Research Article: Alcohol and the Lung

Date Published: , 2017

Publisher: National Institute on Alcohol Abuse and Alcoholism

Author(s): Ashish J. Mehta, David M. Guidot.

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Abstract

Among the many organ systems affected by harmful alcohol use, the lungs are particularly susceptible to infections and injury. The mechanisms responsible for rendering people with alcohol use disorder (AUD) vulnerable to lung damage include alterations in host defenses of the upper and lower airways, disruption of alveolar epithelial barrier integrity, and alveolar macrophage immune dysfunction. Collectively, these derangements encompass what has been termed the “alcoholic lung” phenotype. Alcohol-related reductions in antioxidant levels also may contribute to lung disease in people with underlying AUD. In addition, researchers have identified several regulatory molecules that may play crucial roles in the alcohol-induced disease processes. Although there currently are no approved therapies to combat the detrimental effects of chronic alcohol consumption on the respiratory system, these molecules may be potential therapeutic targets to guide future investigation.

Partial Text

The potential influence of alcohol consumption on airway health and disease has been documented for a long time. Chronic alcohol ingestion constantly subjects the drinker’s airways to high concentrations of alcohol vapor, as best evidenced by the use of alcohol breath tests (i.e., Breathalyzer). The volatile nature of alcohol is exploited in this common field sobriety test, which is reliably used as a surrogate to quantify blood alcohol concentrations. Interestingly, the alcohol vapor found in the airways is not caused by inhalation but is a result of the ready diffusion of alcohol from the airway blood supply across the airway epithelium and into the airways themselves (George et al. 1996). This process explains why alcohol vapor in the breath may be used to determine blood alcohol concentration. The alcohol then is deposited and metabolized in the airways. This process leads to the formation of reactive aldehydes (e.g., acetaldehyde), which in turn can interact and form harmful adducts with proteins and DNA (Sapkota and Wyatt 2015). The formation of these adducts may disrupt normal cellular functions, induce inflammation, and impair healing. Taken together, these findings demonstrate that the airways—including the oral cavity and extending all the way to the alveolar space—are subjected to high concentrations of alcohol and its deleterious metabolites during intoxication.

ARDS is a severe form of lung injury characterized by fluid accumulation in the lung that is not related to heart problems (i.e., noncardiogenic pulmonary edema) as well as by flooding of the alveolar airspaces with protein-like (i.e., proteinaceous) fluid (Ware 2006; Ware and Matthay 2000). ARDS develops in response to inflammatory stresses, including sepsis, trauma, gastric aspiration, pneumonia, and massive blood transfusions (Ware and Matthay 2000). Originally described by Ashbaugh and colleagues (1967), ARDS is characterized by alveolar epithelial and endothelial barrier disruption, dysfunction of the lipoprotein complex (i.e., surfactant) coating the lung surfaces, and intense inflammation. Together, these alterations profoundly disrupt gas exchange and cause severe respiratory failure. Although much has been learned about the underlying pathophysiology of this syndrome over the past four decades, treatment of ARDS remains essentially supportive, and despite aggressive treatment in intensive care units and mechanical ventilation, the mortality rate for ARDS remains unacceptably high at 30 percent to 50 percent (Arcasoy et al. 2005; Villar et al. 2011; Wang et al. 2014; Ware and Matthay 2000).

Lung infections are major causes of morbidity and mortality worldwide. Data from the Centers for Disease Control and Prevention consistently show that pneumonia is one of the top 10 causes of death in the United States and remains the leading cause of death from an infection (Murphy et al. 2013). Alcoholism has been linked to pulmonary infections for over 200 years (Mehta and Guidot 2012). Additionally, recent studies have demonstrated that people who abuse alcohol are not only more likely to develop pneumonia, but also are susceptible to more severe forms of the disease, are more likely to experience complications, and require greater use of resources. A prospective study by Adamuz and colleagues (2011) examined features associated with increased use of health care services and risk for readmission in patients discharged with pneumonia. Interestingly, the only independent risk factor associated with increased health care utilization after discharge was alcohol abuse. Similarly, Chalmers and colleagues (2009) demonstrated in a multivariate regression model that alcohol abuse was among independent risk factors that were significantly associated with the development of certain complications (i.e., complicated para-pneumonic effusion or empyema) in patients with community-acquired pneumonia.

Currently there are no specific therapies that can modify the alcoholic lung in the clinical setting. Clearly, as with all alcohol-related health issues, the ideal treatment would be abstinence in people with underlying AUD and/or a safe level of consumption in people who choose to drink for social reasons. However, this ideal will be impossible to achieve in any meaningful timeframe and it therefore is critical to identify, test, and validate therapeutic strategies that can limit the morbidity and mortality of alcohol-related diseases, including acute lung injury and pneumonia.

 

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