Understanding the link between alcohol and the lungs, as well as how alcohol affects lung function, is essential for individuals who consume alcohol. The airways are lined with tiny hair-like structures called cilia, which play a crucial role in maintaining lung health. Cilia act like microscopic brooms, sweeping mucus, debris, and pathogens out of the lungs. This process, known as mucociliary clearance, is essential for keeping the airways clean and functioning properly. Another potential therapeutic target is Nrf2, which can be activated by plant-derived compounds (i.e., phytochemicals), such as sulforaphane (Hybertson et al. 2011; Jensen et al. 2013).
Increasing the Risk of Aspiration
Additionally, alcohol can interact with medications commonly prescribed for respiratory conditions, such as bronchodilators and steroids, potentially reducing their effectiveness or leading to unwanted side effects. Repeated episodes of aspiration can lead to serious conditions like aspiration pneumonia, which causes inflammation and infection in the lungs. Alcohol affects the reflexes that protect the lungs from aspiration—the accidental inhalation of food, liquid, or stomach acid into the airways. While most alcohol is processed by the liver, a small amount is exhaled through the breath—this is the basis for breathalyzer tests used to measure blood alcohol concentration.
For individuals who smoke, the combination of alcohol and tobacco creates a particularly dangerous synergy. Both substances are known to damage lung tissue, but together, they amplify each other’s harmful effects. When we think about the effects of alcohol on the body, the liver, brain, and heart often come to mind. However, one critical organ that is frequently overlooked in this conversation is the lungs.
The Link Between Alcohol Consumption and Lung Health
- Even if patients seeking treatment for AUD have equally low adherence rates, tens of thousands of individuals could benefit from these relatively simple and inexpensive treatments every year in the United States alone.
- These cellular impairments lead to increased susceptibility to the serious complications from a pre-existing lung disease.
- According to Kershaw, C 2008 page 1, “as of 2001, pneumonia was the sixth most common cause of death in the United States”.
- In another model using mice, Yeligar and colleagues (2012) demonstrated that alcohol induced oxidative stress through the upregulation of specific enzymes called NADPH oxidases, which are an important source of oxidants called reactive oxygen species in alveolar macrophages.
The three main types of lymphocytes are natural killer (NK) cells, T cells, and B cells. Chronic alcohol intake modulates the functions of all three of these lymphocyte populations (Cook 1998; Lundy et al. 1975; Meadows et al. 1992; Spinozzi et al. 1992; Szabo 1999). Research has shown a correlation between alcohol consumption and an increased risk of developing lung cancer.
Potential Therapeutic Strategies for the Alcoholic Lung
Chronic alcohol intake also decreased alveolar binding of PU.1, a transcription factor responsible for GM-CSF activation. When the animals were treated with recombinant GM-CSF, alveolar macrophage bacterial phagocytic capacity, GM-CSF receptor expression, and PU.1 nuclear binding were restored (Joshi et al. 2005). These studies offer the groundwork for understanding the importance of GM-CSF within the lung for the maturation and host immune function of the alveolar macrophage as well as the deleterious impact of chronic alcohol use on these processes. The pathophysiological mechanisms discussed thus far undoubtedly are just components of a highly complex network of alcohol-induced cellular perturbations. In healthy people there is relatively little TGFβ1 in the adult lung; instead, alveolar epithelial integrity and the function of alveolar macrophages are under the influence of GM-CSF.
Alcohol and Acute Lung Injury
Moreover, chronic alcohol ingestion dampens the expression of GM-CSF receptors in alveolar epithelial cells and macrophages (Joshi et al. 2006). This relative imbalance in TGFβ1 and GM-CSF signaling in the alcoholic lung has important implications in the human lung epithelium, and critically ill patients with relatively higher ratios Alcohol and Lung Disease of TGFβ1 to GM-CSF in their alveolar space seem to have a higher mortality (Overgaard et al. 2015). The role of these two signaling molecules is supported by the observation that treatment with recombinant GM-CSF can rapidly restore alveolar epithelial function in alcohol-fed rats, both in vivo and in vitro (Pelaez et al. 2004). These phagocytic cells ingest and clear inhaled microbes and foreign particles from the lungs. The release of cytokines and chemokines by these cells, in turn, mediates the influx of neutrophils into the lungs that occurs in response to infection.
- The article also will briefly review some of the experimental therapies that hold promise for decreasing the enormous morbidity and mortality caused by the “alcoholic lung” in our society.
