Critique 291 – Effects of alcohol consumption from early adolescence on lung function and development of COPD – a retrospective cohort study – June 2025
Authors King M.T., Nielsen L.B., Weinreich U.M.
Citation Eur Clin Resp J. 2025; Mar 19;12(1):2476232. https://doi: 10.1080/20018525.2025.2476232
Author’s Abstract
Background Studies indicate a U-shaped relationship between alcohol consumption (AC) and chronic obstructive pulmonary disease (COPD) with low-moderate AC being protective. We investigated the influence of AC debut (ACD) at different ages on forced expiratory volume in the first second (FEV1), forced vital capacity (FVC) and COPD development.
Methods In a multi-center cohort study, data on AC were collected through a questionnaire and spirometry performed at baseline and follow-up. COPD was defined as FEV1/FVC-ratio <0.7 on post-bronchodilator spirometry. Modelling determined odds ratio (OR) of COPD and mean differences in FEV1 and FVC in stratified age groups of ACD. Never drinkers were used as reference. Adjustments were made for age, sex, smoking parameters, asthma, and education.
Results In total, 4,717 participated in the initial work-up and 2,751 completed follow-up. A higher FEV1 and FVC was found in all groups compared to never drinkers. Highest statistically significant difference in FEV1 and FVC was found in age group 14–16 (0.17 and 0,23 L, respectively). With rising age of ACD a smaller difference in FEV1 and FVC was observed with the smallest difference in age group >25 (0.11 L) and age group 17–18 (0.13 L), respectively. A lower, but not statistically significant OR for COPD in ACD age 14–16 (OR = 0.83) and higher OR in the remaining groups with 21–25 being highest (OR = 1.36) was indicated.
Conclusion This study found higher FEV1 and FVC in all groups drinking alcohol compared to never drinkers with the highest among participants with ACD at age 14–16. The findings on risk of COPD development were not statistically significant.
Forum Summary
This innovative cross-sectional study by King et al. (2025) reports on the association between alcohol consumption and lung function: the authors associated the age at which individuals started alcohol consumption (‘alcohol consumption debut’ or ACD) with future lung function. The authors found better lung function in all groups drinking alcohol compared to never drinkers, with the best outcome among participants with ACD at age 14–16 years. The authors also studied the association between ACD and chronic obstructive pulmonary disease (COPD), a progressive lung disease most often occurring in smokers. COPD is an independent risk factor for lung cancer. The risk of COPD development was not associated with ACD.
Forum members point out that this study in middle-aged Danish moderate drinkers is one of a few studies on the topic of alcohol consumption and lung function and its related diseases, COPD and lung cancer, an issue far from being resolved. The studies to date on this topic are contradictory, and the relation between alcohol consumption and lung function and lung diseases is consequently unclear. In addition, the effects observed in various models applied in this specific study are small; the predicted lung function change associated with ACD is only 5%.
Forum members urge not only for more longitudinal studies, but also for intervention studies testing hypotheses on how alcohol consumption may beneficially affect lung function. Smoking is a major confounding factor, which may, although corrected for, still confound the relationship, like other lifestyle factors such as drinking patterns.
Forum Comments
Background
Chronic obstructive pulmonary disease (COPD) is a type of progressive lung disease characterized by chronic respiratory symptoms and airflow limitation. Global prevalence of COPD in people aged 40 years and older was estimated to be between 7 and 13 %, depending on the definition (Al Wachami et al., 2024). In addition, COPD is an independent risk factor for lung cancer, occurring up to five times more often in smokers with airflow obstruction than those with normal lung function (Young et al., 2009).
The most common cause of the development of COPD is exposure to harmful particles or gases, including tobacco smoke, that irritate the lungs, causing inflammation. Such exposure needs to be significant or long-term. The greatest risk factor for the development of COPD is tobacco smoke. Tobacco smoking causes over 70% of COPD cases in high-income countries and 30% to 40% of cases in low- and middle-income countries[1]. Other risk factors include exposure to indoor and outdoor pollutants, allergens, occupational exposure such as construction dust, and host factors including genetic susceptibility, factors associated with poverty, aging and physical inactivity.
