Fetal Alcohol Syndrome Nip in Research Paper
- Length: 15 pages
- Sources: 10
- Subject: Sports - Drugs
- Type: Research Paper
- Paper: #29466092
Excerpt from Research Paper :
Mainstream smoke is exhaled from a smoker. Some experts say that side-stream smoke can emit higher levels of toxins than mainstream smoke. In response to these new reports, the Environmental Protection Agency classified secondhand smoke as a carcinogen because of its harmful effects on the health of both adults and the children of smokers. In addition, a lot more about the harm of other substances in tobacco smoke remains unknown (Cooper & Moley pp 206-209).
Both active and passive smoking can potentially harm almost every organ of the body (Cooper & Moley, 2008 p 209). Smoking has been linked to cardiovascular disease, cancer, stroke and chronic lung disease. Health costs are enormous to public health in terms of increased deaths, the nature of the addition, and the overall medical expenses and indirect costs. A recent survey of 388 women showed that not many of them associate smoking with miscarriage, ectopic pregnancy and infertility at 95-99%. A secondary analysis of the 1995 National Survey of Family Growth identified lifestyle factors linked with infertility among 824 women-respondents. These factors were increasing age, previous ectopic pregnancy, current smoking, obesity and health status. The study also revealed that active smoking by either partner delays conception at 54%. Although some women decide to quit smoking, they remain exposed passive smoke if their partners continue smoking (Cooper & Moley pp 210-212).
Small for Gestational Age
Fetal tobacco syndrome has been shown to lead to infertility at 25%, miscarriage at 25%, ectopic pregnancy at 90%, cleft lip at 35%, abruption and placenta previa at 60%, preterm labor and PPROM at 70%, small for gestational age or SGA at 100-200%, stillbirth at 100% and pre-eclampsia at 30% (McGowan, 2009 p 32). These adverse effects depend on the dose but they are reversible by quitting tobacco. Smoking is considered the single most avoidable risk factor for these risks. Women who stop smoking 15 weeks before delivery have the same low rates of SGA as non-smokers. But those continue to smoke face the risk of preterm births 3 times and SGA 2 times. These mean that harmful effects may be prevented if smoking is stopped early in pregnancy (McGowan p 33).
Maternity care providers must then exert more effort to encourage pregnant smokers to quit smoking early in pregnancy, at least 15 weeks before due date (McGowan, 2009 p 34). These providers should remember that persistent smokers constitute 10-45% of all pregnant women. They face the risk of SGA at two-fold. Most SGA babies are born full-term. These babies are vulnerable and must be detected at term or scanned at 38 weeks, especially in the presence of other risk factors (McGowan pp 35-37).
Smoking and the Risk of Strabismus
A recent prospective, population-based cohort study found that smoking during pregnancy could increase the risk of strabismus in the unborn child (Torp-Pedersen et al., 2010 p 868). The authors of the study examined the effect of in-utero exposure of maternal smoking and the use of alcohol, coffee, and team on the risk of strabismus. They used the medical records of 97,000 children at the Danish National Birth Cohort who could be developing strabismus between 1996 and 2003. From the total, they identified 1,321 cases, which increased proportionately with the number of cigarettes smoked per day (Torp-Pedersen et al. pp 868-869).
Strabismus is a common eye disorder prevalent in 2-6% of children in Western countries (Torp-Pedersen et al., 2010 p 870). Uncorrected strabismus can progress to amblyopia and to permanent blindness. The findings of the cohort study were consistent with those of another study conducted by Chew et al. On more than 39,000 children born between 1959 and 1966. The increase in strabismus risk was also observed in all types of strabismus. In further support, the use of nicotine replacement did not increase the risk. Maternal smoking during pregnancy was observed to limit fetal growth, induce hypoxia through a number of mechanisms, and impair neurodevelopment. The risk was not noted in the first trimester but it increased up to 43% in the first 2 trimesters or in all 3 trimesters, indicating that it tends to occur later in pregnancy. At the same time, maternal smoking renders the fetus vulnerable to toxins, which could affect its development at different periods. The two types of strabismus, esotropia and exotropia, were both linked with maternal smoking. These cases present a deficit in central fusion, which suggests that maternal smoking may affect the brain centers responsible for central fusion in the developing fetus (Torp-Pedersen et al. pp 871-875).
