FREE ESSAY ON SMOKING ON THE BODY

SMOKING ON THE BODY

Tobacco is one of the leading preventable causes of death in the United States. Nicotine,
which is an alkaloid derived from the tobacco plant, is a potent chemical that has
powerful effects on the human body, especially when administered rapidly or at high
doses. Prenatal exposure to nicotine is associated with adverse reproductive outcomes,
including altered neural structure and functioning, cognitive deficits, and behavior
problems in the offspring (9). At least 20% - 30% of pregnant women are estimated to
smoke cigarettes, although smoking is associated with low birth weight, prematurity and
infant mortality. In the United States, smoking accounts annually for estimated fetal
deaths ranging from 19,000 to 141,000, for 1,900 to 4,800 deaths during or immediately
after parturition, and for 1,200 to 2,200 death from Sudden Infant Death Syndrome (7). 
Maternal smoking has been implicated in long term deficits in infant mental development
and adverse behavioral problems in children such as attention disorder. Nicotine crosses
the human placenta and has direct effects on the developing fetus. Pre-clinical studies
suggest that maternal smoking during pregnancy produces changes on the offspring's neural
functioning, including reductions in uptake of serotonin, alterations in dopaminergic
systems, alterations in peripheral and central noradrenergic neurons, and changes in DNA
and RNA synthesis in the brain (9). Children prenatally exposed to nicotine consistently
score lower in the two subcategories of expressive language and conceptual comprehension.

Evidence from studies of human neonates suggests that maternal smoking during pregnancy
is associated with increased rates of neurobehavioral difficulties. Several studies have
linked maternal smoking during pregnancy with childhood inattention, impulsivity, and
motor hyperactivity in offspring. Similarly, maternal smoking during pregnancy has been
associated with parent-teacher ratings of conduct problems in children and a criminal
record in young adults. A study by Yousef Tzabi suggested that cigarette smoking during
pregnancy may be one of the causes of hyperactivity and learning deficits in children. In
a laboratory study with Sprague-Dawley mice, it was shown that hyperactive male pups that
were exposed to nicotine prenatally had significantly higher nicotinic receptor
concentrations in the cortex than did the controlled pups (8). This study indicates that
hyperactivity in male offspring induced by prenatal nicotine exposure is associated with
an increase in neuronal nicotinic receptors in the cortex. 
A similar study by Lauren S. Wakschlag, on maternal smoking during pregnancy and the risk
of conduct disorder in boys, revealed that mothers who smoked more than half a pack of
cigarettes daily during pregnancy were significantly more likely to have offspring who
met DSM-III-R diagnostic criteria for Conduct Disorder during the preadolescent or
adolescent years than women who did not smoke or smoked only occasionally during
pregnancy. These findings support previous work showing that maternal smoking during
pregnancy is associated with increased rates of preschool and school-age behavior
problems and delinquency in the offspring. 
The relationship between smoking and low birth weight, prematurity, and miscarriage has
been well established. The effects of nicotine are seen in every trimester of pregnancy,
from increased spontaneous abortions in the first trimester to increased premature
delivery rates and decreased birth weights in the final trimester. In 1957, Simpson first
noted in an observational study of 7,499 patients that the incidence of premature
delivery, as defined by a birth weight less than 2,500g, was twice as great for the
smoking mother as compared with the nonsmoking mother (5). A similar study by Walsh
concluded that the smoking mother is at two-fold increased risk for delivering a low
birth weight infant than her nonsmoking counterpart. 
The birth weight of a baby is dependent on two factors: the gestational age of the fetus
at the time of delivery, and the rate of fetal growth up until that point. Nicotine has
been shown to affect both of these factors. The average birth weight of infants
prenatally exposed to nicotine is 100 to 320g lighter than their nonexposed counterparts
(5). Therefore, the rate of delivering a low birth weight or premature infant has
remained consistently increased over the past four decades despite advances in prenatal
and neonatal care.
There is an overall increase of 33% in perinatal and neonatal mortality when women smoke
during their pregnancy. This increase in perinatal mortality is primarily a result of the
increase in low birth weight and premature delivery rate seen with tobacco use in
pregnancy. The risk of spontaneous abortions, as defined by fetal loss before 20 weeks of
gestation, is also 33% higher in smokers compared with controls (5).
A study by T.A. Slotkin, on impaired cardiac function during postnatal hypoxia in rats
exposed to nicotine, proposes that maternal smoking correlates highly with
parturitional/neonatal death including Sudden Infant Death Syndrome (SIDS). Nicotine
exposure of fetal rats reproduces the increased mortality when animals are tested
postnatally with hypoxia. Rats exposed to nicotine prenatally show an impaired
adrenomedullary response, as well as alterations in brain-stem noradrenergic mechanisms
that are likely to participate in cardiorespiratory control (7). Prenatal nicotine
exposure reduces cardiac reactivity to circulating catecholamines and to sympathetic
neuronal stimulation and may promote cardiac cell damage affecting the reactivity to
hypoxia. 
The loss of neonatal hypoxia tolerance caused by fetal nicotine exposure results in part
from interference with the maintenance of cardiac function. In nicotine-exposed rats, the
initial tachycardia was absent and the decline in heart rate was much more rapid and
profound. It was found that prenatal nicotine treatment may alter the differentiation and
function of cardiac cells such that pacemaker diastolic depolarization is blunted during
hypoxia. Nicotine can interfere with catecholamine actions which, when released by
hypoxia, are essential to maintain neonatal heart rate. Prenatal nicotine exposure blunts
the ability of the neonatal adrenal to secrete catecholamines in response to hypoxia. As
the neonatal heart lacks functional sympathetic innervation, there is virtually complete
dependence on circulating catecholamines derived from the adrenal medulla in order to
maintain the heart rate response to hypoxia (7).
If comparable changes are seen in man, then the results provide a casual explanation for
the increased perinatal morbidity and mortality seen in the offspring of smokers. The
fetal environment is relatively hypoxic, and corresponding cardiac functional deficits
would thus contribute to the high incidence of fetal mortality. Just as impaired cardiac
function during hypoxia in neonatal rats can account for the increase in mortality with
prolonged hypoxia, comparable effects in man would provide a mechanism for cardiovascular
collapse and consequent brain damage or death during delivery. 
The consequences of smoking during pregnancy are very dramatic. If clinicians are able to
convince their patients to stop smoking early in their pregnancy, a major impact may be
made on the incidence of low birth weight infants, perinatal morbidity and mortality, as
well as cognitive deficits and behavioral problems in the offspring. A strong statement
has to be made on the issue of tobacco exposure during pregnancy. This could be
accomplished by informing women that their infants may not only be smaller than their
nonsmoking counterparts, but their infants may also have transient or permanent changes
in their lung and brain ultrastructure. A patient who is informed of these possible
long-term effects of nicotine on her child may be more successful with her smoking
cessation.