Perinatal exposure to nicotine and implications for subsequent obstructive lung disease

Abstract

Many diseases are due to gene-environment or epigenetic-environment interactions resulting in a change in the program that controls tissue structure and function. Changes in the in utero and external environment during perinatal development due to parental smoking, or nicotine exposure, may reduce the capacity of the offspring to protect themselves against environmental stressors. Nicotine is genotoxic and also induces reactive oxygen species [ROS] production. It also reduces the antioxidant capacity of the lung. The lungs of the offspring are therefore developing in an environment of an oxidant-antioxidant imbalance with the concomitant adverse effects of the oxidants and nicotine on cell integrity. Consequently, they are more prone to develop respiratory diseases such as asthma and emphysema later in life. The use of NRT by pregnant or lactating females is therefore not an appropriate strategy to quit smoking.