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QCT Textures In COPD May Show Lung Inflammation Distribution, Disease Burden

Quantitative computed tomography (QCT) textures may provide imaging evidence of the spatial heterogeneity of lung inflammation and disease burden in patients with chronic obstructive pulmonary disease (COPD), according to study findings published in Chest.

Researchers analyzed data from the SPIROMICS and COPDGene cohort studies (ClinicalTrials.Gov Identifiers, NCT01969344 and NCT00608764, respectively) to determine whether local textures of the bronchovascular bundles (BVB) and the surrounding regions, quantified by the adaptive multiple feature method, are associated with systemic inflammation, impaired lung function, and all-cause mortality, independent of CT-based emphysema and airway wall thickening.

SPIROMICS participants had high-resolution chest CT scans at total lung capacity (TLC) and residual volume. COPDGene enrolled individuals who were also scanned at multiple lung volumes (TLC and functional residual capacity).

Outcome variables for systemic inflammation included 9 plasma proteomic biomarkers obtained from the Meso Scale Discovery assay: tumor necrosis factor (TNF)-α; interleukin (IL)-2, −6, −8, −10; interferon (IFN)-γ; CCL11 (eotaxin); CCL26 (eotaxin 3); and CCL17. Other biomarkers of systemic inflammation included complete blood counts (CBCs). Multivariable regression analysis was performed to assess the associations of QCT textures with lung function and clinical outcomes in COPD.

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Both BVB and CTDG textures have the potential to serve as visual indicators of inflammation in individuals with or at risk for COPD with significant associations with respiratory morbidity and all-cause mortality.

The analysis included 2118 patients from SPIROMICS and 7077 from COPDGene. Mean ages were 63.0 years in SPIROMICS (52% male) and 60.0 years in COPDGene (54% male).

False discovery rate–corrected univariate analysis with the CBC data identified 5 significant associations with BVB texture in the 2 cohorts. Platelet count, neutrophil count, monocyte count, and neutrophil-to-lymphocyte ratio (NLR) had a significant association with BVB texture after adjustment. CT density gradient (CTDG) was significantly associated with TNF-⍺, NLR, and neutrophil count.

BVB texture was associated with postbronchodilator forced expiratory volume in 1 second (FEV1) (SPIROMICS: b = –0.056; 95% CI, –0.072 to –0.040; P <.001; COPDGene: b = –0.022; 95% CI, –0.029 to –0.015; P <.001) in multivariable regression analysis. BVB texture had a significant association with 6-minute walk distance in SPIROMICS and COPDGene after adjustment.

Among COPDGene participants, CTDG texture had a significant association with FEV1 change (β = –0.967; 95% CI, –1.840 to –0.094; P =.03).

Cox proportional hazards analysis showed that BVB texture had a significant association with all-cause mortality in SPIROMICS and COPDGene. The associations were significant after adjustment for confounding factors, with hazard ratios of 1.084 (95% CI, 1.035-1.135; P <.001) and 1.106 (95% CI, 1.080-1.131; P <.001), respectively. CTDG texture also was significantly associated with all-cause mortality.

Limitations include the descriptive study design and the acquisition of QCT measures and plasma biomarkers at a single time point.

"Both BVB and CTDG textures have the potential to serve as visual indicators of inflammation in individuals with or at risk for COPD with significant associations with respiratory morbidity and all-cause mortality," the investigators stated.

Disclosure: Some of the study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors' disclosures.


COPD And Lung Carbon: A Finding That Surpasses Smoking

People with COPD Show More Carbon in Their Lungs Than Smokers: A Surprising Finding with Environmental and Clinical Implications

A recent study published in ERJ Open Research and reported by The Washington Post revealed that patients with chronic obstructive pulmonary disease (COPD) have levels of carbon—soot-like particles—in their alveolar macrophages more than three times higher than those found in smokers without the disease. This accumulation may be linked to increased inflammation, worsened lung function, and a higher risk of respiratory infections.

A finding based on real tissue

The research team analyzed lung tissue samples from 28 COPD patients and 15 smokers undergoing surgery for lung cancer. They found that macrophages in COPD patients contained large carbon deposits and were significantly larger than in the control group. Furthermore, the higher the carbon load, the worse the lung function (measured via FEV1%) appeared to be.

The presence of carbon suggests not only a failure of the lungs' ability to clear particles but also chronic inflammatory activation, with the release of mediators such as TNFα and CXCL8 observed in in-vitro models.

Why only in COPD and not just from cigarette smoke?

This finding raises key questions: although smoking is a known carbon source, the significantly higher accumulation in COPD cannot be explained by smoking alone. Researchers from the University of Manchester point to multifactorial causes: reduced capacity of macrophages to clear particles and environmental exposure, such as pollution or indoor smoke.

In fact, literature shows that exposure to particulate matter (PM2.5, smoke from wood or coal cooking) can contribute as much or more than active smoking in some cases.

Implications for COPD management

These discoveries offer new insights for prevention and treatment of the disease:

  • More precise assessments: Measuring carbon load in macrophages may serve as a biomarker to estimate inflammation and clinical risk.

  • Environmental control is key: Quitting smoking is not enough—reducing exposure to environmental and household air pollution is critical. Evidence shows that using air purifiers can reduce particulate burden and improve cardiovascular health in COPD patients.

  • Strengthening pulmonary defenses: Developing therapies that enhance macrophage function could improve carbon clearance and reduce chronic inflammation.

    • Expert opinions

    Professor Fabio Ricciardolo (ERS) warned that "this accumulation seems to alter macrophages, triggering inflammation and worsened lung function." Baker and Lea (Manchester) also emphasized that COPD cells are "inherently different" from those in smokers without the disease.

    Conclusion

    This study reshapes our understanding of lung carbon's role in COPD and highlights environmental exposure and immune dysfunction as key pieces of the puzzle. In the future, monitoring these deposits and strengthening lung defenses may improve outcomes and quality of life for millions affected by this chronic disease.





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