Brianna F Moore1, Maggie L Clark2, Annette Bachand2, Stephen J Reynolds2, Tracy L Nelson3, Jennifer L Peel2. 1. Department of Epidemiology, Colorado School of Public Health (CSPH), Aurora, CO. 2. Department of Environmental and Radiological Health Sciences, Colorado State University, Fort Collins, CO. 3. Department of Health and Exercise Science, Colorado State University, Fort Collins, CO.
Abstract
INTRODUCTION: Antioxidant-rich diets may lessen the adverse metabolic responses triggered by exposure to secondhand smoke (SHS), but no studies have investigated these potential interactions. OBJECTIVE: To examine the interaction between diet and exposure to SHS on glycated hemoglobin (HbA1c) levels among 2551 children, ages 12-19 years, who participated in the 2007-2012 National Health and Nutrition Examination Survey (NHANES). METHODS: Exposure to SHS was assessed by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), cotinine, and self-report. Weighted linear regression models evaluated the cross-sectional association between exposure to SHS and HbA1c levels. Additive interaction was assessed by introducing product terms (with SHS) of individual nutrients (dietary fiber, eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA], vitamin C, and vitamin E) to separate models. RESULTS: Over half of the children had NNAL or cotinine levels above the limit of detection (56% and 71%, respectively). The median HbA1c level was 5.2% (95% confidence interval: 5.17%, 5.23%). The interaction results suggest that the effects of exposure to SHS and certain dietary nutrients (EPA, DHA, vitamin C) on HbA1c levels may not be independent. For example, although there was only a slight difference in adjusted mean HbA1c levels across NNAL categories among children with high EPA intakes, the adjusted mean HbA1c level was 0.09% higher for high NNAL as compared to low NNAL among children with low EPA intakes. CONCLUSIONS: Further research is needed to inform public health strategies for limiting increases in HbA1c levels among children. Messages may need to focus both on reducing exposure to SHS and improving diets to obtain the maximum benefit. IMPLICATIONS: Our results suggest that the effects of exposure to SHS and diet on HbA1c levels may not be independent. For example, although there was little effect of exposure to SHS on HbA1c levels among children with high EPA intakes, high exposure to SHS was associated with an increase in HbA1c levels among children with low EPA intakes. Further research is necessary; however, based on these joint effects, strategies for limiting increases in HbA1c levels that focus both on reducing exposure to SHS and improving diets may achieve the largest public health benefits.
INTRODUCTION: Antioxidant-rich diets may lessen the adverse metabolic responses triggered by exposure to secondhand smoke (SHS), but no studies have investigated these potential interactions. OBJECTIVE: To examine the interaction between diet and exposure to SHS on glycated hemoglobin (HbA1c) levels among 2551 children, ages 12-19 years, who participated in the 2007-2012 National Health and Nutrition Examination Survey (NHANES). METHODS: Exposure to SHS was assessed by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), cotinine, and self-report. Weighted linear regression models evaluated the cross-sectional association between exposure to SHS and HbA1c levels. Additive interaction was assessed by introducing product terms (with SHS) of individual nutrients (dietary fiber, eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA], vitamin C, and vitamin E) to separate models. RESULTS: Over half of the children had NNAL or cotinine levels above the limit of detection (56% and 71%, respectively). The median HbA1c level was 5.2% (95% confidence interval: 5.17%, 5.23%). The interaction results suggest that the effects of exposure to SHS and certain dietary nutrients (EPA, DHA, vitamin C) on HbA1c levels may not be independent. For example, although there was only a slight difference in adjusted mean HbA1c levels across NNAL categories among children with high EPA intakes, the adjusted mean HbA1c level was 0.09% higher for high NNAL as compared to low NNAL among children with low EPA intakes. CONCLUSIONS: Further research is needed to inform public health strategies for limiting increases in HbA1c levels among children. Messages may need to focus both on reducing exposure to SHS and improving diets to obtain the maximum benefit. IMPLICATIONS: Our results suggest that the effects of exposure to SHS and diet on HbA1c levels may not be independent. For example, although there was little effect of exposure to SHS on HbA1c levels among children with high EPA intakes, high exposure to SHS was associated with an increase in HbA1c levels among children with low EPA intakes. Further research is necessary; however, based on these joint effects, strategies for limiting increases in HbA1c levels that focus both on reducing exposure to SHS and improving diets may achieve the largest public health benefits.
Authors: Brianna F Moore; Lesley M Butler; Annette M Bachand; Agus Salim; Stephen J Reynolds; Renwei Wang; Tracy L Nelson; Jennifer L Peel; Sharon E Murphy; Woon-Puay Koh; Jian-Min Yuan; Maggie L Clark Journal: Int J Environ Res Public Health Date: 2019-12-17 Impact factor: 3.390