Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2014 Jan;133(1):225-32.e1-5.
doi: 10.1016/j.jaci.2013.04.051. Epub 2013 Jun 24.

Prenatal alcohol exposure and childhood atopic disease: a Mendelian randomization approach

Seif O Shaheen  1 , Clare Rutterford  2 , Luisa Zuccolo  3 , Susan M Ring  4 , George Davey Smith  3 , John W Holloway  5 , A John Henderson  4
Affiliations

Prenatal alcohol exposure and childhood atopic disease: a Mendelian randomization approach

Seif O Shaheen et al. J Allergy Clin Immunol. 2014 Jan.

Abstract

Background: Alcohol consumption in western pregnant women is not uncommon and could be a risk factor for childhood atopic disease. However, reported alcohol intake may be unreliable, and associations are likely to be confounded.

Objective: We aimed to study the relation between prenatal alcohol exposure and atopic phenotypes in a large population-based birth cohort with the use of a Mendelian randomization approach to minimize bias and confounding.

Methods: In white mothers and children in the Avon Longitudinal Study of Parents and Children (ALSPAC) we first analyzed associations between reported maternal alcohol consumption during pregnancy and atopic outcomes in the offspring measured at 7 years of age (asthma, wheezing, hay fever, eczema, atopy, and total IgE). We then analyzed the relation of maternal alcohol dehydrogenase (ADH)1B genotype (rs1229984) with these outcomes (the A allele is associated with faster metabolism and reduced alcohol consumption and, among drinkers, would be expected to reduce fetal exposure to ethanol).

Results: After controlling for confounders, reported maternal drinking in late pregnancy was negatively associated with childhood asthma and hay fever (adjusted odds ratio [OR] per category increase in intake: 0.91 [95% CI, 0.82-1.01] and 0.87 [95% CI, 0.78-0.98], respectively). However, maternal ADH1B genotype was not associated with asthma comparing carriers of A allele with persons homozygous for G allele (OR, 0.98 [95% CI, 0.66-1.47]) or hay fever (OR, 1.11 [95% CI, 0.71-1.72]), nor with any other atopic outcome.

Conclusion: We have found no evidence to suggest that prenatal alcohol exposure increases the risk of asthma or atopy in childhood.

Keywords: ADH; ADH1B; ALSPAC; Alcohol; Alcohol dehydrogenase; Avon Longitudinal Study of Parents and Children (ALSPAC); GWAS; Genome Wide Association Study; Mendelian randomization; PCA; Principal Components Analysis; asthma; atopy; birth cohort; pregnancy; prenatal exposure.

PubMed Disclaimer

References

    1. Starkenburg S., Munroe M.E., Waltenbaugh C. Early alteration in leukocyte populations and Th1/Th2 function in ethanol-consuming mice. Alcohol Clin Exp Res. 2001;25:1221–1230. - PubMed
    1. Waltenbaugh C., Vasquez K., Peterson J.D. Alcohol consumption alters antigen-specific Th1 responses: mechanisms of deficit and repair. Alcohol Clin Exp Res. 1998;22:220S–223S. - PubMed
    1. Oldenburg P.J., Poole J.A., Sisson J.H. Alcohol reduces airway hyperresponsiveness (AHR) and allergic airway inflammation in mice. Am J Physiol Lung Cell Mol Physiol. 2012;302:L308–L315. - PMC - PubMed
    1. Inselman L.S., Fisher S.E., Spencer H., Atkinson M. Effect of intrauterine ethanol exposure on fetal lung growth. Pediatric Res. 1985;19:12–14. - PubMed
    1. Wang X., Gomutputra P., Wolgemuth D.J., Baxi L. Effects of acute alcohol intoxication in the second trimester of pregnancy on development of the murine fetal lung. Am J Obstet Gynecol. 2007;197:269. - PubMed

Publication types

MeSH terms