ENVIRONMENTAL tobacco smoke was associated with greater sleep fragmentation in children evaluated for suspected sleep-disordered breathing.
Children exposed to environmental tobacco smoke had a 67% higher arousal index than unexposed children, according to a prospective study using overnight polysomnography and urinary cotinine testing.
Researchers evaluated 30 children aged 1–12 years who had been referred for suspected sleep-disordered breathing. The cohort had a mean age of 5.8 years, and approximately 73% were boys. Parents completed questionnaires assessing household smoking and sleep, while urine samples collected after polysomnography were analyzed for cotinine, a nicotine metabolite used as a marker of tobacco smoke exposure.
Nearly half of the children had at least one parent who smoked. Among these parents, 82% reported smoking at least 10 cigarettes daily. However, 60% denied that their child experienced environmental tobacco smoke exposure.
Urinary cotinine levels correlated with parent-reported exposure, supporting the questionnaire findings.
Although average sleep duration and sleep efficiency did not differ significantly between the exposed and unexposed groups, analyses based on urinary cotinine revealed measurable associations.
Higher cotinine concentrations correlated with shorter total sleep time and lower sleep efficiency. Cotinine was inversely correlated with sleep duration at r=−0.36 and with sleep efficiency at r=−0.43, with both associations reaching statistical significance.
The findings suggest that continuous biomarker measurements may detect changes in pediatric sleep quality that comparisons between exposure groups do not capture. The higher arousal index among exposed children further indicated that environmental tobacco smoke may interrupt sleep continuity even when total sleep measures appear similar.
Environmental tobacco smoke was not associated with the apnea–hypopnea index, oxygen desaturation index, mean oxygen saturation, or lowest recorded oxygen saturation.
These results suggest that secondhand smoke may impair sleep quality independently of respiratory event frequency or oxygen desaturation. The researchers proposed that nicotine could influence arousal pathways and circadian regulation, while tobacco smoke related airway inflammation may also contribute to disrupted sleep.
The study was limited by its small sample, inclusion of only nonobese children referred for suspected sleep-disordered breathing, and reliance on a single laboratory night. Medical factors including asthma, atopy, prematurity, and medication use were not documented.
Nevertheless, the findings support routinely assessing environmental tobacco smoke exposure when evaluating children with suspected sleep disorders. Reducing exposure may represent a modifiable approach to improving pediatric sleep quality, even when conventional apnea measures are unchanged.
Reference
Arwas N et al. Environmental tobacco smoke and sleep fragmentation in children with suspected sleep apnea. Sci Rep. 2026;16:21616.
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