Copd

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Chronic obstructive pulmonary disease, or COPD, describes a group of lung conditions that make it difficult to empty air out of the lungs because the airways have become narrowed.

See also Asthma

On this page:

What does COPD stand for?

Chronic= it’s a long-term condition and does not go away
Obstructive= your airways are narrowed, so it’s harder to breathe out quickly and air gets trapped in your chest
Pulmonary= it affects your lungs
Disease= it’s a medical condition Two of these lung conditions are long-term (or chronic) bronchitis and emphysema, which can often occur together.

  • Bronchitis means the airways are inflamed and narrowed. People with bronchitis often produce sputum, or phlegm.
  • Emphysema affects the tiny air sacs at the end of the airways in your lungs, where oxygen is taken up into your bloodstream. They break down and the lungs become baggy and full of bigger holes which trap air.

These conditions narrow the airways. This makes it harder to move air in and out as you breathe, and your lungs are less able to take in oxygen and get rid of carbon dioxide.


The airways are lined by muscle and elastic tissue. In a healthy lung, the springy tissue between the airways acts as packing and pulls on the airways to keep them open.


With COPD, the airways are narrowed because:

  • the lung tissue is damaged so there is less pull on the airways
  • mucus blocks part of the airway
  • the airway lining becomes inflamed and swollen

There aretreatmentsto help you breathe more easily and help you keep active, so it’s important to get an early diagnosis.

What causes COPD?COPD usually develops because of long-term damage to your lungs from breathing in a harmful substance, usually cigarette smoke, as well as smoke from other sources and air pollution. Jobs where people are exposed to dust, fumes and chemicals can also contribute to developing COPD.

You’re most likely to develop COPD if you’re over 35 and are, or have been, a smoker or had chest problems as a child.

Some people are more affected than others by breathing in noxious materials. COPD does seem to run in families, so if your parents had chest problems then your own risk is higher.

A rare genetic condition calledalpha-1-antitrypsin deficiencymakes people very susceptible to developing COPD at a young age.

What’s the difference between COPD and asthma?

With COPD, your airways have become narrowed permanently – inhaled medication can help to open them up to some extent. With asthma, the narrowing of your airways comes and goes, often when you’re exposed to a trigger – something that irritates your airways – such as dust, pollen or tobacco smoke. Inhaled medication can open your airways fully, prevent symptoms and relieve symptoms by relaxing your airways.So, if your breathlessness and other symptoms are much better on some days than others, or if you often wake up in the night feeling wheezy, it may be that you have asthma.Because the symptoms are similar and because people who have asthma as children can develop COPD in later life, it is sometimes difficult to distinguish the two conditions. Some people have both COPD and asthma.


What are the symptoms of COPD?

Symptoms include:

  • getting short of breath easily when you do everyday things such as going for a walk or doing housework
  • having a cough that lasts a long time
  • wheezing in cold weather
  • producing more sputum or phlegm than usual

You might get these symptoms all the time, or they might appear or get worse when you have an infection or breathe in smoke or fumes.

If you have COPD that has a severe impact on your breathing, you can lose your appetite, lose weight and find that your ankles swell.

