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These studies suggest that smoking and passive smoking are major risk factors for COPD, driven by oxidative stress, immune response, and inflammation, and that quitting smoking can improve symptoms and prognosis.
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Chronic Obstructive Pulmonary Disease (COPD) is a progressive lung disease characterized by persistent respiratory symptoms and airflow limitation. It is primarily caused by long-term exposure to harmful particles or gases, with cigarette smoking being the most significant risk factor . COPD encompasses conditions such as chronic bronchitis and emphysema, which lead to structural and inflammatory changes in the lungs.
While active smoking is a well-known cause of COPD, passive smoking, or environmental tobacco smoke (ETS), also poses a significant risk. Research indicates that never smokers exposed to ETS have a higher prevalence of COPD. The risk increases with the extent of exposure, particularly in multiple settings such as home and work environments. This highlights the importance of public health measures to reduce ETS exposure.
Cigarette smoke induces oxidative stress and disrupts the immune system, leading to chronic inflammation and lung damage. This oxidative stress results from an imbalance between oxidants and antioxidants, which damages cellular structures and impairs lung function . The immune response to cigarette smoke involves both innate and adaptive immunity, contributing to the chronic inflammatory state observed in COPD.
The pathobiology of COPD involves several cellular and molecular alterations, including apoptosis, abnormal cell repair, and extracellular matrix destruction. These processes are driven by reactive oxygen species and tobacco components, which activate various signaling pathways and cytokine networks . Additionally, cigarette smoke can induce cellular senescence and necroptosis, further exacerbating lung inflammation and damage.
COPD is often associated with systemic inflammation, which can lead to comorbid conditions such as chronic heart failure, metabolic syndrome, and other chronic diseases. This systemic impact underscores the need for comprehensive management strategies that address both pulmonary and extrapulmonary manifestations of COPD.
Psychological factors such as anxiety sensitivity, distress intolerance, and anhedonia are elevated in COPD patients, particularly among current smokers. These factors are associated with greater disease impact and negative responses to COPD symptoms, suggesting their potential as treatment targets. Smoking cessation is crucial for improving COPD outcomes, and interventions should include counseling, nicotine replacement therapy, and strategies to address psychological factors.
Smoking, both active and passive, is a major contributor to the development and progression of COPD. The disease involves complex interactions between oxidative stress, immune response, and cellular changes. Effective management of COPD requires a multifaceted approach, including smoking cessation, addressing psychological factors, and treating comorbid conditions. Public health measures to reduce smoking and ETS exposure are essential to prevent COPD and improve patient outcomes.
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