Exceeding these daily or weekly drinking limits significantly increases the risk of developing AUD and problematic health outcomes (NIAAA 2014). Also, as noted above, chronic alcohol ingestion interferes with Nrf2 signaling in alveolar macrophages (Mehta et al. 2011), thereby disrupting the expression of hundreds of genes that are crucial to combatting oxidative stress. Although the precise role of alcohol-mediated inhibition of the Nrf2–ARE pathway in mediating oxidative stress has not been completely clarified, this pathway represents a strategic target to direct future therapies. Alcohol induces aberrant transforming growth factor beta1 (TGFβ1) expression in the alveolar epithelium and thereby dampens signaling through the granulocyte/macrophage colony-stimulating factor (GM-CSF)–PU.1 and Nrf2–antioxidant responsive element (ARE) signaling pathways. As a consequence, the expression and function of transporters that regulate zinc import and export across the epithelium are disrupted, further inhibiting these zinc-dependent pathways and exacerbating TGFβ1 expression. This results in an increase in redox stress, reduced surfactant levels, and damage to the tight junctions between cells, with severe ramifications for epithelial (and macrophage) function.
Alcohol consumption and your health: What the science says
ARDS develops in response to inflammatory stresses, including sepsis, trauma, gastric aspiration, pneumonia, and massive blood transfusions (Ware Alcohol and Lung Disease 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. One of the molecules involved in disrupting epithelial integrity is the cytokine transforming growth factor β1 (TGF-β1).
Types of T Cells.
The alcohol-induced inhibition of Nrf2–ARE signaling is mediated at least in part by zinc. 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). To supplement the various anecdotal reports of using alcohol in the treatment of airway diseases, early mechanistic investigations demonstrated that alcohol itself seems to have bronchodilating properties in asthmatics. However, the effects differed depending on the alcohol concentration used as well as on the route of administration (i.e., intravenous versus oral) (Ayres and Clark 1983b; Ayres et al. 1982; Brown 1947; Herxheimer and Stresemann 1963). Moreover, these observations directly conflict with findings that many asthmatics actually report exacerbations of their disease after alcohol ingestion (Ayres and Clark 1983a; Breslin et al. 1973; Vally et al. 2000). In an attempt to explain some of these discrepancies, Breslin and colleagues (1973) compared the effects of exposure to different types of alcohol in a clinical study.
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.
- Long-term alcohol use can cause a condition known as “alcoholic lung disease,” characterized by oxidative stress and chronic inflammation in the airways.
- Prolonged alcohol exposure alters the first line of the innate cellular defense, the mucociliary apparatus, against invading pathogens such as RSV.
- One of the molecules involved in disrupting epithelial integrity is the cytokine transforming growth factor β1 (TGF-β1).
- Chen’s research has shown how alcohol affects people of East Asian descent who have a genetic variation, ALDH2, which interferes with their ability to metabolize acetaldehyde.
Tips for Promoting Lung Health
The other main subgroup of T cells, the cytotoxic T cells, has CD8 molecules on their surfaces. This is known as ARLD, which may present as several lung problems, such as pneumonia or TB.
Alcohol and Acute Lung Injury
- The identification of alcohol-driven oxidative stress as a contributor to alveolar macrophage dysfunction has led to promising antioxidant treatment approaches aiming to prevent alcohol-induced lung conditions in rodent models of prolonged alcohol consumption.
- These analyses found that whereas pure alcohol did not appear to induce bronchial reactivity, some alcoholic beverages worsened asthma symptoms.
- Understanding the negative effects of alcohol on lung health is crucial for individuals who consume alcohol.
People have been drinking alcoholic beverages for millennia, and alcohol consumption has played an important role throughout human history, being linked to ancient and modern religions, early medicine, and social occasions and celebrations. Although alcohol consumption is socially accepted across many cultures, heavy and prolonged alcohol intake can lead not only to physical dependence but also to devastating long-term health problems. An estimated 18 million Americans have alcohol use disorder (AUD), including alcoholism and harmful drinking (National Institute on Alcohol Abuse and Alcoholism NIAAA 2014). NIAAA (2014) has established guidelines for low-risk drinking that are age and gender specific. Thus, for men ages 21–64, low-risk drinking is defined as consumption of no more than 4 drinks per day or 14 drinks per week. For women, as well as for men ages 65 and older, drinking levels for low-risk drinking are defined as no more than 3 drinks per occasion or 7 drinks per week.
