CBD Oil Lungs


Buy CBD Oil Online

Effects of cannabis on lung function: a population-based cohort study The effects of cannabis on lung function remain unclear and may be different from those of tobacco. We compared the Studies report that the use of cannabidiol (CBD) can reduce the symptoms of COPD and improve breathing, such as shortness of breath. COPD makes it hard to breathe. Can CBD help people with this condition?

Effects of cannabis on lung function: a population-based cohort study

The effects of cannabis on lung function remain unclear and may be different from those of tobacco. We compared the associations between use of these substances and lung function in a population-based cohort (n = 1,037).

Cannabis and tobacco use were reported at ages 18, 21, 26 and 32 yrs. Spirometry, plethysmography and carbon monoxide transfer factor were measured at 32 yrs. Associations between lung function and exposure to each substance were adjusted for exposure to the other substance.

Cumulative cannabis use was associated with higher forced vital capacity, total lung capacity, functional residual capacity and residual volume. Cannabis was also associated with higher airway resistance but not with forced expiratory volume in 1 s, forced expiratory ratio or transfer factor. These findings were similar among those who did not smoke tobacco. In contrast, tobacco use was associated with lower forced expiratory volume in 1 s, lower forced expiratory ratio, lower transfer factor and higher static lung volumes, but not with airway resistance.

Cannabis appears to have different effects on lung function from those of tobacco. Cannabis use was associated with higher lung volumes, suggesting hyperinflation and increased large-airways resistance, but there was little evidence for airflow obstruction or impairment of gas transfer.

The pulmonary effects of smoking cannabis have not been extensively researched. In common with tobacco, smoking cannabis is associated with airway inflammation and symptoms of bronchitis, although the evidence that it causes airflow obstruction is not conclusive 1–5. Among the reasons for this continuing uncertainty are its illegal status, making it difficult to obtain reliable estimates of cannabis exposure, and the common practice of combining cannabis with tobacco, which makes it difficult to separate the effects of the two substances 6. Thus, although cannabis is widely used throughout the world, there is a paucity of information on its respiratory effects.

Apart from the respective psychoactive components of cannabinoids and nicotine, cannabis and tobacco smoke contain a similar mix of toxic and irritant chemicals 7. However, there are reasons to suspect that their effects on the respiratory system may not be the same. Cannabis smokers tend to smoke fewer cigarettes a day than tobacco smokers, but these tend to be packed more loosely and unfiltered. Differences in depth of inhalation, breath-hold time and leaving a shorter butt may increase the deposition of tar and carbon monoxide absorption from cannabis smoke 8–10. Several case reports of bullous lung disease in young cannabis smokers raise the possibility that cannabis (or the techniques used to smoke it) may have a greater effect on lung parenchyma than tobacco 11–13, although this association has been disputed 14. A recent report comparing smokers of cannabis and tobacco found that, although both cannabis and tobacco smokers had evidence of airflow obstruction on spirometry, cannabis was associated with more lung hyperinflation on lung volume measurement but a lower risk of emphysema on computed tomography (CT) scanning than tobacco 15. Although these findings do not support the suggestion that cannabis smokers are more susceptible to emphysema, they do indicate that cannabis and tobacco may have quite different effects on lung function.

We investigated the impact of cannabis and tobacco smoking on lung function in a population-based birth cohort followed to age 32 yrs.


Participants are members of the Dunedin Multidisciplinary Health and Development Study, a longitudinal study of the health and behaviour of a complete cohort of individuals born in Dunedin, New Zealand, in 1972 and 1973 16. A total of 1,037 individuals (52% male; 91% of eligible births) participated in the age 3 yrs assessment, forming the base sample for the study. Study members represent the full range of socioeconomic status in the general population of the South Island of New Zealand and are primarily of New Zealand/European ethnicity. The cohort has been assessed at ages 3, 5, 7, 9, 11, 13, 15, 18, 21, 26 and, most recently, at 32 yrs, when we assessed 972 participants (96% of the living cohort). The Otago Ethics Committee approved the study. Written informed consent was obtained for each assessment.

Cannabis smoking history was obtained at ages 18, 21, 26 and 32 yrs 17. At each assessment participants were asked how many times they had used marijuana in the previous year. Cumulative exposure to cannabis was calculated as the number of “joint-years” since age 17 yrs. These estimates assume that the number of times marijuana had been smoked in the previous year was representative of all years since the previous assessment. Where data were not collected at a particular assessment, the amount smoked reported at the next assessment was used to calculate cumulative exposure. 1 joint-yr is defined as the equivalent of one joint a day for 1 yr.

