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Impairment in adult lung function has been associated with increased mortality for a wide range of diseases1 and increased morbidity including risk of chronic pulmonary obstructive disease (COPD∥.2 Decrements in lung function have been linked to a number of factors including cigarette smoking, air pollution, lower respiratory tract infection and asthma diagnosis.3 In addition, prenatal factors seem to play an important part in determining adult lung function.
Cigarette smoking is associated with the greatest effect on adult lung function and decline in lung function, with smoking associated with a 28–50 ml/year loss in forced expiratory volume in 1 sec (FEV1).4 This effect on FEV1 seems to be influenced by gender because the effect is greater among adolescent girls than boys5 but reverses in middle age where effects are greater in men than women.4 Both pregnancy and early infancy6–9 have been shown to be risk periods for effects of environmental cigarette smoke. Other work has suggested that exposure to cigarette smoke may be particularly detrimental to lung growth in populations who are already disadvantaged owing to poor rates of fetal growth.10 Cigarette smoke has been shown to have a direct detrimental effect on lung function at birth11 and in the early years.8 However, the question arises of which period is poses the highest risk, fetal or the postnatal.
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