Associations between community-level patterns of prenatal alcohol and tobacco exposure on brain structure in a non-clinical sample of 6-year-old children: a South African pilot study

Abstract

The current small study utilized prospective data collection of patterns of prenatal alcohol and tobacco exposure (PAE and PTE) to examine associations with structural brain outcomes in 6-year-olds, and served as a pilot to determine the value of prospective data describing community-level patterns of PAE and PTE in a non-clinical sample of children. Participants from the Safe Passage Study in pregnancy were approached when their child was ∼6 years old and completed structural brain magnetic resonance imaging (MRI) to examine with archived PAE and PTE data (n=51 children-mother dyads). Linear regression was used to conduct whole brain structural analyses, with FDR correction, to examine: a) main effects of PAE, PTE and their interaction; and b) predictive potential of data that reflects patterns of PAE and PTE (e.g., quantity, frequency, and timing (QFT)). Associations between PAE, PTE and their interaction with brain structural measures demonstrated unique profiles of cortical and subcortical alterations that were distinct between PAE only, PTE only and their interactive effects. Analyses examining associations between patterns of PAE and PTE (e.g., QFT) were able to significantly detect brain alterations (that survived FDR correction) in this small non-clinical sample of children. These findings support the hypothesis that considering QFT and co-exposures is important for identifying brain alterations following PAE and/or PTE in a small group of young children. Current results demonstrate that teratogenic outcomes on brain structure differ as a function PAE, PTE or their co-exposures, as well as the pattern (QFT) or exposure.

Contextualizing the impact of prenatal alcohol and tobacco exposure on neurodevelopment in a South African birth cohort: an analysis from the socioecological perspective

“…These functional correlates of lateral orbitofrontal cortex and nucleus accumbens are consistent with the negative association between PTE and global cognition in children between 9 to 12 years old found in the current literature, suggesting a potential brain-behavior relationship ( Fried et al, 1998 ; Gonzalez et al, 2023 ). Our results are consistent with prior studies from this same birth cohort representing community patterns of PAE and PTE, showing more widespread cortical and subcortical brain alterations with PTE compared to PAE at ages 6 years old ( Uban et al, 2023 ) and ages 8–12 years ( Marshall et al, 2022 ). Compared to alcohol, tobacco use is less likely to be cut back during pregnancy and more likely to be associated with tobacco exposure after pregnancy ( Leech et al, 1999 ; Cornelius and Day, 2000 ).…”

“…The potential for PTE from others' use may be a mechanism for reaching higher doses of exposure, and/or longer durations of exposure across postnatal developmental stages, unlike PAE. Together, these mechanisms for PTE that are unique from those of PAE may explain the more widespread effects on brain development at ages 6 (Uban et al, 2023) and 8-11 years as seen here and in Marshall et al (2022). Interestingly, PTE dose-response relationships did not show significant results after corrections for multiple comparisons (Marshall et al, 2022), suggesting that PTE exposure from the postnatal period, or relating to perinatal tobacco exposure from others around the pregnant person or baby may be driving PTE outcomes more than maternal use in pregnancy alone.…”

Addressing the neurodevelopmental impacts of prenatal substance exposure: insights from a Taiwanese study on methadone maintenance treatment during pregnancy

“…Uban et al's use of structural MRI and quantitative analysis enhances our understanding of the neurobehavioral implications of structural changes observed in the brain (Uban et al, 2024). Our findings suggest that integrating comprehensive developmental assessments can yield a more detailed understanding of how prenatal exposures impact child development over time.…”

Persistent Impact of Antenatal Maternal Anaemia on Child Brain Structure at 6-7 Years of Age: A South African Child Health Study

“…Similarity, antenatal alcohol use may contribute to iron deficiency directly by limiting the intestinal absorption of iron and disrupting iron homeostasis [ 45 , 46 ], and indirectly by negatively impacting nutritional choices [ 56 ]. In turn, antenatal tobacco exposure, which is highly overlapping with alcohol consumption during pregnancy [ 57 , 58 ], is known to increase haemoglobin levels [ 37 ] resulting in the underestimation of functional anaemia in people who smoke. While all of these risk factors were prevalent in this cohort across groups, antenatal alcohol exposure was significantly more common in women who were anaemic during pregnancy suggesting that this interaction may be particularly important.…”