DefinePK

Abstract

Cigarette smoking during pregnancy is a widely recognized public health issue, with a growing body of evidence documenting its harmful effects on the health of the unborn child [1]. While long-term consequences such as low birth weight and respiratory problems are now well-known, the impact on the particularly vulnerable developing nervous system deserves specific and urgent attention. Prenatal exposure to toxic substances from smoking can leave a lasting imprint, compromising the complex neuronal architecture and future cognitive functions. Nicotine, the most well-known component in cigarette smoke, not only easily crosses the placental barrier but is also one of the few lipid-soluble substances capable of passing through the blood-brain barrier by passive diffusion, thus acting directly on the expression of genes and transmitter systems essential for the development of the nervous system [2-4].
In particular, it can act as an agonist on acetylcholine receptors, crucial for neuronal proliferation, differentiation, synaptogenesis, and above all, it can interfere with the development of nerve centers essential for coordinating the vital functions of the fetus. Furthermore, it should be noted that smoke is not just nicotine. Cigarette smoke is a complex mixture of over 7,000 chemical substances, many of which are neurotoxic. Carbon monoxide, for example, reduces the availability of oxygen for the fetus, creating a condition of hypoxia that can irreversibly damage brain cells. Epidemiological studies have consistently shown a correlation between maternal smoking and an increased risk of neurobehavioral and developmental disorders in the child. A higher incidence of Attention Deficit/Hyperactivity Disorder (ADHD), autism spectrum disorders, and cognitive delays is observed in children exposed to smoke in utero [5]. These problems are not simply transient; they often persist into adolescence and adulthood, affecting school performance, social relationships, and overall quality of life.
On the cellular and molecular level, studies have demonstrated the accepted mechanisms of these effects. Exposure to smoke during pregnancy has the capacity to distort the expression of genes governing signal pathways, specifically impairing myelination, which is required to transmit impulses efficiently [6]. Moreover, it has been learned that smoking can cause oxidative stress and inflammation in the fetal brain tissue, which are some of the reasons that lead to cell death and deterioration of the neurons. The problem is not related to the active smoking of the mother alone. Prenatal exposure to secondhand smoke can also be regarded as a major risk factor. There is a need to make sure that the awareness of this problem is conveyed not only to the expectant mothers but also to the partners and all other people who spend time in the same home, so that the atmosphere of the place is totally smoke-free and the fetus can be well taken care of.
In summary, it is not only an ethical and scientific requirement but also scientific to protect the fetal nervous system against exposure to smoke. Each cigarette smoked by a pregnant woman is not only a threat to the pulmonary or cardiac system of the unborn child, but also a potential strike to the wholeness of their brain and the likelihood of delivery without health complications. This should be targeted in information campaigns and health policies, where women and their families are given help that will enable them to stop smoking and give their child the best possible start in life, and a neuro-cognitive future.