Proposed pathophysiologic mechanisms relating gastroesophageal reflux disease to cigarette smoking are reviewed. Acute experiments have shown that smokers have chronically diminished lower esophageal sphincter (LES) pressure and that periods of smoking are associated with an increased rate of reflux events. Reflux occurred primarily by the 'abdominal strain mechanism' rather than by transient LES relaxation. Smoking also caused chronically diminished salivary function that results in prolonged acid clearance time. Thus, smoking potentially increases esophageal acid exposure, both by increases in the number of reflux events, and a prolongation of the esophageal acid clearance time.