The volatile nature of alcohol is exploited in this common field sobriety test, which is reliably used as a surrogate cyclobenzaprine mixed with alcohol to quantify blood alcohol concentrations. Interestingly, the alcohol vapor found in the airways is not caused by inhalation but is a result of the ready diffusion of alcohol from the airway blood supply across the airway epithelium and into the airways themselves (George et al. 1996). This process explains why alcohol vapor in the breath may be used to determine blood alcohol concentration. This process leads to the formation of reactive aldehydes (e.g., acetaldehyde), which in turn can interact and form harmful adducts with proteins and DNA (Sapkota and Wyatt 2015).

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). Aside from smoking, which is a well-known risk factor for developing COPD, little is known about other factors that impact risk for developing airflow obstruction. The term “whiskey bronchitis” is an expression that was often used to describe the high prevalence of bronchitis in alcoholics (Lyons et al., 1986).

Summary of Alcohol and Asthma

Interestingly, Nrf2 also regulates the expression of PU.1, a master transcription factor that mediates GM-CSF–dependent signaling (Staitieh et al. 2015). Accordingly, alcohol-induced reduction of Nrf2 also inhibits binding of PU.1 to its nuclear targets, which can be improved by zinc treatment (Mehta et al. 2011). Thus, alcohol impairs epithelial barrier function in the lung through a complex set of mechanisms with several cycles and feedback mechanisms (see figure 2); however, future studies will almost certainly elucidate further details. Another key function of the alveolar epithelium, namely the synthesis and secretion of surfactant—which is required to maintain alveolar integrity and gas exchange—also is impaired by chronic alcohol ingestion (Holguin et al. 1998).

1. 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).
2. A standard U.S. serving of alcohol is defined as 14 grams (0.6 fluid ounces) of pure ethyl alcohol.
3. In particular, animal models have established that chronic excessive alcohol ingestion causes dysfunction of the mucociliary apparatus, an important host defense mechanism responsible for clearing harmful pathogens and mucus from the lower airways (Happel and Nelson 2005).
4. 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.

Alcohol may also interfere with the effectiveness of antimicrobial agents in the airway and the body’s natural immune response. Researchers have found that heavy drinking reduces levels of an antioxidant in the body called glutathione. This antioxidant helps protect the lungs from damage caused by inhaled toxins such as tobacco smoke. Unless alcohol use in people with AUD is significantly curbed following lung cancer surgery, it can increase the risk of pneumonia by 50%, acute lung injury by 90%, and death by 50%. By contrast, the treatment of AUD prior to lung cancer surgery may improve outcomes and also reduce the risk of alcohol withdrawal by 75%. Interestingly, Myou found that inhaled ethanol did not trigger bronchospasm in Japanese subjects with alcohol-induced asthma.

Diseases Caused By Alcohol

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. As discussed previously, alcohol not only alters the environment of the alveolar space but also directly affects GM-CSF signaling, which regulates the maturation, terminal differentiation, and function of alveolar macrophages.

However, alcohol’s effects on neutrophil phagocytosis and pathogen killing are less clear than the effects on neutrophil recruitment, and the findings to date are inconclusive. 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.

Sexual and reproductive health

Activation of this dual kinase signaling pathway results in faster cilia beat frequency (CBF) in cilia briefly exposed to a moderate alcohol dose compared with controls (Sisson 1995; Sisson et al. 2009; Stout et al. 2007; Wyatt et al. 2003). More recent studies demonstrated that this rapid and transient alcohol-induced increase in NO levels was triggered by the alcohol-induced phosphorylation of heat shock protein 90 (HSP90) (Simet et al. 2013b). Upon phosphorylation, HSP90 increases its association with endothelial nitric oxide synthase (eNOS) in cilia, which then activates the cyclase–kinase cascade, resulting in increased CBF (Simet et al. 2013b). These findings are counterintuitive to the conventional wisdom that alcohol interferes with lung host defenses because stimulation of CBF should protect the lung; however, the clinical observation is that heavy alcohol exposure impairs lung host defenses. Pneumococcal pneumonia, caused by the bacterium Streptococcus pneumoniae, is the most common type of pneumonia in both healthy individuals and heavy alcohol users (Ruiz et al. 1999). In addition, the incidence of infections with Klebsiella pneumoniae also is increased in people with AUD and seems to cause disproportionate rates of lung infection and high mortality in this population (Feldman et al. 1990; Limson et al. 1956).

The exchange of gases between the outside environment and the bloodstream is the primary function of the lung. This requires the bidirectional movement of air through the conducting airways to alveoli where fresh air is exposed to capillary blood from the pulmonary circulation. Matching airflow with blood flow is critical for normal gas exchange and requires a delicate balance between the blood and air distribution systems.