Trevisani and colleagues demonstrated in guinea pigs that alcohol intake triggers airway inflammation via a transient receptor potential vanilloid-1 (TRPV1) resulting in a calcium-dependent release of neuropeptides that contracted airway smooth muscle (Trevisani et al., 2004). The authors suggested that neurogenic airway inflammation may be an important mechanism by which alcohol causes asthma, which might be treatable with inhaled famous alcoholics you never knew about steroids (Antonicelli et al., 2006b). There is even an anecdotal report that suggests small amounts of alcohol present in some inhaled corticosteroid preparations can act as a trigger for asthma for certain individuals (Antonicelli et al., 2006a). In 1963 Herxheimer measured lung vital capacity (VC) in normal subjects and asthmatics following the ingestion of brandy, vodka or pure ethanol (Herxheimer and Stresemann, 1963).
Alcohol-mediated ciliated airway dysfunction
Because alcohol consumption shows a U-shaped curve with cardiovascular mortality (Murray et al., 2002; Rimm et al., 1991), these investigators hypothesized a similar relation between alcohol consumption and COPD mortality. The first study compared twenty-year COPD mortality and pulmonary function to alcohol consumption in three European countries (Tabak et al., 2001b). Analysis of data from 2,953 middle aged men from Finland, Italy and the Netherlands showed reduced virtual meeting schedule COPD mortality in mild drinkers compared to non-drinkers (relative risk of 0.60). In contrast to mild drinkers, COPD mortality was increased in heavy-to-moderate drinkers (relative risk of 1.25). A similar U-shaped risk curve for reduced pulmonary function was observed among non-drinkers, mild drinkers and moderate-to-heavy drinkers. Importantly, the U-shaped risk curve was independent of age, height, body mass index (BMI), smoking status, energy intake or country.
Potential Mechanisms by Which Alcohol Abuse Increases Risk for Pneumonia
Another fundamental mechanism that appears to drive many of the pathophysiological manifestations of the alcoholic lung phenotype is a severe depletion of glutathione stores within the alveolar space. Glutathione is the primary thiol antioxidant found in the alveoli; it serves an essential function in reactions catalyzed by the enzyme glutathione peroxidase, which clears harmful hydrogen peroxide and lipid hydroperoxides that readily form in the oxidizing environment of the lung. In both experimental animal models and humans, chronic alcohol ingestion causes a profound decrease of up to 80 percent to 90 percent in alveolar glutathione levels (Holguin et al. 1998; Moss et al. 2000). Further analyses in experimental models found that alcohol-induced glutathione depletion seems to mediate the defects in alveolar epithelial barrier function.
Alcohol and COPD Medication
The mechanisms responsible for alcohol-induced relaxation of airways are poorly understood and may include receptor-and non receptor-mediated signal transduction pathways involving calcium and/or nitric oxide as second messengers. Many non-alcohol components of alcoholic beverages likely act as triggers for asthma in sensitized individuals and as such are not different from other asthma triggers. Acetaldehyde, the primary metabolite of ethanol, can trigger bronchoconstriction in asthmatics with genetically reduced ALDH2 activity and represents a significant trigger for asthma in certain Asian populations. The sections below examine the epidemiology of alcohol abuse and pneumonia and the potential mechanisms by which alcohol abuse increases the risk for pneumonia.
Clinical Studies of Alcohol and Mucociliary Clearance
The AM is acutely affected by chronic alcohol ingestion and the oxidized lung microenvironment that results from alcohol abuse. Through multifactorial mechanisms, alcohol stimulates oxidative stress within the AM, resulting in impaired phagocytic capacity and decreased bacterial clearance. Experimental manipulations of each of these mechanisms attenuated alcohol-induced oxidative stress and improved AM immune function.
