At present the mechanisms by which the use of tobacco produces a damaging effect on duodenal ulcerous disease are not clearly understood. This paper reports the results of a study of basal and postprandial gastrin and pepsinogen I (PG I) levels of 74 duodenal ulcer (DU) patients and 18 controls in relation to their smoking habits. There was no difference between the UD group and the control group as far as basal gastrin levels were concerned, but there was in the PG I levels (107 +/- 54 ng/ml in UD vs. 69 +/- 30 ng/ml in control) (p less than 0.05). The postprandial gastrin and PG I responses in 34 UD subjects only differed in relation to smoker/non-smoker status; there was no correlation with age less than greater than 35, positive family history or duration of illness. Patients who had had UD less than 10 years showed higher postprandial PG I levels; however, this group included the 83.3% smokers with UD. It was concluded that chronic smoking is clearly related to the existence of hyperpepsinogenemia I, and probably also to postprandial hypergastrinemia in UD sufferers.