Cumulative tobacco exposure was calculated from the reported number of cigarettes smoked per day up to 18 yrs, 18–21 yrs, 21–26 yrs and 26–32 yrs. Where data were not collected for an assessment, the amount smoked reported at the next assessment was used to calculate cumulative exposure. One pack-year is defined as the equivalent of 20 cigarettes a day for 1 yr. Those who had smoked less than one cigarette a day for 1 yr, and fewer than 20 packets in their lifetime, were regarded as nonsmokers 18.

Spirometry has been measured at each assessment since age 9 yrs. At age 32 yrs a broad range of lung function tests, including spirometry, total lung capacity (TLC), functional residual capacity (FRC), residual volume (RV), airway resistance (Raw), specific airway conductance adjusted for thoracic gas volume (sGaw), transfer factor of the lung for carbon monoxide (TL,CO) and alveolar volume (VA) were measured using the plethysmograph and a Sensormedics Vmax 6200 module (Yorba Linda, CA, USA) 19–21. This system uses a heated wire mass flow sensor and methane dilution for measurement of alveolar volume and calculation of TL,CO. A portable spirometer (Spiropro, Sensormedics) was used to test study members (n = 27) who declined to sit in the plethysmograph or were unable to attend the research unit. Spirometry was repeated 10–15 min following inhalation of 200 μg salbutamol via a metered dose inhaler and volumatic spacer device (Allen and Hanburys, Stockley Park, UK). Study members were asked to refrain from use of their inhalers and not to smoke on the day of the assessment. All tests were reviewed by a senior technician to ensure that only acceptable and reproducible results were entered for analysis. Equipment was calibrated daily, and weekly quality control measures using biological controls were performed to ensure accuracy and precision of test equipment.

At age 32 yrs, haemoglobin was measured on a Sysmex XE2100 automated haematology analyser (Sysmex Corporation, Kobe, Japan). Exhaled carbon monoxide was measured before TL,CO measurement using a Micro CO monitor (Micromedical, Rochester, UK) and the average of two tests was recorded.

Height without shoes was measured at each age. Questions were asked about current and prior asthma and asthma symptoms using previously developed questionnaires 22. Current asthma is defined as a reported diagnosis of asthma with symptoms or medication use in the previous 12 months.

Statistical analysis

To assess whether pre-existing differences in lung function influenced the propensity to smoke, regression analyses of cumulative pack-years and joint-years to age 32 yrs were performed using spirometry at age 15 yrs (forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC) as the main predictor. These analyses adjusted for sex and height at age 15 yrs.

Initial analyses of sex–cannabis and sex–tobacco smoking interaction terms found no evidence that the effect of smoking either substance was different for males and females for any of the outcomes. The independent associations between lung function measurements at age 32 yrs and cannabis and tobacco smoking were assessed by linear regression using the measurement of lung function as the dependent variable and estimates of both cannabis and tobacco exposure as independent variables. Analyses included terms for height and sex to adjust for differences in predicted lung function, as recommended by Vollmer et al. 23 except for the FEV1/FVC ratio, which was adjusted for sex only. Analyses of TL,CO also adjusted for pre-test exhaled carbon monoxide and haemoglobin. Analyses of the association of cannabis with lung function were repeated after excluding those with any lifetime history of cigarette smoking.

To assess changes in lung function associated with tobacco and cannabis smoking, regression analyses were repeated for FEV1, FVC and the FEV1/FVC ratio using the estimates of both joint-years and pack-years as predictors with adjustment for the measurements obtained at age 15 yrs. These analyses also adjusted for sex, height at age 32 yrs, change in height between ages 15 and 32 yrs, and current asthma diagnosis.

Because pregnancy may affect lung function, pregnant females were excluded (n = 31). Visual inspection of the residuals from the regression analyses identified one clear outlier who was also excluded. Lung function measurements were approximately normally distributed, except for Raw and sGaw. Repeat analyses after log-transformations of these variables to approximate normal distributions provided similar results (not shown). Analyses were performed using Stata version 10 (StataCorp, College Station, TX, USA).