Studies/papers

Health Outcomes

  • Twitter(X) thread explaining the study
  • "Conclusion: In conclusion, the present findings indicate that increased daily nicotine exposure (via inhalation) when accounting for exposure to non-nicotine constituents of tobacco smoke may increase heart rate but does not increase risk of COPD or CHD and does not appear to adversely impact lung function. We found that, aside from effects on heart rate (which were expected given our knowledge of effects of short-term nicotine use), there was no evidence to suggest that nicotine exposure is responsible for the detrimental effects of smoking on the outcomes that were included in this analysis. Although further research is necessary to explore other health outcomes and triangulate these findings, our results support existing evidence which suggests nicotine use is not a major risk factor in the development of smoking-related disease."
  • Compared with conventional cigarettes, HTPs and ECs offer substantial reduction in exposure to toxic chemicals and have the potential to reduce harm from cigarette smoke when used as tobacco cigarette substitutes. In this review, we examine the available clinical studies and population surveys on the respiratory health effects of ECs and HTPs in COPD patients.
  • As many COPD smokers prefer to smoke, conventional cigarette substitution should be considered as a valuable solution to the persistent problem of smoking, and combustion-free nicotine delivery technologies should be weight as a component of this strategy.
  • Our analysis of existing human studies on the respiratory health impact of ECs/HTPs substitution for COPD patients who smoke, fails to reach a clear conclusion because of the discordant findings and unreliable interpretations driven from surveys and clinical studies of modest quality.
  • This review article highlights the need for large, carefully designed, adequately controlled, long- term follow-up clinical trials to assess the true potential of combustion-free nicotine delivery technologies for sustained smoking cessation and reducing risk of harm from smoking, particularly among smokers with chronic obstructive pulmonary disease (COPD).
  • E-cigarettes and all use categories involving cigarettes were associated with higher COPD prevalence compared to never use, reflecting, in part, the high burden of cigarette exposure in these groups. Cigarette—but not exclusive e-cigarette—use was also strongly associated with higher COPD incidence. Compared to cigarette use, only quitting tobacco was protective against COPD development.
  • A harm reduction approach with the goal of achieving CC switching may be a more pragmatic approach, making EC use particularly appropriate with COPD. EC represent a potentially effective harm reduction tool that is safer than smoking CC [18, 23, 24]. Smokers with COPD, however, tend to be older and may have a higher level of addiction to nicotine than the average smoker and the feasibility and preliminary effectiveness of an EC harm-reduction strategy in a COPD population has not been explored.
  • Our study protocol has a few limitations. First, as a pilot study the protocol is not powered to detect small differences in CPD or CAT Scores between the NRT and EC arms. Second, CAT Score is not the gold standard for the assessment of respiratory health.
  • This study is the first to describe the long-term health effects of HTP use in COPD patients. Consistent improvements in respiratory symptoms, exercise tolerance, quality of life, and rate of disease exacerbations were observed in patients with COPD who abstained from smoking or substantially reduced their cigarette consumption by switching to HTP use.
  • Nearly 60% of COPD patients using HTPs abstained completely from cigarette smoking throughout the duration of the study, whereas those continuing to smoke (dual users) showed a consistent decline in their daily cigarette consumption from the baseline of at least 70% at all study visits.
  • The present study suggests that EC use may ameliorate objective and subjective COPD outcomes, and that the benefits gained appear to persist long term. EC use for abstinence and smoking reduction may ameliorate some of the harm resulting from tobacco smoking in COPD patients.
  • The present study suggests that EC use may ameliorate objective and subjective COPD outcomes and that the benefits gained may persist long-term. EC use may reverse some of the harm resulting from tobacco smoking in COPD patients.
  • The relationship between the identified RNA features and gene ontologies were mapped showing a strong association with stress response, xenobiotics metabolism, and COPD-related terms for 3R4F [combustible cigarette]. In contrast, fewer ontologies were found enriched for the THPs [heated tobacco product] aerosols. “Response to wounding” was a common COPD-related term over-represented for the two THPs but at a reduced significance. Quantification of a cytokine panel post-exposure confirmed a pro-inflammatory effect of cigarette smoke but not for THPs. In conclusion, THPs have a reduced impact on gene expression compared to 3R4F.
  • Report At A Glance: Comparisons of using e-cigarettes vs smoking:
    • There is conclusive evidence that completely substituting e-cigarettes for combustible tobacco cigarettes reduces users’ exposure to numerous toxicants and carcinogens present in combustible tobacco cigarettes.
    • There is substantial evidence that except for nicotine, under typical conditions of use, exposure to potentially toxic substances from e-cigarettes is significantly lower compared with combustible tobacco cigarettes.
    • There is substantial evidence that completely switching from regular use of combustible tobacco cigarettes to e-cigarettes results in reduced short-term adverse health outcomes in several organ systems.
    • There is moderate evidence that risk and severity of dependence are lower for e-cigarettes than combustible tobacco cigarettes.
    • There is moderate evidence from randomized controlled trials that e-cigarettes with nicotine are more effective than e-cigarettes without nicotine for smoking cessation.
    • While the overall evidence from observational trials is mixed, there is moderate evidence from observational studies that more frequent use of e-cigarettes is associated with an increased likelihood of cessation.
    • There is moderate evidence that second-hand exposure to nicotine and particulates is lower from e-cigarettes compared with combustible tobacco cigarettes.
    • There is limited evidence for improvement in lung function and respiratory symptoms among adult smokers with asthma who switch to e-cigarettes completely or in part (dual use).
    • There is limited evidence for reduction of chronic obstructive pulmonary disease (COPD) exacerbations among adult smokers with COPD who switch to e-cigarettes completely or in part (dual use).
    • There is limited evidence suggesting that switching to e-cigarettes will improve periodontal disease in smokers.
  • Although ECs are not risk free, they are much less harmful than conventional tobacco smoking. The emerging clinical evidence suggests that ECs are unlikely to raise significant health concerns for the respiratory tract under normal conditions of use, even in smokers with preexisting lung disease. In particular, recent studies in COPD and chronic asthma suggest that substitution of conventional tobacco cigarettes for ECs can ameliorate subjective and objective disease-related outcomes and exacerbation rates as well as improving success in abstaining from smoking long term.
  • Conclusion: “These findings suggest that ECs use may aid smokers with COPD reduce their cigarette consumption or remain abstinent, which results in marked improvements in annual exacerbation rate as well as subjective and objective COPD outcomes.”

