Impacts of the Secondhand Smoke - Research Paper Example

? Impacts of the Secondhand Smoke Outline Introduction Environmental Tobacco Smoke Exposure or Secondhand Smoke Consequences of Environmental Tobacco Smoke Health Effects of ETS in Young Children ETS and Respiratory illnesses ETS and Asthma Smoking Effects on Placenta and Placental Transfer of Nicotine and Carbon Monoxide Secondhand nicotine exposure and effects on brain functioning Fetal Growth Retardation and Low Birth Weight Conclusion Summary and recommendations Impacts of the Secondhand Smoke Introduction Tobacco use has been found to be the leading preventable cause of illness and death, and it has been estimated that even after controlling for active cigarette smoking, exposure to environmental tobacco smoke (ETS) or secondhand smoke is the third leading preventable cause of illness and death in United States (Desalu Olufemi, Onyedum et al.1). In 2004 alone, exposure to secondhand smoke has caused 379,000 deaths (Oberg, Jaakkola, Woodward et al. 1). The extent of children who are at risk of being exposed to secondhand smoke is substantial. Smoking during pregnancy or postnatal exposure to environmental tobacco smoke or Secondhand Smoker has substantial adverse effects on children, including low birth weight, effects on brain functioning and other respiratory health effects. Environmental Tobacco Smoke Exposure or Secondhand Smoke Environmental tobacco smoke (ETS), also known as secondhand smoke, involuntary smoking, or passive smoke, is a collective mixture of the smoke given off by cigarettes, pipe, or cigars, and the smoke exhaled from smokers (Desalu et al. 1). This mixture contains more than 4,000 substances, including 250 known carcinogens, which are known to cause damage to human health (Desalu et al.1). The effects of exposure to ETS on children have become a major focus of concern. Children have been recognized as a susceptible subpopulation to the effects of ETS since the developing lung is especially vulnerable to ETS. The World Health Organization has estimated that almost half of the children in the world are vulnerable to exposure from environmental tobacco smoke. For children, the home environment is the predominant place for exposure to ETS (USDHHS 6). Throughout the epidemiological literature, the presence of smokers in the home has been utilized as an estimate of the risk of being exposed to ETS. In the United States, the number of children living in homes with a smoker has been estimated to be about 43%, with specific states ranging from 12% to 34% (Kelishadi, Moghtaderi, Khavarian & Famouri, 208). While parental smoking is the main source of ETS exposure for children other family members, caregivers, or visitors may also smoke in the home. Reduction of ETS exposure could take two courses. First, the most effective way to reduce ETS exposure among children would be to have tobacco users who smoke around children to completely quit. While this has been accomplished with parents of children in an outpatient clinic setting of a hospital (Winickoff et at, 140), smoking cessation may not be the most realistic method to reduce ETS exposure in a pediatric cancer population. A second method for reducing ETS exposure would be to encourage parents and others to control their smoking around children. While research suggest that these measures (i.e. smoking in another room, and using an air purifier) are not as effective as smoking cessation, these measures may be more appealing to parents who may blame themselves for their child's diagnosis, given the suggested causal relationship between ETS and childhood cancer (Kelishadi et al. 208-211). While not equally effective, these measures might be easier and more accepted among parents; thereby, the utilization would be broader and more effective in the end. Furthermore, smoking cessation appears to be an indirect effect of ETS reduction interventions. Studies have found that programs that target ETS reduction result in a significant number of parents who reduce the ETS through cessation (Winickoff et al. 140-145). Consequences of Environmental Tobacco Smoke In 1992, the Environmental Protection Agency (EPA) documented the causal association between ETS exposure and its damaging health effects in humans. Throughout the years, this association has been further substantiated and extended in meta-analyses and health agency reports. More recently, a report by the Surgeon General concluded that "there is no risk-free level of exposure to secondhand smoke" (USDHHS 11). Furthermore, nonsmokers' household exposure to ETS has been found to be positively associated with an increased risk for lung cancer (USDHHS 6). The health impact of children’s ETS exposure is particularly alarming. Compared with adults, children have more internal exposure to ETS, as measured by urinary cotinine, for the same level of external exposure. Thus, given the same level of ETS in the environment, children take in more secondhand smoke than adults. Researchers have determined that children exposed to ETS have a small reduction in lung function, higher rates of lower respiratory tract infections, such as bronchitis and pneumonia, and increased incidences of middle ear infections, asthmatic symptoms, colic, sudden infant death syndrome, and symptoms of upper respiratory tract problems (Kelishadi et al. 208). Parents' smoking can affect not only their children's health, but also their children's own tobacco use. Throughout the literature, youngsters' initiation in tobacco use has consistently been associated with the prevalence of other household smokers (i.e., parent or sibling) who models these behaviors (Kelishadi et al. 208). Therefore, limiting