See also  Can I Mix CBD Oil With Melatonin


Reported cannabis and tobacco use at each age are summarised in the online supplementary material. The number of study members who reported using cannabis was higher at ages 21 and 26 yrs than at ages 18 or 32 yrs (table 1 ⇓ in the supplementary material). The number of tobacco smokers was similar at all ages, although the number of heavy smokers increased with age. Cumulative pack-years of tobacco smoking by age 32 yrs correlated with joint-years of cannabis (Spearman’s ρ = 0.49, p <0.0001) (table 1⇓ ). None of the measures of spirometric lung function (FEV1, FVC or FEV1/FVC) at age 15 yrs predicted subsequent pack-years of tobacco consumption or joint-years of cannabis use by age 32 yrs (all p-values ≥0.3).

Cumulative cannabis and tobacco use up to age 32 yrs

Mean values of lung function according to the categories of cannabis and tobacco use are shown in table 2 ⇓ in the online supplementary material. When analysed separately, cannabis and tobacco were both associated with a broad range of lung function measures (tables 3 ⇓ and 4 ⇓ in the supplementary material). However, when the effects of cannabis and tobacco were considered together (i.e. with simultaneous adjustment for exposure to the other substance), different patterns of effects were observed (table 2 ⇓ ). After adjusting for tobacco exposure, cannabis was associated with significantly higher FVC values but there was no significant association with FEV1 or FEV1/FVC ratios. In contrast, tobacco was associated with a nonsignificant trend to lower FEV1 values and significantly lower FEV1/FVC ratios, but there was no association with FVC. The findings for post-bronchodilator spirometry were similar, except that in this analysis the association between tobacco smoking and lower FEV1 values was significant (table 5 in the supplementary material). Both cannabis and tobacco were associated with higher values for TLC, FRC and RV, although the association between tobacco and TLC was of borderline statistical significance (table 2 ⇓ ). Cannabis was significantly associated with higher Raw and lower sGaw. Tobacco was not associated with differences in Raw but was associated with lower sGaw with borderline statistical significance. Cannabis use was not significantly associated with TL,CO, but because of higher values for VA, transfer factor per unit lung volume (TL,CO/VA) were lower. Tobacco was associated with lower total lung TL,CO and lower TL,CO/VA, but not with VA.

Associations of cannabis and tobacco use with lung function at age 32 yrs

Association of cannabis use with lung function at age 32 yrs amongst non-tobacco smokers

Longitudinal analyses of cannabis and tobacco exposure with spirometric lung function

Associations between cannabis exposure and lung function among non-tobacco smokers are shown in table 3 ⇑ . These show a similar pattern of findings to those shown in table 2 ⇑ . Cannabis use was associated with higher values for TLC and VA and with trends to higher values for FVC and RV. Cannabis use was not associated with FEV1, FEV1/FVC or TL,CO among these study members, but was associated with higher Raw and lower sGaw.

Associations between cumulative cannabis and tobacco smoking and spirometric lung function after adjustment for spirometry measurements at 15 yrs are shown in table 4 ⇑ . Cannabis use was significantly associated with higher values for FVC, but was not significantly associated with FEV1 or FEV1/FVC ratios. Tobacco smoking was significantly associated with lower FEV1 values and with lower FEV1/FVC ratios. The pattern of findings for cannabis was similar when tobacco smokers were excluded, except that the association between joint-years and FVC was of borderline statistical significance (table 6 in the supplementary material).


These findings indicate that cannabis is associated with changes in lung function that are independent of the effects of tobacco smoke and appear to be of a different pattern. Both substances were associated with higher values for static lung volumes, indicating a tendency toward hyperinflation and gas trapping, but although cannabis was associated with increased Raw, there was little evidence that it was associated with airflow obstruction (lower FEV1/FVC ratios) once tobacco consumption had been taken into account. Cannabis was also not associated with impairment of the TL,CO. By contrast, tobacco smoking was associated with both airflow obstruction and lower TL,CO but not with Raw.

Cannabis was consistently associated with higher lung volumes, whether measured as FVC by spirometry, static lung volumes (TLC, FRC and RV) by plethysmography or as VA by gas (methane) dilution. This consistency suggests that the findings are unlikely to be an artefact of measurement technique. Moreover, cannabis use was associated with higher values for FVC at age 32 yrs in the analyses that adjusted for FVC at age 15 yrs. It is notable that, although cannabis was not significantly associated with lower TL,CO, the higher values for VA meant that the transfer factor per unit of alveolar volume (TL,CO/VA) was lower in cannabis smokers. The clinical relevance of this is uncertain.

