Dataset Information

Genome-wide by environment interaction studies of maternal smoking and educational score in UK biobank.

ABSTRACT:

Purpose

This study aimed to investigate the associations between maternal smoking (MS) and education score in adult offspring.

Methods

To better understand this link, we performed a two-stage genome-wide by environment interaction studies (GWEIS) of MS and offspring education score in UK Biobank cohort. Specifically, 276 996 subjects from England were enrolled in the discovery study, while 24 355 subjects from Scotland and 14 526 subjects from Wales were enrolled in the replication study. GWEIS were conducted by PLINK 2.0 with MS used as an environmental risk factor.

Results

Significant GWEIS associations ( P < 0.0001) between MS and offspring education score in both the discovery cohort and two replicate cohorts (Scotland population and Wales population) were identified. GWEIS identified 2 independent significant single nucleotide polymorphism-MS interaction, with one variant located in the chromosomal 16 (rs72768988, Position: 22,768,798, P = 1.22 × 10 -8 , β = 6.7662) and the other one located in 2q32.3 region (2 : 196424612_GT_G, Position: 196 424 612, 3.60 × 10 -9 , β = -0.4721).

Conclusion

Our results suggested 2q32.3 region and HECW2 gene could negatively moderate the influence of MS on offspring's educational status.

SUBMITTER: Huang H

PROVIDER: S-EPMC10325563 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature

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Publications

Genome-wide by environment interaction studies of maternal smoking and educational score in UK biobank.

Huang Huimei H Liu Li L Feng Fenling F Sun Hongli H Li Fei F Wu Haibin H Liang Chujun C Chu Xiaomeng X Ning Yujie Y Zhang Feng F

Psychiatric genetics 20230524 4

<h4>Purpose</h4>This study aimed to investigate the associations between maternal smoking (MS) and education score in adult offspring.<h4>Methods</h4>To better understand this link, we performed a two-stage genome-wide by environment interaction studies (GWEIS) of MS and offspring education score in UK Biobank cohort. Specifically, 276 996 subjects from England were enrolled in the discovery study, while 24 355 subjects from Scotland and 14 526 subjects from Wales were enrolled in the replicatio ...[more]

PMID: 37222225

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Project description:BackgroundUnraveling gene-environment interaction can provide a novel insight into early disease prevention. Nevertheless, current understanding of the interplay between genetic predisposition and air pollution in relation to myocardial infarction (MI) risk remains limited. Furthermore, the potential long-term influence of air pollutants on MI incidence risk warrants more conclusive evidence in a community population.ObjectiveWe investigated interactions between genetic predisposition and exposure to air pollutants on MI incidence.MethodsThis study incorporated a sample of 456,354 UK Biobank participants and annual mean air pollution (PM2.5, PM10, NO2, and NOx) from the UK Department for Environment, Food and Rural Affairs (2006-2021). The Cox proportional hazards model was employed to explore MI incidence after chronic air pollutants exposure. By quantifying genetic risk through the calculation of polygenic risk score (PRS), this study further examined the interactions between genetic risk and exposure to air pollutants in the development of MI on both additive and multiplicative scales.ResultsAmong 456,354 participants, 9,114 incident MI events were observed during a median follow-up of 12.08 y. Chronic exposure to air pollutants was linked with an increased risk of MI occurrence. Specifically, the hazard ratios (per interquartile range) were 1.12 (95% CI: 1.10, 1.13) for PM2.5, 1.20 (95% CI: 1.19, 1.22) for PM10, 1.13 (95% CI: 1.12, 1.15) for NO2, and 1.12 (95% CI: 1.11, 1.13) for NOx. In terms of the joint effects, participants with high PRS and high level of air pollution exposure exhibited the greatest risk of MI among all study participants (∼255% to 324%). Remarkably, both multiplicative and additive interactions were detected in the ambient air pollutants exposure and genetic risk on the incidence of MI.DiscussionThere were interactions between exposure to ambient air pollutants and genetic susceptibility on the risk of MI onset. Moreover, the joint effects of these two exposures were greater than the effect of each factor alone. https://doi.org/10.1289/EHP14291.

Dataset Information

Genome-wide by environment interaction studies of maternal smoking and educational score in UK biobank.

Purpose

Methods

Results

Conclusion

Publications

Genome-wide by environment interaction studies of maternal smoking and educational score in UK biobank.

Similar Datasets

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