Further research has shown that although both NAC and procysteine restore cytosolic glutathione in the type II cells of alcohol-fed rats, only procysteine restores mitochondrial glutathione as well (Brown et al. 2001a,b; Guidot and Brown 2000). Overwhelming evidence exists for the central role of oxidative stress and depletion of the antioxidant glutathione in the livers of alcohol-fed experimental animals. It is utilized in multiple important pathways, including the detoxification of potentially damaging compounds, facilitation of the excretion of toxic molecules, and control of the induction of proteins involved in inflammation (Kehrer and Lund 1994; Lieber 1993; Morris and Bernard 1994). Glutathione depletion precedes the development of the typical changes in the liver tissue observed with alcohol-mediated liver damage (Lieber 1993).
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. 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. Prolonged alcohol consumption impairs the cells’ phagocytic capacity (Joshi et al. 2005, 2009), release of cytokines and chemokines (D’Souza et al. 1996), and release of neutrophil chemoattractants (Craig et al. 2009). Although alveolar macrophages are the primary residential innate immune cells and play a pivotal role in the clearance of bacterial and viral pathogens, understanding of and research on their specific function in the context of heavy alcohol consumption and AUD still is lacking.
Subsequent to loss of mitochondrial glutathione, cellular changes occur that are suggestive of acetaldehyde-induced oxidative damage (Fernandez-Checa et al. 1993). Attempts to restore mitochondrial glutathione in the liver cells of alcohol-fed rats with glutathione or the supplement N-acetylcysteine (NAC) have been unsuccessful (Fernandez-Checa et al. 1993). Lieber and colleagues (1990) achieved similar results in a baboon model of cirrhosis. Alcohol alters airway mucociliary clearance, which is dependent upon the dose and duration of alcohol exposure.
Alcohol-related deaths increased among all age groups (during 2020–2021) from just a few years earlier (2016–2017). These are increases of 27% among boys and men, and 35% among girls and women from just a few years earlier (2016–2017). If that casual inflight drink isn’t something you’re quick to forgo, experts offer some tips to minimize sleep and health impacts. Although airplanes are pressurized to minimize the impact, a plane at standard cruising altitude (30,000 to 40,000 feet) would still have a cabin pressure matching that of an altitude above sea level, around 8,000 feet, says Peter Hackett, a high altitude expert and emergency physician. For a healthy person, that amount of elevation gain may not be noticeable, especially because our bodies have natural adaptation mechanisms. In addition, people with COPD also have to consider how any medications they are taking to treat their condition may interact with alcohol.
According to a review of studies from the Mayo Clinic College of Medicine, around 69% of people with lung cancer were drinkers prior to their diagnosis. Those who didn’t were nine times more likely to describe themselves as being in poor health compared to those who did. Glucocorticoids are often used for managing chronic lung conditions, while antibiotics are used to treat bacterial lung infections.
One of the largest analyses, published in 2016 in the American Journal of Epidemiology, reported that heavy alcohol use (defined as over seven drinks per day) modestly increased the risk of lung cancer, but that moderate consumption (one drink or less per day) actually decreased the risk. 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). One clinical study (Burnham et al. 2012) evaluating the effects of 7-day treatment with the Nrf2 activator Protandim® in patients with AUD did not identify any significant improvement in glutathione levels or epithelial function.
But as COPD gets worse, it might be time to take another look at your drinking habits. This can include taking medication, getting a flu shot every year, and getting a pneumonia shot regularly, Schachter says. One out of every four Americans drinks to excess, which will lead to six alcohol poisoning deaths every day.
- Animal studies have shown that chronic alcohol exposure causes significant alveolar macrophage dysfunction, leaving these normally active immune cells poorly equipped to phagocytose or kill invading organisms (Brown et al. 2009; Joshi et al. 2009).
- Bronchoconstriction and wheezing following ingestion of alcoholic beverages is most likely related to non-alcohol congeners present in the beverages or the production of high concentrations of acetaldehyde in susceptible individuals with the low functioning ALDH2 genotype.
- Liver disease, a common consequence of chronic alcohol use, impairs the liver’s ability to detoxify medications.
- For a healthy person, that amount of elevation gain may not be noticeable, especially because our bodies have natural adaptation mechanisms.
- This is likely due to the inability of the airway epithelium to significantly metabolize ethanol into acetaldehyde.