The pattern of lung function changes with cannabis is consistent with a recent report by Aldington et al. 15, who compared lung function tests and CT scan findings in a convenience sample of volunteers who were smokers of either cannabis, tobacco, both or neither. They found that cannabis was associated with hyperinflation on both lung function tests and CT scans but that there was little evidence of emphysema. Aldington et al. 15 also found that cannabis smokers had evidence of airflow obstruction measured by the FEV1/FVC ratio, although this was of marginal statistical significance and less obvious than in tobacco smokers. In our analysis, and in an earlier report from the Dunedin cohort (up to age 26 yrs), we also found an association between cannabis smoking and lower FEV1/FVC ratios, which was of borderline significance after adjusting for tobacco use 24. These findings are in keeping with those of a recent meta-analysis that found no consistent association between long-term cannabis use and airflow obstruction 5.

Our findings also confirm two previous reports of decreased sGaw in cannabis users and indicate that cannabis impacts on large airway function despite having little effect on the FEV1/FVC ratio 15, 25. This finding is not explained by the increase in lung volumes (and therefore the thoracic gas volume used to calculate sGaw) among cannabis smokers since cannabis was also associated with increased Raw without adjustment for lung volume. This observation is compatible with the high prevalence of bronchitic symptoms and evidence of bronchial epithelial injury among cannabis smokers 3, 4. Although increased Raw may plausibly contribute to hyperinflation, the increased Raw among cannabis users did not appear to explain the higher lung volumes: adjusting for Raw made no material difference to the association between cannabis and lung volumes (data not shown).

Considered separately, cannabis and tobacco smoking were associated with a broader range of lung function findings because most smokers used both substances (tables 3 ⇑ and 4 ⇑ in the supplementary material). One potential problem with the combined cannabis–tobacco analyses is whether the regression analyses adequately adjust for the confounding influence of tobacco smoking when assessing the associations with cannabis. The analyses were therefore repeated among those with no tobacco smoking history. Although these analyses also excluded most of the heavy users of cannabis and had smaller sample sizes, the pattern of findings was similar. Among non-tobacco smokers, cannabis was significantly associated with higher values for TLC, Raw and VA, lower values for sGaw, and with nonsignificant trends to higher values for FVC and RV. There was no significant association with the FEV1, FEV1/FVC ratio or TL,CO (table 4 ⇑ ).

Why smoking cannabis might have different effects on lung function from tobacco is unclear. We found that although both substances were associated with increased lung volumes, there was little evidence of airflow obstruction or reduced gas transfer with cannabis use. It is possible that the participants had simply not smoked enough cannabis for it to have a measurable effect on lung function, but this seems unlikely in view of the evidence for increased lung volumes and Raw. Apart from the active ingredients of cannabinoids and nicotine, the inhaled combustion products in cannabis and tobacco smoke are qualitatively similar 7, although cannabis smokers may inhale more tar per cigarette/joint 8–10. One possibility is that delta-9-tetrahydrocannibiol, which is known to act as a short-term bronchodilator 5, also has long-term biological effects. Another possibility is that differences are due to the technique of smoking cannabis. Cannabis smokers tend to inhale more deeply and hold their breath for longer than tobacco smokers 8. It is plausible that this alters the distribution of smoke throughout the lungs and thereby alters the associated physiological effects on lung function. Alternatively, it is possible that some of the findings are due to the repeated deep inhalation and breath-holding techniques themselves.

This study has a number of limitations. Cannabis use was reported for the previous year at the four assessments, rather than for all of the intervening years. Our joint-years variable assumes that the consumption of cannabis was similar for the intervening years. We do not know how much cannabis was used on each occasion or whether the cannabis joints were smoked directly or through a device such as a bong/water pipe. By comparison, tobacco smoking histories were taken for all years of the assessment period, cigarettes tend to vary less in tobacco content 15, and the practice of smoking tobacco through devices such as a bong is very unusual. Hence, the measure of cannabis exposure may be less accurate than that of tobacco, although this measurement error is unlikely to have biased the findings with respect to lung function. Errors in cannabis and tobacco consumption will also have occurred because if data were missing for an assessment, we used the amount reported at the next assessment for the calculation of joint- and pack-years. However, repeating the analysis after excluding those with missing data provided very similar findings. It is also possible that study members were less honest in reporting cannabis use than tobacco use, because it is an illegal substance. However, self-reports of cannabis use correlate well with biological markers of use 26, and our well-established record of confidentiality and nonintervention over 30 yrs of the lives of the study members tends to encourage frank reporting of these behaviours. We cannot rule out the possibility that some smokers mixed cannabis with tobacco in the same joint. Although this is not a common practice in New Zealand 15, any mixing of the two substances is most likely to have obscured the differences in the pattern of lung function changes between the two and is unlikely to explain our findings.

