Environmental exposures are the leading causes of respiratory disease worldwide. Exposures to tobacco smoke and household air pollution consistently rank among the top risk factors not only for respiratory disease burden but also for the global burden of disease (Lim et al., 2012). Less is known, however, about the attributable effects of cannabis use on respiratory disease despite shared similarities with that of cigarette use and the fact that cannabis is the most commonly used inhaled drug in the United States after tobacco, with an estimated 22.2 million people ages 12 years and older reporting current use (CBHSQ, 2015). Moreover, it is estimated that more than 40 percent of current users smoke cannabis on a daily or near daily basis (Douglas et al., 2015). Given the known relationships between tobacco smoking and multiple respiratory conditions, one could hypothesize that long-term cannabis smoking leads to similar deleterious effects on respiratory health, and some investigators argue that cannabis smoking may be even more harmful than that of tobacco smoking. Indeed, data collected from 15 volunteers suggest that smoking one cannabis joint can lead to four times the exposure to carbon monoxide and three to five times more tar deposition than smoking a single cigarette (Wu et al., 1988). This may be, in part, because cannabis smokers generally inhale more deeply and hold their breath for longer than do cigarette smokers (Wu et al., 1988) and because cannabis cigarettes do not commonly have filters as tobacco cigarettes often do. On the other hand, cannabis cigarettes are not as densely packed as tobacco cigarettes (Aldington et al., 2008), and cannabis users usually smoke fewer cannabis cigarettes per day than tobacco users smoke tobacco cigarettes per day. CBG is extremely effective against the symptoms of Bronchitis due to its anti-inflammatory and analgesic properties.Use CBG Oil for Bronchitis The bronchodilating activity of oral cannabinoids was evaluated in three double-blind experiments that involved the study of dose-response and interactive relationships and the potential development of tolerance. Data indicated that delta 8-tetrahydrocannabinol (delta 8-THC), cannabinol (CBN), and c …
NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.
National Academies of Sciences, Engineering, and Medicine; Health and Medicine Division; Board on Population Health and Public Health Practice; Committee on the Health Effects of Marijuana: An Evidence Review and Research Agenda. The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research. Washington (DC): National Academies Press (US); 2017 Jan 12.
The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research.
National Academies of Sciences, Engineering, and Medicine; Health and Medicine Division; Board on Population Health and Public Health Practice; Committee on the Health Effects of Marijuana: An Evidence Review and Research Agenda.
7 Respiratory Disease
It is unclear whether cannabis use is associated with chronic obstructive pulmonary disorder, asthma, or worsened lung function.
Environmental exposures are the leading causes of respiratory disease worldwide. Exposures to tobacco smoke and household air pollution consistently rank among the top risk factors not only for respiratory disease burden but also for the global burden of disease (Lim et al., 2012). Less is known, however, about the attributable effects of cannabis use on respiratory disease despite shared similarities with that of cigarette use and the fact that cannabis is the most commonly used inhaled drug in the United States after tobacco, with an estimated 22.2 million people ages 12 years and older reporting current use (CBHSQ, 2015). Moreover, it is estimated that more than 40 percent of current users smoke cannabis on a daily or near daily basis (Douglas et al., 2015). Given the known relationships between tobacco smoking and multiple respiratory conditions, one could hypothesize that long-term cannabis smoking leads to similar deleterious effects on respiratory health, and some investigators argue that cannabis smoking may be even more harmful than that of tobacco smoking. Indeed, data collected from 15 volunteers suggest that smoking one cannabis joint can lead to four times the exposure to carbon monoxide and three to five times more tar deposition than smoking a single cigarette (Wu et al., 1988). This may be, in part, because cannabis smokers generally inhale more deeply and hold their breath for longer than do cigarette smokers (Wu et al., 1988) and because cannabis cigarettes do not commonly have filters as tobacco cigarettes often do. On the other hand, cannabis cigarettes are not as densely packed as tobacco cigarettes (Aldington et al., 2008), and cannabis users usually smoke fewer cannabis cigarettes per day than tobacco users smoke tobacco cigarettes per day.
