Low dose prenatal tobacco and alcohol result in long lasting changes on electroencephalogram

1. In this cohort study, children with low dose prenatal alcohol and tobacco exposure were found to have differences in electroencephalogram activity even at 11 years of age.

2. Males were particularly vulnerable to the effects of prenatal alcohol exposure compared to females. 

Evidence Level Rating: 2 (Good)

Tobacco and alcohol consumed during pregnancy have teratogenic effects on the fetus, even when consumed in low amounts. In this cohort study, researchers sought to further characterize the effects of PAE and PTE on neurodevelopment in childhood. The study utilized data from the Safe Passage Study conducted by the Prenatal Alcohol and SIDS and Stillbirth (PASS) Network, and involved 649 participants who had electroencephalogram (EEG) recordings obtained at 4, 5, 7, 9, or 11 years old. Maternal data of pregnant people aged 16 years or older were additionally obtained to characterize PAE and PTE. This was then correlated with EEG band powers (theta, alpha, beta, and gamma), via linear regression models. In children with PAE, the association between PAE and heightened alpha EEG power is noted (0.116 [95% CI, 0.023 to 0.209] μV2, P = 0.02), with a dose-dependent effect in continuous exposure after the first trimester (0.211 [95% CI, 0.005 to 0.417] μV2, P = 0.04). Notably, mothers included in the study had quit drinking early into their pregnancy, suggesting that even low and early doses of PAE can result in teratogenicity. Likewise, PTE was associated with decreased beta power, as well as gamma power, compared with children from non-smoking mothers. Interestingly, there appeared to be a sex-related difference where males were particularly susceptible to PTE compared to females. Study findings suggest that even minor exposures to prenatal alcohol and tobacco can result in long-lasting differences in neurodevelopment that can be objectively identified on EEG. This study exists as the first of its kind to utilize a large cohort of EEG data and quantified prenatal exposure data, though the latter did rely on self-reporting. Nonetheless, the study provides further confirmatory evidence to the teratogenicity of prenatal alcohol and tobacco exposure.

Click to read the study in JAMA Network Open

Image: PD

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