Obesity and related disorders have become a significant burden worldwide. In 2014, the World Health Organization estimated that ~2 billion people around the world were overweight and of those, 600 million people were obese. Obesity is also associated with metabolic conditions such as hypertension, cardiovascular disease, and type 2 diabetes. The additional health care costs for the treatment of these conditions are estimated to be $2 trillion annually worldwide. Thus, understanding the factors that are contributing to this epidemic becomes timely and important. The causal factors associated with obesity were traditionally ascribed to positive energy balance. More recently, evidence linking obesity with certain genetic mutations and the balance of bacterial flora in the gut microbiome is mounting. However, the prevalence of obesity and overweight in infants and in other animal species that live in urban areas indicates that there may be other environmental factors that should not be overlooked. In this chapter, we review the possible contributions of chemical obesogens to the obesity epidemic and other obesity comorbidities such as cardiovascular diseases. We discuss in vitro approaches currently used to determine the molecular mechanisms through which chemicals might act as obesogens as well as in vivo approaches using animal models to test the capability of obesogens to promote obesity. Since obesity is a condition with a developmental origin, we particularly focus on the effect of obesogens during in utero development and the potential transgenerational consequences of this exposure. We review the current knowledge about two different obesogens: the organotin tributyltin (TBT), whose mode of action is at least partly understood, and the estrogenic chemical bisphenol A (BPA), whose widespread use makes exposure ubiquitous. We provide an overview of the direction this field is following to better understand the relationship between obesogen exposure and the obesity epidemic.