Recent research published in JAMA Network Open explores the association of in utero exposure to alcohol (PAE) and tobacco (PTE) with brain activity during childhood. This comprehensive cohort study examines how prenatal exposures impact EEG measurements in children aged 4 to 11 years, reinforcing public health messages about the risks of alcohol and tobacco consumption during pregnancy.

Study Design and Participants

The study is part of the Safe Passage Study, conducted from August 2007 to January 2015, and includes data from the Environmental Influences on Child Health Outcomes Program. A subset of 649 participants, aged 4 to 11 years, contributed a total of 795 EEG recordings. The EEG data were collected from September 2018 through November 2022. Data analysis was performed between November 2022 and November 2023.

Exposures and Classifications

Maternal self-reported alcohol and tobacco consumption during pregnancy were recorded at multiple points:

• At recruitment.
• Between 20-24 weeks’ gestation.
• Between 28-32 weeks’ gestation.
• After 34 weeks’ gestation.

Classifications of PAE and PTE were categorised as follows:

• PAE: Continuous drinking, quit-early drinking, and nondrinking.
• PTE: Continuous smoking, quit-early smoking, and nonsmoking.

Main Outcomes and Measures

The primary outcomes measured were EEG band powers (theta, alpha, beta, gamma). Linear regression models were used to estimate the associations between PAE, PTE, and EEG estimates.

Key Findings

General Findings

• PAE and Brain Activity: Prenatal alcohol exposure (PAE) was associated with increased low-frequency brain activity.
• PTE and Brain Activity: Prenatal tobacco exposure (PTE) was linked to decreased high-frequency brain activity.

Specific Results

1. Alpha Power:
   • Children in the quit-early drinking cluster had increased alpha power (0.116 [95% CI, 0.023 to 0.209] μV²; P = .02) compared to those without PAE.
   • The increase was approximately double for children exposed to continuous drinking (0.211 [95% CI, 0.005 to 0.417] μV²; P = .04).
2. Beta and Gamma Power:
   • Children in the continuous smoking cluster had decreased beta power (-0.031 [95% CI, -0.059 to -0.003] μV²; P = .03) and gamma power (-0.020 [95% CI, -0.039 to -0.000] μV²; P = .04) compared to the nonsmoking cluster.

Sex-Stratified Models

Exploratory sex-stratified models revealed more nuanced findings:

1. Male Participants and Alpha Power:
   • Boys in the quit-early PAE cluster had greater alpha power (0.159 [95% CI, 0.003 to 0.315] μV²; P = .04) compared to those with no PAE.
   • This increase was approximately double for boys with continuous PAE (0.354 [95% CI, 0.041 to 0.667] μV²; P = .03).
2. Male Participants and Beta/Gamma Power:
   • Boys in the continuous PTE cluster had decreased beta power (-0.048 [95% CI, -0.090 to -0.007] μV²; P = .02) and gamma power (-0.032 [95% CI, -0.061 to -0.002] μV²; P = .04) compared to those with no PTE.

The findings from this study underscore the significant impact that prenatal exposure to alcohol and tobacco can have on brain development, as evidenced by alterations in EEG activity during early and middle childhood. These results highlight the importance of avoiding alcohol and tobacco consumption during pregnancy to promote healthier neurodevelopmental outcomes in offspring.

Source: Practice Update