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Dai and colleagues used an integrative combination of cognitive testing measures, namely the National Institutes of Health Toolbox Cognition Battery, morphometric assays, and structural MRI to evaluate differences between users and nonusers. In regard to race and ethnicity, 2.1% of the cohort were Asian; 20.3% Hispanic; 14.9% non-Hispanic Black; and 52.1% non-Hispanic White. Slightly more than one-fourth (27.3%) of the cohort had parents who were college graduates, and 13.7% of those with parents who had an annual income of less than $25,000.
At the 2-year follow-up, wave 1 tobacco users continued to exhibit lower scores for Oral Reading Recognition (b = –2.1; SE, 0.5; P <.001), Picture Sequencing Memory (b = –3.0; SE, 0.7; P <.001), and lower crystalized cognition composite scores (b = –2.7; SE, 0.8; P = .005) than nonusers. In sMRI analyses, tobacco ever users demonstrated significantly lower whole-brain measures, including total cortical surface area at wave 1 (b = –5014.8 mm3; SE, 7043.9; P = .002) and cortical volume at wave 1 (b = –174,621.0 mm3; SE, 5857.7; P = .003) and at follow-up (b = –21,790.8 mm3; SE, 7043.9; P = .002) and total intracranial volume (b = –38.,442.8 mm3; SE, 12,057.7; P = .009) at wave 1.
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In a related editorial, Steven R. Laviolette, PhD, University of Western Ontario, wrote, "The findings reported by Dai and colleagues raise many important questions for future clinical and preclinical investigations. Notably, it will be important to determine how persistent these pathophysiological outcomes remain beyond the windows of prepubertal and adolescent brain maturation. In addition, it will be critical to identify the specific molecular mechanisms and biomarkers underlying these enduring, tobacco-induced pathophysiological outcomes."2
He added that the characterization of the underlying mechanisms may promote similar identification of better strategies of intervention and reversal for "neuropsychiatric phenotypes caused by pediatric, adolescent, and perhaps even prenatal nicotine exposure. In addition, advances in genomic and transcriptomic assays may provide improved understanding of the underlying genetic factors that may predispose individuals to a greater risk of accessing nicotine products during critical periods of brain development and of the factors that may render certain individuals at increased risk of severe neuropathological and neurocognitive outcomes after exposure to nicotine during the developmental windows."
REFERENCES
1. Dai HD, Doucet GE, Wang Y, et al. Longitudinal assessments of neurocognitive performance and brain structure associated with initiation of tobacco use in children, 2016 to 2021. JAMA Netw Open. 2022;5(8):e2225991. doi:10.1001/jamanetworkopen.2022.25991.
2. Laviolette SR. Understanding the association of childhood tobacco use with neuropathological outcomes and cognitive performance deficits in vulnerable brains. JAMA Netw Open. 2022;5(8):e2226001. doi:10.1001/jamanetworkopen.2022.26001.