The committee responsible for the 1999 Institute of Medicine (IOM) report Marijuana and Medicine: Assessing the Science Base (IOM, 1999, p. 6) concluded that cannabis smoking was an important risk factor in the development of respiratory disease and recommended that “studies to define the individual health risks of smoking marijuana should be conducted, particularly among populations in which marijuana use is prevalent.” The literature search conducted by the current committee did not identify any fair- or good-quality systematic reviews for cannabis use and respiratory disease published since 2011 (the cutoff established by the current committee); however, the committee identified—and elected to include—a systematic review by Tetrault et al. (2007) that provides a detailed synthesis of the available literature through 2005. A review by Tashkin (2013) and a position statement by Douglas et al. (2015), which summarized current evidence of the link between cannabis smoking and respiratory disease, were also considered by the committee. Fourteen primary articles published since 1999 that were not included in the systematic review from Tetrault et al. (2007) provided additional evidence on the association between smoking cannabis and respiratory diseases (Aldington et al., 2007; Bechtold et al., 2015; Hancox et al., 2010, 2015; Kempker et al., 2015; Macleod et al., 2015; Papatheodorou et al., 2016; Pletcher et al., 2012; Tan et al., 2009; Tashkin et al., 2012; Van Dam and Earleywine, 2010; Walden and Earleywine, 2008; Weekes et al., 2011; Yadavilli et al., 2014).
Pulmonary function refers to lung size and function. Common measures of pulmonary function include forced expiratory volumes, lung volumes, airways resistance and conductance, and the diffusion capacity of the lung for carbon monoxide (DLCO). Spirometry values include the measurements of forced expiratory volumes, including forced expiratory volume at 1 second (FEV1), forced vital capacity (FVC), and FEV1/FVC. The latter is a measure of airflow obstruction and, when combined with bronchodilator therapy, is used in the diagnosis of chronic obstructive pulmonary disorder (COPD).
Is There an Association Between Cannabis Use and Pulmonary Function?
Tetrault et al. (2007) systematically reviewed the evidence found in 34 publications, of which 12 reported on the effects of airway response and 14 reported on the effects of pulmonary function. The authors found that short-term exposure to cannabis smoking resulted in bronchodilation. Specifically, acute cannabis smoking was consistently associated with improvements in specific airway conductance, peak flow measurements, and FEV1, as well as reversed bronchospasm from challenges by either methacholine or exercise. Any short-term benefits, however, were offset by the effects of long-term cannabis smoking. Specifically, regular cannabis smoking was associated with a lower specific airway conductance on average by 16 percent and also with a lower FEV1. There was also a dose–response effect between average daily quantity of cannabis and a lower specific airway conductance. However, the clinical significance of the association between regular cannabis smoking and a lower specific airways conductance is not known. Other studies that examined the association between long-term cannabis smoke exposure and pulmonary function have inconsistently found lower or no change in FEV1, FVC, FEV1/FVC, DLCO, and airway hyperresponsiveness (Tetrault et al., 2007).
Aldington et al. (2007) examined the cross-sectional relationship between long-term cannabis smoking and pulmonary function in a convenience sample of 339 participants in the Wellington Research Study. The inclusion criteria for cannabis and tobacco smokers were a lifetime exposure of at least 5 joint-years of cannabis (defined as smoking 1 joint per day for 1 year) or at least 1 pack-year of tobacco, respectively. Cannabis smoking was based on self-report. The researchers did not find an association between long-term cannabis smoking and pulmonary function variables. However, when cannabis smoking was analyzed in terms of joint-years, Aldington et al. (2007) found a significantly lower FEV1/FVC, lower specific airways conductance, and a higher total lung capacity per joint-year smoked in cannabis smokers compared to nonsmokers. Based on their analyses, the authors estimated that the negative association between each cannabis joint and a lower FEV1/FVC was similar to that of 2.5 to 5 tobacco cigarettes. The committee identified a couple of problems with the analyses and the presentation of the results in the paper by Aldington et al. (2007). First, the authors reported main effects only from their analysis of covariance. A more conservative analysis would have considered the examination of interaction effects between cannabis smoke (or joint-years) and tobacco smoke (or pack-years) in a regression model to better dissect the contribution of cannabis smoke (or joint-years) versus tobacco smoke (or pack-years). Second, the authors incorrectly labeled the association with continuous measures of pulmonary function with cannabis smoke (or joint-years) as odds ratios (ORs) in tables 3 and 4; however, their methods correctly state that a multivariable analysis of covariance methods was used for continuous data.