Alcohol reaches the airway passages both by the bronchial circulation and by direct inhalation (Sisson, 2007). Thus, an effect on airway flow is plausible with implications for COPD. Some data, mostly from small studies, suggest that low doses of alcohol may have a bronchodilator effect by relaxing smooth muscle tone.
In COPD, lung airway flow (LAF), which encompasses the normal movement of air through the respiratory system during inhalation and exhalation, is significantly impaired and restricted. This is due to various factors, primarily involving inflammation, narrowing of airways, and destruction of lung tissue. LAF is assessed by the spirometry lung function test, which, therefore, also assists in the diagnosis of COPD. Spirometry measures forced expiratory volume (FEV1) which is the volume exhaled in the first second, forced vital capacity (FVC), which is the maximal amount of air that the patient can forcibly exhale after taking a maximal inhalation, and peak expiratory flow (PEF), a measure of how quickly air can be exhaled.
ISFAR previously commented on studies on the association of more moderate alcohol consumption with lung function and COPD (Kaluza et al., 2019; Siedlinski et al., 2012). For example, an early study on lung function (Siedlinski et al., 2012) focussed on dietary factors, and resveratrol and white wine specifically. This study, however, was poorly adjusted, and the non-drinker control group was not defined. A later, larger study by Kaluza et al. (2019) on the association between alcohol consumption and COPD was adjusted for many more lifestyle factors and confounding factors, showing protective associations for alcohol, although mainly for wine and beer consumption.
This paper by King et al. (2025) reports on the issue of alcohol consumption and lung function and COPD in an innovative way: the authors associated the age at which alcohol consumption started (‘alcohol consumption debut’ or ACD) with lung function, namely FEV1, FVC and COPD development. The paper concludes that higher FEV1 and FVC were found in all groups drinking alcohol compared to never drinkers, with the highest among participants starting to consume alcohol at age 14–16 years. Their findings on the risk of COPD development were not statistically significant. Siu et al. (2010) also found that, independent of smoking and evident lung or heart disease, light to moderate drinkers of alcohol had better FEV1, FVC, and FEV1/FVC than abstainers did. Although this association does not prove causality, drinking moderate amounts of alcoholic beverages may have some benefit for lung function. Speculative mechanisms of a potential benefit from moderate alcohol drinking include anti-inflammatory effects (Pratt and Vollmer, 1984), improved mucociliary clearance (Elliott et al., 2001, Sisson, 2007), direct bronchodilation (Sisson, 2007) and antioxidant effects (Schünemann et al., 2002).
Although the analyses were not always clearly independent of smoking, earlier cross-sectional reports consistently show impaired LAF in heavy drinkers (Hrubec et al., 1973, Emirgil et al., 1974, Banner, 1980, Lyone et al., 1986, Garschick et al., 1989). One of these older papers reporting on the association between lifetime alcohol consumption and COPD was a small epidemiological study, of which 55% were alcoholics (Garshick et al., 1989). Population studies of chronic LAF among light to moderate drinkers, however, have shown conflicting results independent of smoking status (Cohen et al. 1980, Lebowitz 1981, Pratt and Vollmer, 1984, Tabak et al., 2001, Murray et al., 2002, Schünemann et al., 2002, Sisson et al. 2005). A large US study comparing the prevalence of LAF with alcohol consumption in 15,294 adults, for example, showed no relationship with light to moderate alcohol consumption but did show increased airflow obstruction in former heavy drinkers (Sisson et al. 2005), while another smaller US study showed no overall relationship between alcohol and LAF, but lung function was better among wine drinkers, especially drinkers of white wine (Schünemann et al., 2002). Conversely, the Canadian Lung Health Study in 5887 smokers with airways obstruction found a significant protective effect of moderate drinking in men, but not in women, for both hospitalizations and deaths (Murray et al., 2002). A 20-year mortality study among 2953 middle-aged men from several European countries showed a U-shaped relation between alcohol and COPD mortality (Tabak et al., 2001).