See also  CBD Oil Maine

The study also has a number of strengths. Both cannabis and tobacco smoking were assessed on a number of occasions throughout early adult life in a population-based cohort with minimal loss to follow-up. We have a comprehensive assessment of lung function at age 32 yrs and, although plethysmography was only performed at the most recent assessment, we have measurements of spirometry pre-dating the exposure to cannabis and tobacco to investigate whether baseline lung function influenced the propensity to smoke (e.g. a “healthy smoker” effect). This analysis provided no evidence for an association between spirometry at age 15 yrs and subsequent use of tobacco or cannabis.

In conclusion, cannabis and tobacco smoking are each associated with a distinct pattern of lung function changes in young adults. Cannabis was associated with evidence of hyperinflation and increased large airway resistance, with little evidence of airflow obstruction or impairment of gas transfer, whereas tobacco was associated with airflow obstruction, gas trapping and lower transfer factors. These findings suggest that smoking cannabis and tobacco have different physiological consequences for the lungs.

Support statement

This research was supported by UK Medical Research Council (London, UK) grants G0100527, G0601483, US National Institutes of Mental Health (Bethesda, MD, USA) grants MH45070 and MH49414, and the William T. Grant Foundation (New York, NY, USA). The Dunedin Multidisciplinary Health and Development Research Unit is funded by the Health Research Council of New Zealand (Auckland, New Zealand). M.R. Sears holds the AstraZeneca Chair in Respiratory Epidemiology at McMaster University (Hamilton, ON, Canada) and A. Caspi is a Royal Society-Wolfson Merit Award holder.

Statement of interest


We are grateful to the study members and their families and friends for their continued support. We also thank P.A. Silva, the study founder.


This article has supplementary material accessible from www.erj.ersjournals.com

For editorial comments see page 3.

  • Received April 19, 2009.
  • Accepted June 26, 2009.
  • © ERS Journals Ltd


Roth MD, Arora A, Barsky SH, et al. Airway inflammation in young marijuana and tobacco smokers. Am J Respir Crit Care Med 1998 ; 157 : 928 –937.

Fligiel SE, Roth MD, Kleerup EC, et al. Tracheobronchial histopathology in habitual smokers of cocaine, marijuana, and/or tobacco. Chest 1997 ; 112 : 319 –326.

Taylor DR, Poulton R, Moffitt TE, et al. The respiratory effects of cannabis dependence in young adults. Addiction 2000 ; 95 : 1669 –1677.

Tashkin DP, Baldwin GC, Sarafian T, et al. Respiratory and immunologic consequences of marijuana smoking. J Clin Pharmacol 2002 ; 42 : 71S –81S.

Tetrault JM, Crothers K, Moore BA, et al. Effects of marijuana smoking on pulmonary function and respiratory complications: a systematic review. Arch Intern Med 2007 ; 167 : 221 –228.

Hoffmann D, Brunnemann KD, Gori GB, et al. On the carcinogenicity of marijuana smoke. Recent Adv Phytochem 1975 ; 9 : 63 –81.

Wu TC, Tashkin DP, Djahed B, et al. Pulmonary hazards of smoking marijuana as compared with tobacco. N Engl J Med 1988 ; 318 : 347 –351.

Tashkin DP, Gliederer F, Rose J, et al. Tar, CO and Δ9THC delivery from the 1st and 2nd halves of a marijuana cigarette. Pharmacol Biochem Behav 1991 ; 40 : 657 –661.

Tashkin DP, Gliederer F, Rose J, et al. Effects of varying marijuana smoking profile on deposition of tar and absorption of CO and Δ-9-THC. Pharmacol Biochem Behav 1991 ; 40 : 651 –656.

Johnson MK, Smith RP, Morrison D, et al. Large lung bullae in marijuana smokers. Thorax 2000 ; 55 : 340 –342.

Beshay M, Kaiser H, Niedhart D, et al. Emphysema and secondary pneumothorax in young adults smoking cannabis. Eur J Cardiothorac Surg 2007 ; 32 : 834 –838.

Hii SW, Tam JD, Thompson BR, et al. Bullous lung disease due to marijuana. Respirology 2008 ; 13 : 122 –127.

Tan C, Hatam N, Treasure T. Bullous disease of the lung and cannabis smoking: insufficient evidence for a causative link. J R Soc Med 2006 ; 99 : 77 –80.

