Abstract
Tobacco smoking during pregnancy remains common, especially in indigenous communities, and likely contributes to respiratory illness in exposed offspring. It is now well established that components of tobacco smoke, notably nicotine, can affect multiple organs in the fetus and newborn, potentially with life-long consequences. Recent studies have shown that nicotine can permanently affect the developing lung such that its final structure and function are adversely affected; these changes can increase the risk of respiratory illness and accelerate the decline in lung function with age. In this review we discuss the impact of maternal smoking on the lungs and consider the evidence that smoking can have life-long, programming consequences for exposed offspring. Exposure to maternal tobacco smoking and nicotine intake during pregnancy and lactation changes the genetic program that controls the development and aging of the lungs of the offspring. Changes in the conducting airways and alveoli reduce lung function in exposed offspring, rendering the lungs more susceptible to obstructive lung disease and accelerating lung aging. Although it is generally accepted that prevention of maternal smoking during pregnancy and lactation is essential, current knowledge of the effects of nicotine on lung development does not support the use of nicotine replacement therapy in this group.
Highlights
Recent epidemiological studies have shown that lung function and susceptibility to respiratory diseases throughout life can be programmed by environmental factors operating during fetal and early postnatal life
The Mn-Zn SOD activity of the developing lungs is reduced by nicotine exposure which further reduces the ability of the lungs to be protected against the point mutations in DNA induced by oxidants; this will increase the susceptibility of exposed lungs to changes in the “program” that controls lung development, maintenance and aging
Since rapid cell proliferation is associated with rapid shortening of the telomeres [108], it is conceivable that premature aging of the type II cells will occur in the lungs of the nicotine exposed rats. This may result in an increased vulnerability of the alveolus, which is supported by the observation that loss of type II cells has a detrimental effect on the alveolus [106]. It appears that the negative impact of maternal nicotine exposure during gestation and lactation on the growth, development and repair processes of the lungs of the offspring causes lung structure to more rapidly deteriorate with age than in animals that were not exposed to nicotine
Summary
Recent epidemiological studies have shown that lung function and susceptibility to respiratory diseases throughout life can be programmed by environmental factors operating during fetal and early postnatal life. Prenatal and early postnatal exposure to tobacco smoke has a wide range of adverse health effects, including an increased risk of low birthweight and perinatal complications, the Sudden Infant Death. In infants prenatally exposed to maternal smoking, tidal and forced expiratory flow rates are reduced, suggesting that small airway development has been affected [9,10]. This is supported by studies in guinea pigs which showed that maternal. Maternal smoking may increase the risk of low FEV1 and COPD in adults [17], but it is presently unclear whether such effects are due to prenatal smoking or exposure to environmental tobacco smoke during infancy and childhood
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