Nicotine exposure (by smoking, using patches or being exposed to passive smoke) during pregnancy has harmful effects on at least three major types of fetal cells during early pregnancy. Nicotine's toxic effect on the development and function of fetal placental, nervous system and pancreatic cells is described.
Embryonic and Placental Cells
Nicotine exposure inhibits the normal development of placenta cells which are essential to forming a strong fetal-placental interface in the uterus. Women who smoke during pregnancy are more likely to experience a catastrophic tearing of the placenta from the uterus (placenta abruptia), or inappropriate growth of the placenta over the cervical opening (placenta previa), both conditions which increase the risk of pregnancy loss and fetal death. Preterm labor and stillbirth are also more common in smokers due to the toxic effects of nicotine on placental development and blood vessel function. Nicotine constricts the blood vessels of the placenta, causing the fetal cells to get less nutrients and less oxygen resulting in the birth of lower birth weight babies.
Fetal Nervous System
Nicotine interacts with cholinergic receptors in the developing fetal brain to inhibit nerve cell growth which reduces the number of connections (synapses) between nerve cells. Smokers are 50 percent more likely than non-smokers to have children with learning difficulties and or mental retardation. The nervous system has numerous receptors that can bind to nicotine and are therefore vulnerable to its toxic effects. Nicotine prevents the normal development of the fetal cholinergic nervous system which negatively affects the normal contraction and dilation of muscle cells in various organs including eye, heart, lung, intestines, stomach, blood vessels and bladder. Some studies suggest that some forms of hearing loss in children may be due to exposure of the developing auditory cells to nicotine.
Fetal Pancreatic Cells
The beta cells of the pancreas are responsible for secreting insulin to regulate glucose entry into all the cells of the body. If the pancreas is damaged, it is unable to produce sufficient levels of insulin, which can result in type 2 diabetes, a chronic disease. Animal studies have demonstrated that nicotine acts to reduce the quantity of fetal beta cells by increasing the programmed cell death (apoptosis) rate and decreasing the proliferation rate. This combined effect is enough to decrease the number of functioning beta cells by 25 percent, which has serious implications for development of a functioning pancreas.