Aldington S, Williams M, Nowitz M, et al. The effects of cannabis on pulmonary structure, function and symptoms. Thorax 2007 ; 62 : 1058 –1063.

Hancox RJ, Poulton R, Greene JM, et al. Associations between birth weight, early childhood weight gain, and adult lung function. Thorax 2008 ; 64 : 228 –232.

Thomson WM, Poulton R, Broadbent JM, et al. Cannabis smoking and periodontal disease among young adults. JAMA 2008 ; 299 : 525 –531.

Ferris BG. Epidemiology Standardization Project (American Thoracic Society). Am Rev Respir Dis 1978 ; 118 : 1 –120.

American Thoracic Society: Standardization of Spirometry, 1994 Update. Am J Respir Crit Care Med 1995 ; 152 : 1107 –1136.

Coates AL, Peslin R, Rodenstein D, et al. Measurement of lung volumes by plethysmography. Eur Respir J 1997 ; 10 : 1415 –1427.

American Thoracic Society: Single-breath carbon monoxide diffusing capacity (transfer factor). Recommendations for a standard technique–1995 update. Am J Respir Crit Care Med 1995 ; 152 : 2185 –2198.

Sears MR, Greene JM, Willan AR, et al. A longitudinal, population-based, cohort study of childhood asthma followed to adulthood. N Engl J Med 2003 ; 349 : 1414 –1422.

Vollmer WM, Johnson LR, McCamant LE, et al. Methodologic issues in the analysis of lung function data. J Chronic Dis 1987 ; 40 : 1013 –1023.

Taylor DR, Fergusson DM, Milne BJ, et al. A longitudinal study of the effects of tobacco and cannabis exposure on lung function in young adults. Addiction 2002 ; 97 : 1055 –1061.

Tashkin DP, Coulson AH, Clark VA, et al. Respiratory symptoms and lung function in habitual heavy smokers of marijuana alone, smokers of marijuana and tobacco, smokers of tobacco alone, and nonsmokers. Am Rev Respir Dis 1987 ; 135 : 209 –216.

Martin GW, Wilkinson DA, Kapur BM. Validation of self-reported cannabis use by urine analysis. Addict Behav 1988 ; 13 : 147 –150.

Does CBD Help Shortness of Breath?

Studies report that the use of cannabidiol (CBD) can reduce the symptoms of COPD and improve breathing, such as shortness of breath.

A study based on the neurophysiology of dyspnea (difficulty breathing) and the location of cannabinoid receptors in the central nervous system (CNS) states that cannabinoids will alleviate the unpleasantness of breathlessness in people without causing respiratory depression.

Patients with chronic obstructive pulmonary disease (COPD) may need a long and gradual therapy depending on specific characteristics. During the early stages of COPD, many individuals utilize oxygen treatment to delay the disease’s progression. In more severe situations, surgical procedures, such as lung transplants, may be required.

Studies have reported that the use of cannabidiol (CBD) has reduced the symptoms of COPD and improved breathing. CBD has been examined for its anti-inflammatory properties and effectiveness as a bronchodilator (causes widening of airways for better breathing). Both outcomes suggest that CBD may help relieve some of the symptoms of COPD. More studies, however, are needed to support the effect of CBD on the shortness of breath.

2 health benefits of CBD

  1. Bronchodilation
    • Cannabidiol (CBD) has been found in several recent studies to have considerable bronchodilatory activities. According to scientists, CBD can widen the airways, decreasing resistance and increasing airflow into the lungs.
    • When researchers were looking for novel asthma medicines, they looked at these qualities. CBD’s bronchodilatory actions, however, may provide similar alleviation to those suffering from acute chronic obstructive pulmonary disease (COPD) symptoms.
    • CBD may help COPD patients avoid low levels of oxygen in the blood and shortness of breath by increasing airways. This, in turn, may decrease the progression of the disease and lessen the severity of its negative effects.
  2. Anti-inflammatory properties
    • Since 2009, medical experts have been investigating CBD’s powerful anti-inflammatory capabilities. In a 2014 study, CBD was shown to enhance lung function and decrease inflammation in animal studies.
    • According to the researchers in the 2014 study, the results reported that cannabidiol can become a viable therapeutic tool for the attenuation and treatment of inflammatory lung illnesses in the future, implying that CBD might be an effective therapy for COPD.

What is the impact of CBD in cannabis on asthma?

As previously stated, people with asthma should avoid inhaling cannabis by smoking or vaping.

