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Updated: Jul 10, 2025

Methods to Evaluate Cytotoxicity and Immunosuppression of Combustible Tobacco Product Preparations
Published on: January 10, 2015
Inflammatory marker levels in children with tobacco smoke exposure
E Melinda Mahabee-Gittens1, Georg E Matt2, Matthew J Mazzella3
1Division of Emergency Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Insights
Parent-reported tobacco smoke exposure (TSE) in children is linked to increased C-reactive protein (CRP) levels. Higher IL-8 levels were observed in children with TSE and bacterial infections, highlighting the impact of smoke exposure on pediatric health.
Area of Science:
- Environmental Health
- Pediatric Health
- Immunology
Background:
- Tobacco smoke exposure (TSE) can cause inflammation and immunosuppression.
- These effects may alter inflammatory markers and contribute to pediatric illnesses.
Purpose of the Study:
- To investigate associations between child TSE patterns and inflammatory markers (CRP, IL-8, IL-10).
- To examine relationships between discharge diagnoses and inflammatory markers in pediatric patients exposed to smoke.
Main Methods:
- Saliva samples analyzed for cotinine, CRP, IL-8, and IL-10 in 115 pediatric emergency department patients.
- Parental reports of child TSE and medical record review for discharge diagnoses were used.
- Linear regression models adjusted for demographic and socioeconomic factors.
Main Results:
- Parent-reported TSE was positively associated with C-reactive protein (CRP) levels.
- Child age showed positive associations with CRP and IL-8 levels in the context of reported TSE.
- Children with bacterial diagnoses exhibited higher IL-8 levels compared to other groups.
Conclusions:
- Parent-reported child TSE correlates with increased CRP expression in ill children.
- Elevated IL-8 levels in children with TSE and bacterial infections are supported by findings.
- Further research is recommended to explore these associations in pediatric populations.
Background:
Tobacco smoke exposure (TSE) has inflammatory and immunosuppressive effects which may be associated with altered levels of inflammatory markers and pediatric illnesses.
Objective:
The primary objective was to examine the associations of cotinine-confirmed and parent-reported child TSE patterns and discharge diagnoses with C-reactive protein (CRP), IL-8, and IL-10 in 0-11-year-old pediatric emergency department (PED) patients who lived with ≥ 1 smoker.
Methods:
Saliva samples were obtained from 115 children with a mean (SD) age of 3.5 (3.1) years during the PED visit (T0). Saliva was analyzed for cotinine, CRP, IL-8, and IL-10. Parents self-reported their children's TSE patterns; children's medical records were reviewed to identify and categorize discharge diagnoses. Linear regression models were utilized to find T0 associations of cotinine-confirmed and parent-reported child TSE patterns, and PED diagnoses with each inflammatory marker. All models were adjusted for child race/ethnicity, child sex, annual household income, and housing type. The TSE models also adjusted for child discharge diagnosis.
Results:
At T0, the geometric mean (GeoM) of cotinine was 4.1 ng/ml [95 %CI = 3.2-5.2]; the GeoMs of CRP, IL-8, and IL-10 were 3,326 pg/ml [95 %CI = 2,696-4,105], 474 pg/ml [95 %CI = 386-583], and 1.1 pg/ml [95 %CI = 0.9-1.3], respectively. Parent-reported child TSE patterns were positively associated with ln-transformed CRP levels, while adjusting for the covariates (β^ = 0.012 [95 %CI:0.004-0.020], p = 0.037). In the parent-reported child TSE pattern model, there were significant positive associations between the covariate of child age with CRP and IL-8 levels (p = 0.028 and p < 0.001, respectively). Children with a bacterial diagnosis had higher IL-8 levels (p = 0.002) compared to the other diagnosis groups.
Conclusions:
Results indicate that parent-reported child TSE increases the expression of CRP in ill children and supports prior work demonstrating that IL-8 is higher in children with TSE who have bacterial infections. These findings should be examined in future research with ill children with and without TSE.
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