Ashley L Merianos1, Roman A Jandarov2, Jane C Khoury3, E Melinda Mahabee-Gittens4. 1. School of Human Services, University of Cincinnati, Cincinnati, Ohio. Electronic address: ashley.merianos@uc.edu. 2. Division of Biostatistics and Bioinformatics, Department of Environmental Health, College of Medicine, University of Cincinnati, Cincinnati, Ohio. 3. Division of Biostatistics and Epidemiology, Cincinnati Children's Hospital Medical Center, College of Medicine, University of Cincinnati, Cincinnati, Ohio. 4. Division of Emergency Medicine, Cincinnati Children's Hospital Medical Center, College of Medicine, University of Cincinnati, Cincinnati, Ohio.
Abstract
PURPOSE: We investigated the association between tobacco smoke exposure (TSE) as measured by serum cotinine and lipoprotein cholesterols and adiposity in adolescents. METHODS: We performed a secondary analysis of 1999-2012 National Health and Nutrition Examination Survey data including participants 12-19 years old. We examined TSE: unexposed (<.05 ng/mL), passively exposed (.05-2.99 ng/mL), and actively exposed (≥3 ng/mL); lipid profiles: total cholesterol, high-density lipoprotein cholesterol (HDL-C), non-HDL-C, low-density lipoprotein cholesterol (LDL-C), and triglycerides; and adiposity: body mass index z-score (BMIZ), waist circumference (WC), and waist-to-height ratio (WHtR). Covariates were age, sex, race/ethnicity, income, diet, and physical activity. Multiple regression models were used to assess the association between TSE and lipid profile variables separately, and then TSE and adiposity measures separately, adjusting for covariates. We performed logistic regression to examine the association of TSE with body mass index and WHtR classifications. RESULTS: Of the 11,550 participants, 41.7% were unexposed to tobacco smoke, 40.5% were passively exposed, and 17.8% were actively exposed. Compared with unexposed, participants with active TSE had lower total cholesterol, lower HDL-C, and higher triglycerides; higher BMIZ, higher WC, and higher WHtR; participants with passive TSE had lower HDL-C, higher total cholesterol, and higher LDL-C; higher BMIZ, higher WC, and higher WHtR. Participants actively exposed were at increased odds of being obese or WHtR ≥.65, and those passively exposed were at increased odds of being overweight, obese, or WHtR ≥.65. CONCLUSIONS: Active TSE and passive TSE are differentially associated with factors within the lipid profile and adiposity, independent of covariates. TSE prevention efforts should start as early as childhood and continue throughout adolescence and adulthood.
PURPOSE: We investigated the association between tobacco smoke exposure (TSE) as measured by serum cotinine and lipoprotein cholesterols and adiposity in adolescents. METHODS: We performed a secondary analysis of 1999-2012 National Health and Nutrition Examination Survey data including participants 12-19 years old. We examined TSE: unexposed (<.05 ng/mL), passively exposed (.05-2.99 ng/mL), and actively exposed (≥3 ng/mL); lipid profiles: total cholesterol, high-density lipoprotein cholesterol (HDL-C), non-HDL-C, low-density lipoprotein cholesterol (LDL-C), and triglycerides; and adiposity: body mass index z-score (BMIZ), waist circumference (WC), and waist-to-height ratio (WHtR). Covariates were age, sex, race/ethnicity, income, diet, and physical activity. Multiple regression models were used to assess the association between TSE and lipid profile variables separately, and then TSE and adiposity measures separately, adjusting for covariates. We performed logistic regression to examine the association of TSE with body mass index and WHtR classifications. RESULTS: Of the 11,550 participants, 41.7% were unexposed to tobacco smoke, 40.5% were passively exposed, and 17.8% were actively exposed. Compared with unexposed, participants with active TSE had lower total cholesterol, lower HDL-C, and higher triglycerides; higher BMIZ, higher WC, and higher WHtR; participants with passive TSE had lower HDL-C, higher total cholesterol, and higher LDL-C; higher BMIZ, higher WC, and higher WHtR. Participants actively exposed were at increased odds of being obese or WHtR ≥.65, and those passively exposed were at increased odds of being overweight, obese, or WHtR ≥.65. CONCLUSIONS: Active TSE and passive TSE are differentially associated with factors within the lipid profile and adiposity, independent of covariates. TSE prevention efforts should start as early as childhood and continue throughout adolescence and adulthood.
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