Misperceptions/Misinformation

  • Search this page for COPD

Studies with comments or retracted studies

  • One of the studies used in the meta-analysis has been retracted.
  • "The study provides zero evidence on any risk associated with e-cigarette use, whether absolute risk or in comparison with smoking. The question that was supposed to be addressed in this metanalysis CANNOT be examined with the studies included in their analysis." (Farsalinos)
  • See Also: "The methods look impressive, but the devil is in the dirty details buried in the nearly 100 pages supplemental material. The authors have done an admirable job collecting studies and organizing them, but the conclusions reached are untenable, and unsupportable at least for now." (Cummings)
  • Inaccurate and misleading meta-analysis of E-cigarettes and population-based diseases: "We demonstrate that the meta-analysis by Glantz et al. had three principal deficits that were avoidable: (1) mixing unjustified and incomprehensible disease outcomes, such as erectile dysfunction with fatal CVDs and influenza with COPD; (2) using survey datasets containing no temporal information about smoking/vaping initiation and disease diagnosis; (3) using longitudinal studies that didn’t account for changes in vaping and smoking during follow-up waves. The meta-analysis by Glantz et al. is misleading and inaccurate. The deficits are only apparent to investigators thoroughly experienced with the data from the source studies. We conclude that Glantz et al. failed to meet basic criteria for the quality of source studies; the results of their meta-analysis are invalid." (Rodu, Plurphanswat, and Rodu)
  • Comparing smoking-related disease rates from e-cigarette use with those from tobacco cigarette use: a reanalysis of a recently-published study: "The claim in the original meta-analysis that the studies had a low risk of bias is demonstrably incorrect, and even the biased data suggests that switching to e-cigarettes may reduce disease risk similarly to quitting. Biases may also explain the somewhat higher risk observed in those who smoked and vaped than in those smoking exclusively. Very limited unbiased data found no significant effect of vaping on the diseases considered. Though more good studies are urgently needed, the conclusions of Glantz et al. are not supported by the currently available evidence." (Lee, Farsalinos)
  • Observational studies of exposure to tobacco and nicotine products: Best practices for maximizing statistical precision and accuracy: The case study discussed below (Glantz et al., 2024) includes two cautionary examples which selected case-control designs and subsequently reported that CC use was not associated with increased risk of cardiovascular harm (with former CC use being associated with reduced risk in one study). In other words, they attributed the entirety of risk associated with tobacco product use to EC use. (Cohen, Cook)
  • When meta-analysis misleads: the need for methodological integrity in e-cigarette research: Together, these findings suggest that many of the alarming conclusions drawn were overstated. This is especially true when the analyses fail to disentangle the effects of vaping from those of smoking, a mistake that continues to plague much of the current literature. (Polosa, Geraci, Adebisi)
  • The Updated Meta-Analysis of E-Cigs & Health Outcomes: Still Critically Flawed: A highly-criticized meta-analysis of e-cigs &health outcomes was just updated. Not only does it still perpetuate critical flaws in the underlying studies, but it's interpreted with double-standards. (Selya)
    • Referring to: Glantz SA, Nguyen N, Oliveira da Silva AL. Population-Based Disease Odds for E-Cigarettes and Dual Use versus Cigarettes. NEJM Evid. 2024 Mar;3(3):EVIDoa2300229. Epub 2024 Feb 27. PMID: 38411454. doi: 10.1056/EVIDoa2300229
