Lung function trajectory from childhood to the fourth decade of life (Am J Respir Crit Care Med. 2016;194:607-12)

As low lung function in childhood and early adulthood is associated with increased risk of development of chronic obstructive pulmonary disease later in life, it is important to understand the natural history of progression of lung function changes over time. The cohort of individuals enrolled in the Tucson Children’s Respiratory Study which was started in the early 1980s to understand the effect of lung function on wheezing and risk of asthma later in life, have provided important longitudinal data on lung function. Among this non-selected birth cohort of 1246 participants, 599 had 2 or more spirometry results between 11 and 32 years of age, for a total of 2142 observations. The authors were able to identify lung function trajectories that included a) normal lung function throughout, b) persistently low lung function, and c) decline from normal to low lung function later in life. For individuals in the persistently low lung function trajectory, the authors found that they had history of maternal asthma, higher incidence of early life infection with respiratory syncytial virus, and physician diagnosed active asthma at 32 years of age. All of these individuals had evidence of small airway dysfunction in infancy and at 6 years of age as well. The authors concluded that this distinct group of individuals with a low lung function trajectory may have been established at birth and predisposes them to chronic obstructive pulmonary disease later in life.

Obesity is a risk factor for asthma, and with rising incidence of obesity in urban pediatric populations, it is important to understand its effect on the lung function of children. Airway dysanapsis is defined as the physiologic divergence between the growth of the lung parenchyma and the size of the airways, and can be recognized by spirometry that demonstrates normal Forced Expired Volume in one second (FEV1) and Forced Vital Capacity (FVC), and an abnormal FEV1/FVC ratio. Even though increase in airway length tracks with lung volumes, but airway caliber growth does not. Therefore, dysanapsis can be seen in healthy individuals with expiratory flow limitation and obesity in children has also been associated with reduced FEV1/FVC ratio. The authors evaluated for dysanapsis in obese children by analyzing longitudinal and cross-sectional pulmonary function data from various sources and included populations with and without asthma. The authors defined dysanapsis as normal to high z-score for FVC (>0.674 or 75th percentile), normal z-score for FEV1 (>-1.645, 5th percentile or lower limit of normal) and low FEV1/FVC (<0.80). They found that obesity was associated with dysanapsis both in cross-sectional and longitudinal data sets, and they found higher lung volumes and lower flows, along with ventilation inhomogeneity in these children. For obese children with asthma, they found that dysanapsis was associated with severe disease exacerbations and use of systemic steroids. The authors concluded that obese children show relative airflow obstruction throughout airways of all sizes, and their lung volumes show larger vital capacity, residual volume (RV) and Total Lung Capacity (TLC), but normal RV/TLC ratio suggesting that there is no air trapping. This suggests that dysanapsis or asymmetric growth of lungs and airways can have significant impact on obese children with asthma and may partly explain the decreased response to asthma medications in this group.