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Published on: October 8, 2013
Passive smoking induces nasal biofilms in children
Samy Elwany1, Mohamed A Gamea2, Iman Talaat3
1Department of Otolaryngology, Alexandria Faculty of Medicine, Alexandria, Egypt.
Insights
Children exposed to secondhand smoke may develop nasal biofilms, increasing their risk of respiratory infections. This study found a link between passive smoking and biofilm formation in children
Area of Science:
- Otolaryngology
- Pediatric Respiratory Medicine
- Microbiology
Background:
- Passive exposure to cigarette smoke is linked to childhood respiratory issues.
- The relationship between secondhand smoke and nasal biofilm formation in children is unknown.
- Household passive smoking is a potential trigger for nasal biofilm development.
Purpose of the Study:
- To investigate the hypothesis that household passive smoking induces nasal biofilm formation in children.
- To explore the association between passive smoke exposure and the presence of nasal biofilms.
Main Methods:
- 20 children (6-12 years) with passive smoke exposure underwent inferior turbinate reduction.
- A control group of 20 children with no smoke exposure also had surgery.
- Nasal biopsies from the inferior turbinate were analyzed using electron microscopy.
Main Results:
- Nasal biofilms were found in 11/20 children exposed to passive smoke, with S. aureus in ten.
- Only one child in the control group had a nasal biofilm.
- Longer smoke exposure, higher cotinine levels, and parental smoking intensity correlated with biofilm formation.
Conclusions:
- Children exposed to household passive smoke may develop nasal biofilms.
- Nasal biofilm development could heighten susceptibility to sinonasal and respiratory infections.
- This preliminary report highlights a potential link between passive smoking and pediatric sinonasal health.
Objectives:
Passive exposure of children to cigarette smoke has been implicated in several recalcitrant respiratory childhood disorders. However, to our knowledge, no information is available regarding the connection between passive exposure to tobacco smoke and the formation of nasal biofilms in children. The present study was therefore geared at investigating the hypothesis that exposure of children to household passive smoking may induce the formation of nasal biofilms.
Methods:
The study included 20 children between the ages of 6 and 12 years with a positive history of prolonged exposure to household passive smoke, and who required inferior turbinate reduction together with other procedures. Another 20 children who required similar surgeries but with negative history of exposure to household smoking formed the control group. None of children, in the study and control groups, had evidence of adenoids or infective rhinosinusitis. At the time of surgery, a tiny biopsy was taken from the lower border of the inferior turbinate. The specimens were processed for scanning and transmission electron microscopy.
Results:
The nasal mucosa of 11 out of 20 children with positive history of exposure to passive smoking showed biofilm formation. Ten of these biofilms grew S. aureus. On the other hand, only one child in the control group showed nasal biofilm. Longer exposure to tobacco smoke and higher urinary cotinine levels were associated with more frequent biofilm formation. Likewise, children of heavy smokers developed biofilms more frequently than other children. On the other hand, the age of the children and nasal allergy had no effect on the chances of biofilm formation.
Conclusions:
This is a preliminary report showing that children exposed to household passive cigarette smoking may develop nasal biofilms. Development of these biofilms may increase susceptibility of affected children to persistent sinonasal and possibly other respiratory infections.
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