Alcohol and the Lung Alcohol Research: Current Reviews

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. Although the mechanisms remain to be delineated, treatment with recombinant GM-CSF restores GM-CSF receptor expression and signaling and normalizes both alveolar epithelial barrier function (Joshi et al. 2006) and alveolar macrophage immune function (Joshi et al. 2005). GM-CSF treatment is widely used to improve bone marrow recovery following chemotherapy for malignancies. However, the major site of GM-CSF production actually is in the airway epithelium, where its actions are partially blocked by alcohol abuse.

What Are the Effects of Alcohol on the Body?

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). Over time, this can start to affect the lungs, making the body more vulnerable to lung infections and damage. 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. Though studies are lacking as to how much dehydration impacts hypertension, animal studies conducted by Monash University reported that chronic dehydration not only worsens high blood pressure in mice but also increases the risk of severe kidney damage. Pure ethanol is a moderately effective and transient bronchodilator and likely relaxes airway smooth muscle tone.

Systems Biology and the Study of Alcoholic Lung Disease

The first reported use of intravenous (IV) alcohol for the treatment of asthma appeared in 1947 when Brown infused 5% ethanol into children with severe asthma attacks who were unresponsive to conventional asthma therapy (Brown, 1947). Five of the six patients improved with the alcohol infusion and no adverse reactions were reported. This report suggested that pure alcohol, when administered intravenously and, in the absence of any other ingredients, acted as a bronchodilator and could be used as a treatment of asthma. A later report noted that asthmatics cleared intravenous alcohol from the bloodstream significantly faster than controls (Sotaniemi et al., 1972) and was confirmed by a subsequent report (Korri and Salaspuro, 1988).

Chemo Drugs and Alcohol

When this happens, the body will respond by narrowing blood vessels, causing blood pressure to rise. But that’s rarely a consideration when the sun is out, and there’s a cold bottle of chablis in the fridge. What makes alcohol so pleasant also makes it easy to overindulge, and when we do, the body works hard to deal with the effects.

More on COPD

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. Exceeding these daily or weekly drinking limits significantly increases the risk of developing AUD and problematic health outcomes (NIAAA 2014). Airflow obstruction diseases continue to increase in prevalence and that chronic obstructive pulmonary disease (COPD) will become the third most common cause of death in the United States by the year 2020 (Mannino et al., 2003).

Trouble breathing and drinking alcohol: Is it COPD?

These T cells are characterized by the presence of a molecule called CD4 on their surface and therefore also are called CD4+ cells. When they become activated, CD4+ cells secrete various cytokines to facilitate different types of immune responses. For example, type 1 CD4+ cells are characterized by the secretion of interferon γ (IFN-γ); they act primarily against pathogens that are found within cells. Conversely, type 2 CD4+ cells do not produce IFN-γ but various types of interleukins.

Thus, although the total number of circulating B cells does not differ significantly between people with and without AUD, people with AUD have elevated levels of circulating IgA, IgM, and IgG (Spinozzi et al. 1992). In the lungs of people with AUD, however, Ig levels are reduced as determined by bronchoalveolar lavage (BAL) (Spinozzi et al. 1992). Replacement IgG therapy only partially restored Ig levels in these people, although it decreased the rates of pulmonary infections (Spinozzi et al. 1992). Alcohol-related lung damage is most common among those who are heavy drinkers or have been abusing alcohol for an extended amount of time.

Although the evidence is far from conclusive, if true, it could add lung cancer to the growing list of other cancers thought to be linked to alcohol. 1Delayed-type hypersensitivity responses are excessive immune reactions that occur only a few days after the body has been exposed to the pathogen. These responses are not mediated by immune molecules produced by B cells (i.e., antibodies) but by T cells.

Thus, some studies indicate that alcohol has no effect on neutrophil phagocytosis or pathogen killing (Nilsson et al. 1996; Spagnuolo and MacGregor 1975), whereas other studies demonstrate that acute alcohol exposure impairs functional activities of neutrophils. For example, Davis and colleagues (1991) found that alcohol-fed rats failed to clear bacteria from the lungs and had increased mortality. Some of this discrepancy likely is related to differences in the bacterial pathogens studied. Thus, Jareo and colleagues (1995) noted impaired neutrophil killing of selected strains of S. Pneumoniae in vitro and a complete absence of killing of other bacterial strains in alcohol-exposed animals. In human studies, BACs as low as 0.2 percent (i.e., approximately 2.5 times the legal intoxication level) impaired neutrophil degranulation and bactericidal activity (Tamura et al. 1998).

The first careful in vitro experiments that examined the effects of modest concentrations of alcohol on CBF in tracheal tissues were done in airway tissue from unanaesthetized sheep during fiberoptic bronchoscopy (Maurer and Liebman, 1988). These investigators found that CBF was stimulated by low concentrations of alcohol (0.01–0.1% or ≈ 2–20 mM), not changed by modest concentrations of alcohol (0.5–1.0% or ≈ 100–200 mM) and slowed at higher concentrations of alcohol (2% or ≈ 400 mM). This transient alcohol stimulation effect on cilia was recapitulated in vivo in alcohol-fed rats (Wyatt et al., 2004). In this model, 1 week of feeding 36% alcohol increased baseline CBF 40% over control animals and was comparable to stimulation with an exogenous beta agonist. These findings indicate that brief exposure to alcohol stimulated ciliary motility both in vitro and in vivo.

