COPD and alcohol: Links and risks

What this suggests is that alcohol may contribute to the development of lung cancer independently, most presumably in people with a genetic predisposition for the disease. The link between lung cancer and alcohol consumption has long been considered controversial. There has been debate about the nature of this relationship, with some studies arguing that there is no association and others contending that alcohol may have a protective benefit in certain cases.

While no change in any pulmonary function was noted in the normal subjects at any concentration of IV alcohol, concentration-dependent bronchodilation occurred in all of the asthmatics. At the highest concentration (8%) IV alcohol caused a 33% increase in airway conductance in the asthmatics, which was roughly one third of the response that inhaled salmeterol, a beta-agonist, could induce in the same patients. While this study was small, it demonstrated the modest bronchodilator properties of IV ethanol. Clinicians and physiologists commonly believe that the alcohol present in exhaled air during alcohol consumption comes from alcohol that is vaporized from the alveolar-capillary interface of the pulmonary circulation. Careful studies by George and colleagues show that almost all of the exhaled alcohol is derived from the bronchial and not the pulmonary circulation (George et al., 1996).

Tuberculosis and AUD

These findings were the first to suggest that the nonalcohol components and additives of alcoholic beverages may be responsible for inducing asthma, rather than alcohol itself. Similar findings were seen in later studies that examined the effects of red wine in asthma (Dahl et al. 1986; Vally et al. 2000). However, researchers have not yet been able to determine conclusively if alcohol ingestion has any clinically significant effects on asthma.

Alcohol withdrawal

Acetaldehyde, the primary metabolite of ethanol, can trigger bronchoconstriction in asthmatics with genetically reduced ALDH2 activity and represents a significant trigger for asthma in certain Asian populations. Lastly, there are animal data suggesting that alcohol can promote neurogenic-driven airway inflammation. Trevisani and colleagues demonstrated in guinea pigs that alcohol intake triggers airway inflammation via a transient receptor potential vanilloid-1 (TRPV1) resulting in a calcium-dependent release of neuropeptides that contracted airway smooth muscle (Trevisani et al., 2004). The authors suggested that neurogenic airway inflammation may be an important mechanism by which alcohol causes asthma, which might be treatable with inhaled steroids (Antonicelli et al., 2006b). There is even an anecdotal report that suggests small eco sober house amounts of alcohol present in some inhaled corticosteroid preparations can act as a trigger for asthma for certain individuals (Antonicelli et al., 2006a).

Alcohol’s Effects on the Body

By Lynne Eldridge, MD Lynne Eldrige, MD, is a lung cancer physician, patient advocate, and award-winning author of “Avoiding Cancer One Day at a Time.” What this suggests is that having a genetic predisposition for AUD may predispose you to lung cancer as well. Unlike some carcinogens, such as tobacco smoke, alcohol is thought to promote the growth of an existing tumor rather than initiate the onset of cancer. This includes malignancies such as liver cancer, colon cancer, rectal cancer, breast cancer, and head and neck cancers. In 2010, alcohol was classified as a carcinogen (cancer-causing agent) by the U.S.

What are the signs of alcohol-related lung disease?

1. A similar U-shaped risk curve for reduced pulmonary function was observed among non-drinkers, mild drinkers and moderate-to-heavy drinkers.
2. ARLD can refer to any lung problems that chronic alcohol consumption has influenced, including pneumonia, tuberculosis (TB), and acute respiratory distress syndrome (ARDS).
3. Alcohol induces aberrant transforming growth factor beta1 (TGFβ1) expression in the alveolar epithelium and thereby dampens signaling through the granulocyte/macrophage colony-stimulating factor (GM-CSF)–PU.1 and Nrf2–antioxidant responsive element (ARE) signaling pathways.
4. Importantly and perhaps not as well known, alcohol intake is also clearly linked to a variety of airway diseases likely playing pathogenic, treatment and protective roles.
5. 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.
6. Thus, G-CSF levels rise significantly within 3 hours of pulmonary bacterial infections, peaking at 12 hours, and plateauing around 18 hours post-infection within the lung and systemic circulation.

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). Acuteon-chronic, or chronic + binge alcohol feeding produces alcoholic steatohepatitis in mice (Bertola et al., 2013). To validate these findings, indices of liver injury and inflammation were measured in liver tissue 9 hours after oral gavage of ethanol or isocaloric control (Figure 1A). Compared to animals receiving an isocaloric control liquid diet and isocaloric control binge, animals fed an ethanol containing liquid diet developed mild hepatic steatosis, as indicated by fatty droplets in the liver tissue (Figure 1B, bottom left).

It’s characterized by chronic inflammation, fluid accumulation, and the clogging of airways in the lungs, leading to severe breathing difficulties and reduced oxygen supply to the body. In addition to messing with their ability to deliver oxygen to the cells of our body, alcohol interferes with another important function of the lungs — their role in the immune system. The respiratory tract is lined with cilia, tiny hair-like structures that help keep the airways clean by sweeping our pathogens and harmful particles along with mucus. 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.