Papatheodorou et al. (2016) analyzed cross-sectional data from 10,327 adults who participated in the National Health and Nutrition Examination Survey (NHANES) between 2007 and 2012. Cannabis smoking was based on self-report, but the researchers could not quantify joint-years. Cannabis smokers were categorized as never smokers (n = 4,794), past cannabis smokers (n = 4,084), cannabis smokers in the past 5–30 days (n = 555), and cannabis smokers in the past 0–4 days (n = 891). Current cannabis smokers were heavier tobacco smokers than were past and never smokers of cannabis, as measured by mean pack-years. In multivariable analyses, the investigators found that current smokers had a smaller FEV1/FVC than never smokers (−0.01 and −0.02, respectively), and they observed moderate to large increases in FEV1 (49 mL and 89 mL, respectively) and FVC (159 mL and 204 mL, respectively) when comparing current smokers to never smokers. There was also an important decrease in exhaled nitric oxide among current smokers when compared to never smokers (−7 percent versus −14 percent), but it is unclear if this effect was confounded by the high prevalence of tobacco smoking in current cannabis users or if it represented a true decrease in exhaled nitric oxide due to cannabis smoking. The study by Papatheodorou et al. (2016) has some shortcomings. First, the researchers’ analyses were based on cross-sectional data. Second, cannabis use was obtained by self-report and there may have been a bias of underreporting. Finally, there was a lack of data on the method of smoke inhalation and the frequency of cannabis smoking, thus not allowing for an analysis of the relationship between the frequency of cannabis use and pulmonary function.
Pletcher et al. (2012) analyzed longitudinal data from 5,115 adults in the Coronary Artery Risk Development in Young Adults (CARDIA) study and concluded that occasional and low cumulative cannabis smoking was not associated with adverse effects on pulmonary function. The investigators noted that there was a trend toward decreases in FEV1 over 20 years only in the heaviest cannabis smokers (≥20 joint-years). Similar to the findings of Papatheodorou et al. (2016), CARDIA investigators found a higher-than-expected FVC among all categories of cannabis smoking intensity. Despite the large sample size, the study by Pletcher et al. (2012) had a small number of heavy cannabis smokers. Other limitations include the risk of bias due to the self-reporting of cannabis use, a lack of data on the method of cannabis smoke inhalation, and bias due to unmeasured confounders as cannabis smoking was not the main objective of this study.
The study by Hancox et al. (2010) analyzed data of a cohort of 1,037 adult participants in Dunedin, New Zealand, followed longitudinally since childhood and asked about cannabis and tobacco use at ages 18, 21, 26, and 32 years. Cumulative exposure to cannabis was quantified as joint-years since age 17 years. Spirometry was conducted at 32 years. Cumulative cannabis use was associated with higher FVC, total lung capacity, and functional residual capacity and residual volume, but not with lower FEV1 or FEV1/FVC.
A small feasibility study by Van Dam and Earleywine (2010) found that the use of a cannabis vaporizer instead of smoking cannabis in 12 adult participants who did not develop a respiratory illness was associated with improvements in forced expiratory volumes at approximately 1 month after the introduction of the vaporizer; however, this study did not have a control group.
Discussion of Findings
Overall, acute cannabis smoking was associated with bronchodilation, but many of the authors agreed that any benefits may be offset when cannabis is smoked regularly. The current findings are inconclusive on a variety of pulmonary function measurements, and the findings may be affected by the quality of the studies, a failure to adjust for important confounders, including tobacco and other inhaled drugs, and other occupational and environmental exposures. The committee’s findings are consistent with those reported in another recent review (Tashkin, 2013) and a position statement (Douglas et al., 2015).
The majority of studies, including those evaluated in the systematic review, relied on self-report for cannabis smoking. Many studies failed to control for tobacco smoking and occupational and other environmental exposures; did not control for the dose or duration of cannabis smoking; and did not use joint-years and instead based heavy cannabis smoking on having exceeded a specific threshold of joints. Even among studies that used joint-years, it is unclear how generalizable their findings are, given the potential high variability in lung-toxic content from joint to joint. Prior studies have inconsistently documented decreases or no change in FEV1, FEV1/FVC, DLCO, and airway hyperresponsiveness. Moreover, neither the mechanism nor the clinical significance of the association between cannabis smoking and pulmonary function deficits is known beyond the possible impact of a high FVC in lowering the FEV1/FVC ratio. While elevated lung volumes could be indicators of lung pathology, an elevated FVC by itself has not been associated with any lung pathology.
7-1(a) There is moderate evidence of a statistical association between cannabis smoking and improved airway dynamics with acute use, but not with chronic use.
7-1(b) There is moderate evidence of a statistical association between cannabis smoking and higher forced vital capacity (FVC).
