Most recent research on infants has focused on behavior. Using the Brazelton Neonatal Behavioral Assessment Scale, one study [5••
] compared 25 infants of women who smoked at least five cigarettes per day to 25 infants of nonsmokers. Urine cotinine levels significantly correlated with infant irritability, attention, and decreased response to inanimate auditory stimuli. Paternal smoking, in the absence of maternal use, was also significantly correlated with infant cotinine level and irritability.
Another study [6
] examined 962 mother/infant pairs from the Providence Cohort of the National Collaborative Perinatal Project using the Graham-Rosenblith Behavioral Examination of the Neonate. Prenatal tobacco exposure (PTE) was associated with increased irritability and hypertonicity controlling for maternal socioeconomic status (SES), age, race, and infant birthweight. This study represented the largest investigation of the effects of maternal smoking on examiner-assessed neonatal behavior.
In a pilot study, Stroud et al
] compared 28 infants with PTE to 28 infants of nonsmokers aged 10–27 days. Infants with PTE had a greater need for handling and scored lower on self-regulation. In contrast to prior studies, there were no effects of PTE on abstinence withdrawal symptoms or muscle tone. The authors concluded that effects at this age included poorer infant self-regulation and an increased need for external intervention.
Infant temperament at 9 months was studied in a cohort of over 18 000 infants [8•
]. Infants of heavy smokers scored least well on the Carey Infant Temperament Scale, whereas women who quit smoking had infants with higher scores on the easy temperament scale. These findings remained robust after controlling for sociodemographic factors that correlated with maternal pregnancy smoking status.
Six-month-old infants with PTE had less focused attention, lowered reactivity to basic sensory stimulation, and more distractibility compared to nonexposed infants (Wiebe, unpublished data), and the author concluded that PTE leads to deficits in information processing and self-regulation. An additional study by the same author and colleagues evaluated the genetic aspects of PTE-associated neurobehavioral deficits [9•
]. This study examined early infant neurobehavior of 119 mothers and their infants. PTE status was based on self-report and maternal and meconium cotinine. The dopamine receptor D2 genotypes of the infants were identified. Nonexposed infants with the A1+ genotype had a heightened response to novelty. Among PTE infants with this variant, however, the response to novelty was dampened, which suggests that genetic variability and PTE interact to affect infant development.
In a study of infant cognition, speech-processing ability was assessed between eight PTE and eight non-PTE infants [10•
]. Using event-related potentials, exposed infants discriminated fewer syllables and processed them more slowly than nonexposed infants. Thus, PTE may lead to changes in brain physiology that affect basic perceptual skills.
A study from the animal literature reported on gestational exposure and visual recognition memory. Golub et al
] examined rhesus monkeys that were exposed to environmental tobacco smoke (ETS) from gestation day 50 to delivery. In parallel with the human literature, the exposed group showed less novelty preference in the visual recognition task. However, unlike the human literature, no effects were found on the auditory function test. The authors concluded that ETS exposure during pregnancy had adverse effects on cognitive function in nonhuman primates.