Detrimental effects of secondhand smoke exposure on infants with cystic fibrosis
Related Experiment Video
Updated: May 2, 2026

Impact Assessment of Repeated Exposure of Organotypic 3D Bronchial and Nasal Tissue Culture Models to Whole Cigarette Smoke
Published on: February 12, 2015
Benjamin T Kopp1, Lisa Sarzynski, Sabrina Khalfoun
1Section of Pediatric Pulmonology, Nationwide Children's Hospital, Columbus, Ohio; Center for Microbial Pathogenesis, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio.
Insights
Secondhand smoke (SHS) exposure in infants with cystic fibrosis (CF) is linked to poorer growth and increased respiratory issues. Early parental smoking cessation is crucial to prevent these complications.
Area of Science:
- Pediatric Pulmonology
- Environmental Health
- Genetics and Disease
Background:
- Secondhand smoke (SHS) exposure poses risks to children's respiratory, immune, and nutritional health.
- Limited data exists on SHS effects in infants with cystic fibrosis (CF).
Purpose of the Study:
- To investigate the impact of SHS exposure on growth, lung function, and microbiology in infants with CF.
Main Methods:
- Retrospective chart review of 75 infants with CF from 2008-2012.
- Comparison of growth, lung function, chest CT imaging, and microbiology between SHS-exposed and non-exposed infants at 4 and 12 months.
Main Results:
- SHS-exposed infants with CF showed decreased growth between 4 and 12 months.
- SHS exposure correlated with increased bronchodilator responsiveness and air trapping.
- Increased detection of methicillin-resistant Staphylococcus aureus (MRSA) and anaerobic bacteria in SHS-exposed infants.
Conclusions:
- SHS exposure in CF infants is associated with impaired growth and altered lung function.
- SHS exposure increases the risk of MRSA and anaerobic bacterial colonization.
- Urgent parental smoking cessation interventions are recommended to mitigate SHS-related complications in CF infants.
Rationale:
Secondhand smoke (SHS) has deleterious respiratory, immune, and nutritional effects in children, but there is little data regarding the effects of SHS exposure in infants with cystic fibrosis (CF).
Methods:
A retrospective chart review was undertaken from 2008 to 2012 of 75 infants with CF. Growth, lung function, Chest CT imaging, and microbiologic characteristics were compared between 4 and 12 months for SHS and non-SHS exposed patients.
Results:
SHS exposed infants with CF had decreased growth between 4 and 12 months compared to non-SHS exposed infants. SHS exposure was associated with increased bronchodilator responsiveness and air trapping, but no other lung function or radiologic differences. SHS exposure was also associated with increased methicillin resistant Staphylococcus aureus (MRSA) and anaerobic growth on respiratory culture. There was no difference in Pseudomonas aeruginosa between groups. There were no differences in antibiotic use or hospitalizations between the groups.
Conclusions:
SHS exposure in CF infants is associated with diminished growth, increased air trapping and bronchodilator responsiveness, and propensity to culture MRSA and facultative anaerobic bacteria, suggesting the need for early, aggressive parental smoking cessation interventions to prevent SHS exposure complications.
Related Concept Videos
Cystic Fibrosis: Pathogenesis
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...
Chronic Obstructive Pulmonary Disease II: Emphysema
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features
Upper Respiratory Drugs: Antitussives, Expectorants, and Mucolytics
Antitussives include codeine, dextromethorphan (Robitussin), and benzonatate (Tessalon). Codeine and dextromethorphan exert their effects centrally by suppressing the cough reflex center in the medulla. Benzonatate operates peripherally within the respiratory tract by...
Cystic Fibrosis: Management
Sinus disease and chronic...
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
Chronic Inflammation