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
COPD is a clinical syndrome that consists of lower airway inflammation and damage that impairs airflow. Ranked as the fourth-leading cause of death worldwide by the World Health Organization, COPD has been estimated to cause more than 3 million deaths worldwide annually and has an estimated global prevalence of 10 percent in adults (Buist et al., 2007; Diaz-Guzman and Mannino, 2014). COPD is diagnosed with spirometry and is defined by a post-bronchodilator forced expiratory volume at 1 second divided by forced vital capacity (FEV1/FVC) 1/FVC below the 5th percentile of a reference population (lower limit of normal). The committee responsible for Marijuana and Medicine: Assessing the Science Base (IOM, 1999) suspected, but did not conclude, that chronic cannabis smoking causes COPD.
Is There an Association Between Cannabis Use and COPD?
There is no discussion about the association between cannabis and COPD in the systematic review by Tetrault et al. (2007). In the position statement of the American Thoracic Society (Douglas et al., 2015), workshop members concluded that there was minimal impairment in occasional cannabis smokers when controlling for tobacco use. In contrast, there was a trend toward higher prevalence in heavier users based on studies of lung function decline (Pletcher et al., 2012; Tashkin et al., 1987); however, workshop members determined that this association was incompletely quantified.
The study by Aldington et al. (2007) examined high-resolution computed tomography scans among the subgroups of participants with cannabis smoking only, cannabis and tobacco smoking, tobacco smoking only, and never smokers. They found inconsistent results: a decreased mean lung density, which is suggestive of emphysematous changes (mean percent of area below −950 Hounsfield units in three slices at 2.4 percent [95% confidence interval (CI) = 1.0%–3.8%] for cannabis smokers, but −0.6 percent [−2.0%–0.8%] for tobacco smokers when compared to nonsmokers), but almost no evidence of macroscopic emphysema (1.3% versus 16.5% versus 18.5% versus 0% in cannabis-only smokers versus cannabis and tobacco smokers versus tobacco-only smokers versus non-smokers, respectively).
Tan et al. (2009) analyzed cross-sectional data collected in 878 adults ages 40 years and older from Vancouver, Canada, who participated in the Burden of Obstructive Lung Disease study on COPD prevalence. Current smoking of either tobacco or cannabis was defined as any smoking within the past year. Participants who had smoked at least 50 marijuana cigarettes but had no history of tobacco smoking were not at significantly greater risk of having COPD or more respiratory symptoms. There was inconsistent evidence for whether synergy from combined cannabis and tobacco smoking might affect the odds of having COPD or worse respiratory symptoms.
Specifically, the mean estimates for the tobacco and cannabis smoking versus tobacco-only smoking groups do not appear to be different, and the 95% CI for the tobacco and cannabis smoking group appears to overlap significantly with the tobacco-only smoking groups when evaluating either COPD or respiratory symptoms as the outcome.
Yadavilli et al. (2014) examined data from 709 participants over a 33-month period for hospital readmissions of COPD in illicit drug users and tobacco smokers. These investigators found that cannabis users had similar readmission rates to ex-tobacco or current tobacco users (mean readmissions at 0.22 versus 0.26) and much lower readmission rates than other illicit drug users (mean readmissions at 1.0). The unit for mean readmissions was not specified in either the tables or methods of this paper. The limitations of the study by Yadavilli et al. (2014) include a lack of spirometry data on all patients to confirm diagnosis of COPD, the self-report of tobacco use, the risk for potential underreporting of illicit drug use, and the lack of outpatient visit frequency.
Kempker et al. (2015) analyzed data from the 2007–2010 NHANES cohorts, similar to the work done by Papatheodorou et al. (2016). Kempker et al. (2015), however, also examined the information on cumulative lifetime use of cannabis available in the 2009–2010 NHANES cohort. Main findings were that 59 percent reported using cannabis at least once during their lifetime, and 12 percent reported use during the last month. When evaluating cumulative lifetime cannabis use, those with >20 joint-years had a two times higher odds (OR, 2.1; 95% CI = 1.1–3.9) of having a pre-bronchodilator FEV1/FVC 1, which would spuriously reduce the ratio FEV1/FVC. Beyond the limitations noted above for the paper by Papatheodorou et al. (2016), who also used NHANES data, the authors were limited to use pre-bronchodilator spirometry instead of using post-bronchodilator spirometry as commonly done in COPD studies.
