Alcohol and Lung Injury: A Dangerous Combination

Alcohol abuse alters the proper functioning of the human body in ways which contribute to the development of a number of illnesses on the long term. Alcohol is a substance which is metabolized inside the human body. In large quantities alcohol has a number of negative effects on the body systems affecting them irreparably in many cases. The respiratory system is vital to life but it is also fragile and hypersensitive. Alcohol abuse interferes with the respiratory functions of the lung attacking them both at a cellular and molecular level. The effects of alcohol abuse can be seen outside and inside the lungs, with and without a microscope.  

Alcohol is one of the most commonly used drugs worldwide. It is estimated that the prevalence of alcohol use is 66% in the United States. Epidemiological studies show that 13% of Americans will meet the diagnostic criteria for alcohol dependence during their lifetime. The prevalence of alcohol abuse and dependence in hospitalized patients worldwide is similar.  

Epidemiological evidence has shown that alcohol abuse independently increases the risk of developing the Acute Respiratory Distress Syndrome or ARDS by as much as three to four times as demonstrated by Dr. Moss’ seminal paper published in 1996 on the subject. Based on these observations and under the direction of Dr. Guidot, it has been shown in experimental models as well as in clinical studies, for the first time, that chronic alcohol abuse causes changes in the alveolar epithelium that render the lung susceptible to acute edematous injury in response to sepsis trauma, and other inflammatory insults. 

We have shown that chronic alcohol ingestion decreases the levels of the antioxidant glutathione within the alveolar space by as much as 80 to 90%, and, as a consequence, impairs alveolar epithelial surfactant production and barrier integrity, decreases alveolar macrophage function, and renders the lung susceptible to oxidant-mediated injury. These changes are often subclinical and may not manifest as detectable lung impairment until challenged by an acute insult such as sepsis or trauma. However, even otherwise healthy alcoholics show evidence of severe oxidant stress in the alveolar space that correlates with alveolar epithelial and macrophage dysfunction (correlates with dysfunctions of both the epithelial and the macrophage cells of the lung air sacs).  

All our data indicate that chronic alcohol intake 1) Impairs surfactant production and increases oxidant-mediated necrosis in alveolar epithelial cells 2) Increases oxidant- and cytokine-mediated apoptosis in alveolar epithelial cells in vitro and in vivo. 3) Increases protein leak across the alveolar barrier and decreases alveolar liquid clearance in vivo. 4) Increases activation of metalloproteinases and degrades the alveolar matrix during endotoxemia. (5) Renders the lung intrinsically susceptible to injury during endotoxin-mediated acute inflammation; 6) decreases functional surfactant in the alveoli and increases respiratory failure during sepsis in vivo. 7) In the cecal ligation and perforation model there is increase in the expression and activation of transforming growth factor- within the alveolar space where it can increase epithelial permeability. 

Mankind is yet to fully discover how the human body works. However, there are medical certainties which are supported by both live and in vitro studies. And one of these medical certainties is the fact that alcohol abuse is a decisive factor in the development of lung injury. People are affected to a higher or lower degree depending on numerous added factors including the fact that each human body is unique, physically and structurally.