An investigation into the effect of maternal exposure to nicotine and copper on neonatal lung development
In the 20th century, where tobacco smoking continues to be the leading preventable cause of death, an alarming number of people continue to smoke, despite awareness of the implications of exposure for themselves and those around them. Campaigns for the promotion of effective tobacco legislation and awareness are continuously being confronted by the tobacco industry’s reluctance to put the health of their consumers before company profits, leading to a ripple effect of misinformation, serious health risks and economic implications, at least for the consumers. Pregnant women are especially a concern because exposure to tobacco smoke affects not only the smoking mother but has serious implications for the health of her unborn child. Some mothers try to quit smoking by using nicotine replacement therapy. However, recent studies implicate nicotine as the causative factor for some of the cigarette smoke associated respiratory diseases. Therefore, the aim of this study was to investigate the effect of: 1) maternal exposure to nicotine (1mg/kg BW/day) during all the phases of lung development, or from the onset of the phase of rapid alveolarisation and, 2) whether copper supplementation (1mg/kg BW/day) will prevent the adverse effects of maternal nicotine exposure, on lung development in the offspring. The latter aim is based on studies in our laboratory which suggested that nicotine may impair lysyl oxidase activity by reducing the lung copper content in the lungs of rats that were exposed to nicotine via the placenta and mother’s milk. It was found that although maternal nicotine exposure had no significant effect on the growth parameters of the offspring, it did have an effect on the development of the lung, and indeed compromised the ability of the lung to act as an organ of gaseous exchange. This included alveolar destruction due to damage to the connective tissue framework of the lung, and consequently a decrease in the surface area available for gas exchange. The changes occurred after the lungs reached maturation and resembled microscopic emphysema. Copper supplementation did not prevent the lung from damage caused by maternal nicotine exposure but appeared to lessen the severity of disease progression. The late development of the lung lesions in the offspring suggests that maternal nicotine exposure changes the program that regulates ageing and maintenance of the lungs, such that the lungs are more susceptible to damage and disease. Pregnant women who smoke, or use nicotine replacement therapy, will therefore increase the risk of the offspring to develop respiratory disease, even if the offspring never smoke themselves.
Tobacco, Smoking, Maternal, Nicotine, Copper
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