Sudden infant death syndrome (SIDS) is the sudden death of an infant under 12 months of age, which remains unexplained after complete autopsy and investigation. Prior research has suggested that SIDS is related to multiple risk factors involving sleep position, age, and preexisting biological vulnerabilities. These risk factors may contribute to a failure of an infant’s autonomic nervous system (ANS) to maintain homeostatic control upon a direct physiological challenge, resulting in a sudden death. A practical way to study correlations between altered ANS functioning and homeostatic control in the developing infant is through the analysis of interactions between the cardiovascular and respiratory systems upon prenatal exposure to adverse substances. This study investigates the cardiorespiratory physiology of infants born in Cape Town, South Africa who were prenatally exposed to alcohol and tobacco smoke (with respect to age and sleep state). These substances have been shown to interact with, and likely impair functioning, of brainstem regions involved in homeostatic control. My primary hypothesis is that infants will exhibit changes in cardiorespiratory physiology and interactions upon prenatal exposure to alcohol and tobacco smoke, thus reflecting some ANS impairment. The overall findings in this study provide evidence of alterations in cardiorespiratory physiology in infants at risk for SIDS that converge with those from the epidemiological literature.
