Secondhand Smoke Exposure Measured in Urinary Cotinine Levels and Severity of Pediatric Sleep Apnea

Abstract

Exposure to secondhand smoke has been associated with numerous health problems in children, including obstructive sleep apnea. Secondhand smoke exposure may be a risk factor for increased pediatric sleep apnea severity. To assess the association of secondhand smoke exposure (SHSe), quantified by urinary cotinine levels, with severity of obstructive sleep apnea (OSA) in children. This was a prospective cohort trial including pediatric patients from 3 to 16 years of age with sleep-disordered breathing who underwent a polysomnogram at a tertiary-level children's hospital in the US in either March 2014 to October 2016 or March 2020 to March 2021. Urine specimens were analyzed for cotinine, an important metabolite of nicotine. Each child's caregiver completed a validated SHSe questionnaire. Data were analyzed from February to June 2023. OSA and secondhand smoke. SHSe and severity of pediatric OSA, quantified by urinary cotinine levels and obstructive apnea hypopnea index (AHI) scores. Secondary outcomes were association of urinary cotinine levels with nadir oxygen saturation, sleep-related quality of life measured by the OSA-18 questionnaire, and caregiver-reported smoking habits (collected through a questionnaire). The study included 116 patients with a median (IQR) age of 6 (5-9) years, among whom 51 (45%) had obesity. The median (IQR) AHI was 3.0 (1.2-8.0), with 28 children (30.0%) having severe disease (AHI >10). Thirty-four children (29.0%) were found to have a positive result for urine cotinine screening, with a mean (SD) level of 11.7 (9.4) ng/mL. The percentage of children with SHSe was less than anticipated. There was no association identified between urinary cotinine levels and either AHI (ρ = -0.04; 95% CI, -0.22 to 0.15) or nadir oxygen saturation (ρ = -0.07; 95% CI, -0.26 to 0.11). Furthermore, SHSe was not associated with the presence of severe OSA (odds ratio, 0.70; 95% CI, 0.26 to 1.90). Children whose caregivers reported indoor SHSe were more likely to have a detectable urinary cotinine level (odds ratio, 20.3; 95% CI, 6.67 to 61.8). This cohort study did not identify any clinically meaningful association between SHSe, quantified by urinary cotinine level, and pediatric OSA severity. Future research with a larger number of children with SHSe is needed to confirm these findings and determine whether SHSe affects OSA treatment outcomes in children.