COMMENTARY

Can a CT Scan Determine Lung Age?

Aaron B. Holley, MD

Disclosures

October 10, 2016

What Happens to the Lungs in Aging?

Just like every other organ in our body, the lungs change with age. On the basis of a wealth of published data, we know that lung size peaks somewhere around 20 years of age.[1] A long, steady decline follows. This decline affects exercise capacity[2] and is accelerated by tobacco use, chronic obstructive pulmonary disease (COPD), and other environmental exposures.[3,4,5]

A recent study[6] in the American Journal of Respiratory and Critical Care Medicine sought to characterize age-related lung changes using CT. Patients from the Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS), a multicenter project that enrolls participants across four categories (never-smokers and ever-smokers without COPD, with mild/moderate COPD, and with severe COPD), were evaluated.[7] Using novel CT imaging techniques to differentiate air trapping from emphysema, the investigators quantified both and used air trapping as a surrogate for small-airways disease (SAD) using parametric response mapping (PRM).

They found that SAD increases with age—each decade, the portion of the lung fields consistent with SAD increased by 2.7% on CT. Absolute values and change per decade were much lower for emphysema. SAD and emphysema both increased at a faster rate in patients diagnosed with COPD.

Of interest, the investigators also found that the proportion of SAD on CT was associated with an increased forced vital capacity (FVC) but had no effect on forced expiratory volume in 1 second (FEV1). As a consequence, more SAD leads to a lower FEV1/FVC because the denominator increases. A decline in FEV1/FVC is a known consequence of the aging process.[1]

Separating SAD From Emphysema

Much is left unsaid, however. It's not clear how SAD would lead to an increase in FVC without having an effect on FEV1. Air trapping typically leads to a reduction in FVC,[8] and loss of small-airways volume is associated with increased elastance and less distensibility.[9,10] The investigators admitted that they could not differentiate SAD from reduced elastance owing to loss of structural integrity at the level of the alveoli. In short, they are right when they state that tissue confirmation is necessary to properly characterize the pathology they are identifying using PRM.[6]

PRM was recently used by another group who conducted their research in patients from COPDGene.[3] The software system was different, but the Hounsfield units used to identify emphysema and SAD were identical. The authors of the COPDGene study concluded that SAD as measured by PRM is associated with FEV1 decline.[3]

What does all this mean? It's hard to say at this time. I agree with the SPIROMICS investigators when they say that understanding normal changes in the aging lung is important. PRM is powerful and provides the opportunity to characterize the lung in new and interesting ways. Confirmatory histologic data would be welcome, and the authors say they are forthcoming.[6]

Because we are getting closer to being able to target the small airways with inhaled therapies,[11] the ability to differentiate SAD from emphysema or other structural abnormalities is critical. In summary, advanced imaging techniques have tremendous potential. Studies such as this one place us closer to being able to use them clinically.

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