetic polymorphisms of interest, 
      environmental and lifestyle-related chemicals examined, and the study design used 
      to estimate the gene-environment interactions. It was also found that a 
      consistently increasing number of European and worldwide large-scale birth cohort 
      studies on environmental health risks have been conducted since approximately 
      1996. CONCLUSION: There is some evidence to suggest the importance of 
      gene-environment interactions on adverse fetal growth. The current knowledge on 
      gene-environment interactions will help guide future studies on the combined 
      effects of maternal-child genetic polymorphisms and exposure to environmental and 
      lifestyle-related chemicals during pregnancy.
FAU - Kobayashi, Sumitaka
AU  - Kobayashi S
AUID- ORCID: 0000-0002-0396-8637
AD  - Center for Environmental and Health Sciences, Hokkaido University.
FAU - Sata, Fumihiro
AU  - Sata F
AD  - Center for Environmental and Health Sciences, Hokkaido University.
AD  - Health Center, Chuo University.
FAU - Kishi, Reiko
AU  - Kishi R
AD  - Center for Environmental and Health Sciences, Hokkaido University.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Japan
TA  - Environ Health Prev Med
JT  - Environmental health and preventive medicine
JID - 9609642
RN  - EC 1.14.11.33 (Alpha-Ketoglutarate-Dependent Dioxygenase FTO)
RN  - EC 1.14.11.33 (FTO protein, human)
SB  - IM
MH  - Alpha-Ketoglutarate-Dependent Dioxygenase FTO
MH  - Female
MH  - Fetal Development
MH  - *Gene-Environment Interaction
MH  - Humans
MH  - Life Style
MH  - *Maternal Exposure/adverse effects
MH  - Polymorphism, Genetic
MH  - Pregnancy
PMC - PMC9251623
OTO - NOTNLM
OT  - Developmental origins of health and disease
OT  - Environmental chemical
OT  - Epidemiology
OT  - Fetal growth
OT  - Gene-environment interaction
OT  - Lifestyle-related chemical
OT  - Polymorphism
OT  - Precision medicine
OT  - Precision public health
OT  - Smoking
COIS- The authors declare that they have no competing interests.
EDAT- 2022/06/09 06:00
MHDA- 2022/06/11 06:00
PMCR- 2022/06/09
CRDT- 2022/06/08 21:02
PHST- 2022/06/08 21:02 [entrez]
PHST- 2022/06/09 06:00 [pubmed]
PHST- 2022/06/11 06:00 [medline]
PHST- 2022/06/09 00:00 [pmc-release]
AID - 21-00033 [pii]
AID - 10.1265/ehpm.21-00033 [doi]
PST - ppublish
SO  - Environ Health Prev Med. 2022;27:24. doi: 10.1265/ehpm.21-00033.