To determine whether perinatal smoking exposure is associated with gastroesophageal reflux (GER)-related changes in sleep-wakefulness states in neonates.

Thirty-one neonates, referred for the investigation of suspected GER, were recruited and underwent multichannel impedance–pH monitoring and synchronized 8- to 12-hour polysomnography. The infants' exposure to tobacco smoke was estimated by means of a urine cotinine assay. The total number, frequency (h⁻¹), and mean duration (minutes) of GER-pH (reflux events detected by the pH electrode only) and GER-imp (reflux events with bolus movement detected by impedance) events were determined. Intergroup differences (smoking-exposed group vs nonexposed group) were probed with nonparametric, unpaired Mann–Whitney U tests. A χ² test was used to assess a possible intergroup difference in bolus retrograde migration during GER-imp events.

According to the urine cotinine assay, 21 of the 31 neonates had been exposed to cigarette smoke during the perinatal period. The number (and frequency) of GER-imp was significantly greater (P = .016) in the exposed group (29 [0-90]) than in the nonexposed group (12 [2-35]). Migration of the esophageal bolus from the distal segment to the most proximal segment was significantly more frequent (P = .016) in the exposed group (83% of GER) than in the nonexposed group (41%). The GER pattern associated with smoking exposure was particularly obvious during Rapid eye movement sleep.

The more frequent occurrence and greater proximal migration of GER-imp in the smoking-exposed group (especially during rapid eye movement sleep) may have clinical relevance. Smoking exposure is a preventable risk factor for limiting the occurrence of GER in neonates.