Fetal Nicotine Syndrome Research Paper

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Fetal Alcohol Syndrome

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Fetal Nicotine Syndrome

Nicotine has been linked to many adverse conditions affecting fetal development and other disorders later in life. Many previous studies established that smoking accounts for sudden infant death, structural, cardio-respiratory and functional dysfunctions of the fetus as well as low weight and preterm births. Some studies connected tobacco smoke with the failure to conceive and behavioral problems later in life. Pharmacological and non-pharmacological therapies are in place for the cessation of smoking. Public policy, community efforts and the media have waged a successful campaign against it with a few measures left needed to fill some gaps in regulation.

Background

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Fetal nicotine syndrome is a malformation complex in pregnant women who smoke 5 cigarettes a day and which affects their infants (De Ruvo, 2009). Nicotine has long been the prime suspect linking maternal cigarette smoking during pregnancy and sudden infant death syndrome or SIDS (Eugenin et al., 2008 p 13907). SIDS is a recognized leading cause of death among infants in developed countries. Causes are still unknown but most evidence attributes it to the respiratory failure. Nicotine is a neuroteratogen content of tobacco, blamed for cardio-respiratory dysfunctions in infants during pregnancy. Nicotine moves from the mother to the placenta and into the fetus. It then interacts with functional nicotine receptors. Earlier studies on animals found that prenatal nicotine causes hypoventilation, increases the likelihood of sleep apnea and reduces hypoxia-induced ventilatory reflexes. This present study used pregnant mice to determine the effect of nicotine in unborn mice. Results showed that exposure to nicotine reduced the unborn mice's respiratory rhythm and reduced their central chemoreception. The ventilatory failure is similar to that in SIDS (Eugenin et al., 2008 pp 13908-17).

History

TOPIC: Research Paper on Fetal Nicotine Syndrome Assignment

The Developmental Origins of Health and Disease or DOHaD suggest that fetal adaptations in the womb during the developmental stage influence the structure and function of organs (Swanson et al., 2009 p 391). A review of environmental exposures, which can lead to fetal mal-adaptations, was conducted on tobacco smoke, anti-depressant medications and shortage of folic acid. The DOHaD approach was used to determine and explain the long-term effects of the exposures. The approach was drawn from the hypothesis advanced by David Barker through his published observations in 1986, 1989 and 1993. It assumes that a pregnant woman's exposure to stress or toxins, the manner of feeding given to the infant and how fast he grows determine his risks for chronic disease in adult life. Increasing evidence points to the influence of events during the earliest stages of development of the fetus to vulnerability to certain disorders. These disorders include diabetes, cardiovascular disease, asthma, cancers, osteoporosis and neuro-psychiatric conditions (Swanson et al. pp 392-394).

Earliest research dating back in 1957 observed that women who smoked during pregnancy suffered from preterm birth at 11% (Swanson et al., 2009 p 394). This was twice the rate of non-smoking women. Debates ensued for decades on whether the association was causal. In 1992, more findings on lifestyle factors and their effects on pregnancy offered greater evidence to the observation than mere causal association for smoke-related stunted fetal growth. The findings said that tobacco smoke can bring on chronic hypoxia from increased placenta resistance, decreased uterine blood flow, and increased carboxymemoglobin. Smoking can also lead to under-nutrition by suppressing the appetite and food consumption. The National Collaborative Perinatal Project of Births from 1960 to 1966 documented pregnancy outcomes as detrimental effects on neonatal behavior, underweight or obesity, and complications of diabetes or hypertension. This was bolstered by the results of interventions, such as the Generation R Study, on 7,098 women in Rotterdam. It revealed no abnormal effects on infant birth weight in women who stopped smoking at the start of pregnancy. Those who stopped after 32 weeks increased gestational age and reduced preterm birth. Those who stopped before 15 weeks prevented preterm births in comparable levels as non-smoking mothers. These suggested that maternal smoking affects fetal growth and gestation in the late stages of pregnancy. The study also observed that many pregnant women continue to smoke despite these findings and warnings (Swanson et al. pp 393-397).

The Surgeon General's Office report and a recent meta-analysis investigation said that secondhand smoke reduces birth weight, although it does not affect gestation or increases the risk of preterm birth (Swanson et al., 2009 p 398). According to earlier studies, prenatal environmental tobacco smoke and maternal smoking during pregnancy raised the likelihood of neuro-developmental and behavioral disorders in fetuses in later life. Prominent among these disorders is attention deficit hyperactivity disorder or ADHD, which is 2.5 times for children exposed to prenatal environmental tobacco smoke. Programs to suppress environmental tobacco have been introduced in some countries. But these have not been effective because of their high public health costs (Swanson et al. pp 399-402).

