Authors’ reply

Thank you for your interest in our study. Although emphysema has been determined to be an independent predictor of lung cancer development, the underlying phenomenon is not satisfactorily elucidated.1 The most likely chain of events is structural reshaping of the lung elicited by a chronic inflammatory process as a result of exposure to multiple chemical compounds in tobacco smoke and air pollutants.

Here, we address your doubts and queries in the order they appear in your letter.

First, we demonstrated that emphysema modifies the features of a solitary pulmonary nodule (SPN), as documented in Tables 3 and 4. Note that there was a tendency for SPN to have bigger diameter in the emphysema coexisting with nodules (E + N) group in comparison with the group with nodules without emphysema (median [IQR], 12 [3] mm vs 10 [15] mm, respectively; P = 0.047). Additionally, nonsolid nodules were more numerous in the E + N group (36.5% vs 21.1%, respectively; P = 0.01), whereas solid and part-solid SPNs prevailed in the group with nodules without emphysema. Moreover, the multiple SPNs were more abundant in the E + N group (71.9% vs 56.3%; P = 0.02).

Understandably, individuals with emphysema were characterized by older age and higher cumulative tobacco consumption.

Second, query regarding the difference in SPN morphology, size, and number between the 2 groups remains a question open to debate. From the clinical point of view, our findings confirm the need to incorporate additional factors beyond participants’ age and pack-years smoked when considering a target screening cohort. Emphysema is included into the set of risk factors but is not a variable used in risk assessment prediction models like the Bach model, LDCRAT (Lung Cancer Death Risk Assessment Tool), or others. Quite recently, Tammemägi et al2 proposed to include the result of the initial low-dose computed tomography into the prediction regression equation. Yong et al,3 with the use of prediction tests, showed that the number needed to screen to detect 1 patient with cancer was lower in the participants with radiological emphysema.

Third, our cohort did not include patients with emphysema and idiopathic pulmonary fibrosis. It is an in-depth question since both diseases are risk factors listed to include a screenee into group 2 according to the guidelines of the National Comprehensive Cancer Network.4 Nonetheless, most likely, an individual with concomitant occurrence of these disorders would not be a candidate for screening due to respiratory insufficiency.

Fourth, unfortunately, lack of pathological information pertaining to the nodules is the limitation of our study. This, in turn, is due to the relatively small size of our cohort. This means we know pathological outcome only for those patients with SPNs who underwent diagnostic workup. In our study, we focused only on the baseline low-dose computed tomography. In further reports we plan to focus on the consecutive low-dose computed tomography rounds.

We hope that this response has, at least to some extent, clarified your queries.