Secondhand smoke exposure and serum cytokine levels in healthy children
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Published on: August 7, 2017
Karen M Wilson1, Sarah C Wesgate, Jennifer Pier
1Department of Pediatrics, University of Colorado School of Medicine, Aurora, CO, USA. karen.wilson@childrenscolorado.org
Insights
Secondhand smoke (SHS) exposure in children is linked to lower levels of key immune signaling molecules, including IL-1β and interferon-gamma (IFN-γ). This suggests SHS may suppress immune responses in young children.
Area of Science:
- Pediatric Immunology
- Environmental Health
- Toxicology
Background:
- Secondhand smoke (SHS) exposure is a known risk factor for childhood morbidity.
- Immune system alterations may underlie the link between SHS and illness in children.
- Limited research exists on SHS effects on children's immune responses.
Purpose of the Study:
- To investigate the association between SHS exposure and serum cytokine levels in healthy children.
- To quantify differences in cytokine concentrations based on SHS exposure levels.
Main Methods:
- Recruited 40 healthy children aged 1-6 years undergoing routine procedures.
- Assessed SHS exposure via parent interview; excluded children with asthma.
- Measured serum cytokines using Luminex assays and cotinine levels via ELISA; analyzed data using mixed-effects models.
Main Results:
- 65% of children had detectable SHS exposure (16 intermediate, 10 high).
- SHS-exposed children showed lower concentrations of IL-1β, IL-4, IL-5, and IFN-γ compared to unexposed children.
- Significant reductions in IL-1β and IFN-γ were observed in any SHS exposure group; high exposure correlated with lower IL-4.
Conclusions:
- SHS exposure is associated with decreased expression of certain pro-inflammatory cytokines, including IFN-γ, in children.
- Further research is required to elucidate the acute and chronic immunological impacts of SHS on children.
Introduction:
Exposure to secondhand smoke (SHS) is associated with morbidity in children. Alterations in immune responses may explain this relationship, but have not been well-studied in children. Our objective was to determine the association between SHS exposure and serum cytokine levels in healthy children.
Methods:
We recruited 1-6 year old patients undergoing routine procedures. A parent interview assessed medical history and SHS exposure. Children with asthma were excluded. Blood was collected under anesthesia. We used Luminex Multiplex Assays to test for a panel of cytokines; cotinine was determined using an enzyme-linked immunosorbent assay. Children were categorized as no, intermediate, or high exposure. A mixed-effects model was fit to determine differences in cytokines by exposure level.
Results:
Of the 40 children recruited, 65% (N=26) had SHS exposure; 16 intermediate, and 10 high. There were no differences by demographics. In bivariate analyses, children exposed to SHS had lower concentrations of IL-1β, IL-4, IL-5, and IFN-γ than those with no exposure. In the mixed-effects model, children with any SHS exposure had significantly lower concentrations of IL-1β (0.554 pg/mL vs. 0.249 pg/mL) and IFN-γ (4.193 pg/mL vs. 0.816 pg/mL), and children with high exposure had significantly lower mean concentrations of IL-4 (8.141 pg/mL vs. 0.135 pg/mL) than children with no exposure.
Conclusions:
This study suggests that SHS exposure decreases expression of some pro-inflammatory cytokines in SHS exposed children, including IFN-γ. Further research to describe the acute and chronic effects of SHS on the immune systems of children is needed.
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