Passive smoking or environmental tobacco smoking (ETS) is the indoor pollution variable that has been most intensively studied. Not only does smoking in the presence of a child have an effect on the manifestation of respiratory symptoms but also has an adverse effect on the developing fetus of mothers who smoke. [Burr 1999, Burr et al., 1999]. Exposure to cigarette smoke in utero and in the immediate post natal period is also a major risk factor for sudden infant death syndrome (SIDS) (see below). During childhood, wheezing is the most pronounced symptom [Diez et al., 2000, OIE et al., 1999, Zacharasiewicz 1999]. ETS, particularly in utero, leads to a decrease in pulmonary function, increased asthmatic symptoms and an increase in bronchial hyper responsiveness [Lodrup Carlsen 2002, Lodrup Carlsen et al., 2001, Bogacka 2002, Liard et al., 2002]. Whereas postnatal or environmental tobacco smoke (ETS) exposure has a significant influence or respiratory morbidity in the young [Taylor & Wadsworth 1987] the effects of prenatal exposure are likely to be more long lasting. Studies which have assessed lung function soon after birth, when the effects of ETS would be expected to be small have shown evidence of reduced airway function [Hanrahan et al 1992, Young et al 1991]. Whereas it is clearly not possible to identify the exact mechanisms of these effects in humans, animal studies have shown that fetal ETS significantly reduces cell division in the lung as evidenced by reduced DNA, alveolar number and connective tissue within the lung [Collins et al1985, Vidic et al 1989].
A recent systematic review demonstrated a consistent relationship between parents’ smoking and respiratory illnesses and symptoms and middle ear disease in children with odds ratios between 1.2 and 1.6 [Cook & Strachan, 1999]. The odds are greater for preschool children and higher for maternal compared with paternal smoking. The latter observation might be explained by increased exposure to maternal rather than paternal smoking among preschool children. Alternatively, a prenatal effect of maternal smoking on the developing fetal lungs might be responsible. One of the difficulties of disentangling the interrelationships of prenatal and postnatal tobacco smoke exposure on children’s respiratory symptoms in epidemiological studies is the observation that prenatal maternal smoking is almost always associated with postnatal tobacco smoke exposure. However whatever the mechanism it is clear that environmental tobacco smoke exposure (ETS) is an important and potentially remediable cause of respiratory morbidity in the young.
Several studies have demonstrated an association between prenatal tobacco smoke exposure and decrements in pulmonary function in infants soon after delivery and before the onset of symptoms. Such decrements appear to be associated with respiratory symptoms during the first year after birth [Martinez et al, 1988; Stick et al, 1996; Dezateux et al, 1999] and it seems likely that in utero smoke exposure causes growth restraint of fetal airways. The longer term effects of such fetal growth restraint have yet to be determined. Recent studies have attempted to examine the differential effects of intrauterine and postnatal tobacco smoke exposure on the outcomes of asthma and wheezing in later childhood. Gilliland and colleagues (2001) have demonstrated associations between in utero exposure and physician diagnosed asthma in later childhood but, although current or past environmental (postnatal) exposure was related to wheezing symptoms, there was not a significant relationship with asthma. The authors speculated that environmental exposure may act as a cofactor for attacks of wheezing but did not appear to be a factor that induced asthma in this population.
Parental smoking has also been demonstrated in several case control and cohort studies [Mitchell, 1995] to be significantly associated with sudden infant death syndrome (SIDS). Maternal smoking was associated with increased risk and a dose response effect has been demonstrated in several studies, suggesting a casual relationship, and, although smoking rates vary with socio-economic status, the risk appears to be consistent across socio-economic groups. Fleming and colleagues (1996) in a study of sudden infant death after the ‘Back to Sleep’ campaign in the United Kingdom calculated an odds ratio of SIDS for maternal smoking during pregnancy of 2.1 with an additional independent effect of paternal smoking. The mechanisms for this effect has not been elucidated but fetal lung growth restraint or effects of smoking on neurological responses to thermal, hypoxic or hypercapnic stress have been postulated. ETS also contributes to exacerbation of allergic symptoms [Baier et al., 2002, Diez et al., 2000]. Pre- and post natal ETS exposure increases a child’s sensitisation to food allergens [Kulig et al., 1999, 1999] and changes in the nasal mucous membrane have been observed in genetically predisposed children [Vinke et al., 1999].
Many studies have concentrated on the respiratory health effects of passive exposure to tobacco smoke in children. However, active smoking by children remains a significant health problem. A recent survey of 14-16 year old children revealed that 30% had been active smokers in the previous 12 months, with 14.1% reporting regular smoking [Withers et al, 2000].