Early Tobacco Use in Children Leads to Poorer Cognitive Performance, Reduced Brain Structure

Article

Those who had used tobacco at any time demonstrated multiple significantly lower whole-brain measures than nonusers, including total cortical surface area, cortical volume, and total intracranial volume.

Hongying Daisy Dai, PhD, University of Nebraska Medical Center

Hongying Daisy Dai, PhD

Data from a large-scale study of more than 10,000 children aged 9 to 10, findings showed that initiating tobacco use was associated with inferior cognitive performance and reduced brain structure with sustained effects at 2-year follow-up.1

There were 116 children who reported ever using tobacco products, deemed the ever user group. This group exhibited lower scores on the Picture Vocabulary Test (mean, b = –2.9; SE, 0.6; P <.001), lower crystalized cognition composite scores (b = –2.4; SE, 0.5; P <.001), and total cognition composite scores (b = –2.9; SE, 0.5; P = .01). At the 2-year follow-up, tobacco ever users had lower cortical volume in frontal, parietal, and temporal lobes than nonusers.

"Electronic cigarettes and smokeless tobacco products should not be treated as harm reduction alternatives for youth," lead investigator Hongying Daisy Dai, PhD, University of Nebraska Medical Center, and colleagues, concluded.1 "Comprehensive intervention strategies and tobacco control policies are needed to prevent tobacco initiation."

A total of 11,729 children from 21 US sites enrolled in the Adolescent Brain Cognitive Development (ABCD) study were included wave 1 from October 2016 to October 2018, and followed up 2 years later from August 2018 to January 2021. Participants were asked to complete a survey about their tobacco use, and products such as electronic cigarettes (e-cigarettes), cigarettes, cigars, smokeless tobacco, hookah, pipes, and nicotine replacement.

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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.
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