The impact of prenatal alcohol and/or tobacco exposure on brain structure in a large sample of children from a South African birth cohort. (26th September 2022)

• Record Type: Journal Article
• Authors: Marshall, Andrew T.; Bodison, Stefanie C.; Uban, Kristina A.; Adise, Shana; Jonker, Deborah; Charles, Weslin; Donald, Kirsten A.; Kan, Eric; Ipser, Jonathan C.; Butler‐Kruger, Letitia; Steigelmann, Babette; Narr, Katherine L.; Joshi, Shantanu H.; Brink, Lucy T.; Odendaal, Hein J.; Scheffler, Freda; Stein, Dan J.; Sowell, Elizabeth R.
• Is Part Of: Alcoholism. Volume 46:Number 11(2022)
• Page Start: 1980
• Page End: 1992
• Publication Date: 2022-09-26
• Subjects: alcohol use -- neuroimaging -- prenatal exposure delayed effects -- South Africa -- tobacco use; Alcoholism -- Periodicals; Alcoholism -- Periodicals; Alcoolisme; Electronic journals; Périodique électronique (Descripteur de forme); Ressource Internet (Descripteur de forme); 616.861005
• DOI: 10.1111/acer.14945
• Languages: English
• ISSNs: 0145-6008

Abstract

Abstract: Background: Neuroimaging studies have emphasized the impact of prenatal alcohol exposure (PAE) on brain development, traditionally in heavily exposed participants. However, less is known about how naturally occurring community patterns of PAE (including light to moderate exposure) affect brain development, particularly in consideration of commonly occurring concurrent impacts of prenatal tobacco exposure (PTE). Methods: Three hundred thirty‐two children (ages 8 to 12) living in South Africa's Cape Flats townships underwent structural magnetic resonance imaging. During pregnancy, their mothers reported alcohol and tobacco use, which was used to evaluate PAE and PTE effects on their children's brain structure. Analyses involved the main effects of PAE and PTE (and their interaction) and the effects of PAE and PTE quantity on cortical thickness, surface area, and volume. Results: After false‐discovery rate (FDR) correction, PAE was associated with thinner left parahippocampal cortices, while PTE was associated with smaller cortical surface area in the bilateral pericalcarine, left lateral orbitofrontal, right posterior cingulate, right rostral anterior cingulate, left caudal middle frontal, and right caudal anterior cingulate gyri. There were no PAE × PTE interactions nor any associations of PAE and PTE exposure on volumetrics that survived FDR correction. Conclusion: PAE was associated with reduction in the structure of the medial temporal lobe, a brain region critical for learning and memory. PTE had stronger and broader associations, including with regions associated with executive function, reward processing, and emotional regulation, potentially reflecting continued postnatal exposure to tobacco (i.e., second‐hand smoke exposure). These differential effects are discussed with respect to reduced PAE quantity in our exposed group versus prior studies within this geographical location, the deep poverty in which participants live, and the consequences of apartheid and racially and economically driven payment practices that contributed to heavy drinking in the region. Longer‐term follow‐up is needed to determine potential environmental and other moderators of the brain findings here and assess the extent to which they endure over time. Abstract : We analyzed brain structure of 332 8‐ to 12‐year‐old children from the Prenatal Alcohol, SIDS and Stillbirth (PASS) Network who had varying levels of prenatal alcohol (PAE) and/or tobacco exposure (PTE). PAE was associated with thinner parahippocampal cortices; PTE's impact was more regionally expansive. Such PAE and PTE effects reflect highly complex downstream outcomes, which require consideration in terms of the amount of exposure, the deep poverty in which participants live, and the legacy of the dop system.