Discussion of Findings
It is unclear whether regular cannabis use is associated with the risk of developing COPD or exacerbating COPD. Current studies may be confounded by tobacco smoking and the use of other inhaled drugs as well as by occupational and environmental exposures, and these studies have failed to quantify the effect of daily or near daily cannabis smoking on COPD risk and exacerbation. There is no evidence of physiological or imaging changes consistent with emphysema. The committee’s findings are consistent with those of a recent position statement from the American Thoracic Society Marijuana Workgroup which concluded that there was minimal impairment in light and occasional cannabis smokers when controlled for tobacco use and that the effects in heavy cannabis smokers remain poorly quantified (Douglas et al., 2015). The review by Tashkin (2013) concluded that the lack of evidence between cannabis use and longitudinal lung function decline (Pletcher et al., 2012) argues against the idea that smoking cannabis by itself is a risk factor for the development of COPD. This is further supported by the findings of Kempker et al. (2015), who concluded that smoking cannabis was not associated with lower FEV1 after adjusting for tobacco smoking. However, smoking cannabis was associated with a higher FVC, which may have led to a spuriously lower FEV1/FVC. Therefore, their analyses also do not support an association between heavy cannabis use (>20 lifetime joint-years) and obstruction on spirometry. The position statement by Douglas et al. (2015) concluded that the lack of solid epidemiologic association suggests that regular cannabis smoking may be a less significant risk factor for the development of COPD than tobacco smoking.
Cross-sectional studies are inadequate to establish temporality, and cohort studies of regular or daily cannabis users are a better design to help establish COPD risk over time. Better studies are needed to clearly separate the effects of cannabis smoking from those of tobacco smoking on COPD risk and COPD exacerbations, and better evidence is needed for heavy cannabis users.
7-2(a) There is limited evidence of a statistical association between occasional cannabis smoking and an increased risk of developing chronic obstructive pulmonary disease (COPD) when controlled for tobacco use.
7-2(b) There is insufficient evidence to support or refute a statistical association between cannabis smoking and hospital admissions for COPD.
RESPIRATORY SYMPTOMS, INCLUDING CHRONIC BRONCHITIS
Respiratory symptoms include cough, phlegm, and wheeze. Chronic bronchitis is defined as chronic phlegm production or productive cough for 3 consecutive months per year for at least 2 consecutive years (Medical Research Council, 1965). Chronic bronchitis is a clinical diagnosis and does not require confirmation by spirometry or evidence of airflow obstruction. The committee responsible for Marijuana and Medicine: Assessing the Science Base (IOM, 1999) concluded that acute and chronic bronchitis may occur as a result of chronic cannabis use.
Is There an Association Between Cannabis Use and Respiratory Symptoms, Including Chronic Bronchitis?
The systematic review by Tetrault et al. (2007) summarized information from 14 studies that assessed the association between long-term cannabis smoking and respiratory symptoms. Nine of these studies were cross-sectional, 3 were case series, 1 was a case-control study, and 1 was a longitudinal cohort study. Data were relatively consistent in both cross-sectional and cohort studies in indicating that long-term cannabis smoking worsens respiratory symptoms, including cough (ORs, 1.7–2.0), increased sputum production (ORs, 1.5–1.9), and wheeze (ORs, 2.0–3.0). Other studies have reported effects on more episodes of acute bronchitis and pharyngitis, dyspnea, hoarse voice, worse cystic fibrosis symptoms, and chest tightness.
Aldington et al. (2007) reported higher prevalence of wheeze (27 percent versus 11 percent), cough (29 percent versus 5 percent), chest tightness (49 percent versus 35 percent), and chronic bronchitis symptoms (19 percent versus 3 percent) among cannabis smokers than among nonsmokers. There were no clear additive effects observed in the combined cannabis and tobacco smoking groups on respiratory symptoms.
Hancox et al. (2015) conducted a study in a cohort of 1,037 adults (52 percent male) in the Dunedin Multidisciplinary Health and Development Study. Cannabis and tobacco smoking histories were obtained at the ages of 18, 21, 26, 32, and 38 years. At each assessment, participants were asked how many times they had used cannabis in the previous year. Frequent cannabis users were defined as those who reported using marijuana ≥52 times over the previous year. Quitters were defined as a frequent cannabis user at the previous assessment but less than frequent at the current assessment. Because it was possible to quit frequent cannabis use more than once during the follow-up from 18 to 38 years of age, only the first recorded episode of quitting was used in analyses. In this study, the investigators found that frequent cannabis use was associated with morning cough (OR = 1.97, p <0.001), sputum production (OR = 2.31, p <0.001), and wheeze (OR = 1.55, p <0.001), but not dyspnea (p = 0.09) (see Figure 7-1). Quitters (open triangles) also had fewer respiratory symptoms than those who did not quit (solid squares).
