An known. Therefore, smoking during pregnancy might affect

An impressive amount of literature describes the adverse effects of smoking during pregnancy. Even before pregnancy, cigarette smoking is of influence since it is dose dependently associated with a decrease in fertility. Cigarette smoking during pregnancy is associated with a higher frequency of obstetric complications, such as spontaneous abortions, ectopic pregnancies, preterm birth, placenta previa, abruptio placentae, and premature rupture of membranes. Smoking during pregnancy may be responsible for 15% of all preterm births and a 150% increase in overall perinatal mortality. Even in non-smoking pregnant women, high exposure to ETS is associated with an increased risk for preterm birth. The relation between smoking and ectopic pregnancy might be causal, with a highly significant adjusted odds ratio of 2.5 or more for women who smoke more than 20 cigarettes a day.Fetal breathing movements are essential for normal growth and structural maturation of the fetal lungs. Animal studies show that exposure to cigarette smoke during pregnancy leads to a reduction in fetal breathing movements. Prolonged absence or impairment of fetal breathing movements is likely to result in hypoplasia of the fetal lungs with fewer saccules. This results in a reduced surface potentially available for gas exchange. Moreover, in utero cigarette smoke exposure decreased alveolar attachment points to the airways and caused changes in airway dimensions in guinea pigs. These observations may be applicable to humans since nicotine caused a reduction in the incidence of fetal breathing movements in normal and abnormal human pregnancies. Consequently, reduced lung growth in children of smoking mothers may begin antenatally. Lung function tests in infants born to smoking mothers confirm reduced airway patency, whereas the effect of prenatal smoke exposure most likely plays a greater role on lung function in childhood than postnatal and childhood exposure. How long the impaired lung function that results from exposure in utero continues to be significant is still not known. Therefore, smoking during pregnancy might affect adult lung function, which is suggested to be “programmed” in fetal life.Low birth weightActive smoking by pregnant women induces early morphological changes of the placenta, resulting in a reduced volume of maternal intervillous space and a reduced volume and surface area of fetal capillaries. These morphological changes lead to a reduction in oxygen diffusion across the placenta and seem to be the result of an all-or-none effect, rather than a dose dependent effect. Hence, the fetus suffers from chronic hypoxic stress as a consequence of smoking. These factors contribute to a reduced birth weight and length, and a smaller head circumference at birth. In developed countries maternal smoking is the major factor for low birth weight. It is estimated that smoking during pregnancy reduces birth weight by 10–15 g per cigarette smoked daily. However, this is not a linear relation; the sharpest declines in birth weight occurred at low levels of exposure. Therefore, the effect of a reduction of cigarette smoking during pregnancy is small compared to the effect of smoking cessation. It has even been suggested that high exposure to ETS in non-smoking pregnant women is negatively associated with birth weight. Recently, Wang and co-workers concluded that the direct effects of smoking during pregnancy on birth weight and gestational age may even be stronger depending on the individual susceptibility. They investigated whether the association between maternal cigarette smoking and infant birth weight differs by polymorphisms of two maternal metabolic genes. Without consideration of genotype, continuous maternal smoking during pregnancy was associated with a mean reduction of 377 g in birth weight. When both metabolic genes were considered, the greatest reduction in birth weight (?1285 g) was found among smoking mothers with polymorphisms of both genes (which occurs in almost 10% of the population). Among never-smokers genotype did not independently confer an adverse effect.SMOKING AND CHILDRENSudden infant death syndromeExposure to ETS during infancy is a major risk factor for sudden infant death syndrome (SIDS). A systematic review concluded that after adjusting for confounders, such as sleeping position and economic status, maternal smoking doubles the risk for SIDS. The effect of prenatal and postnatal smoking was similar. The relation is dose dependent and almost certainly causal.Prenatal smoking is almost invariably associated with postnatal smoking. Therefore, it is difficult to resolve the role of prenatal smoking per se using epidemiological studies. The fact that infants who died from SIDS had a higher nicotine concentration in their lung tissue compared with non-SIDS cases supports the statement that postnatal ETS exposure is important. Possible reasons for the association between passive smoking and SIDS are abnormalities in brain development, with a tendency to central apnoea and disturbed respiratory control mechanisms, including a reduced ventilatory response to hypoxia. Other possible explanations are an abnormal pulmonary development in neonates and the promotion of respiratory infections.InfectionsIn a systematic review a causal relation was found between parental smoking and an increased risk of acute lower respiratory illness in infancy. Most likely this is the result of both prenatal and postnatal passive smoking, but it is difficult to distinguish the independent contributions. On the other hand, the increased risk associated with smoking by other household members in families where the mother does not smoke suggests that exposure to ETS after birth contributes to acute chest illness in young children. There is a positive dose-response relation, which is stronger with maternal smoking compared to smoking by other household members. This