In the last decade, the incidence of diabetes in Canada has nearly doubled and is now estimated to affect one in three individuals. Type 2 diabetes (T2D) is a serious public health problem: governments and health care professional are working to control its propagation, offer better treatment alternatives and reduce its impact on patient quality of life. Insulin resistance is an early event in the development of T2D. Due to its mass and important role in the maintenance of glucose homeostasis, skeletal muscle is believed to play a central role in the development of insulin resistance. The development of this metabolic disorder is multifaceted with obesity, physical activity and diet receiving the most research interest. It is recognized that mitochondrial dysfunction, increased oxidative stress and inflammation are implicated in the development of insulin resistance in muscle. Recently, the environmental hypothesis has been advanced to explain the increased number of patients with T2D. Various persistent organic pollutants (POPs), such as polychlorinated biphenyls (PCBs), bisphenol A (BPA) and p, p-dichlorodiphenylchloroethane (DDT) are being investigated in their relation to T2D. However, despite the importance of skeletal muscle in the development of insulin resistance and T2D, very few studies have focused on the effect of POPs on skeletal muscle energy metabolism. This review will highlight the implication of POPs in the development of diabetes and present work being done to asses POPs’ involvement in observed metabolic disarrangements, specifically at the level of skeletal muscle.