Abstract
Nicotine and the related oxidant/antioxidant imbalance cause point mutations in the DNA molecule thereby changing the program that controls lung growth and maintenance. It has also been shown that maternal nicotine exposure during gestation and lactation induces a persistent inhibition of glycolysis. These changes are thought to contribute to the faster aging of the lungs of the offspring of mothers that were exposed to nicotine. The lungs of these animals are more susceptible to damage as the animals age. The gradual deterioration can be attributed to increased numbers of senescent cells together with slower cell proliferation and thereby compromising the ability of the lung to adequately replace old cells. Remodeling of the airways of the offspring of nicotine exposed mothers results in a higher incidence of asthma and an increase in the susceptibility to lung cancer. The lower FEV1 of female rats than male rats that were exposed to nicotine during gestation and lactation suggests remodeling of the airways of the females are more severe than in males. The rapid metabolic and structural aging of the lungs of the animals that were exposed to nicotine via the placenta and mother’s milk is likely due to “programming” induced by nicotine and an imbalance in the oxidant/antioxidant capacity of the mother and fetus. Restoration of the oxidant/antioxidant balance prevents the adverse effects of nicotine on the lungs of the offspring. Although restoration of the oxidant/antioxidant balance protects the lungs of the offspring it is not advisable for pregnant or lactating mothers to use nicotine replacement therapy during gestation and lactation in an effort to quit smoking.
Keywords: Lung development, nicotine, premature aging, programming, gestation and lactation, nicotine replacement therapy (NRT), smoking, pulmonary absorption, Progeny, maternal nicotine exposure
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