Dioxin-metabolizing genes in relation to effects of prenatal dioxin levels and reduced birth size: The Hokkaido study

Kobayashi, Sumitaka; Sata, Fumihiro; Miyashita, Chihiro; Sasaki, Seiko; S, Ban; Araki, Atsuko; Goudarzi, Houman; Kajiwara, Jumboku; Todaka, Takashi; Kishi, Reiko

doi:10.1016/j.reprotox.2016.12.002

Cited by 13 publications

(10 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One previous study did not observe an association between SNPs (including rs2158041, rs7811989, and rs2040623) of the maternal AHR gene and NTD or between NTD and the interaction between maternal genes and indoor air pollution 26 . Another later study did not find that the AhR rs2066853 polymorphism modified the effect of prenatal dioxin levels on birth size 40 . The polymorphism of the AHR gene affected the expression of the protein 41 .…”

Section: Discussionmentioning

confidence: 93%

Assessment of interaction between maternal polycyclic aromatic hydrocarbons exposure and genetic polymorphisms on the risk of congenital heart diseases

Liu

et al. 2018

Sci Rep

View full text Add to dashboard Cite

The major causes of congenital heart diseases (CHDs) are the interactions of genetic and environmental factors. We conducted a case–control study in 357 mothers of CHDs fetuses and 270 control mothers to investigate the association of maternal PAHs exposure, AHR, CYP1A1, CYP1A2, CYP1B1 and CYP2E polymorphisms, the interaction between PAHs exposure and genetic variants with the risk of CHDs. The higher level PAHs exposure was associated with the risk of CHDs (aOR = 2.029, 95% CI: 1.266, 3.251) or subtypes. The haplotypes of AHR or CYP1A2 were associated with the risk of CHDs: AHR: C-G-A-C: aOR = 0.765; T-A-G-A: aOR = 1.33; CYP1A2: A-T:aOR = 1.75; C-C: aOR = 0.706. When exposed to higher level PAHs, the risk of CHDs among the mothers carrying rs2158041 “C/T or T/T” genotype or rs7811989 “G/A or A/A” genotype in AHR was 1.724 (χ2 = 7.209, P = 0.007) or 1.735 (χ2 = 7.364, P = 0.007) times greater than the aOR in the mothers carrying wild genotype. The multiplicative-scale interactions between PAHs exposure and polymorphisms of CYP1A2 rs4646425 (P = 0.03) or CYP2E1 rs915908 (P = 0.0238) on the risk of CHDs were observed. Our study suggests that maternal AHR polymorphisms may modify the association of PAHs exposure with CHDs, CYP1A2 or CYP2E1 polymorphisms significantly interact with PAHs exposure on CHDs.

show abstract

Section: Discussionmentioning

confidence: 93%

Assessment of interaction between maternal polycyclic aromatic hydrocarbons exposure and genetic polymorphisms on the risk of congenital heart diseases

Liu

et al. 2018

Sci Rep

View full text Add to dashboard Cite

show abstract

“…The effects of maternal smoking during pregnancy and maternal genetic polymorphisms on infant birth weight were examined in the Sapporo and Hokkaido cohorts [ 22 , 59 – 63 ]. The results are shown in Table 11 .…”

Section: Resultsmentioning

confidence: 99%

“…Maternal polymorphisms in the AhR (G>A, Arg554Lys) and CYP1A1 (T>C, MspI) genes were associated with maternal dioxin concentration [ 60 ]. Moreover, among 29 dioxin congeners, reduced infant birth weight was associated with increased levels of certain dioxin congeners [ 59 ] (Fig. 1 ).…”

Section: Resultsmentioning

confidence: 99%

“…

Fig. 1 Association of maternal PCDD and PCDF congeners and maternal GSTM1 (non-null/null) genotypes with reduction of infant birth weight in the multiple linear regression model ( N = 421) [ 59 ] …”

Section: Resultsmentioning

confidence: 99%

“…Our findings on gene polymorphisms suggest that the presence of maternal smoking [ 22 , 61 – 63 ] and dioxin exposure [ 59 ] during pregnancy affects not only the genes encoding chemical metabolizing enzymes but also the genes encoding DNA repair possibly resulting in adverse fetal health effects, such as infant birth size. Our findings suggest that there are populations genetically susceptible to the effects of exposure to environmental chemicals.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

The Hokkaido Birth Cohort Study on Environment and Children’s Health: cohort profile—updated 2017

Kishi

Araki

Minatoya

et al. 2017

Environ Health Prev Med

Self Cite

View full text Add to dashboard Cite

The Hokkaido Study on Environment and Children’s Health is an ongoing study consisting of two birth cohorts of different population sizes: the Sapporo cohort and the Hokkaido cohort. Our primary study goals are (1) to examine the effects of low-level environmental chemical exposures on birth outcomes, including birth defects and growth retardation; (2) to follow the development of allergies, infectious diseases, and neurobehavioral developmental disorders and perform a longitudinal observation of child development; (3) to identify high-risk groups based on genetic susceptibility to environmental chemicals; and (4) to identify the additive effects of various chemicals, including tobacco smoking. The purpose of this report is to update the progress of the Hokkaido Study, to summarize the recent results, and to suggest future directions. In particular, this report provides the basic characteristics of the cohort populations, discusses the population remaining in the cohorts and those who were lost to follow-up at birth, and introduces the newly added follow-up studies and case-cohort study design. In the Sapporo cohort of 514 enrolled pregnant women, various specimens, including maternal and cord blood, maternal hair, and breast milk, were collected for the assessment of exposures to dioxins, polychlorinated biphenyls, organochlorine pesticides, perfluoroalkyl substances, phthalates, bisphenol A, and methylmercury. As follow-ups, face-to-face neurobehavioral developmental tests were conducted at several different ages. In the Hokkaido cohort of 20,926 enrolled pregnant women, the prevalence of complicated pregnancies and birth outcomes, such as miscarriage, stillbirth, low birth weight, preterm birth, and small for gestational age were examined. The levels of exposure to environmental chemicals were relatively low in these study populations compared to those reported previously. We also studied environmental chemical exposure in association with health outcomes, including birth size, neonatal hormone levels, neurobehavioral development, asthma, allergies, and infectious diseases. In addition, genetic and epigenetic analyses were conducted. The results of this study demonstrate the effects of environmental chemical exposures on genetically susceptible populations and on DNA methylation. Further study and continuous follow-up are necessary to elucidate the combined effects of chemical exposure on health outcomes.

show abstract

Effects of Persistent Organic Pollutants (POPs) in the Ecosystem and Human Health: Focusing on Chlorinated Chemicals

Araki

Miyashita

Kobayashi

et al. 2022

The Handbook of Environmental Chemistry

View full text Add to dashboard Cite

Dioxin-metabolizing genes in relation to effects of prenatal dioxin levels and reduced birth size: The Hokkaido study

Cited by 13 publications

References 48 publications

Assessment of interaction between maternal polycyclic aromatic hydrocarbons exposure and genetic polymorphisms on the risk of congenital heart diseases

Assessment of interaction between maternal polycyclic aromatic hydrocarbons exposure and genetic polymorphisms on the risk of congenital heart diseases

The Hokkaido Birth Cohort Study on Environment and Children’s Health: cohort profile—updated 2017

Effects of Persistent Organic Pollutants (POPs) in the Ecosystem and Human Health: Focusing on Chlorinated Chemicals

Contact Info

Product

Resources

About