Dutta Joytri, Singh Sabita, Greeshma Mandya V, Mahesh Padukudru Anand, Mabalirajan Ulaganathan
Molecular Pathobiology of Respiratory Diseases, Cell Biology and Physiology Division, Council of Scientific and Industrial Research (CSIR)-Indian Institute of Chemical Biology (IICB), Kolkata 700091, WB, India.
Academy of Scientific and Innovative Research (AcSIR), Sector-19, Kamla Nehru Nagar, Ghaziabad 201002, UP, India.
Diagnostics (Basel). 2024 Sep 27;14(19):2154. doi: 10.3390/diagnostics14192154.
Chronic Obstructive Pulmonary Disease (COPD) is a major global health challenge, primarily driven by exposures to tobacco smoke and biomass smoke. While Tobacco-Smoke-Induced COPD (TSCOPD) has been extensively studied, the diagnostic challenges and distinct pathogenesis of Biomass-Smoke-Induced COPD (BSCOPD), particularly in low- and middle-income countries, remain underexplored. To explore the differences in clinical manifestations, pulmonary function, and inflammatory profiles between BSCOPD and TSCOPD and highlight the diagnostic complexities of BSCOPD. This review analyzes the current literature comparing BSCOPD with TSCOPD, focusing on distinctive pathophysiological mechanisms, inflammatory markers, and oxidative stress processes. BSCOPD presents differences in clinical presentation, with less emphysema, smaller airway damage, and higher rates of pulmonary hypertension compared to TSCOPD. BSCOPD is also characterized by bronchial hyperresponsiveness and significant hypoxemia, unlike TSCOPD, which exhibits severe airflow obstruction and emphysema. Additionally, the inflammatory profile of BSCOPD includes distinct mucous hypersecretion and airway remodeling. The unique genetic, epigenetic, and oxidative stress mechanisms involved in BSCOPD complicate its diagnosis and management. Biomass smoke's underrecognized impact on accelerated lung aging and exacerbation mechanisms emphasizes the need for targeted research to refine diagnostic criteria and management strategies for BSCOPD. : Further research should focus on identifying specific biomarkers and molecular pathways to enhance early diagnosis and improve clinical outcomes in populations exposed to biomass smoke.
慢性阻塞性肺疾病（COPD）是一项重大的全球健康挑战，主要由接触烟草烟雾和生物质烟雾所致。虽然烟草烟雾诱导的COPD（TSCOPD）已得到广泛研究，但生物质烟雾诱导的COPD（BSCOPD）的诊断挑战和独特发病机制，尤其是在低收入和中等收入国家，仍未得到充分探索。为了探究BSCOPD和TSCOPD在临床表现、肺功能和炎症特征方面的差异，并突出BSCOPD的诊断复杂性。本综述分析了当前比较BSCOPD和TSCOPD的文献，重点关注独特的病理生理机制、炎症标志物和氧化应激过程。与TSCOPD相比，BSCOPD在临床表现上存在差异，肺气肿较少、气道损伤较小且肺动脉高压发生率较高。BSCOPD还具有支气管高反应性和显著低氧血症的特征，而TSCOPD则表现为严重气流阻塞和肺气肿。此外，BSCOPD的炎症特征包括明显的黏液分泌过多和气道重塑。BSCOPD所涉及的独特遗传、表观遗传和氧化应激机制使其诊断和管理变得复杂。生物质烟雾对加速肺衰老和加重机制的未被充分认识的影响强调了开展针对性研究以完善BSCOPD诊断标准和管理策略的必要性。未来的研究应专注于识别特定生物标志物和分子途径，以加强对接触生物质烟雾人群的早期诊断并改善临床结局。