Safety is vital and comes first for anybody who uses cannabis, especially those with chronic illnesses. Determine the safest technique of consuming cannabis, as well as the lowest feasible amount that gives the best relief, with the doctor.

See also  Can CBD Gummies Cause Diarrhea

Cannabis should be used carefully. If one feels too high, they should try sleeping it off or waiting it out. Do not overdo it. Although cannabis has medical use, it can have negative side effects.

Cannabis contains more tetrahydrocannabinol (THC) and fewer cannabidiols (CBD), whereas hemp contains more CBD and less THC. However, CBD in both works the same and has the same effects on the body.


What is CBD?

Cannabidiol (CBD) is one of the hundreds of molecules called cannabinoids present in the cannabis plant. It is now accessible in a broad range of products, including tincture drops, capsules, chocolates, pastries, and even coffee. CBD is available in liquid forms, which are warmed and inhaled using a specific apparatus (a process called “vaping”).

Marijuana and hemp are the same species of cannabis plants, but the Agriculture Improvement Act of 2018 has made hemp lawful on the federal level because it contains less than 0.3 percent tetrahydrocannabinol (THC), whereas marijuana contains more than 0.3 percent of THC. CBD can be extracted from hemp, which means its potential health advantages may now be researched more thoroughly.

CBD appears to offer a variety of therapeutic benefits according to research. Some supporters are now praising CBD’s ability to alleviate symptoms of chronic obstructive pulmonary disease (COPD), a disorder that damages the airways and makes it difficult to breathe regularly.

Because of the Agriculture Improvement Act of 2018, many CBD-containing products have emerged, and consumers may now take CBD in a variety of ways, such as:

COPD: Can CBD Help?

If you have COPD, you may have been asked a surprising suggestion recently: Have you considered CBD? CBD (short for cannabidiol) is a chemical found in marijuana and other forms of the cannabis plant that’s now available in a wide variety of products, including tincture drops, capsules, candy, cookies, and even coffee. CBD is also sold in liquids that are warmed and inhaled with a special device (known as “vaping”).

Research shows that CBD appears to have various medicinal properties. Now some proponents are touting CBD’s potential to ease symptoms of COPD, or chronic obstructive pulmonary disease, a condition that affects your airways, making it hard to breathe normally. Can CBD help you catch your breath? As products laced with this cannabis extract pop up in convenience stores and pharmacies in many states (though a few prohibit or place tight restrictions on sales of CBD), you might be tempted to give one a try. Here’s what you should know before you buy.

What Is CBD?

There are about 540 chemicals in cannabis, but the two you may have heard of are tetrahydrocannabinol (THC) and CBD, which are known as cannabinoids. THC is the stuff in pot that makes you feel “high.” CBD doesn’t have that effect and is generally considered safe.

You can also find CBD in hemp, a related cannabis plant that has very little THC. While you can buy marijuana legally in many states, the federal government still considers it an illicit drug. But CBD derived from hemp can be sold legally in most of the United States, with some exceptions. (Hemp seed oil is also available. It contains some CBD but little THC.)

The FDA has approved a prescription drug made with CBD, Epidiolex, to treat some forms of epilepsy and a condition called tuberous sclerosis complex, which causes growth of benign (noncancerous) tumors. But many people use CBD to self-treat a variety of conditions, including pain, insomnia, anxiety, and others. There isn’t much research on whether CBD helps with these health problems, though some evidence is beginning to build. For example, a handful of early studies in both animals and humans suggests that CBD could help ease anxiety, though more research is needed.

Does CBD Work for COPD?

Doctors don’t know if CBD can relieve symptoms of COPD or any other form of lung disease. “There’s not any research that says CBD is effective for COPD,” says April Hatch, a nurse at Cannabis Care Team in Kansas City, MO. She works with patients interested in cannabis-based therapies.

The belief that CBD might ease COPD symptoms may have sprung from research done decades ago, which showed that smoking pot actually relaxed the airways and improved breathing in healthy people and people with asthma. But that benefit was short-lived, and routine pot smoking is known to promote breathing problems, like coughing and wheezing.

Some lab studies have offered early signs that CBD could alter certain biological changes that cause COPD. With COPD. Your lungs become highly inflamed. The inflammation doesn’t go away and leads to irreversible blockages in your airways. CBD does seem to fight inflammation, at least in studies on animals. And a 2020 study in the Journal of Cannabis Research found that cannabis oil (which contained CBD and THC) appeared to act as an anti-inflammatory when exposed to human lung cells in a laboratory.