Pneumoniae challenge; after that, however, neutrophil recruitment remained elevated even 40 hours post-challenge compared with nondrinking rats. This observation suggests that in individuals with heavy alcohol exposure, the host neutrophils drooling: causes and treatments arrive late at the infected lung but stay longer (Sisson et al. 2005). These findings highlight that alcohol intoxication impairs neutrophil recruitment into infected tissues and the lung and also hinders neutrophil clearance from the lung.

Alcoholic lung disease and other lung issues can happen to any chronic heavy drinker, regardless of age or previous health status. Studies have found that after you stop drinking, alcohol can stay in your blood for up to six hours and in your breath for hours. It can take the liver several days to recover after a binge and sometimes up to weeks or months if the damage is severe. The implications may be more serious among people who are older or suffering from preexisting conditions, like heart or lung diseases, says Piano. Theoretically, she says, an increase in heart rate or a drop in oxygen saturation levels could cause an “acute physiologic consequence,” such as heart failure.

“People spend much less time in the deeper stages of sleep and in REM sleep,” he says. Lower oxygen levels cause people to wake up more frequently and experience periods of breathing punctuated by periods of apnea, a phenomenon called periodic breathing. 4Relative risk is the risk of an event (or of developing a disease) relative to exposure. Relative risk is a ratio of the probability of the event occurring in the exposed group versus the control (nonexposed) group.

In contrast to these few clinical studies, a larger body of literature indicates both short and long term effects of alcohol on the mucociliary apparatus. As a first step to identify candidate genes that might explain how alcohol-induced oxidative stress renders the lung susceptible to acute lung injury, the authors compared lungs from control- and alcohol-fed rats using genetic analysis. In addition, alcohol vs marijuana is one safer than the other the expression of a protein involved in immune system regulation, transforming growth factor β1 (TGFβ1), also was markedly increased in the alcohol-fed rat lungs (Bechara et al. 2004). Soon after the association between alcohol abuse and ARDS was reported, researchers began to design studies of the mechanisms by which chronic alcohol ingestion increases susceptibility to acute lung injury.

1. Tuberculosis infection and produce interferon γ (INF-γ), an important cytokine that stimulates cell-mediated immunity (Junqueira-Kipnis et al. 2003).
2. This is not to suggest that they “treat” hypertension, but they are considered “safe” and can help you maintain ample hydration in addition to the water you drink each day.
3. Rats fed alcohol for six weeks demonstrated slowed cilia beating and desensitization of airway PKA activity (Wyatt et al., 2004).
4. Ten of these 12 (83.3 percent) patients died, whereas the mortality in the rest of the cohort was only 22 percent.

Other mechanisms that activate the gut-liver axis may have similar results when superimposed on alcohol intoxication. During alcohol-induced lung immune dysfunction, the upper airway is the first checkpoint to fail in the clearance of respiratory pathogens due to differential post-translational modifications of novel proteins that control cilia function. Proteomic approaches are needed to identify drug overdose: definition treatment prevention and more novel alcohol targets and post-translational modifications in airway cilia for therapeutic interventions. When inhaled pathogens are not cleared in the upper airway, they enter the alveolar space, where they are phagocytized and cleared by AMs. With chronic alcohol ingestion, oxidative stress pathways in the AM are stimulated, thereby impairing AM immune capacity and pathogen clearance.

But the bad news is, once alcohol is in your bloodstream there is nothing you can do to speed up alcohol metabolism. Once alcohol has entered the bloodstream it starts to be processed, mainly by the liver (90-98 per cent) and also by the kidneys (2-10 per cent). A 2006 study found that the use of a carbonated mixer had varying effects on the alcohol absorption rate. Two thirds of the 21 subjects studied absorbed the alcohol with the carbonated mixer at a faster rate, with the remaining third showing either no change or a decrease in rate.

Acute lung injury involves the rapid development of noncardiogenic pulmonary edema, and patients with impaired alveolar epithelial fluid clearance are three times more likely to die from ARDS than patients with a maximal ability to clear lung fluid (Ware and Matthay 2001). Although the fluid balance in the lungs is regulated by the concerted actions of both epithelial and endothelial barriers (Mehta et al. 2004), it is the alveolar epithelium which primarily prevents protein and fluid flow into airspaces (Mutlu and Sznajder 2005). A pathological hallmark of ARDS is heterogeneous damage of the alveolar epithelium, with complete loss of the epithelial surface in some areas, whereas other alveoli remain relatively intact. Therefore, at a cellular level the extent of the alveolar epithelial damage may not be as widespread or as uniform as chest X-rays may suggest, and preservation and repair of the alveolar epithelium are key to survival. 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).

For example, oral GSH treatment in alcohol-drinking mice was able to restore GSH pools, reverse alcohol-induced Nox increases, and restore alveolar macrophage function (Yeligar et al. 2012, 2014). These results suggest that GSH is a vital component in restoring alcohol-induced alveolar macrophage function by decreasing Nox proteins and restoring GSH pools. While alcoholics represent a minority of the drinking public, these results are informative. Banner observed that nearly half of the patients admitted to an alcohol detoxification unit had airflow obstruction on spirometry and almost all had in gas diffusion impairment that could not be explained on the basis of cigarette smoking (Banner, 1973). The findings were confirmed by Emirgil and correlated to symptoms of chronic bronchitis and shortness of breath in a similar group of alcoholics (Emirgil et al., 1974).