124 - Impact of tobacco smoke exposure on the pediatric nasal microbiome

Poster Number: 124
Publication Number: 124.108

Karen M. Wilson, University of Rochester School of Medicine and Dentistry, Rochester, NY, United States; Hilary Monaco, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Cordelia R. Elaiho, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Bian Liu, Icahn School of Medicine at Mount Sinai, New York, NY, United States; Joseph M. Collaco, Johns Hopkins Medical Institutions, Baltimore, MD, United States; Sharon McGrath-Morrow, Childrens Hospital of Philadelphia, Philadelphia, PA, United States; Jose C. Clemente, Icahn School of Medicine at Mount Sinai, New York, NY, United States

Background: Tobacco smoking is known to change the composition of the microbiome, and emerging evidence suggests that tobacco smoke exposure (TSE) may alter the microbiome of exposed children, potentially increasing their risk of atopy and other diseases.

Objective: To examine the differences in the nasal microbiome of children with and without tobacco smoke exposure.

Design/Methods: Methods: We recruited children in three categories: 1) inpatients with asthma or bronchiolitis (IP); 1-2 year old outpatients (Y-OP), 4-5 year old outpatients (O-OP) at Mount Sinai Hospital, and 1-5 year olds with bronchopulmonary dysplasia (BPD) at Johns Hopkins Hospital (JHH). After consent, parents completed a questionnaire including demographics, health status, tobacco smoke exposure, and factors potentially impacting the microbiome (eg breastfeeding and antibiotic use).  TSE was defined by exposure to second hand smoke within the last 3 months, within the last 24 hours and in the home, and confirmed by salivary/urine cotinine. A nasal swab was collected to sample the nasal microbiome and 16S sequencing performed. Microbiome diversity was assessed and taxonomic data was analyzed for association with smoke exposure and adjusted for false discovery rate.

Results: A total of 236 children were recruited (32 IP, 79 Y-OP, 78 O-OP, 47 BPD; Table 1). Across all patients, nasal microbiome alpha diversity, as measured by Shannon index, Faith’s Phylogenetic Diversity and Observed OTUs, showed no difference between collection sites, by patient type or age. Similarly, beta diversity, as measured by Bray-Curtis dissimilarity and Unweighted UniFrac, showed no difference between collection site, patient type or age.  Among patients with TSE, inpatient status but not outpatient was associated with lower alpha diversity of the nasal microbiome. We did not observe differences in beta diversity among patients with TSE compared to those without TSE, even when controlling for patient type or grouping by age. We find several taxa were associated with TSE, including depletion of a member of the Prevotellaceae family.Conclusion(s): There were no significant differences associated with collection site, indicating our protocols are robust to sampling biases. Alpha diversity was reduced in inpatients with TSE, which could be driven by their acute illness. The finding of taxa differentially enriched with respect to TSE further suggests that tobacco smoke may modify nasal microbiome composition which could potentially alter immune responses to respiratory illnesses.