- The over-exuberant response by AMs may have implications for the severity of illness among individuals with pulmonary infections.
Alcohol-induced alveolar macrophage dysfunction likely occurs primarily as a result of alcohol-induced increases in oxidative stress, which is reflected by depletion of the antioxidant glutathione (GSH) in BAL fluid (Brown et al. 2007; Yeh et al. 2007). Impaired secretion of granulocyte monocyte colony-stimulating factor (GM-CSF) by type II alveolar cells likely also contributes to alcohol-induced oxidative stress (Joshi et al. 2005). Schematic illustration of the mechanisms by which alcohol abuse increases the risk of pneumonia.
Researchers will continue working to unravel the complex relationship between alcohol consumption and the human body. And there are other medications you might be taking, like antihistamines or antianxiety medications, that make you sleepy. Alcohol will only add to that, making you even more drowsy, and that could make it harder for you to breathe. If your respiratory how to stop binge drinking system is damaged and you’re taking medication that could affect your ability to breathe, Han says adding alcohol could raise your risk for other problems. But there’s plenty of research showing that drinking too much can cause serious problems with your lungs. She doesn’t recommend that patients go out and start drinking to decrease their risk of COPD, she adds.
Difficulty absorbing vitamins and minerals from food can cause fatigue and anemia, a condition where you have a low red blood cell count. A damaged pancreas can also prevent your body from producing enough insulin to use sugar. Drinking too much alcohol over time may cause inflammation of the pancreas, resulting in pancreatitis. Pancreatitis can activate the release of pancreatic digestive enzymes and cause abdominal pain. Impulsiveness, loss of coordination, and changes in mood can affect your judgment and behavior and contribute to more far-reaching effects, including accidents, injuries, and decisions you later regret. Dehydration-related effects, like nausea, headache, and dizziness, might not appear for a few hours, and they can also depend on what you drink, how much you drink, and if you also drink water.
It is unknown how concurrent alcohol exposure impacts these consequences of RSV infection. In summary, these studies demonstrate that alcohol exposure compromises innate defenses against viral pathogens such as RSV in part by disrupting airway ciliary function. Alcohol use disorder can cause a susceptibility to infection after major trauma to the lungs / respiratory system. It creates an increased risk of aspiration of gastric acid, microbes from the upper part of the throat, decreased mucous-facilitated clearance of bacterial pathogens from the upper airway and impaired pulmonary host defenses. This increased colonization by pathogenic organisms, combined with the acute intoxicating effects of alcohol and the subsequent depression of the normally protective gag and cough reflexes, leads to more frequent and severe pneumonia from gram-negative organisms.
This includes worsening acute lung injury following a serious accident or trauma, and acute respiratory distress syndrome (ARDS). The stimulation of ciliary motility by biologically relevant concentrations of alcohol was surprising since higher ciliary motility should enhance mucociliary clearance and did not fit with the conventional wisdom that lung clearance is impaired in heavy drinkers. The consequence of prolonged exposure to alcohol was desensitization of the mucociliary apparatus, meaning that cilia could no longer be stimulated during stress, such as following aspiration of bacteria. This hypothesis better fit the notion that airway mucociliary clearance is impaired in chronic drinkers. Whether these mechanisms were operative in vivo required studies of cilia in animals. The conducting airways of the lung, including the trachea, bronchi and bronchioles, function to distribute air throughout the lung and represent the proximal and often rate-limiting component of the air distribution system.
The applicability of the frog palate as a model of human airways is uncertain and the extremely high concentrations of alcohol used in these experiments are not relevant to human alcohol consumption. Another study in cultured human bronchial epithelial cells found that alcohol caused a concentration- and time-dependent increase in the expression of the tracheo-bronchial mucin (TBM) gene (Verma and Davidson, 1997). This finding suggests that alcohol regulates mucin expression in the airway epithelium at a biologically relevant concentration. Seeking to verify that the relationship between alcohol intake and pulmonary glutathione deficiency in the rat were relevant for humans, Moss and colleagues (2000) measured lung glutathione levels in 19 otherwise healthy alcoholic subjects.