The observed association of aspirin ingestion and symptomatic esophageal hiatus hernia is ascribed by me to injury of the esophageal mucosa during delayed passage of ingested aspirin from mouth to stomach. Physiologic alterations attributable to esophageal hiatus hernia act to prolong contact between swallowed material and the esophageal mucosa. This prolongation of contact between swallowed aspirin and the esophageal mucosa predisposes patients with esophageal hiatus hernia, and who are aspirin-users, to develop symptomatic esophagitis. Clinical data obtained from human subjects are presented which show that swallowed material may become trapped for extended periods in the esophagi of patients with esophageal hiatus hernia. Also, the capability of aspirin to injure alkaline mucosa by direct contact, in the absence of acid, is demonstrated.