Environmental Toxins

Heavy metals, like lead and mercury, organic solvents, alcohol and ionizing radiation are confirmed environmental teratogens (Gardella & Hill, 2000). Exposure to them can lead to pregnancy loss. Suspected teratogens include caffeine, cigarette smoking, insecticide and hyperthermia, the impact of which is still unknown. A teratogen is a substance, organism, or physical agent, which produces a permanent structural or functional abnormality, or causes growth retardation or death in an embryo or fetus when exposed prenatally. Teratogens include radiation, infections, maternal metabolic imbalances, drugs, environmental chemicals, hypoxia, hyperthermia, trauma and surgical procedures. Teratogens produce structural defects, spontaneous abortion, growth retardation, microcephaly, major and minor malformations, metabolic dysfunctions, cognitive dysfunctions or disability, altered social behavior, malignancy, reduced fertility, increased perinatal sicknesses and altered offspring sex ratios (Gardella & Hill).

Cigarette smoking decreases fertility (Gardella & Hill, 2000). It also increases the incidence of spontaneous abortion, abruptio placentae, placenta previa and bleeding during pregnancy and premature rupture of placental membranes, low birth weight, and overall mortality from all causes, specifically SIDS. The connection between spontaneous abortion and maternal smoking has not been accurately established. But current studies strongly suggest that 10-20 cigarettes a day pose a relative risk of miscarriage at a ratio of 1.1-1.3. A study of 1,500 karyotyped spontaneous abortions found that 50% of the women smoked. A large retrospective study of more than 47,000 women also showed that spontaneous abortion occurred in those who smoked more than 10 cigarettes a day. The teratogenicity of environmental factors depends on the fetal gestational age at the time of exposure, amount of toxin reaching the fetus, duration of exposure, impact of other factors to which the mother and the fetus are exposed, genetic differences between them, and interrelationship between frequency of exposure and effect, and the adverse outcome, such as spontaneous abortion (Gardella & Hill).

Preterm Births and Nicotine

Psychological social stress and increased risk of preterm birth have been associated although the connection has not been explained (Denney et al., 2008 p 625). Clinical depression has been reported in 16% of pregnant women and 35% of them presented depressive symptoms. The incidence of preterm birth seemed to increase with depression. Depression, in turn, has been associated with an increase in smoking as well as drugs and alcohol. Cigarette smoking has been found to increase the risk of preterm birth to less than twofold. The in vivo effects of thousands of chemical agents in cigarette smoke have yet to be understood to shed light to the connection. But at present, nicotine and carbon monoxide are known to be powerful vasoconstrictors. They are also associated with placental damage and sub-optimal utero-plancental blood flow. These effects depress fetal growth and preterm deliveries caused by abruption and intrauterine growth restriction. Smoking may also elicit a systemic inflammatory response and spontaneous preterm birth through the inflammatory response and induce labor (Denney et al. pp 626-638).

Health Effects

Tobacco smoke affects all facets of fertility in both genders and influences a couple's inability to have children (Cooper & Moley, 2008 p 204). Women are more potentially vulnerable to environmental toxins like tobacco smoke on account of their complex reproductive cycle. The negative effects can seep in into any part of the reproductive process -- ovulation, fertilization, movement of gametes and embryos, and implantation and throughout the duration of pregnancy. Abundant data reflect on the impact of tobacco smoke throughout the entire in vivo fertilization process, which can extend even if the effect is transient. Increased embryo toxicity, congenital abnormalities, behavioral disorders, decreased fertility and link with adult disease call for prompt action. The reduction of infertility is now a national health objective of the Healthy People 2010, a response to that call. Preventing it by identifying and addressing dangerous lifestyle habits is far better than treating it (Cooper & Moley pp 211-212).

Tobacco smoke consists of more than 4,000 chemicals, many of which are carcinogenic and dangerous toxins (Cooper & Moley, 2008 p 205). Among these are nicotine, tar, polycyclic aromatic hydro-carbons, metals, carbon monoxide and hydrogen cyanide, which are associated with many disease conditions. Both active smoking and secondhand or passive smoke have been primary targets of health care interventions. Secondhand smoke is… [END OF PREVIEW] . . . READ MORE

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