Author: James Anderson

Alcohol and Airways Function in Health and Disease PMC

In contrast, a more recent study in permeabolized canine smooth airway cells by Hanazaki and colleagues found that alcohol promotes concentration-dependent airway smooth muscle relaxation and increased sensitivity to calcium, independent of regulatory myosin light chain phosphorylation (Hanazaki et al., 2001). This study suggests a direct effect of alcohol on calcium-regulated smooth muscle tone and is consistent with the observation that alcohol is a bronchodilator. 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.

1. These include prominent roles for the second messengers calcium and nitric oxide, regulatory kinases including PKG and PKA, alcohol and aldehyde -metabolizing enzymes such as ALDH2.
2. Restoring the redox balance in the lung could reverse many of these alcohol-induced defects and improve alveolar macrophage immune function (Brown et al. 2007; Yeligar et al. 2014).
3. Joshi et al. (2005, 2006) subsequently found that chronic alcohol ingestion decreases the expression of GM-CSF receptors in the airway epithelium and macrophages and, in turn, dampens intracellular signaling to the protein responsible for GM-CSF gene expression.
4. As of 2001, pneumonia was the sixth most common cause of death in the United States, with over 1 million people requiring hospitalization for pneumonia per year (Niederman et al. 1998).

Another alcohol vapor exposure is in the form abusing “alcohol-with-out-liquid” (AWOL). With AWOL alcohol is aerosolized through a nebulizer and has become fashionable in Europe and Asia as way to become intoxicated without the side effects of drinking (Press, 2004). The increase in the use of ethanol-supplemented fuels and the abuse potential of AWOL will likely stimulate more research in this interesting area. At this point it is safe to say that our knowledge about the influence of inhaled alcohol on airway function is unsatisfactory. This is in contrast to our knowledge of alcohol intake and asthma from population studies.

This same finding was reproduced in mice ingesting alcohol in their drinking water (Elliott et al., 2007). Taken together, these studies fully recapitulated the in vitro findings of alcohol-desensitization of ciliary kinases. At this juncture, alcohol downregulation of airway ciliary PKA represents the most likely mechanism that causes alcohol-induced impairment of mucociliary clearance. The mucociliary apparatus consists of mucus secreting cells, sero-mucinous bronchial glands and ciliated cells that line the conducting airways from the trachea to the terminal bronchi deep in the lung. This system traps inhaled particles and debris in secreted mucus, which is then propelled up and out of the lung via the escalator-like function of the waves created by beating cilia. Normal mucociliary clearance ensures a sterile environment in the lung below the vocal cords (Laurenzi et al., 1965; Laurenzi et al., 1963; Laurenzi et al., 1961).

This may reflect a compensatory response to excess AT1 activation during chronic alcohol ingestion. The implication that a pure alcohol infusion acted as a bronchodilator and did not worsen asthma was important since some atopic patients report bronchospasm following ingestion of alcoholic beverages. This point was made in a small but elegant study by Breslin in 1973 of eleven subjects with asthma who reported worsening of their asthma symptoms following the ingestion of an alcoholic beverage (Breslin et al., 1973). The authors were able to provoke bronchospasm in the laboratory in six of the eleven subjects challenged with the offending alcoholic beverage precipitating a ≥ 15% reduction in the forced expiratory flow in the first second (FEV1) on spirometry. Importantly, in three of these patients, drink-precipitated bronchospasm was not triggered by an oral ingestion of an equivalent amount of pure alcohol in water implicating the non-alcohol components of the beverage as the likely asthma trigger.

Chemo Drugs and Alcohol

For example, drinking alcohol will increase the intoxicating effects of both anxiety and pain medications, which may dramatically slow your breathing to the point of being life-threatening. Those who have concerns about their lung health or alcohol consumption can speak with their doctor for further advice and guidance. According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), AUD is a medical condition in which a person has difficulty controlling their alcohol intake despite negative effects on their health, work life, and social life. The Recovery Village aims to improve the quality of life for people struggling with substance use or mental health disorder with fact-based content about the nature of behavioral health conditions, treatment options and their related outcomes.

Pancreatitis can activate the release of pancreatic digestive enzymes and cause abdominal pain. Alcohol use can begin to take a toll on anyone’s physical and mental well-being over time. These effects may be more serious and more noticeable if you drink regularly and tend to have more than 1 or 2 drinks when you do. If you drink, you’ve probably had some experience with alcohol’s effects, from the warm buzz that kicks in quickly to the not-so-pleasant wine headache, or the hangover that shows up the next morning. Since those effects don’t last long, you might not worry much about them, especially if you don’t drink often.

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As mentioned above, Joshi and colleagues (2005) recently demonstrated that chronic alcohol ingestion impairs GM-CSF–dependent alveolar epithelial cell and macrophage function. These discoveries were initiated by the finding that, when delivered via the upper airway, GM-CSF restored alveolar epithelial barrier function and fluid transport in alcohol-fed rats, even when bacteria-released toxins were present in the blood (Pelaez et al. 2004). Joshi et al. (2005, 2006) subsequently found that chronic alcohol ingestion decreases the expression of GM-CSF receptors in the airway epithelium and macrophages and, in turn, dampens intracellular signaling to the protein responsible for GM-CSF gene expression.

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.

Alcoholic lung disease

This review focuses on our current understanding of alcohol’s impact on airway functions based on clinical and experimental research. What emerges is that alcohol has a considerable and largely unrecognized influence on airway function in health and disease. Much of this impact stems from the unique vapor characteristics of alcohol and its interplay with the bronchial circulation. Lung issues are often the result of heavy or chronic alcohol use and cannot be reversed with a quick fix. Although there are several treatment strategies being researched for alcoholic lung damage, the most effective way to prevent further lung damage is to stop drinking. However, in recent years, more research has also been conducted on the effects of alcohol on the lungs; specifically, how heavy drinking can increase the risk for mild to severe lung-related issues.

We publish material that is researched, cited, edited and reviewed by licensed medical professionals. The information we provide is not intended to be a substitute for professional medical advice, diagnosis or treatment. It should not be used in place of the advice of your physician or other qualified healthcare providers. 6Alveolar epithelial type II cells synthesize, secrete, and recycle all components of the substance (i.e., surfactant) that serves to maintain the stability of pulmonary tissue by reducing the surface tension of fluids that coat the lung. Of all the patients who developed ARDS, 51 percent were alcoholics, compared with 49 percent in the second study. The exchange of gases between the outside environment and the bloodstream is the primary function of the lung.

Alcohol has long been known to be a risk factor for pneumonia, but even more recent is the discovery of how chronic alcohol use can increase the risk for acute conditions. This includes worsening acute lung injury following a serious accident or trauma, and acute respiratory distress syndrome (ARDS). 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.