Critique
This study adds to the limited and contradictory information available on the relationship between alcohol consumption and lung function, COPD, and lung cancer. However, this retrospective study suggests that lifelong alcohol consumption improves lung function, which in turn may beneficially affect COPD risk (that was on average improved but not statistically significant). This middle-aged Danish population was drinking moderately, with an average consumption of approximately 6 units per week, a unit consisting of 12 g of alcohol. The authors point out that this outcome needs confirmation in a prospective study.
It will be interesting to follow this population for a longer time. Not only to further substantiate these outcomes, but also to show that lung function improvement will beneficially affect COPD outcome and that longer follow-up may show an association with lung cancer. The latter may be best observed in a subpopulation of COPD patients, since lung cancer is more common in these patients (Young et al., 2009). Also, an association between alcohol consumption and lung cancer is not established. Lung cancer in never-smokers was associated with alcohol consumption (Fehringer et al., 2017); a pooled analysis of an international consortium on lung cancer showed that alcohol consumption was inversely associated with lung cancer risk, with evidence most strongly supporting lower risk for light and moderate drinkers relative to non-drinkers. This was, however, not confirmed in other studies, meta-analyses, such as (García-Lavandeira et al., 2016) nor for lung cancer in wine drinkers (Bertola et al., 2025).
The King et al. (2025) study included many participants, but only a small portion was present at follow-up. Unfortunately, reasons for non-enrolment and loss to follow-up were not specified. Unfortunately, it seems that participants who did not report their ACD, obtained the highest proportion of COPD, and these were lost to follow-up, leading to an unequal distribution of groups.
The study defined the group of never drinkers as those who never drank > 1 unit per month. A clear definition of this group is important in light of the discussions on sick quitters potentially affecting the beneficial effects of moderate alcohol consumption. It is, however, unclear whether alcohol consumption was checked twice (at baseline and follow-up), how differences in answers were dealt with, and whether temporary alcohol abuse was specifically asked for in the questionnaire. Alcohol consumption debut (ACD) was defined as consistently drinking > 1 unit per month. Thus, alcohol consumption seemed to be assessed in some detail both at baseline and follow-up. Also, the questionnaire inquired about average weekly alcohol intake across different types of alcoholic beverages (beer, wine, strong wine, and spirits). The authors consider their approach of using ACD as a strength of the study, given that it avoids the sick quitters bias by using lifetime never drinkers as the reference group.
Interestingly, the authors analysed their results using adjusted and unadjusted models, both with similar outcomes, that is, earlier and later ACD are associated with better lung function as compared to never-drinkers. Adjustment for factors such as age could over-adjust for outcome parameters, because age, for example, may fully or partially mediate the association between ACD and lung function. Consequently, the effects observed in the adjusted model are smaller and not always statistically significant for all ACDs. However, the percentage of predicted lung function change is similar in both models, viz, up to approximately 5%.
All in all, the associations between alcohol consumption and lung function and lung disease are still not yet clear and need further investigation.
Specific Comments from Forum Members
Forum member Harding muses that he “found it hard to see what conclusions could be drawn from this study. Previously published epidemiology in this area indicates an unclear picture, with some showing a U-shaped relationship between alcohol consumption and some not. This study found that the findings on the risk of COPD from alcohol consumption were not statistically significant. So, the picture remains unclear.
I did detect some bias in the language used. The last sentence is, ‘To our knowledge, this is the first study on the effects of age of ACD (when subjects started to drink alcohol) on FEV1, FVC (measures of lung function) and COPD (disease outcome), warranting further research, preferably prospective, to confirm our findings. What ‘findings’? Why your findings? What about other people’s findings? And ‘confirm’? One of the principles of the scientific method is that experiments must be repeatable, i.e., other workers demonstrably get the same outcome with the same method. Epidemiological studies are by their nature not repeatable. They are all one-offs.
