Respiratory disease is a major component of the global burden of disease, with a reduction in deaths from childhood pneumonia but an increase in chronic respiratory disease over the past few decades [1-3]. There is an increasing recognition that low lung function poses a major risk for acute and chronic lung disease. Lung function tracks closely along centiles throughout childhood [4, 5], with lung function at birth determining lung function in later life [6]. Childhood asthma is associated with low lung function [7, 8], with the deficit seen on the first occasion that it is measured. Low lung function in childhood, with failure to reach predicted peak lung function in early adult life, is a major risk factor for chronic obstructive pulmonary disease (COPD), responsible for about 50% of cases in adults [9, 10]. Airway obstruction, generally indicated by a ratio of the forced expiratory volume in 1 s (FEV1) to the forced vital capacity (FVC) of <0.7 following bronchodilator inhalation, is a hallmark of COPD [11]. Indeed, the reliance on forced spirometry (so named to indicate the forced expiration required) may be one of the reasons that the major impact of early-life factors on COPD has been under-recognised [6]. Forced spirometry can be challenging in young children [12], with reported success rates varying from 30% to >80% [12, 13]. Young children find several aspects of spirometry difficult, including: taking a full breath in to total lung capacity; achieving a rapid onset of forced expiration; blowing hard enough to achieve expiratory flow limitation; and maintaining forced expiration to residual volume [12]. Given these difficulties, it is easy to understand why FVC may be underestimated in young children. In addition, in healthy young children, FEV1 approximates FVC, with a FEV1/FVC ratio of about 94% in children aged 5-7 years [14]. Thus, the physiological meaning of FEV1 differs in young children. This, together with the