Alcohol and Asthma: Is It Safe?

Later more elegant in vivo studies in mice and kittens by Laurenzi demonstrated profound effects caused by injections of intraperitoneal (IP) alcohol on mucociliary clearance (Laurenzi and Guarneri, 1966). IP alcohol, at 5–21% concentrations that induced coma, caused concentration- and time-dependent slowing of clearance of inhaled staphylococci in mice. At the highest concentration of IP alcohol used (21%) clearance was slowed five-fold compared to control mice and there was a strong direct correlation between the reductions of airway clearance with the blood alcohol concentrations. Importantly, in the same study the investigators directly observed tracheal clearance of inert carbon particles following IP alcohol injection of anesthetized kittens. Alcohol caused a rapid and reversible concentration-dependent slowing of airway particle clearance compared to control kittens. This important study established that alcohol clearly impairs mucociliary clearance.

1. Drinking alcohol can also have negative effects on the peripheral nervous system (PNS).
2. While this is not the most common health complication of drinking, alcohol consumption—even moderate amounts—can impair your breathing abilities, especially if you have lung disease.
3. These findings highlight that alcohol intoxication impairs neutrophil recruitment into infected tissues and the lung and also hinders neutrophil clearance from the lung.
4. These results corroborate findings that infection in the setting of alcohol exposure increases the risk of complications such as ARDS.

As discussed in this review, genetic analysis has helped to identify potential candidate genes involved in alcohol-induced lung dysfunction that might explain the newly identified association between alcohol abuse and acute lung injury in humans. Although several genes of interest were identified and pursued as has been discussed, the vast majority of the genes that displayed significantly altered expression in the alcohol-fed rat lung have not yet been evaluated. In fact, the full power of genomic and proteomic tools, which are used to study an organism’s genes and/or proteins, only now are being applied to complex lung diseases.

CPAP is a type of treatment for OSA that works by pumping air through a mask and into the airway. The pressurized stream of air helps hold the 11 ways to curb your drinking airway open while a person sleeps. OSA is much more common than CSA and involves the airway being blocked by tissues in the mouth and throat.

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. Another fundamental component contributing to alcohol’s effects on the lungs is oxidative stress and the resulting alterations in alveolar macrophage function.

Alcohol use disorder

According to the National Heart, Lung, and Blood Institute, an estimated 25 million people in the United States have asthma. A number of triggers can cause an asthma attack, and different people can have different triggers. However, it is not clear that the presence of histamine in alcohol or any other external trigger can cause symptoms. Fermenting alcohol produces histamine, which is present in all alcohol types, including liquor, beer, and wine. The study, using participants in Australia, asked more than 350 adults to fill out a questionnaire on their allergy triggers related to alcohol. As there is no cure for asthma, it is important for people to know their triggers and to take steps to prevent an attack.

Alcohol and Sleep Apnea

An excellent review of alcoholic drinks as triggers for asthma has been previously published (Vally et al., 2000). Indeed, the alcoholic with pneumonia as the prototype of the immunocompromized host is well known to every first year medical student (Chomet and Gach, 1967). An ever-expanding body of evidence points to multiple immune mechanisms by which alcohol intake compromises lung defenses and has been previously reviewed (Bomalaski and Phair, 1982; Happel and Nelson, 2005). While innate and acquired lung immune mechanisms how to build alcohol tolerance: the best tips from real experts are vitally important, the effects of alcohol intake on the functions of lung airways are poorly understood. Importantly and perhaps not as well known, alcohol intake is also clearly linked to a variety of airway diseases likely playing pathogenic, treatment and protective roles. This review first will discuss key aspects of the epidemiology and pathophysiology of AUD and lung health, before focusing more in-depth on lung infections and acute lung injury, which comprise the majority of alcohol-related lung diseases.

Epidemiology of Alcohol Abuse and Acute Lung Injury

People with more severe asthmatic symptoms should be more cautious when drinking. Alcohol consumption can have a direct effect on your asthma, but is it the alcohol that’s causing you to have an asthma attack? Learn more about the connection and if you should still drink alcoholic beverages.