In this particular study, pulmonary inflammation in alcohol-exposed mice persisted for more than 7 days after infection, compared with 3 to 5 days in the control animals. Moreover, some alcohol-exposed mice showed severe inflammation with hemorrhage and edema. These results corroborate findings that infection in the setting of alcohol exposure increases the risk of complications such as ARDS. The goal of these treatments clearly would not be to make it safe(r) to consume excessive amounts of alcohol. There also may be some concerns about alcoholic patients’ compliance with chronic oral treatments, such as zinc and SAMe supplements. However, many patients with AUD seek care for their addiction precisely because they are motivated to become or remain healthy and, consequently, are likely to adhere to their treatment regimen.
Because acetaldehyde accumulates more quickly in people with the ALDH2 variant, they are at an increased risk of alcohol-related diseases, including cancer and heart disease, even at lower levels of alcohol consumption. One potential explanation for the disparate findings in the literature regarding alcohol’s role in airway disease is that some forms (i.e., phenotypes) of asthma may be more sensitive to the effects of alcohol than others. Interestingly, alcohol-induced respiratory symptoms are more common in patients with aspirin-exacerbated respiratory disease than in aspirin-tolerant asthmatics (Cardet et al. 2014). These findings suggest that the potential irritant versus bronchodilator effects of alcohol may vary by disease subtype; however, further investigation is necessary to validate these observations. To promote optimal lung health, individuals who consume alcohol should practice moderation, adopt a healthy lifestyle, and seek professional help if needed.
What are the signs of alcohol-related lung disease?
Excessive alcohol intake can disrupt the normal functioning of immune cells, impairing their ability to recognize and destroy invading pathogens. This weakened immune response leaves individuals more vulnerable to respiratory infections, such as pneumonia, bronchitis, and influenza. Investigations into alcohol lung infections and injury have utilized both in vitro and in vivo animal models, which have, importantly, led to human translational studies. For example, in this Special Issue, in vitro studies of LL-37 have been translated into human studies.
Alcoholic lung disease
These cells act as the lungs’ first line of defense, engulfing and destroying harmful pathogens. One of the most common and deadliest conditions afflicting individuals with AUD is bacterial pneumonia. Dr. Benjamin Rush, the first Surgeon General of the United States, described some of the earliest links of alcohol abuse to pneumonia over two centuries ago, reporting that pneumonia was more common in drinkers than nondrinkers (Jellinek 1943; Rush 1810). Two centuries later, the correlation between alcohol abuse and lung infections still remains strong. According to the Centers for Disease Control and Prevention (CDC), people who abuse alcohol are 10 times more likely to develop pneumococcal pneumonia and 4 times more likely to die from pneumonia than nondrinkers (Lujan et al. 2010). By understanding the harmful effects of alcohol on the lungs, individuals can make informed decisions about their alcohol consumption and take steps to prioritize their lung health.
In 1885, Sir William Osler reported alcohol as one of the greatest predisposing factors to the development of pneumonia (Osler, 1892). Compared to people who do not misuse alcohol, individuals with a history of alcohol misuse are twice as likely to develop sepsis, and those with sepsis are twice as likely to develop acute respiratory syndrome (Jong, Hsiue, Chen, Chang, & Chen, 1995; Joshi & Guidot, 2007; Moss, 2005). Alcohol-induced lung injury and immune dysfunction contribute to a higher incidence of respiratory infections, leading to increased morbidity and mortality in excessive alcohol misusers (Moss, 2005).
It’s important to note that smoking and alcohol consumption can have a synergistic effect, significantly increasing the risk of developing COPD. Individuals who both smoke and consume alcohol are at a higher risk compared to those who engage in either behavior alone. Alcohol consumption can weaken the immune system, making it less effective in fighting off infections. The immune system plays a crucial role in protecting the body against harmful pathogens, including viruses and bacteria that can cause respiratory infections.