is explained by a higher degree of postnatal exposure from the mother as principal care giver, and the fact that intra-uterine lung growth might already have been disturbed as a result of maternal smoking during pregnancy.In the first two years of life, passive smoking is associated with a higher incidence of respiratory infections in general, including respiratory syncytial virus bronchiolitis. In addition, passive smoking is a risk factor for developing pulmonary tuberculosis in children immediately following infection, and a risk factor in meningococcal disease. This could possibly be the result of a direct effect of cigarette smoke on host defences since smoking is negatively associated with cell mediated and humoral immunity, and smoking increases bacterial adherence and the risk of inflammation and other infections The observation that smokers are more likely to be carriers of meningococci is consistent with the increased risk of invasive meningococcal disease.Middle ear disease and adenotonsillectomy in childrenIn a systematic quantitative review, Strachan and Cook concluded that there is probably a causal relation between parental smoking and both acute and chronic middle ear disease in children. In particular, chronic middle ear disease is 20–50% more frequent in children exposed to ETS. There is no association between exposure to ETS and adenotonsillectomy in children. A possible explanation for the relation between ETS exposure and these and other infections, is a direct effect of cigarette smoke on host defences.Lung functionThere is compelling evidence that maternal smoking reduces lung function in young children and that the effect is present at birth and attributable to effects of maternal smoking during pregnancy and early postnatal exposure on the child’s lung development. In infants born to smoking mothers lung function tests show a reduction in forced expiratory flows compared to infants born to non-smoking mothers. This reduction in forced expiratory flows, used as a measure of airway patency, could amount to 51% compared to infants whose mothers did not smoke during pregnancy.In a pooled analysis of school age children, exposure to ETS was associated with a reduction of 1.4% in forced expiratory volume in one second (FEV1). Parameters for airway patency of the peripheral airways, the mid and end expiratory flow rates, show a decrease of 5.0% and 4.3% respectively, in those exposed to ETS. These small, but significant, deficits in spirometric indices are almost certainly causally associated with maternal smoking, and much of the effect may be due to maternal smoking during pregnancy and/or neonatal exposure. Smoking by the father only had no significant effect on the children’s lung function. A dose-response relation was not always shown, perhaps due to the fact that parents tend to smoke less as their children develop respiratory symptoms. When the independent effect of prenatal and postnatal tobacco smoke exposure on children’s lung function was studied, the effect of maternal smoking during pregnancy was larger than that of current smoking.Wheezing and asthmaPrenatal maternal smoking increases the risk for symptomatic paediatric asthma, and postnatal maternal smoking is associated with an increased incidence of wheezing illness up to the age of 6 years. Surprisingly, the long term prognosis of early wheezing illness was better if the mother smoked. The excess incidence of wheezing in smoking households appears to be largely non-atopic “wheezy bronchitis”, which has a relatively benign prognosis. Therefore, postnatal ETS exposure can be considered as a co-factor provoking wheezing attacks, rather than a cause of the underlying asthmatic tendency. The reason why prenatal passive smoking is associated with paediatric asthma, and postnatal passive smoking is associated with non-atopic “wheezy bronchitis”, remains to be elucidated. Possibly, a reduction in lung function as a result of prenatal passive smoking makes the children more susceptible for respiratory symptoms, and therefore enables the diagnosis of paediatric asthma. Furthermore, the distinction between wheezy bronchitis and asthma can be very difficult, and it seems conceivable that they can co-exist as well. Among children with established asthma, parental smoking is associated with more severe disease.In school age children (5–16 years), parental smoking has no influence on the prevalence of allergic asthma. Nevertheless, parental smoking does have an effect on respiratory symptoms, both in children with asthma and in children without asthma. Wheeze, cough, phlegm, and breathlessness are 20–40% more frequent in children exposed to ETS. There is a clear dose-response relation, which also becomes apparent when there is a reduction in symptoms as the parents stop smoking, and as the children grow older, and therefore spend less time with their parents.CONCLUSION AND IMPLICATIONSPrenatal and postnatal passive smoking have a wide range of effects on mortality and morbidity in children (boxes 1 and 2). Prenatal passive smoking has lifetime consequences since it influences placental and fetal development, reduces birth weight, and affects lung and brain development. A low birth weight is associated with an increase in the incidence of coronary heart disease, stroke, hypertension, type 2 diabetes mellitus, insulin resistance, serum lipids, and premature pubarche. Lung function tests in infants and older children born to smoking mothers show reduced airway patency, probably reflecting underdevelopment of lungs and airways. The reduced lung growth and the increased risk for respiratory infections due to passive smoking are possible explanations for the increased risk for SIDS. Furthermore, prenatal passive smoking is thought to be a risk factor for a variety of neurodevelopmental and behavioural problems, such as reduced general intellectual ability and attention deficit and hyperactivity disorder.References: