LONG-TERM NEUROBEHAVIORAL EFFECTS OF PRENATAL EXPOSURE TO MATERNAL SMOKING
Investigations of the long-term effects of prenatal exposure to maternal smoking have inherent difficulties. Animal studies demonstrate conclusively that prenatal smoke exposure alters brain chemistry. Neuronal cell proliferation and differentiation, nicotine receptor gene expression, and cholinergic (activated by or capable of liberating acetylcholine, which is involved in the transmission of nerve impulses in the body), catecholaminergic (has important physiological effects as neurotransmitters and hormones and include epinephrine, norepinephrine, and dopamine), and peripheral autonomic pathways exhibit permanent changes after prenatal smoke exposure.
In human subjects, isolation of variable is problematic. Like studies of fetal alcohol or drug exposure, accurate ascertainment of dose, duration, and timing of maternal smoking exposure is difficult. Depending on the formulation of the cigarette, various compounds in addition to nicotine cross the placenta to enter the circulation of the fetus. Co-incident exposures, especially if covert, confound interpretation of outcomes.