The impact of perinatal nicotine exposure on fetal lung development and subsequent respiratory morbidity.

Maternal smoking during pregnancy remains as a significant public health crisis as it did decades ago. Although its prevalence is decreasing in high-income countries, it has worsened globally, along with a concerning emergence of electronic-cigarette usage within the last two decades. Extensive epidemiologic and experimental evidence exists from both human and animal studies, demonstrating the detrimental long-term pulmonary outcomes in the offspring of mothers who smoke during pregnancy. Even secondhand and thirdhand smoke exposure to the developing lung might be as or even more harmful than firsthand smoke exposure. Furthermore, these effects are not limited only to the exposed progeny, but can also be transmitted transgenerationally. There is compelling evidence to support that the majority of the effects of perinatal smoke exposure on the developing lung, including the transgenerational transmission of asthma, is mediated by nicotine. Nicotine exposure induces cell-specific molecular changes in lungs, which offers a unique opportunity to prevent, halt, and/or reverse the resultant damage through targeted molecular interventions. Experimentally, the proposed interventions, such as administration of peroxisome proliferator-activated receptor gamma (PPARγ) agonists can not only block but also potentially reverse the perinatal nicotine exposure-induced respiratory morbidity in the exposed offspring. However, the development of a safe and effective intervention is still many years away. In the meantime, electropuncture at specific acupoints appears to be emerging as a more practical and safe physiologic approach to block the harmful pulmonary consequences of perinatal nicotine exposure.