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There is a great deal of interest in the early life determinants of lung function as possible determinants of obstructive airways disease through the rest of the life course. Failure to attain maximal lung function in early adult life either alone or coupled with accelerated decline during adulthood could contribute to the substantial burden of morbidity and mortality associated with obstructive airway disease and COPD in later life.1 Longitudinal studies of lung function in unselected populations have suggested that decrements of FEV1 established in the first few years after birth track to adulthood,2 thus pointing to early childhood as a critical period in lung function development. In this context, longitudinal cohort studies of populations that have lung function measurements during this critical period are of particular interest. Turner and colleagues report results from one of these, a birth cohort established in Perth, Western Australia, in 1987–1990 with repeat measures of lung function from shortly after birth to 18 years of age.3 The authors investigated whether factors associated with wheezing illnesses in childhood were associated with altered trajectories of lung function to age 18 years. The major influences identified were maternal asthma, atopy during infancy and maternal smoking when pregnant.
Infant lung function was measured in this cohort at three times during the first 12 months after birth and subsequent spirometry was repeated on three further occasions at 1 and 18 years. Due to its longevity, the Perth infant study used rather than a raised volume method to measure infant lung function. Therefore, FEF25–75, a notoriously variable measurement, was selected as the most comparable measure from later spirometric variables. The authors also presented …
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