Can Drinking Alcohol Trigger an Asthma Attack?

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. 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. Overall, these alterations in host defense and immune dysfunction explain how chronic excessive alcohol ingestion predisposes to pulmonary infection. It is important to realize, however, that the effects of alcohol on alveolar macrophage innate immune function are just one facet of the complex pathophysiology of alcohol and the lung’s immune system. Alcohol also impairs neutrophil migration to the infected lung, and abnormalities in this and other components of the adaptive immune response clearly are involved but are beyond the scope of this brief review. Alcohol’s effects on TGFβ1 also interface with its effects on antioxidant levels.

This effect was partially reduced by histamine or the alpha-adrenergic blockade, but completed abolished by calcium channel blockade, suggesting a calcium flux mediated alcohol-triggered airway smooth muscle contraction in this model. The high concentrations of alcohol used in this study undermine the applicability of these findings. 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 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.

Alcohol misuse can lead to neurological damage that can affect multiple areas of a person’s health and well-being. The best way to avoid the issue is to limit alcoholic consumption to 2 or fewer drinks per day for males and 1 or fewer for females. According to a 2017 review, muscle myopathy is common in alcohol use disorder. In addition, about 40 to 60 percent of people who experience chronic alcohol misuse also experience alcohol-related myopathy. If alcoholic drinks do contain substances that cause a reaction, the amount a person drinks may also contribute to worsening asthma symptoms.

This comes from clinical studies of the utility of estimating blood alcohol concentration (BAC) with the breath test (Breathalyzer) in patients with chronic obstructive pulmonary disease (COPD). A study of ten older male patients with COPD, given a standard alcohol drink, found that exhaled Breathalyzer alcohol levels in the COPD patients did not correlate with BACs compared to the linear relationship of Breathalyzer levels with BACs in normal subjects (Russell and Jones, 1983). A second study showed that Breathalyzer levels significantly underestimated BACs in patients with COPD as a function of age (Wilson et al., 1987). These findings were confirmed in a third study that demonstrated poor correlation between exhaled alcohol concentrations and BACs in patients with COPD and asthma (Honeybourne et al., 2000).

Alcoholic neuropathy

In a case-control study, Lyons performed pulmonary function tests and assessed respiratory symptoms on 27 alcoholic subjects and case-matched control subjects (Lyons et al., 1986). They found there was no difference in pulmonary function or symptoms between the two groups and could account for all abnormal function on the basis of smoking alone. A subsequent study of 111 alcoholics and controls by Garshick found that lifetime alcohol consumption was a predictor of chronic cough and sputum production but not wheeze (Garshick et al., 1989). Using a linear regression model that included age, smoking history measured in pack/years, and interactions between pack/years and alcohol intake, Garshick found that lifetime alcohol consumption was also a predictor of lower FEV1 on spirometry. Interestingly, they found that the interaction between alcohol and smoking consumption was in a direction opposite to the independent effects of alcohol and smoking on lung function and suggested that alcohol might exert a protective effect in heavy smokers.

However, if alcoholic cardiomyopathy is caught early and the damage isn’t severe, the condition can be treated. It’s very important to stick with the treatment plan and how much does a drug and to stop drinking alcohol during recovery. Alcoholic cardiomyopathy is most common in men between the ages of 35 and 50, but the condition can affect women as well.

During acute inflammatory stresses such as sepsis and trauma, TGFβ1 is released and activated in the alveolar space, where it can cause the alveolar epithelial barrier dysfunction described above (Bechara et al. 2004). Therefore, the experimental findings to date implicate the pathophysiological sequence in the alcoholic lung shown in figure 2. 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.

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).

Careful studies by George and colleagues show that almost all of the exhaled alcohol is derived from the bronchial and not the pulmonary circulation (George et al., 1996). During alcohol ingestion, alcohol freely diffuses from the bronchial circulation directly through the ciliated epithelium where it vaporizes as it moves into the conducting airways (George et al., 1996). Indeed, alcohol vapor excreted into the airways in this manner forms the basis of the breath test used to estimate blood alcohol levels (Hlastala, 1998).