There is a growing awareness that inflammation plays a contributory role in numerous pathologies, including pancreatic carcinogenesis. Inflammatory states are characterized by the creation of reactive oxygen species and the induction of cell cycling for tissue growth and repair. The initiation, promotion and expansion of tumors may be influenced by numerous components that function in the inflammatory response. Recognized risk factors for pancreatic cancer include cigarette smoking, chronic/hereditary pancreatitis, obesity and type II diabetes. Each risk factor is linked by the fact that the inflammatory state significantly drives its pathology. This article will outline how inflammatory mechanisms are etiologically linked to pancreatic adenocarcinoma.