smoking & ETS exposure in families can result in less health problems for children, and possibly diminish the risk of children's future use of tobacco. Health Effects of ETS in Young Children Environmental Tobacco Smoke is associated with a significant increase in morbidity and mortality among children especially for ages 5 years and younger (Oberg et al. 1). SS consists of a complex mixture of exhaled mainstream smoke and non-inhaled, side stream smoke from cigarettes (Desalu et al. 1). It is now very clear that ETS poses serious health effects especially to young children living with smoking adults at home. ETS and Respiratory illnesses One of the health effects associated with secondhand smoke is increased respiratory infection seen in children. Researchers showed that risk of respiratory illness is increased in infants and children whose parents smoked. Infants exposed to maternal smoking had an increased incidence of lower respiratory tract infection (Wright, Holberg, Martinez, & Taussig 207-214). In a study by Wright et al. (207-214), infants whose mothers smoked at least one pack per day had 2.8 times the risk of developing a lower respiratory infection. Considering the increased risk for respiratory illnesses in children exposed to secondhand smoke, ETS clearly poses as a serious pediatric health problem. ETS and Asthma Another health effect associated with ETS is an increased incidence of asthma among children exposed to ETS (Oberg et al. 1). According to Oberg et al. secondhand smoke has caused 36,900 deaths from asthma alone. Martinez, Cline, & Burrrows (21-26) found the risk of asthma was 2.5 times higher in children exposed to maternal smoking when the mother had less than 12 years of education. However, in another study (Morgan & Martinez 1185-1203), researchers did not find any correlation between asthma risks with maternal smoking. Similar to respiratory illnesses, risk of developing asthma is found to be dose respondent to the level of ETS exposure when other risk factors such as low socioeconomic status were present (Gigging et al, 2581-2590.). Although the mechanism for the ETS/asthma connection is unclear, research involving Italian school children has linked the development of asthma through immune mechanisms (Martinez et al 21-26). It is thought that ETS increases bronchial reactivity, IgE levels, eosinophilia, and sensitization to aero allergens and augments the exposed child's level of atopy and risk for asthma (Gigging et al, 2581-2590). Exposure to ETS has also been associated with increased asthma-related trips to the emergency room and related costs. Children who are exposed to secondhand smoke have more visits to the emergency room than those who are not exposed (Kelishadi et al. 208). Based on the findings of mentioned studies, it can be concluded that there is enough evidence to conclude that “passive smoking is associated with additional episodes and increased severity of asthma in children who already have the disease" (United States National Cancer Institute 15). Smoking Effects on Placenta and Placental Transfer of Nicotine and Carbon Monoxide The unborn fetus in the human uterus is totally dependent on its mother's health and nutrients. The placenta, a fetal organ that provides nutrients to the developing fetus, is a vital organ for the maintenance of pregnancy and functions as a multifactorial organ (liver, kidney, lung, ovary, pituitary and hypothalamus) (Subramoney et al. 576). It acts as a potential barrier between the maternal and fetal compartments, and it is capable of metabolizing potential toxic substances into less detrimental or more detrimental compounds (Subramoney et al. 576). There are clearly substances that act directly on the placenta to inhibit its ability to function as an organ of exchange (Matt & Borzelleca, 10). Nicotine, carbon monoxide, cyanide and nitrites have been shown to inhibit active uptake of amino acids by the placenta. The placenta must supply the fetus with a variety of essential nutrients for growth; this means adequate blood perfusion through the placental circulation. Substances that cause vasoconstriction can have deleterious consequences to fetal well being. Cigarette smoke has been shown to decrease placental blood flow. Part of this appears to result from nicotine, which may act directly to cause vasoconstriction or indirectly by releasing endogenous serotonin, a potent inhibitor of placental perfusion. Cigarette smoking impairs placental perfusion and the consequences are increased risk of pre-eclampsia, intrauterine growth retardation (IUGR), premature delivery and perinatal mortality. The mechanisms by which these outcomes occur appears to be correlated with decreased placental blood flow and amino acid transport (Matt & Borzelleca 1). Secondhand nicotine exposure and effects on brain functioning According to Mansvelder & McGehee (606-617) higher percentages of nicotine inhaled during smoking is absorbed in the lungs. With the pervasiveness of SHS exposure producing potentially high levels of nicotine from SHS, it is conceivable that SHS may not only impact smoking-related behaviors, but have psychobehavioral outcomes on nonsmokers as well. With regard to brain functioning, nicotine can act as both a stimulant and a depressant. Nicotine's reinforcing effects have been associated with the activation of the mesolimbic dopamine pathway; particularly the ventral tegmental area (VTA) and nucleus accumbens (Nacc) resulting in persistent smoking behaviors (Mansvelder & McGehee 606-617). Prenatal nicotine exposure is known to produce cognitive and behavioral impairments in children, as well as an increased susceptibility to initiate