Author: John Carter

Alcohol and Lung Disease

This injury results in leakage of proteinaceous fluid into the normally dry alveolar spaces, causing a significant impairment in gas exchange. Clinically, patients exhibit bilateral pulmonary edema and severe hypoxemia necessitating mechanical ventilation. While alcoholism does not directly cause ARDS, experimental evidence demonstrates that chronic alcohol exposure leaves the alveolar epithelium more leaky and primed for injury.

  1. In healthy individuals, this process ensures that pathogens and debris are continuously cleared from the lower airways.
  2. And, it’s well known that quitting alcohol can be as hard for some as quitting cigarettes.
  3. Although five studies found both negative and positive effects of alcohol intake on pulmonary function, these associations were no longer found when adjusting for covariates, such as smoking, socioeconomics and age 24, 29, 32, 44, 47.
  4. In fact, it has been reported that 87.6% of adults in the United States will consume alcohol at some point (SAMHSA, 2013).
  5. However, these changes have previously been considered insufficient to directly cause histologic damage to the lung.

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While 29.8% of non-drinkers in the study were never-smokers, 30.3% of heavy drinkers were current or former smokers who smoked more than 20 cigarettes per day. As such, it is difficult to ascertain how much heavy drinking contributes to the risk among people who are already at high risk due to smoking. It is well established that smoking has a huge effect on the pulmonary function 49. We know that the prevalence of respiratory disease in alcoholics is high, but as seen in this review the results regarding the effect of alcohol on pulmonary function are inconsistent and a major reason for this is the co-existing use of tobacco and alcohol.

Negative or no effects of heavy alcohol consumption on pulmonary function

This damage may result from various lung conditions, such as viral infections, pneumonia, and acute lung injury. According to a 2015 review in the Permanente Journal, heavy alcohol consumption (over three drinks per day) increases the risk of lung cancer in never-smokers by 30%. The literature currently cannot confirm the hypothesis of the U-shaped curve, but there are strong indications of a negative effect of a heavy alcohol consumption and a positive effect of a low to moderate consumption.

Nevertheless, the statistical power of this study was low and crucial environmental factors influencing pulmonary health were not adequately described. After a person drinks alcohol, besides going into the bloodstream, some of it will diffuse out into the lungs and end up in the breath. This damage happens not only in the lungs but also in the nasal passages and sinuses, causing inflammation and making them less able to fight off infection.

Impact on Respiratory Function

That is, low alcohol consumption appears to have a protective benefit while high consumption increases the cancer risk. Four studies expressed alcohol consumption in terms of grams per day or week 23, 25, 35, 48. Three of these studies further subdivided the subjects into different categories in terms of their alcohol consumption with varying definitions for each study 23, 25, 35.

Alcohol is the fifth leading risk factor for premature death and disability worldwide (Lim et al., 2012), contributing to the development of over 200 disease states (WHO, 2014). Although the liver is considered to be the major target of alcohol toxicity, alcohol also damages several distal organs. The lung is recognized as a target of chronic alcohol abuse, and alcohol-related susceptibility to lung injury is estimated to account for tens of thousands of deaths in the United States each year (Kershaw and Guidot, 2008). Alcohol consumption is well known to negatively impact the lung and to increase the risk of upper respiratory tract infections and pneumonia (Joshi and Guidot, 2007, Samokhvalov et al., 2010).

Can you drink alcohol if you have COPD?

In addition to its inhibitory effect on the cough reflex, studies have shown that chronic alcohol exposure can decrease ciliary beat frequency and thereby interfere with the mucociliary escalator (15). The combined effect of alcoholism on these nonimmunological host defense systems leaves individuals much more vulnerable to the development of pulmonary infections. Alcohol exposure has important consequences throughout the entire respiratory system, spanning from the oropharynx to the lung parenchyma, which are outlined in Figure 1. Clinical studies show that alcoholics have a much higher incidence of severe pneumonia caused by more virulent gram-negative organisms (12, 13), and many of these observations can be explained by changes that occur in the upper airway. Most clinical practitioners can attest to the fact that alcoholics have very poor oral hygiene.

Pulmonary Mechanics Measurements

Despite ongoing debate and gaps in research, it seems clear that heavy drinking is something that needs to be addressed if you are at risk of lung cancer. While there is nothing to suggest that alcohol causes lung cancer outright, the statistics strongly suggest that heavy drinkers are more likely to develop the disease—even if they don’t smoke. In 2020, research from the University of Liverpool Institute of Translational Medicine strongly suggested that alcohol use disorder (AUD, a.k.a. alcoholism) is an independent risk factor of lung cancer, especially squamous cell lung carcinoma. The study contends that the same genetic variations that can predispose a person to alcohol abuse may also increase a person’s risk of lung cancer. The articles were transferred to the software program Covidence and checked for duplicates 20.

This enhanced liver injury and inflammation correlated with increased levels of plasma ALT and AST, markers of liver injury. While ethanol feeding alone did not affect plasma ALT or AST, chronic + binge ethanol exposure significantly increased ALT and AST levels, to 68 ± 7 and 81 ± 6 IU/L, respectively. Although the effects of chronic + binge ethanol feeding have been well-characterized in the liver, the effects of this pattern of alcohol exposure on the lung are unknown. Therefore, the effects of this pattern of ethanol exposure on general lung morphology were characterized (Figure 2A, left). Ethanol-containing liquid diet alone, ethanol binge alone, and chronic + binge administration did not cause any overt pathological changes to the lung tissue, including the lung parenchyma and major airways. However, an increase in lung tissue cellularity was observed in lung tissue after chronic + binge alcohol exposure (Figure 2A, left).

First, experimental models have consistently shown that alcohol is responsible for depletion of the antioxidant glutathione, which causes oxidative stress in the lung and impairs alveolar macrophage maturation and function (18). In these studies, treatment with glutathione precursors both reverses oxidative stress and restores alveolar macrophage immune function. Clinical studies have confirmed the presence of glutathione depletion in human alcoholic subjects (19).

We aim to explore the potential protective effect of small to moderate amounts of alcohol and the harmful effect of larger doses to investigate whether existing literature can confirm the theory of the U-shaped association. To determine if the influx of neutrophils into the lung tissue was persistent, the number and type of cells in the bronchoalveolar lavage fluid (BALF) were examined 9 h and 24 h post-binge. Total BAL cell accumulation was not significantly affected by any treatment 9 h after ethanol or control binge.

Second, alcohol abuse alters intracellular signaling of granulocyte macrophage colony-stimulating factor (GM-CSF), which is a peptide that essential for alveolar macrophage terminal differentiation, maturation, and function. Animal models of alcohol ingestion have demonstrated a decrease in GM-CSF receptor expression on the cell surface of alveolar macrophages (20). These alcohol-mediated defects prevent proper maturation and normal functioning of the alveolar macrophage, both of which can be reversed by treatment with exogenous GM-CSF.