The effects of tobacco smoke exposure on lung function in children are dependent on the source, timing and dose of exposure and may be modified by the sex of the child and the child’s asthma status. There is evidence that both passive exposure at different developmental stages and active smoking during adolescence have detrimental effects on pulmonary function in cross-sectional studies and on the rate of growth of pulmonary function in longitudinal analyses.

In their series of systematic quantitative reviews of the effects of tobacco smoke exposure, Cook and Strachan analysed 22 cross-sectional studies and concluded that ETS exposure, particularly from the mother, was associated with small decrements in forced expiratory volume in 1 s (FEV1) and mid-expiratory flow rates in school-aged children.35 The findings of subsequent studies have been consistent with this conclusion. A large, international study of 6–12-year-old children reported measurable effects of current ETS exposure on both FEV1 and Maximal midexpiratory flow (MMEF), although the effect sizes were even greater for prenatal exposure.

Other studies of the relative contributions of prenatal and postnatal exposure to pulmonary function outcomes in children have also provided support for a stronger effect of maternal smoking in pregnancy than subsequent or current smoking when lung function was assessed in school-aged children.36,37 Decreased lung function growth during adolescence has been reported in association with both early exposure to maternal smoking in the first 5 years of life and current maternal smoking, although the effect was attenuated in older children (11–18 years) compared with a younger age group (6–10 years).38 These data suggest that
the effects of maternal smoking during pregnancy on pulmonary function shortly after birth16 track through to later childhood but that there is a small additional, independent effect of postnatal ETS exposure.

Interactions between ETS exposure and asthma have been suggested by an analysis of the NHANES III data, in which the presence of two or more smokers in the home was an independent risk factor for reduced mid-expiratory flow rates in asthmatic girls, although small effects were observed in children without asthma who were exposed to smoke.39 Gilliland and colleagues had previously reported an interaction between asthma and in utero tobacco smoke exposure on children’s lung function, suggesting that there might be synergy between the toxic effects of tobacco smoke on the developing airway and airway inflammation associated with asthma.

The majority of studies that have reported pulmonary function outcomes in children in relation to ETS exposure suggest that there is a greater effect on mid-expiratory flow rates, reflecting the function of the smaller airways, than on FEV1. There is also a suggestion of differential effects of exposure on lung and airway development in boys and girls.41 In addition, although the measured effect sizes have tended to be small, they remain important for a number of reasons: small decrements in lung function growth will affect maximally attained pulmonary function in adulthood 42 and may therefore contribute to the burden of chronic obstructive airways disease43,44; passive exposure to ETS is highly prevalent, resulting in large population attributable risks5; and there are likely to be additive or multiplicative effects of active smoking on a background of cumulative passive exposure through childhood. Smoking during adolescence has been associated with dose-dependent reductions of both FEV1 and mid-expiratory flow, and children who smoke before the age of 16 years are more likely to develop bronchitis and emphysema than those smokers who start later, possibly due to greater cumulative lifetime exposure.