Contrary to popular opinion, the blame for the obesity epidemic cannot be attributed solely to diet broadly, but relates directly to pesticide and toxic chemical exposures, including residues in food, that may lead to Type 2 diabetes, heart disease, high blood pressure, kidney failure, a breakdown of cartilage and bone within joints, and other metabolic disorders. An increasing body of research shows that exposure to certain pesticides and environmental contaminants initiates various changes in metabolism leading to obesity—not only in the exposed person, but also in offspring. According to medical researchers, obesity “is a complex disease which has reached pandemic dimensions” and has multigenerational effects. The prevalence of obesity increased three-fold from 1980 to 2019.    

>>Tell EPA not to register pesticides that contain obesogens. Tell USDA's Food and Nutrition Service to require organic school lunches.

Environmental obesogens are endocrine-disrupting chemicals that “may increase adipose tissue deposition, expand adipocytic size, regulate appetite and satiety, and slow metabolism to induce the occurrence of obesity.” A recent review of the literature finds, “Environmental obesogens have the potential to induce adipogenesis, increase energy storage, and interfere with appetite and homeostasis within the neuroendocrine system, thereby promoting the development of obesity. Since the obesogen hypothesis was proposed in 2006, more than 50 chemicals have been identified as environmental obesogens. Furthermore, the increasing usage of newly developed chemical products has led to the detection of increasing amounts of new contaminants in the environment, which may have obesogenic effects and cause potential risks to human health.” 

The current list of identified environmental obesogens includes pesticide active ingredients such as chlorpyrifos, atrazine, organotins, and triclosan, as well as contaminants and other ingredients that may be found in pesticide products such as dioxins, phthalates, per- and polyfluoroalkyl substances (PFAS), alkylphenols, and polyaromatic hydrocarbons (PAHs). In addition to the effects of a single obesogen, two or more obesogens may have a synergistic effect, as shown by the interaction of tributyltin (TBT) and perfluorooctanesulfonate (PFOS).  

The inability of the Environmental Protection Agency (EPA) to prevent exposure to obesogens through the use of pesticides is one more failure of the agency to carry out its mandated consideration of endocrine disrupting pesticides. It is evidence of a failed pesticide regulatory system that does not consider and promote nontoxic and beneficial alternatives, such as organic agriculture—which the agency could do under its mandate to protect against “unreasonable adverse effects” to people and the environment in the Federal Insecticide, Fungicide and Rodenticide Act (FIFRA).

While childhood obesity is recognized as a serious problem, the National School Lunch Program of the U.S. Department of Agriculture (USDA)—although improved by the Healthy, Hunger-Free Kids Act of 2010—still provides lunches laced with obesogenic pesticides. To take meaningful steps against childhood obesity, school lunches must be organic. 

>>Tell EPA not to register pesticides that contain obesogens. Tell USDA's Food and Nutrition Service to require organic school lunches. 

The targets for this Action are the U.S. Environmental Protection Agency, the U.S. Department of Agriculture (Food and Nutrition Service), and the U.S. Congress.  

Thank you for your active participation and engagement!