The role of smoking in the pathogenesis of gastrooesophageal reflux disease has been controversial since the early 1970s when Stanciu reported the two to be 92% epidemiologically associated (a study subsequently challenged by inconsistencies in the observational data). Mechanistically, reflux disease is caused by excessive oesophageal acid exposure, which is potentially attributable to excessive reflux events and/or prolonged acid clearance. Currently, the best available pH monitoring data confirm that smoking increases oesophageal acid exposure. Smoking reduces lower oesophageal sphincter (LOS) pressure and predisposes to strain-induced reflux. Consistent with this, smoking has been shown to cause an increased number of reflux events that are not attributable to increased transient LOS relaxations, but rather are associated with deep inspiration and coughing. Once reflux occurs, acid is cleared from the oesophagus by a two-step process consisting of oesophageal peristalsis followed by neutralization of the residual acid by swallowed saliva. Smoking prolongs acid clearance by decreasing salivation. The effects of smoking on LOS tone and acid clearance are most likely mainly due to nicotine but are incompletely understood. Transdermal nicotine has similar effects to smoking on LOS pressure and salivation. Thus, although perhaps not a dominant risk factor, smoking and nicotine impact on pathophysiological variables of gastro-oesophageal reflux disease. In itself, smoking cessation is unlikely to cure severe gastrooesophageal reflux disease, but, along with appropriate pharmacological therapy, it may be beneficial.