- We are very excited to introduce this Special Issue of Alcohol devoted entirely to the subject of alcohol and its effects on lung injury and immune defense.
- Engaging in exercise can help improve lung capacity and strengthen respiratory muscles.
- Specifically, Nrf2 function depends on adequate zinc levels, and alcohol interferes with the transporter molecules that mediate zinc absorption from the diet as well as its transport into the alveolar space (Joshi et al. 2009).
With so much data and so many variables, public health recommendations concerning alcohol differ around the world. Surgeon General’s Advisory reported that among 100 women who have less than one drink per week, about 17 will develop an alcohol-related cancer. Among 100 women who have one drink a day, 19 will, and among 100 women who have two drinks a day, about 22 will. When newer, larger studies account for these and other variables, the protective effect of alcohol tends to disappear. The findings were widely publicized and promoted by the alcohol industry, and they gained traction in the medical community.
In experimental models, alveolar macrophages from alcohol-fed animals exhibit zinc deficiency in the fluid of the epithelial lining and have decreased intracellular zinc levels compared with alveolar macrophages from control-fed animals (Joshi et al. 2009). These findings have been confirmed in alveolar macrophages collected from otherwise-healthy people with underlying AUD, even though these individuals had normal serum levels of zinc (Mehta et al. 2013). Zinc is important for diverse immune functions, and its severe deficiency within the alveolar space may be one mechanism by which alcohol impairs innate immune functions within the lung. This role is further supported by findings that restoration of zinc bioavailability in the alveolar space also restores the phagocytic capacity of alveolar macrophages (Joshi et al. 2009).
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.
Alcohol has unique effects on the ciliated airways because it is rapidly and transiently absorbed from the bronchial circulation directly across the ciliated epithelium of the conducting airways. However, when the exhaled air cools as it reaches the trachea, the alcohol vapor condenses and is dissolved back into the fluid in periciliary airway lining (George et al. 1996). NK cells do not need previous exposure to their target cells to recognize, bind to, and destroy these targets (e.g., cancer and virus-infected cells) (Vivier et al. 2008). Tuberculosis infection and produce interferon γ (INF-γ), an important cytokine that stimulates cell-mediated immunity (Junqueira-Kipnis et al. 2003). Alcohol consumption in mice reduces the in vitro killing capacity of NK cells compared with control animals not exposed to alcohol (Meadows et al. 1992). If individuals are concerned about the impact of alcohol on their lung health or are experiencing alcohol-related lung problems, it is crucial to seek professional help.
Pneumonia is a form of acute respiratory infection that affects the lung parenchyma and oxygenation. When a patient with pneumonia is an alcoholic, the mortality rate exceeds by 50% if they are placed into intensive care (ICU). According to Kershaw, C 2008 page 1, “as of 2001, pneumonia was the sixth most common cause of death in the United States”.
They observe an alcohol-stimulated release of damaged mitochondrial DNA in cultured alveolar epithelial cells, which could alter phagocytosis in alveolar macrophages. Reciprocally, they find that such alcohol-induced exosomes from macrophages reduce barrier function in the epithelium. The alcohol-induced dysregulation of lung neutrophil recruitment and clearance is only part of the problem in people with AUD, because alcohol also has harmful effects on other aspects of neutrophil functioning. However, alcohol’s effects on neutrophil phagocytosis and pathogen killing are less clear than the effects on neutrophil recruitment, and the findings to date are inconclusive.
The experimental evidence that alcohol can cause a profound defect in the physical barrier of the alveolar epithelium led to the question of why alcohol abuse alone, in the absence of an acute stress such as sepsis, does not cause pulmonary edema. Additional studies revealed that alcohol causes a concurrent, and perhaps compensatory, increase in salt and water transport across the epithelium. This transport is mediated by specific epithelial sodium channels located in the apical membrane and by protein pumps (i.e., Na/K-ATPase complexes) in the basolateral membrane of the epithelial cells. The expression and function of both the Na/K-ATPase complexes and epithelial sodium channels are increased in the alveolar epithelium of alcohol-fed animals (Guidot et al. 2000; Otis et al. 2008). In the presence of an acute inflammatory stress, such as sepsis or aspiration, however, the paracellular leak increases dramatically, and the alveoli flood with proteinaceous edema fluid that overwhelms the already upregulated transepithelial pumping mechanisms.
