• H Brown Robert, A Wise Robert, Gregory Kirk, M Bradley Drummond, and Wayne Mitzner.
• Department of Anesthesiology, Johns Hopkins University, Baltimore, MD; Department of Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, MD; Environmental Health Sciences, Division of Physiology, Johns Hopkins University, Baltimore, MD. Electronic address: rbrown@jhsph.edu.
• Chest. 2015 Oct 1; 148 (4): 9951002995-1002.

BackgroundWith body growth from childhood, the lungs can enlarge by either increasing the volume of air in the periphery (as would occur with inspiration) or by increasing the number of peripheral acinar units. In the former case, the lung tissue density would decrease with inflation, whereas in the latter case, the lung density would be relatively constant as the lung grows. To address this fundamental structural issue, we measured the CT scan density in human subjects of widely varying size at two different lung volumes.MethodsFive hundred one subjects were enrolled in the study. They underwent a chest CT scan at full inspiration and another scan at end expiration. Spirometry, body plethysmography, and diffusing capacity of the lung for carbon monoxide were also measured.ResultsThere was a strong correlation between the size of the lungs measured at full inspiration on CT scan and the mean lung density (r = -0.72, P = .001). People with larger lungs had significantly lower mean lung density. These density changes among different subjects overlapped the density changes within subjects at different lung volumes.ConclusionsLung structure in subjects with larger lungs is different from that in subjects with smaller lungs. Tissue volume does not increase in proportion to lung size, as would be required if larger lungs just had more alveoli. These observations suggest that the growth of the lung into adulthood is not accompanied by new alveoli, but rather by enlargement of existing structures. The presence of greater air spaces in larger lungs could impact the occurrence and pathogenesis of spontaneous pneumothorax or COPD.

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