The Impact of Smoking on the Body

Mechanisms of nicotine-induced damage

As with any environmental adverse factors, the severity of pathological changes from smoking directly depends on the dose of the toxic substance and the duration of its exposure to tissues.

The primary damaging effect of nicotine is due to its potent vasoconstrictive (blood vessel-narrowing) action. Chronic spasm of capillaries and arterioles leads to persistent microcirculation disorders. Simultaneously, tobacco smoke causes a systemic decrease in cellular metabolism. As a result, tissues are deprived of oxygen and nutrients, which forms the basis for the development of chronic hypoxia.

In obstetric and perinatal practice, the ability of tobacco smoke components to easily cross the placental barrier is of particular importance. In effect, the fetus becomes a passive smoker and is subjected to a direct chemical assault.

Toxicokinetics of tobacco smoke in the fetus

Having crossed the placenta, nicotine begins to accumulate in almost all tissues and internal organs of the fetus. Due to the immaturity of the child's enzyme systems and excretory organs, toxins are eliminated from its body significantly slower than from the mother's bloodstream.

Carbon monoxide contained in the smoke poses a particular hazard. It binds to hemoglobin, forming carboxyhemoglobin—a compound incapable of carrying oxygen. It has been proven that the concentration of carboxyhemoglobin in the bloodstream of a developing fetus is two to three times higher than the corresponding figure in the blood of the pregnant woman herself. This repeatedly amplifies oxygen starvation in developing systems.

Impact on intrauterine development and pregnancy complications

A crucial postulate of pathologically based physiology: nicotine itself does not possess teratogenic effects—that is, it does not provoke gross anatomical anomalies or congenital malformations. However, its embryotoxic effect is colossal.

Pronounced spasm of uteroplacental vessels leads to the development of chronic placental insufficiency. This condition blocks the mechanisms of active transport of vital amino acids from the maternal organism to the child. As a consequence, marked fetal growth restriction (FGR) occurs.

The risk of developing severe obstetric complications increases manifold if a woman smokes 20 or more cigarettes per day. These complications include:

• Spontaneous abortions at various gestational ages.
• Premature placental abruption.
• Pronounced fetal hypoxia during the gestation period.
• Neonatal asphyxia in the intranatal period.

That is why a strict clinical rule is the complete cessation of active and passive smoking during pregnancy—the patient must be clearly informed about the risks to the child's life.

The role of smoking in adult vascular pathologies

In addition to affecting embryogenesis, smoking is a powerful catalyst for vascular catastrophes in adulthood. In the treatment of such pathologies as cerebral atherosclerosis or hypertension, non-pharmacological measures play no less a role than the administration of pharmacological drugs.

Complete tobacco cessation is considered a mandatory step. Eliminating the constant vasoconstrictive factor reliably improves cerebral blood flow, increases the efficacy of vasotropic and antiplatelet therapy, and inhibits the further progression of atherosclerotic lesions of the vascular wall.

Class and exam questions

What else to study on this topic

• Teratogenic effects of alcohol and the development of fetal alcohol syndrome
• The impact of ionizing radiation on embryogenesis depending on the stage of development
• Mechanisms of embryotoxicity of heavy metals and organic solvents
• Causes and consequences of acute and chronic fetal hypoxia
• Pharmacological treatment of cerebral atherosclerosis and hypertension
• Pathogenesis of mental disorders of infectious origin

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