tobacco use. The cognitive and behavioral impairments from nicotine exposure are associated with neurotoxic processes in the developing brain; but more pertinent, pre and postnatal nicotine exposure can produce an upregulation of nicotine receptors in the brain, similar to active tobacco use. Nonhuman studies have shown that early (periadolescence) nicotine exposure increases subsequent intravenous nicotine self-administration with accompanying neurologic changes and increased sensitivity to the addictive effects of the drug (e.g. Li et al. 135-139). Furthermore, in assessing the effects of tobacco smoke inhalation in rats, Fa and colleagues (p. 3639) found that exposure to smoke from a burned cigarette (1.0 mg nicotine) stimulated the dopaminergic neurons in the mesolimbic system. However, no stimulation was observed in rats exposed to smoke from lower nicotine concentrations (one cigarette containing 0.1 mg nicotine) (Fa et al., 3637-3639) Another study found duration-of-exposure dependent decreases in gamma-aminobutyric acid (GABA) receptor expression in the hippocampus of rats that were passively exposed to tobacco smoke (Li et al. 135-139). These findings support the hypothesis that tobacco smoke exposure has effects on GABA receptors; and consequently, learning and memory (Li et al. 135-139). However, the magnitude of functional effects from passive tobacco smoke exposure appear to be contingent upon the amount of the nicotine content in the smoke (Fa et al., 3637-3639). Similarly, passive exposure to inhalants produces concentration dependent neural and behavioral effects. Passive nicotine exposure can result in behavioral and cognitive effects similar to drug administration through more direct routes. There are relatively few clinical studies that have assessed the functional effects of nicotine from passive or side-stream tobacco smoke exposure on the brain and/or behavior. However, more extensive studies of the behavioral effects of passive or side­ stream exposure have been conducted with marijuana. These studies indicate that SHS exposure can engender functional changes in the brain with corresponding behavioral outcomes. Fetal Growth Retardation and Low Birth Weight Niebyl reports that more than fifty studies confirmed that smokers' babies weigh, on the average, 200 g. less at birth than babies of comparable nonsmokers, and the proportion of babies weighing less than 2,500 g. usually doubles with maternal smoking. It has been estimated that if smoking were eliminated, the number of low-birthweight infants would be reduced by 20 to 40%. Niebyl points that the reduction of birth weight is dose related, that is, the more the women smokes during pregnancy, the lower is her baby's birth weight. Wilcox's (1098-1104) study found that the infants of Missouri mothers who smoked at least one pack of cigarettes a day were, on average, 320 g. lighter than unexposed infants (3,180 g. compared with 3,500 g.). Wilcox also found that smoking produced lighter infants among both upper class and lower class women, and that the effect of smoking on infant survival among the upper classes appeared to be less perhaps because upper social class women experience the smoking effect on fetal growth and less of the smoking effect on weight specific mortality or preterm delivery (Wilcox 1098-1104). The above findings show the serious nature of ETS exposure among infants and children. Infants thrive physically due to intimate contact with their mothers during the early part of their lives. The health effects seen in young children exposed to ETS indicate a need for helping and assisting family members, especially mothers, to quit smoking or smoke away from the children. Conclusion From this literature review it is clear that exposure to secondhand smoke is related to various disease conditions. ETS has been linked with increased respiratory infections in children, increased asthma prevalence and susceptibility to develop asthma, smoking effects on Placenta, effects on brain functioning, fetal growth retardation and low birth weight. Despite the known harmful effects of secondhand smoke on young children, it is distressing to know that many children in the U.S. are regularly exposed to ETS at home. Since the major site of ETS exposure for young children under 5 years old is the home, efforts to reduce secondhand smoke exposure among young children are clearly called. Reducing secondhand smoke exposure is indeed a public health challenge that remains in the coming decades. Governments around the world have limited the hazards of second-hand smoke (SHS) through legislation to ensure smoke-free workplaces (Fernandez, Fu, Pascual et al. 1). However a lot needs to be done to protect young children from SHS. To reduce the ETS exposure among children, there is a need to educate parents about dangers of secondhand smoke for their children and to increase efforts to reduce the ETS exposure among children. Emmons et al. indicate that there is a need to "implement policies to ensure parent's access to smoking cessation interventions and to educate about the impact of smoking on their children's health." (P. 329) Work Cited Desalu, Olufemi O., Onyedum, Cajetan C., Adewole, Olufemi O., Fawibe1, Ademola E, & Salami, Alakija K. “Secondhand smoke exposure among nonsmoking adults in two Nigerian cities” Annals of African Medicine, (2011), 10(2), 103-111. 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Wright, A.L., Holberg, C., Martinez, F.D., & Taussig, L.M. Relationship of parental smoking to wheezing and non-wheezing lower respiratory tract illnesses in infancy: Group Health Medical Associates. (1991). Journal of Pediatrics, 118,207-214. Read More