Abstract
Obesity rates and consequent type 2 diabetes are rising at epidemic rates in the United States and in many other countries around the world.1 Chemical exposures as possible risk factors for obesity and diabetes have received less attention than other risk factors such as eating habits and lifestyle, genetics, family history of diabetes, race/ethnicity, and socioeconomic status.1,2 Nonetheless, epidemiological studies have illustrated how exposure to environmental chemicals, including chemicals identified as potential endocrine disrupting chemicals (EDCs) (e.g., organochlorine pesticides) may increase the risks of obesity and diabetes.3–12 EDCs are compounds that mimic or interfere with the normal action of endocrine hormones such as estrogens, androgens, and thyroid, hypothalamic, and pituitary hormones.2 Humans are exposed to EDCs through direct contact with chemicals such as insecticides, herbicides, and fungicides and indirectly through ingestion of contaminated food and water. Examples of other EDCs include bisphenol A13,14 (used to make polycarbonate plastic water bottles, baby bottles, the linings of metal food and soft-drink cans, thermal receipt paper, and dental sealants) and phthalates15 (plasticizers found in polyvinyl chloride tubing, plastic, cosmetics, shampoos, soaps, pesticides, paint, and other items). There is particular concern about EDCs “that are lipophilic, resistant to metabolism, and/or are able to bioconcentrate up the food chain; [t]his is because these substances become stored in body fats and can be transferred to the developing offspring via the placenta or egg [during pregnancy].”2 The timing of exposure to EDCs is also crucial to the outcome being studied, and exposures during early life stages (e.g., fetal, infant, and pubertal) are particularly important.16 In animal studies, researchers have begun to evaluate how exposure to organophosphorus (OP) pesticides may increase the risks of obesity, insulin resistance, and diabetes.1,17–19 …
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