  • "The study by Osei et al. is deficient and unreliable, because it used the Behavioral Risk Factor Surveillance Survey, which contains no information about when participants started to smoke or vape, or when they were diagnosed with chronic obstructive pulmonary disease (COPD)." (Rodu)
  • Referring to: Osei, A. D., Mirbolouk, M., Orimoloye, O. A., Dzaye, O., Uddin, S. M. I., Benjamin, E. J., Hall, M.E., DeFilippis, A.P., Bhatnagar, A., Biswal, S.S., Blaha, M. J. (2020). Association Between E-Cigarette Use and Chronic Obstructive Pulmonary Disease by Smoking Status: Behavioral Risk Factor Surveillance System 2016 and 2017. American Journal of Preventive Medicine. https://doi.org/10.1016/j.amepre.2019.10.014
  • "The study by Wills et al. is deficient and unreliable, because it used the Behavioral Risk Factor Surveillance Survey, which contains no information about when participants started to smoke or vape, or when they were diagnosed with chronic obstructive pulmonary disease (COPD)." (Rodu)
  • Referring to: Wills TA, Choi K, Pokhrel P, Pagano I. Tests for confounding with cigarette smoking in the association of E-cigarette use with respiratory disorder: 2020 National-Sample Data. Prev Med. 2022 Aug;161:107137. doi: 10.1016/j.ypmed.2022.107137. Epub 2022 Jul 9. PMID: 35820496; PMCID: PMC9328844.
  • "The problem is that vegetable glycerin (glycerol) is not a lipid it is an alcohol. It cannot cause the lipoid pneumonia symptoms mentioned." (Bates)
  • "Endogenous lipoid pneumonia from VG (or PG) inhalation is a speculation and implausible...The experience in the US over the past several months clearly shows that the culprit for the acute lung intoxication cases are black market THC oils which were sold as THC oils, not e-cigarette products." (Farsalinos)
  • "visual assessment of lung HRCT scans showed no pathological findings in people vaping daily for more than 3.5 years. In particular, no CT features compatible with early signs of COPD (i.e. parenchymal micronodules, ground-glass opacity, or macroscopic emphysema) or lipoid pneumonia or popcorn lung disease were present." (Polosa)
  • Referring to: Eissenberg T, Maziak W. Are Electronic Cigarette Users at Risk for Lipid-mediated Lung Injury? Am J Respir Crit Care Med. 2020 Apr 15;201(8):1012-1013. doi: 10.1164/rccm.201910-2082LE. PMID: 31917600; PMCID: PMC7159422.
  • Prof John Britton, Director of the UK Centre for Tobacco & Alcohol Studies and Consultant in Respiratory Medicine, University of Nottingham, said:
    • “This paper provides an unsystematic overview on evidence relating to the likely relative risks of nicotine use, and of questionable reliability: for example, that e-cigarette use increases the risk of chronic obstructive pulmonary disease by 194% but COPD is a disease with a lead time of decades, so to attribute a risk directly to e-cigarettes – which have been widely used for less than a decade and are almost exclusively used by former smokers – is inappropriate.”
  • Multiple Comments:
    • "One of the essential criteria of causal inference is that exposure to the cause precedes disease onset. Three of the diseases Glantz studies — COPD, chronic bronchitis and emphysema — take decades to become clinically apparent and would have been present, even though undiagnosed, in many of his cases long before his study began in 2014, and indeed even before e-cigarettes first became available in the US in about 2007. His findings are also flawed by the fact that most vapers have smoked, and since smoking is a strong cause of chronic lung disease, vapers inevitably carry an increased risk of lung disease long after quitting smoking. Glantz claims to have allowed for this statistically but his approach is simplistic: he lacks the detail of lifetime duration and intensity of smoking required. On these grounds alone his conclusion is specious." (Britton)
