You are here:
Influences of chemical and non-chemical stressors on childhood obesity
Tulve, N., S. Darney, K. Lichtveld, S. Gaston, K. Thomas, J. Cashdollar, K. Hibbert, N. Louie, AND I. Hahn. Influences of chemical and non-chemical stressors on childhood obesity. 29th Annual Scientific Conference of the International Society of Environmental Epidemiology, Sydney, AUSTRALIA, September 24 - 28, 2017.
To be presented at ISEE 2017
Background/Aim: Children are exposed to diverse chemical and non-chemical stressors in their built, natural, and social environments; and these are thought to contribute to their health and well-being during each developmental stage throughout life. Here we focus on growing evidence that interacting stressors in children’s environments contribute to recent and marked increases in childhood overweight/obesity/obesity-related metabolic dysfunction. Additionally, inherent characteristics (age, sex, genetics) and lifestage-specific activities and behaviors need to be considered along with the stressors. Our objective is to show evidence of the interrelationships between chemical and non-chemical stressors, inherent characteristics, and activities/behaviors in addressing childhood overweight/obesity/obesity-related metabolic dysfunction. Methods: Literature reviews, data mining, meta-analyses, and laboratory work collected information on chemical and non-chemical stressors and their links to childhood overweight/obesity/obesity-related metabolic dysfunction. In vitro evaluations of the obesogenic potentials of chemicals were conducted with the 3T3-L1 pre-adipocyte culture system. Results: A literature survey identified many stressors associated with childhood obesity. In our individual stressor meta-analyses, smoking in the home/during pregnancy, early life antibiotic use, bisphenol A, family income, access to supermarkets, diet, and stress had significant (p<0.05) results and increased odds of the child being overweight/obese. Hours of television and sedentary behavior also increased the odds of the child being overweight/obese. Breastfeeding was associated with reduced odds (p<0.05). Cross-sectional analyses suggested childhood metabolic dysfunction may be associated with interactions between endocrine-disrupting chemicals and selected non-chemical stressors such as family income. Cell culture analyses illustrated the influence of perfluorinated chemicals on adipocyte differentiation and function. Conclusions: Our analyses suggest that childhood overweight/obesity/obesity-related metabolic dysfunction result from interactions of many chemical and non-chemical stressors in combination with inherent characteristics and children’s activities and behaviors. Further research is required to infer causal associations.