So, what is needed is not more epidemiology, but the testing of a hypothesis of how alcohol consumption might influence lung function, by designing an experiment to find out if it actually does or doesn’t.”
Forum member Ellison states “I agree with the comments of other Forum members. However, it is clear that cigarette smoking is the major factor in the development of pulmonary disease. As for effects of alcohol consumption, the pattern of drinking (especially the type of beverage and if the drinking is regular or just on week-ends, with or without binges, with or without food, etc.), as well as details on the cultural and family influences and socio-economic and genetic factors are often not well known and thus difficult to adjust for in epidemiologic studies. This was often the case in the present analyses, and thus it is not surprising that its results lacked statistical significance for many factors. Nevertheless, the additional information provided by these authors can be useful in seeking to learn the true relation between alcohol consumption and lung disease.”
References
Al Wachami, N., Guennouni, M., Iderdar, Y., et al. (2024). Estimating the global prevalence of chronic obstructive pulmonary disease (COPD): a systematic review and meta-analysis. BMC Public Health, 24(1), 297. https://doi.org/10.1186/s12889-024-17686-9
Banner, A.S. (1980) Alcohol and the lung. Chest, 77(4), 460–1. https://doi.org/10.1378/chest.77.4.460
Bertola, C., Gobbetti, C., Baccarini, G., & Fabiani, R. (2025). Wine Consumption and Lung Cancer Risk: A Systematic Review and Meta-Analysis. Nutrients, 17(8). https://doi.org/10.3390/nu17081322
Cohen, B.H., Celentano, D.D., Chase, G.A., et al. (1980) Alcohol consumption and airway obstruction. American Reviews on Respiratory Disease, 121(2):205–15. https://doi.org/10.1164/arrd.1980.121.2.205.
Emirgil, C., & Sobol, B.J. (1977) Pulmonary function in former alcoholics. Chest, 72(1):45–51. https://doi.org/10.1378/chest.72.1.45
Emirgil, C., Sobol, B.J., Heymann, B., & Shibutani, K. (1974) Pulmonary function in alcoholics. The American Journal of Medicine, 57(1), 69–77. https://doi.org/10.1016/0002-9343(74)90770-0.
Fehringer, G., Brenner, D. R., Zhang, Z. F., et al. (2017). Alcohol and lung cancer risk among never smokers: A pooled analysis from the International Lung Cancer Consortium and the SYNERGY study. International Journal of Cancer. https://doi.org/10.1002/ijc.30618
García-Lavandeira, J. A., Ruano-Ravina, A., & Barros-Dios, J. M. (2016). Alcohol consumption and lung cancer risk in never smokers. Gaceta Sanitaria, 30(4), 311–317. https://doi.org/10.1016/j.gaceta.2016.03.017
Garshick, E., Segal, M. R., Worobec, T. G., Salekin, C. M., & Miller, M. J. (1989). Alcohol consumption and chronic obstructive pulmonary disease. The American Review of Respiratory Disease, 140(2), 373–378. https://doi.org/10.1164/ajrccm/140.2.373
Hrubec, Z., Cederlof, R., Friberg, L., Horton, R., & Ozolins, G. (1973) Respiratory symptoms in twins: effects of residence-associated air pollution, tobacco and alcohol use, and other factors. Archives of Environmental Health, 27(3), 189–95. https://10.1080/00039896.1973.10666350
Kaluza, J., Harris, H. R., Linden, A., & Wolk, A. (2019). Alcohol consumption and risk of chronic obstructive pulmonary disease: A prospective cohort study of men. American Journal of Epidemiology, 188(5), 907–916. https://doi.org/10.1093/aje/kwz020
King, M. T., Nielsen, L. B., & Weinreich, U. M. (2025). Effects of alcohol consumption from early adolescence on lung function and development of COPD – a retrospective cohort study. European Clinical Respiratory Journal, 12(1), 2476232. https://doi.org/10.1080/20018525.2025.2476232
Lange, P., Groth, S., Mortensen, J., et al. (1988) Pulmonary function is influenced by heavy alcohol consumption. American Reviews of Respiratory Disease, 137(5), 1119–23. https://doi.org/10.1164/ajrccm/137.5.1119
Lebowitz, M.D. (1981) Respiratory symptoms and disease related to alcohol consumption. American Reviews of Respiratory Disease, 123(1), 16–9. https://doi.org/10.1164/arrd.1981.123.1.16.
