Search resultsAlcohol and airways function in health and disease
Title
Alcohol and airways function in health and disease
Publication type
Journal Article
Year of Publication
2007
Authors
Journal
Alcohol
Volume
41
Issue
5
Pagination
293 - 307
Date published
2007
ISBN
07418329 (ISSN)
Keywords
acetaldehyde, Acetaldehyde dehydrogenase 2, airway conductance, alcohol, alcohol blood level, alcohol consumption, Aldehyde Dehydrogenase, aldehyde dehydrogenase isoenzyme 2, ALDH2, Animals, asthma, bronchodilatation, calcium, cAMP, Central Nervous System Depressants, chronic bronchitis, chronic obstructive lung disease, chronic obstructive pulmonary disease, cigarette smoke, Cilia, ciliary dyskinesia, ciliary motility, concentration (parameters), COPD, disease exacerbation, emphysema, endothelial nitric oxide synthase, Ethanol, forced expiratory flow, human, Humans, Inhalation Exposure, Lung epithelium, lung function, lung volume, mortality, Mucociliary clearance, mucus, nitric oxide, nonhuman, pathogenesis, pathophysiology, phosphotransferase, PKA, PKG, Pulmonary Disease, Chronic Obstructive, respiratory airflow, respiratory epithelium, Respiratory Mechanics, respiratory system, review, salmeterol, second messenger, signal transduction, smoking, smooth muscle, smooth muscle contraction, spirometry, volatilization
Abstract
The volatility of alcohol promotes the movement of alcohol from the bronchial circulation across the airway epithelium and into the conducting airways of the lung. The exposure of the airways through this route likely accounts for many of the biologic effects of alcohol on lung airway functions. The effect of alcohol on lung airway functions is dependent on the concentration, duration, and route of exposure. Brief exposure to mild concentrations of alcohol may enhance mucociliary clearance, stimulates bronchodilation, and probably attenuates the airway inflammation and injury observed in asthma and chronic obstructive pulmonary disease (COPD). Prolonged and heavy exposure to alcohol impairs mucociliary clearance, may complicate asthma management, and likely worsens outcomes including lung function and mortality in COPD patients. Nonalcohol congeners and alcohol metabolites act as triggers for airway disease exacerbations especially in atopic asthmatics and in Asian populations who have a reduced capacity to metabolize alcohol. Research focused on the mechanisms of alcohol-mediated changes in airway functions has identified specific mechanisms that mediate alcohol effects within the lung airways. These include prominent roles for the second messengers calcium and nitric oxide, regulatory kinases including PKG and PKA, alcohol- and acetaldehyde-metabolizing enzymes such as aldehyde dehydrogenase 2. The role alcohol may play in the pathobiology of airway mucus, bronchial blood flow, airway smooth muscle regulation, and the interaction with other airway exposure agents, such as cigarette smoke, represents opportunities for future investigation.