Background: Tobacco smoke exposure increases the risk and severity of lower respiratory tract infections in children, yet the mechanisms remain unclear. We hypothesized that tobacco smoke exposure would modify the lower airway microbiome. Methods: Secondary analysis of a multicenter cohort of 362 children between ages 31 days and 18 years mechanically ventilated for >72 h. Tracheal aspirates from 298 patients, collected within 24 h of intubation, were evaluated via 16 S ribosomal RNA sequencing. Smoke exposure was determined by creatinine corrected urine cotinine levels ≥30 µg/g. Results: Patients had a median age of 16 (IQR 568) months. The most common admission diagnosis was lower respiratory tract infection (53%). Seventy-four (20%) patients were smoke exposed and exhibited decreased richness and Shannon diversity. Smoke exposed children had higher relative abundances of Serratia spp., Moraxella spp., Haemophilus spp., and Staphylococcus aureus. Differences were most notable in patients with bacterial and viral respiratory infections. There were no differences in development of acute respiratory distress syndrome, days of mechanical ventilation, ventilator free days at 28 days, length of stay, or mortality. Conclusion: Among critically ill children requiring prolonged mechanical ventilation, tobacco smoke exposure is associated with decreased richness and Shannon diversity and change in microbial communities. Impact: Tobacco smoke exposure is associated with changes in the lower airways microbiome but is not associated with clinical outcomes among critically ill pediatric patients requiring prolonged mechanical ventilation.This study is among the first to evaluate the impact of tobacco smoke exposure on the lower airway microbiome in children.This research helps elucidate the relationship between tobacco smoke exposure and the lower airway microbiome and may provide a possible mechanism by which tobacco smoke exposure increases the risk for poor outcomes in children.
|Original language||English (US)|
|State||Accepted/In press - 2023|
Bibliographical noteFunding Information:
This study was supported by NICHD Collaborative Pediatric Critical Care Research Network.
Supported in part, by the following cooperative agreements from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), and Heart Lung Blood Institute (NHLBI), National Institutes of Health (NIH): UG1HD083171 (P.M.M.), 1R01HL124103 (P.M.M. and M.K.S.), UG1HD049983 (J.C.), UG01HD049934 (R. Reeder, C. Locandro), UG1HD050096 (K.L.M.), UG1HD083166 (P.S.M.), UG1HD049981 (M.M.P.), and K23HL138461-01A1 (C.L.). NIH/NIEHS funded Human Heath Exposure Analysis Resource (HHEAR) under grant numbers U2CES026555, U2CES026560, and U2CES026553.
© 2023, The Author(s), under exclusive licence to the International Pediatric Research Foundation, Inc.