Inflammation mediates the association between furan exposure and the prevalence and mortality of chronic obstructive pulmonary disease: National Health and Nutrition Examination Survey 2013-2018.

BACKGROUND: Although extensive research has established associations between chronic obstructive pulmonary disease (COPD) and environmental pollutants, the connection between furan and COPD remains unclear. This study aimed to explore the association between furan and COPD while investigating potential mechanisms. METHODS: The study involved 7,482 adults from the National Health and Nutrition Examination Survey 2013-2018. Exposure to furan was assessed using blood furan levels. Participants were categorized into five groups based on quartiles of log10-transformed blood furan levels. Logistic regression and restricted cubic spline regression models were used to assess the association between furan exposure and COPD risk. Mediating analysis was performed to assess the contribution of inflammation to the effects of furan exposure on COPD prevalence. Cox regression was used to assess the association between furan exposure and the prognosis of COPD. RESULTS: Participants with COPD exhibited higher blood furan levels compared to those without COPD (P < 0.001). Log10-transformed blood furan levels were independently associated with an increased COPD risk after adjusting for all covariates (Q5 vs. Q1: OR = 4.47, 95% CI = 1.58-12.66, P = 0.006, P for trend = 0.001). Inflammatory cells such as monocytes, neutrophils, and basophils were identified as mediators in the relationship between furan exposure and COPD prevalence, with mediated proportions of 8.73%, 20.90%, and 10.94%, respectively (all P < 0.05). Moreover, multivariate Cox regression analysis revealed a positive correlation between log10-transformed blood furan levels and respiratory mortality in COPD patients (HR = 41.00, 95% CI = 3.70-460.00, P = 0.003). CONCLUSIONS: Exposure to furan demonstrates a positive correlation with both the prevalence and respiratory mortality of COPD, with inflammation identified as a crucial mediator in this relationship.

Development of a Diagnostic Nomogram to Predict CAP in Hospitalized Patients with AECOPD.

The purpose of this study was to establish a nomogram for predicting community-acquired pneumonia (CAP) in hospitalized patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD). The retrospective cohort study included 1249 hospitalized patients with AECOPD between January 2012 and December 2019. The patients were divided into pneumonia-complicating AECOPD (pAECOPD) and non-pneumonic AECOPD (npAECOPD) groups. The least absolute shrinkage and selection operator (LASSO) regression and multivariate logistic regression were utilized to identify prognostic factors. A prognostic nomogram model was established, and the bootstrap method was used for internal validation. Discrimination and calibration of the nomogram model were evaluated by receiver operating characteristic (ROC) curve, calibration curve, and decision curve analysis (DCA). Logistic and LASSO regression analysis showed that C-reactive protein (CRP) >10 mg/L, albumin (Alb) <40 g/L, alanine transferase (ALT) >50 U/L, fever, bronchiectasis, asthma, previous hospitalization for pAECOPD in the past year (Pre-H for pAECOPD), and age-adjusted Charlson score (aCCI) ≥6 were independent predictors of pAECOPD. The area under the ROC curve (AUC) of the nomogram model was 0.712 (95% CI: 0.682-0.741). The corrected AUC of internal validation was 0.700. The model had well-fitted calibration curves and good clinical usability DCA curve. A nomogram model was developed to assist clinicians in predicting the risk of pAECOPD.China Clinical Trials Registry: ChiCTR2000039959.