Association with Behavioral Problems
Children who are exposed to prenatal tobacco smoke face a 90% higher risk of abnormal behavior in later life than those not exposed (Ruckinger et al., 2010 p 150). Those post-natally exposed had only a 30% relative risk. The abnormal behavior tends to surface in school age. This was the basic finding of a prospective birth cohort study conducted on 6,000 children born between 1995 and 1998 in two cities in Germany and their parents in determining the relative risk of behavioral problems posed by in utero tobacco smoke. It validated earlier knowledge on the adverse effects of in utero or postnatal tobacco smoke, not only intrauterine growth retardation, SIDS, and asthma, but also of behavioral problems later in life (Ruckinger et al. pp 151-152).
The present study used data derived from the German Infant Nutritional Intervention or GINI, which also conducted a follow-up of the respondents (Ruckinger et al., 2010 p 153). It found tobacco smoke as the most influential exposure that conduces to hyperactivity or inattention in later life, as demonstrated in attention deficit hyperactivity disorder or ADHD. Studies on this subject revealed that in utero tobacco exposure produces more externalizing problems than internalizing problems. It was hypothesized that neurotoxicity occurs through hypoxic effects on the fetal placental unit and teratologic effects of tobacco smoke on the developing nervous system. Studies noted that the fetal brain is protected from many neurotoxicants but not nicotine. Nicotine can cross the placental barrier. It acts as a neurotransmitter on nicotinic receptors ( Koren, 1995 as qtd in Ruckinger et al.). Continuously high nicotine levels change non-adrenaline and dopamine response, which is characteristic of ADHD and demonstrated by the hyperactivity and lack of arousal modulation in animal tests. Smoking also indirectly lowers birth weight and perinatal problems, which contribute to antisocial behavior in later life (Ruckinger et al. pp 153-154).
Tobacco Smoke and Developmental Disabilities (Graff et al. 2007) pp 596-603
The National Research Council and the Oregon Environmental Council emphasized that toxic chemical exposure during the prenatal and postnatal development of a child can have lifetime adverse nervous system effects (Graff et al., 2007 p 596). Lead, for example, can lead to lower intelligence, hyperactivity, learning disabilities and attention disorders. Environmental tobacco smoke, secondhand smoke or ETS comes from the burning end of a cigarette, pipe or cigar. It is exhaled by the smoker and the vapor compounds diffuse through the cigarette wrapper. ETS has more than 4,000 substances, more than 50 of which are considered carcinogenic to humans and animals. Nicotine is one of the components of cigarette smoke and a widely admitted neuro-developmental toxicant. Nicotine is taken into the body when tobacco smoke is inhaled. From the lungs, it is absorbed into the blood stream at a high 92%. It is then broken down into cotinine, a metabolite. Children exposed to ETS have been observed to develop increased respiratory illnesses and symptoms, such as asthma, lower respiratory ailments and serous otitis media. They are more vulnerable to conditions like lipid profiles, cancer, dental caries, infectious illness and SIDS. They tend to be behind in math, reading and visual-spatial reasoning even if their exposure to ETS is at very low levels (Graff et al. pp 597-598).
With the decline of smoking among U.S. adults, children's exposure to ETS also decreased (Graff et al., 2007 p 599). The blood cotinine content in non-smoking children aged 4-17 ranged from 87% to 58% between 1988 and 1994 and between 1999 and 2002, respectively. Children in families living below the poverty line were more likely to live with a smoker (Federal Interagency Forum on Child and Family Statistics, 2005 as qtd in Graff et al.). Children with difficulty or abnormal swallowing and gastro-esophageal reflux are more vulnerable to recurrent aspiration. This, in turn, makes them more susceptible to higher rates of asthma, respiratory inflammation, and respiratory infections. Exposure to ETS in children with developmental disabilities and higher rates of respiratory illnesses puts them at a greater risk than those without developmental disabilities (Graff et al. pp 600-602).
The establishment of a smoke-free environment is recommended to protect children from ETS (Graff et al., 2007 p 602). All family members, visitors and childcare providers should quit smoking. Many health providers lack the knowledge and skills needed to advise parents to stop smoking, however (Graff et al. pp 602-603).
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