The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease
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The pathogenesis of chronic obstructive pulmonary disease (COPD) is related to a chronic innate and adaptive inflammatory immune response to inhaled toxic particles and gases, primarily as a result of the tobacco smoking habit. This inflammatory immune process develops in the lungs of everyone that smokes, and there is an association between the extent and severity of this tissue response and the severity of airflow limitation present in the fraction of the smoking population that develops COPD. This infiltration of inflammatory immune cells into the lung tissue is inextricably linked to a tissue repair and remodeling process that enlarges the bronchial mucus glands, thickens the walls and narrows the lumen of conducting airways <2 mm in diameter. ⋯ This tissue destruction begins in the respiratory bronchioles in very close proximity to the small conducting airways that become the major site of obstruction in COPD. The mechanism(s) that allow small airways to thicken in such close proximity to lung tissue undergoing emphysematous destruction remain a puzzle that needs to be solved. As the accumulation of tissue responsible for thickening the small conducting airways is a very different pathological process from the emphysematous destruction of surrounding gas exchanging tissue, we need a better understanding of the pathogenesis of both processes and better methods of separating their relative contribution to airflow limitation in individuals to adequately prevent and treat COPD.
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Int. J. Tuberc. Lung Dis. · Apr 2008
ReviewPathogenesis of COPD. Part II. Oxidative-antioxidative imbalance.
Chronic obstructive pulmonary disease (COPD) represents a serious global health problem that affects the aged. This State of the Art article summarises previous studies on oxidative-antioxidative imbalance in patients with stable COPD or in acute exacerbations. Recent literature in this field reports conflicting findings. ⋯ A few studies have shown higher erythrocyte superoxide dismutase (SOD) activity in COPD patients and healthy smokers than those in healthy non-smokers. In contrast, we found no differences in erythrocyte SOD activity and elevated erythrocyte catalase activity in Chinese patients with COPD compared with healthy smokers matched for age and pack-years smoked. Possible reasons for such discrepancies could be related to differences in inter-individual variations in antioxidant capacity as a result of different populations and also differences in methodologies between studies.
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Chronic obstructive pulmonary disease (COPD) is mostly caused by cigarette smoking and affects up to 25% of smokers. Air pollution and occupational exposure to dust and fumes can also induce COPD. COPD is characterised by airflow limitation that is not fully reversible and chronic inflammation of the lung. ⋯ However, this hypothesis was never fully confirmed in humans and may only explain the degenerative stage of the disease, emphysema. The role of tissue-forming cells in the pathogenesis of COPD has not been adequately studied and indicates a deregulated synthesis of growth factors and cytokines in COPD. Finally, recent studies indicate that alpha-1-antitrypsin activity plays a role in all forms of COPD.
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Int. J. Tuberc. Lung Dis. · Jan 2008
ReviewGlobal perspective on tobacco control. Part II. The future of tobacco control: making smoking history?
Serious efforts to reduce the harm caused by tobacco use throughout populations require implementation policies and interventions capable of reaching all smokers and potential smokers. While the Framework Convention on Tobacco Control promises to accelerate the adoption of comprehensive tobacco control policies throughout the world, its extensive 'optional' language provides considerable latitude for governments unwilling to implement rigorous controls. This paper examines four broad areas in which important debates and policy advances will be necessary to ensure population-wide impact of tobacco control: harm reduction; demand reduction strategies involving particularly the use of news generation in increasing the coverage of tobacco and health issues; denormalisation of tobacco use, especially among health workers in nations where use remains high; and further efforts to regulate the tobacco industry, particularly in regard to plain packaging, under-the-counter retail sales and the regulation of tobacco products.
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Int. J. Tuberc. Lung Dis. · Jan 2008
ReviewGlobal perspective on tobacco control. Part I. The global state of the tobacco epidemic.
Tobacco smoking is losing adherents in some countries, and a number of international developments may dramatically change the choices people make concerning tobacco. However, the growth of chronic obstructive pulmonary disease (COPD) in the world is nevertheless assured-tobacco consumption is rising globally because of increased consumption in many low-income countries. Risk of COPD is strong wherever smokers are found, and even among former smokers, it remains high for decades. ⋯ Smoking-related COPD rates will continue to be high for some time. The future of COPD is related most dramatically to low- or middle-income countries, where more than four in five current smokers in the world live. The predictable health consequences of smoking, including an enormous burden in COPD, have only begun to emerge.