Allergic rhinitis, microbiota and passive smoke in children: A pilot study

Abstract

Background Allergic rhinitis (AR) is one of the most common allergic diseases affecting children. Objective assessment of nasal obstruction is possible through active anterior rhinomanometry (AAR). Several factors, such as passive smoke exposure (PSE), are triggers for worsening nasal obstruction and chronic inflammation. PSE affects bacterial eubiosis in the upper respiratory tract. This study evaluates the influence of PSE and cotinine levels on both nasal obstruction and local microbiome composition in children with AR. Methods Fifty patients (aged between 6 and 16 years) with AR monosensitized grass pollen were enrolled. They underwent skin prick tests, a nasal swab to evaluate the microbial composition of the anterior nostrils, a basal AAR, a post‐decongestion AAR, and spirometry. Serum cotinine levels were assessed to evaluate PSE. Results A significantly lower percentage of mean nasal flow (mNF%) was observed before and after hydrazine administration in subjects exposed to passive smoke (Exp group) compared with the non‐exposed group. In contrast, higher cotinine levels were observed in the Exp group than in the controls. PSE has been associated with a decrease in biodiversity and a change in the nasal microbiome composition; instead, although to a different extent, the abundance of specific taxa resulted in being correlated to cotinine levels and nasal flow. Conclusion Children with AR exposed to passive smoke with positive serum cotinine could represent a risk factor for developing nasal obstruction and microbial dysbiosis, suggesting their possible role in pathophysiological processes.

The Impact of Smoking on Microbiota: A Narrative Review

“…Smoking—even when passive—seems to have the strongest effect on the overall microbial community composition, since it can simultaneously deplete members of the normal commensal airway flora and enrich potential pathogens, with various mechanisms which resembles the ones reported for the oral cavity [ 35 , 37 , 38 ]. First of all, cigarette smoke contains potential respiratory pathogens, including Acinetobacter , Clostridium , Klebsiella , Pseudomonas aeruginosa , and Serratia spp.…”

“…First of all, cigarette smoke contains potential respiratory pathogens, including Acinetobacter , Clostridium , Klebsiella , Pseudomonas aeruginosa , and Serratia spp. Moreover, smoking enhances bacterial adhesion to respiratory epithelial cells, disrupts the mucociliary clearance, and impairs the host immune responses [ 35 , 37 , 38 ]. The pathogenetic effect of tobacco smoke on the respiratory tract is a consolidated axiom.…”

(R)Evolution in Allergic Rhinitis Add-On Therapy: From Probiotics to Postbiotics and Parabiotics

“…Fetal–maternal microbiota interchange occurs already during intrauterine life. Many prenatal factors (diet, atopy, smoking status, antibiotic) and the genetic background of the infant may influence the colonization process that occurs in a predetermined order [ 16 , 18 ]. Subsequently, even if the type of delivery is widely considered a significant step in the first microbiota settlement, recently, several studies have proposed a rearrangement of infant microbiota mainly determined by body niches and not by the delivery type.…”

Tobacco Smoke Exposure is Characterized by a Distinct Nasal Rhinotype in a Pediatric Population

“…For example, chronic rhinosinusitis is associated with higher levels of Staphylococcus aureus in infants 16 . In allergic rhinitis, the sinonasal microbiome of adults has higher diversity during the allergic season 16 , while children who reported tobacco smoke exposure had lower diversity in the anterior nostrils 17 . Early asthma diagnosis is associated with nasopharynx colonization of Streptococcus in infants 18 .…”