Lyons, D.J., Howard, S.V., Milledge, J.S., & Peters, T.J. (1986) Contribution of ethanol and cigarette smoking to pulmonary dysfunction in chronic alcoholics. Thorax, 41(3), 197–202. https://doi.org/10.1136/thx.41.3.197
Murray, R.P., Connett, J.E., Tyas, S.L., et al. (2002) Alcohol volume, drinking pattern, and cardiovascular disease morbidity and mortality: is there a U-shaped function? American Journal of Epidemiology, 155(3), 242–48. https://doi.org/10.1093/aje/155.3.242.
Schünemann, H.J., Grant, B.J., Freudenheim, J.L., et al. (2002) Evidence for a positive association between pulmonary function and wine intake in a population-based study. Sleep Breath, 6(4), 161–73. https://doi.org/10.1007/s11325-002-0161-6.
Siedlinski, M., Boer, J. M. A., Smit, H. A., Postma, D. S., & Boezen, H. M. (2012). Dietary factors and lung function in the general population: wine and resveratrol intake. The European Respiratory Journal, 39(2), 385–391. https://doi.org/10.1183/09031936.00184110
Sisson, J.H. (2007) Alcohol and airways function in health and disease. Alcohol, 41(5), 293–307. https://doi.org/10.1016/j.alcohol.2007.06.003.
Sisson, J.H., Stoner, J.A., Romberger, D.J., et al. (2005) Alcohol intake is associated with altered pulmonary function. Alcohol, 36(1), 19–30. https://doi.org/10.1016/j.alcohol.2005.05.002
Siu, S.T., Udaltsova, N., Iribarren, C., & Klatsky, A.L. (2010) Alcohol and lung airways function. Permanente Journal, 14(1), 11-8. https://doi.org/10.7812/TPP/09-089.
Young, R. P., Hopkins, R. J., Christmas, T., Black, P. N., Metcalf, P., & Gamble, G. D. (2009). COPD prevalence is increased in lung cancer, independent of age, sex and smoking history. The European Respiratory Journal, 34(2), 380–386. https://doi.org/10.1183/09031936.00144208
Comments on this critique by the International Scientific Forum on Alcohol Research were provided by the following members:
Henk Hendriks, PhD, Netherlands
Creina Stockley, PhD, MBA, Independent consultant and Adjunct Senior Lecturer in the School of Agriculture, Food and Wine at the University of Adelaide, Australia
Richard Harding, PhD, Formerly Head of Consumer Choice, Food Standards and Special Projects Division, Food Standards Agency, UK
R. Curtis Ellison, MD, Section of Preventive Medicine/Epidemiology, Boston University School of Medicine, Boston, MA, USA
Erik Skovenborg, MD, specialized in family medicine, member of the Scandinavian Medical Alcohol Board, Aarhus, Denmark
Lynda H. Powell, MEd, PhD, Chair, Dept. of Preventive Medicine, Rush University Medical School, Chicago, IL, USA
[1] https://www.who.int/news/item/15-11-2023-smoking-is-the-leading-cause-of-chronic-obstructive-pulmonary-disease
Proudly powered by WordPress. Theme by Infigo Software.