    • "Donald Kenkel and colleagues at Cornell University conducted a replication of the analysis using econometric techniques...When we use a more flexible empirical specification, among respondents who had never smoked combustible tobacco, we find no evidence that current or former e-cigarette use is associated with respiratory disease. The statistical associations between e-cigarette use and respiratory disease are driven by e-cigarette users who are also current or former smokers of combustible tobacco. A striking feature of the data is that almost all e-cigarette users were either current or former smokers of combustible tobacco." (Bates)
  • Referring to: Bhatta DN, Glantz SA. Association of E-Cigarette Use With Respiratory Disease Among Adults: A Longitudinal Analysis. Am J Prev Med. 2020 Feb;58(2):182-190. doi: 10.1016/j.amepre.2019.07.028. Epub 2019 Dec 16. PMID: 31859175; PMCID: PMC6981012.
  • "​It is literally true that they "find no evidence...", but that is because this study is completely ill-suited to drawing any policy conclusions about e-cigarettes and COPD. Despite hinting at the limitations of cross-sectional data, the authors draw a negative-sounding conclusion without addressing the key question of how respiratory health changes for a given smoker who uses e-cigarettes to quit or cut down once they are ill from smoking or as a way of preventing COPD." (Bates)
  • Referring to: Bowler RP, Hansel NN, Jacobson S, Graham Barr R, Make BJ, Han MK, O'Neal WK, Oelsner EC, Casaburi R, Barjaktarevic I, Cooper C, Foreman M, Wise RA, DeMeo DL, Silverman EK, Bailey W, Harrington KF, Woodruff PG, Drummond MB; for COPDGene and SPIROMICS Investigators. Electronic Cigarette Use in US Adults at Risk for or with COPD: Analysis from Two Observational Cohorts. J Gen Intern Med. 2017 Dec;32(12):1315-1322. doi: 10.1007/s11606-017-4150-7. Epub 2017 Sep 7. PMID: 28884423; PMCID: PMC5698219.
  • "The mice were severely overdosed with nicotine, up to the lethal levels for mice, and a huge amount above what any human vaper would get...Regarding the relevance to human health, nicotine poisoning poses normally no risk to vapers or smokers because if nicotine concentrations start to rise above their usual moderate levels, there is an advance warning in the form of nausea which makes people stop nicotine intake long before any dangerous levels can accrue. (Mice in these types of experiments do not have that option)." (Hajek)
  • Referring to: Garcia-Arcos I, Geraghty P, Baumlin N, Campos M, Dabo AJ, Jundi B, Cummins N, Eden E, Grosche A, Salathe M, Foronjy R. Chronic electronic cigarette exposure in mice induces features of COPD in a nicotine-dependent manner. Thorax. 2016 Dec;71(12):1119-1129. doi: 10.1136/thoraxjnl-2015-208039. Epub 2016 Aug 24. PMID: 27558745; PMCID: PMC5136722.

Articles, Blogs, Op-eds, Press Releases, Videos, Podcasts, etc

  • Filter Magazine
  • This sharing of lived experience demonstrates how people who smoke are stigmatized by the healthcare system.
  • Filter Magazine
  • "Women who smoke are also more likely than men to develop severe COPD at younger ages. Each year, more women than men die from COPD. Women over the age of 35 who smoke now have a greater risk of dying from heart disease compared to men."
  • MedicalXpress
  • "The study, conducted by a team of researchers led by Nathan Harrison, a behavioral scientist and Ph.D. student from Flinders University, in Australia, aimed to identify and synthesize existing interventions to combat stigma associated with lung cancer and smoking-related respiratory diseases, including chronic obstructive pulmonary disease (COPD)."

External Links

Rise and Vape Podcast double issue on Asthma and COPD

Episode 1 Asthma


Episode 2 COPD