This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Tobacco smoke contains over 4000 chemicals and 60 carcinogens, thus the mechanisms by which maternal smoking causes fetal and infant harm are likely to be multi-factorial. Studies suggest that infants born to smokers have altered auditory processing, which has been correlated with deficits in reading and spelling in school-aged children. Nicotine exerts its effects mostly via specific receptors in both neuronal and non-neuronal tissue which may, in turn modulate expression of cytokines, which act as mediators. However the roles played by nicotinic receptors and cytokines in fetal development have not been well studied. Objective:1.To determine if maternal smoking during pregnancy is associated with infant abnormalities in the auditory component of the Brazelton Neonatal Behavioral Assessment Scale (BNBAS),a scale devised to test auditory function.2. To determine if maternal smoking increases/alters nicotinic receptor (nAChR) expression in umbilical cord blood and cord tissue,a non-neuronal tissue that is more readily available .3.To determine if maternal smoking causes an increased level of the inflammatory cytokine interleukin-8(IL-8) in fetal circulation, which in turn may be related to neuronal injury and auditory dysfunction in infants and in turn will serve as a potential biomarker to predict which babies are at risk.4. Differences in nAChR expression and IL-8 production will be correlated with auditory functioning in newborn infants of smokers and non-smokers.