Childhood obesity and environmental chemicals

Abstract

Childhood and adolescent rates of obesity and overweight are continuing to increase in much of the world. Risk factors such as diet composition, excess caloric intake, decreased exercise, genetics, and the built environment are active areas of etiologic research. The obesogen hypothesis, which postulates that prenatal and perinatal chemical exposure can contribute to risk of childhood and adolescent obesity, remains relatively underexamined. This review surveys numerous classes of chemicals for which this hypothesis has been explored. We focus on human data where they exist and also discuss the findings of rodent and cell culture studies. Organochlorine chemicals as well as several classes of chemicals that are peroxisome proliferator-activated receptor agonists are identified as possible risk factors for obesity. Recommendations for future epidemiologic and experimental research on the chemical origins of obesity are also given.

Figure 1

Maternal chemical exposures are associated with childhood obesity. Maternal exposure to chemicals may target offspring through gametes, placenta, or milk. Potential target tissues of obesogens in offspring can arise through all three germ cell layers of the blastocyst, which continue to differentiate post-natally.