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Publication Detail

Title: The Association of Environmental Tobacco Smoke Exposure and Inflammatory Markers in Hospitalized Children.

Authors: Mahabee-Gittens, E Melinda; Merianos, Ashley L; Fulkerson, Patricia C; Stone, Lara; Matt, Georg E

Published In Int J Environ Res Public Health, (2019 11 21)

Abstract: BACKGROUND: Environmental tobacco smoke (ETS) exposure is associated with altered cytokine levels in children. We sought to examine ETS exposure prevalence and the relationship between ETS exposure and cytokine levels in a sample of hospitalized children. (2) Methods: Inflammatory markers (IL-8, IL-1β, IL-10, and TNF-α) and cotinine were measured in saliva of hospitalized, nonsmoking children (N = 112). To assess the association between ETS exposure and immune system response, we built a multivariate regression model including the four inflammatory markers as the response variables and cotinine, age, sex, and discharge diagnosis as explanatory variables while assessing possible interaction effects. (3) Results: Mean age (SD) was 5.8(5.0) years; Geometric Mean (GeoM) cotinine = 1.8 [95% CI = 1.4-2.2]. Children with non-inflammatory other diagnoses had lower IL-10 (p = 0.003) and TNF-α (p = 0.009) levels than children with inflammatory other diagnoses. Children with asthma (p = 0.01) and bacterial illnesses and/or pneumonia (p = 0.002) had higher IL-8 levels. Independent of diagnosis, there was a significant curvilinear association between cotinine and IL-1β (p = 0.002) reflecting no association for cotinine levels <5 ng/mL and a positive association for >5 ng/mL. (4) Conclusions: Children with higher ETS exposure levels have higher IL-1β levels regardless of age, sex, and diagnosis. ETS exposure may increase pro-inflammatory immune responses in children and may interfere with native immune responses and the ability to heal and fight infection.

PubMed ID: 31766400 Exiting the NIEHS site

MeSH Terms: Adolescent; Asthma/chemically induced*; Biomarkers/analysis; Child; Child, Hospitalized/statistics & numerical data; Child, Preschool; Cotinine/analysis*; Environmental Exposure/adverse effects*; Female; Humans; Infant; Infant, Newborn; Inflammation/chemically induced*; Interleukin-1beta/analysis*; Male; Saliva/chemistry*; Tobacco Smoke Pollution/adverse effects*

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