Diane L. Carlisle, PhD

In the United States, each year approximately 1 in 10 newborns is exposed to cigarette smoke during gestation. Cigarette smoke exposure during this critical time of organogenesis and subsequent organ growth and maturation causes morbidity and mortality after birth. In the lung, prenatal cigarette smoke exposure causes decreased lung function at birth and into childhood as well as increased incidence of asthma and allergies. The mechanisms by which cigarette smoke has these effects is not known; however, it is modeled in non-human primates exposed during pregnancy to nicotine, a major component of cigarette smoke. These studies find that although there are thousands of chemicals in cigarette smoke, NHP infants subjected to nicotine alone via a maternal exposure during development have increased thickness of the inner airway wall and altered complexity of branching, decreased respiratory volumes, and altered response to airway challenges. This is possible because nicotine easily crosses the placenta and accumulates in amniotic fluid with average concentrations of 150 nM. The physiological alterations described above that are caused by nicotine exposure may be linked to altered regulation of proliferation and apoptosis during organogenesis and organ growth. Our preliminary data demonstrate that nicotine may affect differentiation by altering the expression of a key regulators of proliferation and apoptosis during development.