Author: Gary Jackson

Alcohols Effects on Lung Health and Immunity PMC

This effect was blocked by a β-adrenergic blocker and was not reproduced in isolated first passage cultured airway epithelial cells. These findings suggested that autonomic innervation and functional β-adrenergic receptors participate in alcohol-induced relaxation of airway smooth muscles. The applicability of this study, however, is uncertain since most of the bronchoreactivity of asthma occurs in the small airways and not the trachea.

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). 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.

Lung Function

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). The formation of these adducts may disrupt normal cellular functions, induce inflammation, and impair healing. Taken together, these findings demonstrate that the airways—including the oral cavity and extending all the way to the alveolar space—are subjected to high concentrations of alcohol and its deleterious metabolites during intoxication. 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).

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. 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).

Alcohol and Chronic Obstructive Pulmonary Disease (COPD)

Alcohol can affect the upper part of the airways, including the nose, sinuses, voice box and throat. Additionally, chronic use of alcohol makes people more vulnerable to other viral infections, not just RSV. One out of every four Americans drinks to excess, which will lead to six alcohol poisoning deaths every day.

• 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.
• These chemical changes compound the negative mechanical and microbiological effects of alcoholism on the respiratory system.
• Alcohol-induced suppression of G-CSF–driven neutrophil production combined with impaired bacterial clearance likely account for the high severity and mortality of bacterial infections among the alcohol-fed mice observed in these studies.
• Alcohol-induced failure of the mucociliary system could interfere with the clearance of pathogens from the airways and thereby may contribute to the increased risk of pulmonary infections in people with chronic heavy alcohol use (Sisson 2007).
• 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.
• The effects of heavy alcohol use on measures of pulmonary function can be temporary or long-lasting, and there is no way to know when your breathing issues will become irreversible.