PRENATAL tobacco exposure accelerates cortical thinning in frontal brain regions during early adolescence, while prenatal alcohol exposure shows no significant association with cortical development, new research has shown.
Understanding how prenatal substance exposure influences long-term brain development is critical, as these exposures occur during a period of rapid neurogenesis yet their effects may only manifest years later. This cohort study addresses a gap by examining longitudinal cortical changes rather than single time points, providing insights into developmental trajectories long after initial exposures.
The study analysed 5,417 youths aged 9–12 years from the Adolescent Brain Cognitive Development (ABCD) Study across 21 US sites, with cortical thickness and surface area measured approximately two years apart. Prenatal exposures were categorised using caregiver reports of tobacco (PTE) and alcohol (PAE) use during pregnancy. Statistical analysis revealed PTE correlated with baseline cortical thickness in bilateral parahippocampal and left lateral orbitofrontal cortices (e.g., right parahippocampal: |rp| = 0.04; P < .001). Crucially, PTE was linked to accelerated cortical thinning in medial/anterior frontal regions (e.g., right rostral middle frontal: |rp| = 0.04; P < .001), with this thinning associated with increased externalising behaviours and sleep problems. PAE showed no structural or developmental associations. Post hoc analyses indicated weaker effects when tobacco use continued post-pregnancy recognition or without concurrent alcohol use.
These findings demonstrate that prenatal tobacco, but not alcohol, exposure alters cortical development trajectories in early adolescence, with tangible behavioural consequences. Clinically, this highlights the need for early screening for prenatal tobacco exposure in paediatric assessments, enabling targeted support for at-risk youths through behavioural interventions or neurodevelopmental monitoring. Future research should integrate biomarker-based exposure verification (e.g., cotinine) and explore whether interventions can mitigate these neurodevelopmental impacts. For practice, recognising PTE as a risk factor for accelerated cortical thinning could inform family counselling and preventive strategies during prenatal care.
Reference
Marshall AT et al. Prenatal tobacco and alcohol exposure and cortical change among youths. JAMA Netw Open. 2025;8(6):e2516729.