“The problem with these kinds of studies is that they only offer hints that CBD might help relieve breathing problems,” says pulmonologist Andrew Martin, MD, chair of pulmonary medicine at Deborah Heart and Lung Center in Browns Mills, NJ. Unfortunately, he says, some experimental medicines that look promising in the lab end up having no effect when given to real people.

And that’s just what seems to have happened when scientists have tested whether CBD improves breathing in people with and without COPD. In a 1984 study, large doses of CBD given to healthy men failed to relax and widen their airways. In a very small 2011 study that included just four people with COPD, treatment with a drug called Sativex, which has THC and CBD, didn’t improve scores on a test that measures breathing. Interestingly, though, after treatment with the medication, they reported being less out of breath.

In another small study from 2018, researchers had people with advanced COPD inhale vaporized cannabis to see if it gave them more lung power when pedaling exercise cycles. It didn’t help, though in fairness the strain of pot used in the study contained only a very small amount of CBD. Once again, the people who inhaled cannabis said they felt less anxious, though that came at a cost, since they also felt high.

If You Decide to Try CBD

If you’re still thinking of giving CBD a try for your COPD symptoms or any other reason, talk to your doctor first. You might be surprised by their response.

“I have no objections to the use of cannabinoids,” says Martin, who doesn’t think they’ll help, but probably won’t hurt — if you use the right products. “As a lung physician, I cannot recommend that you smoke cannabis to get your CBD,” he says. That includes inhaling cannabis or CBD oil with a vaping device, which he worries could be harmful to the lungs.

“If taking CBD makes you feel better and decreases your anxiety,” he says, “use the edible version.”

Hatch suggests you only buy CBD products from a retailer that can provide a document known as a certificate of analysis. This shows the product has been tested in a lab, is free of contaminants, and contains the amount of CBD listed on the label.

Chances are, your local convenience store can’t or won’t provide those documents, so if possible purchase CBD at a medical marijuana dispensary, Hatch says. Research shows that taking 10 milligrams three times a day is an appropriate starting dose, she says, adding that it may take weeks or even months to notice a benefit. If you feel CBD isn’t helping, ask your doctor what you can do to improve your symptoms.

Show Sources

Lung Health Institute: “Can CBD Cure My Lung Disease?”

Cannabis and Cannabinoid Research: “A Cross-Sectional Study of Cannabidiol Users,” “An Update on Safety and Side Effects of Cannabidiol: A Review of Clinical Data and Relevant Animal Studies.”

CDC: “What is COPD?”

National Center for Complementary and Integrative Health: “Cannabis (Marijuana) and Cannabinoids: What You Need To Know.”

ProCon.org: “States with Legal Cannabidiol (CBD).”

Iranian Journal of Psychiatry: “Chemistry, Metabolism, and Toxicology of Cannabis: Clinical Implications.”

Biomolecules: “Cannabidiol: A Potential New Alternative for the Treatment of Anxiety, Depression, and Psychotic Disorders.”

National Conference of State Legislatures: “State Medical Marijuana Laws.”

FDA: “FDA Regulation of Cannabis and Cannabis-Derived Products, Including Cannabidiol (CBD).”

Congressional Research Service: “Defining Hemp: A Fact Sheet.”

April Hatch, RN, Cannabis Care Team, Kansas City, MO.

Annals of American Thoracic Society: “Effect of Vaporized Cannabis on Exertional Breathlessness and

Exercise Endurance in Advanced Chronic Obstructive Pulmonary Disease.”

Archives of Internal Medicine: “Effects of Marijuana Smoking on Pulmonary Function and Respiratory Complications: A Systematic Review.”

Clinical And Translational Medicine: “Inflammation in chronic obstructive pulmonary disease and its role in cardiovascular disease and lung cancer.”

Cell Death & Disease: “Cannabidiol (CBD): a killer for inflammatory rheumatoid arthritis synovial fibroblasts.”

Journal of Cannabis Research: “ Effects of cannabis oil extract on immune response gene expression in human small airway epithelial cells (HSAEpC): implications for chronic obstructive pulmonary disease (COPD).”

Andrew Martin, MD, chair of pulmonary medicine, Deborah Heart and Lung Center, Browns Mills, NJ.

Chronic Respiratory Disease: “Cannabinoid effects on ventilation and breathlessness: A pilot study of efficacy and safety.”

How useful was this post?

Click on a star to rate it!

Average rating / 5. Vote count:

No votes so far! Be the first to rate this post.