Passive and Active Tobacco Exposure and Children's Lipid Profiles

Despite reductions in smoking rates, exposure to cigarette smoke remains common among US children and adolescents. In adults, active smoking and secondhand smoke (SHS) exposure have been linked to adverse changes in lipid profiles and increases in inflammatory markers. Evidence that such changes are present before adulthood remains limited, and the extent to which active smoking and SHS exposure affect these cardiovascular measures in children has not been thoroughly assessed.

We employed data from 2008 individuals aged 12-19 years from the 2005-2010 National Health and Nutrition Examination Survey. Comparisons of the lipid and inflammatory marker levels among active smokers, those exposed to SHS (as determined by serum cotinine levels), and those unexposed to tobacco smoke were made using linear regression with multiple propensity score adjustment.

Compared to unexposed children, lipid and inflammatory marker profiles did not differ among those exposed to SHS exposure. Among active smokers, differences compared to unexposed children were observed in triglyceride levels ( β=8.5 mg/dL, P = .01), the ratio of triglycerides to high-density lipoprotein ( β=0.2, P = .045), and low-density lipoprotein cholesterol ( β=-4.1 mg/dL , P = .03), though these did not reach levels of confirmatory statistical significance.

After accounting for sociodemographic characteristics and medical comorbidities, serum lipids and markers of systemic inflammation were not associated with SHS exposure. Tobacco smoke exposure in children may require longer durations of compounded effect before serum lipid abnormalities are detected.

This paper adds detail to the study of secondhand smoke's effects on lipid profiles of children and adolescents. Prior research on this topic for these age groups has been limited, and this study provides national, cross-sectional data to show that both secondhand smoke and active smoking in childhood and adolescence is not associated with changes in lipid profiles or markers of inflammation. Tobacco smoke exposure may require longer durations of compounded effect before abnormalities are detected.