In Utero Exposure to Alcohol and Tobacco and Electroencephalogram Power During Childhood

Author:

Pini Nicolò12,Sania Ayesha12,Rao Shreya12,Shuffrey Lauren C.3,Nugent J. David12,Lucchini Maristella12,McSweeney Marco4,Hockett Christine56,Morales Santiago7,Yoder Lydia4,Ziegler Katherine56,Perzanowski Matthew S.8,Fox Nathan A.4,Elliott Amy J.56,Myers Michael M.9,Fifer William P.129

Affiliation:

1. Department of Psychiatry, Columbia University Irving Medical Center, New York, New York

2. Division of Developmental Neuroscience, New York State Psychiatric Institute, New York

3. Department of Child and Adolescent Psychiatry, NYU Grossman School of Medicine, New York, New York

4. Department of Human Development and Quantitative Methodology, University of Maryland, College Park

5. Center for Pediatric & Community Research, Avera Research Institute, Sioux Falls, South Dakota

6. Department of Pediatrics, University of South Dakota School of Medicine, Sioux Falls

7. Department of Psychology, University of Southern California, Los Angeles

8. Department of Environmental Health Sciences, Mailman School of Public Health at Columbia University, New York, New York

9. Department of Pediatrics, Columbia University Irving Medical Center, New York, New York

Abstract

ImportancePrenatal alcohol exposure (PAE) and prenatal tobacco exposure (PTE) are risk factors associated with adverse neurobehavioral and cognitive outcomes.ObjectiveTo quantify long-term associations of PAE and PTE with brain activity in early and middle childhood via electroencephalography (EEG).Design, Setting, and ParticipantsThis cohort study included participants enrolled in the Safe Passage Study (August 2007 to January 2015), from which a subset of 649 participants were followed up in the Environmental Influences on Child Health Outcomes Program. From September 2018 through November 2022, EEG recordings were obtained at ages 4, 5, 7, 9, or 11 years. Data were analyzed from November 2022 to November 2023.ExposuresMaternal self-reported consumptions of alcohol and tobacco during pregnancy were captured at the recruitment interview and at up to 3 visits during pregnancy (20-24, 28-32, and ≥34 weeks’ gestation). Classifications of PAE (continuous drinking, quit-early drinking, and nondrinking) and PTE (continuous smoking, quit-early smoking, and nonsmoking) were previously obtained.Main Outcomes and MeasuresEEG band powers (theta, alpha, beta, gamma) were extracted from the EEG recordings. Linear regression models were used to estimate the associations of PAE and PTE with EEG estimates.ResultsThe final sample included 649 participants (333 [51.3%] female) aged 4, 5, 7, 9, or 11 years. Children whose mothers were in the quit-early drinking cluster had increased alpha power (0.116 [95% CI, 0.023 to 0.209] μV2; P = .02) compared with individuals without PAE. The magnitude of this increase was approximately double for children exposed to continuous drinking (0.211 [95% CI, 0.005 to 0.417] μV2; P = .04). Children whose mothers were 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 with the nonsmoking cluster. In exploratory sex-stratified models, male participants in the quit-early PAE cluster had greater EEG power in the alpha band (0.159 [95% CI, 0.003 to 0.315] μV2; P = .04) compared with those with no PAE, and the difference was approximately double for male participants with continuous PAE (0.354 [95% CI, 0.041 to 0.667] μV2; P = .03). Male participants in the continuous PTE cluster had decreased beta (−0.048 [95% CI, −0.090 to − 0.007] μV2; P = .02) and gamma (−0.032 [95% CI, −0.061 − 0.002] μV2; P = .04) power compared with those with no PTE.Conclusions and RelevanceThese findings suggest that even low levels of PAE and PTE were associated with long-term alterations of brain activity.

Publisher

American Medical Association (AMA)

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