Prevalence of symptoms before and after quitting regular cannabis use (open triangles) and among those who used cannabis for two consecutive phases (solid squares). Vertical bars show 95% confidence level. SOURCE: Hancox et al., 2015.
Limitations of the study by Hancox et al. (2015) include its reliance on self-reported data of cannabis use without objective confirmation, the classification of nonusers as those with
Walden and Earleywine (2008) conducted a cross-sectional Internet survey of 5,987 adults worldwide who used cannabis at least once per month. They quantified frequency, amount, and degree of usual and maximal intoxication, and they also asked about respiratory symptoms using a composite score produced from the answers to six standard questions about cough, morning phlegm, dyspnea, chest wheezing other than during colds, and nighttime awakenings because of chest tightness. They found that the frequency of use, the amount used (in quarter bags per month), and the degree of usual intoxication were all positively associated with more respiratory symptoms. Limitations for this study include its recruitment of participants from organizations that advocate drug policy reform, its reliance on self-reported data of cannabis or tobacco use without objective confirmation, and the lack of data about cannabis use for medical versus recreational purposes.
Tashkin et al. (2012) followed 299 participants from a longitudinal cohort study for at least two visits over 9.8 years and examined the relationship between symptoms for chronic bronchitis and cannabis use. They found that current cannabis users were more likely to have cough (OR = 1.7), sputum (OR = 2.1), increased bronchitis episodes (OR = 2.3), and wheeze (OR = 3.4) when compared to never users. They also found that current cannabis users were more likely to have cough (OR = 3.3), sputum (OR = 4.2), or wheeze (OR = 2.1) than former users. Similar to the studies by Hancox et al. (2015) and Walden and Earleywine (2008), these findings demonstrated the benefit of cannabis smoking cessation in resolving preexisting symptoms of chronic bronchitis. The limitations of this study include its reliance on self-reported data of cannabis or tobacco use without objective confirmation and high rates of loss to follow-up or variable follow-up periods.
A small feasibility study by Van Dam and Earleywine (2010) of 12 adult participants who did not develop a respiratory illness during the trial found that the use of a cannabis vaporizer instead of smoking cannabis was correlated with the resolution of cannabis-related respiratory symptoms at approximately 1 month after the introduction of the vaporizer; however, this study did not have a control group.
Discussion of Findings
Regular cannabis use was associated with airway injury, worsening respiratory symptoms, and more frequent chronic bronchitis episodes. There were no clear additive effects on respiratory symptoms observed from smoking both cannabis and tobacco. Cannabis smoking cessation was temporally associated with the resolution of chronic bronchitis symptoms, and a small feasibility study suggests that use of a vaporizer instead of smoking cannabis may lead to the resolution of respiratory symptoms. The committee’s findings are consistent with those reported in a recent review (Tashkin, 2013) and position statement (Douglas et al., 2015).
The majority of studies relied on self-report for cannabis smoking. Many studies failed to control for tobacco, occupational, and other environmental exposures; did not control for the dose or duration of the cannabis smoke exposure; and did not use joint-years and instead based heavy cannabis exposure on exceeding a specific threshold of cigarettes. Even among studies that used joint-years, it is unclear how generalizable the findings are, given the potential high variability in tetrahydrocannabinol (THC) content from joint to joint and from year to year.
7-3(a) There is substantial evidence of a statistical association between long-term cannabis smoking and worse respiratory symptoms and more frequent chronic bronchitis episodes.
7-3(b) There is moderate evidence of a statistical association between cessation of cannabis smoking and improvements in respiratory symptoms.
Asthma is a clinical syndrome that is associated with airways inflammation, airflow limitation, bronchial hyperresponsiveness, and symptoms of episodic wheeze and cough. It is predominantly an allergic disease. Worldwide, asthma is thought to affect 300 million people, and it is responsible for more disability-adjusted life-years lost than diabetes mellitus. Asthma was not specifically addressed in Marijuana and Medicine: Assessing the Science Base (IOM, 1999).
Is There an Association Between Cannabis Use and Asthma?
The systematic review by Tetrault et al. (2007) referred to only one study that described the association between cannabis use and asthma exacerbations. Upon retrieving this study, the committee found that this was a letter to the editor which reported findings of a case-control study of 100 participants ages 18–55 years, with and without asthma, admitted to the emergency department. In this study, the authors found no association between THC and asthma (Gaeta et al., 1996).
Bechtold et al. (2015) reported on a follow-up of a cohort of boys who participated in the Pittsburgh Youth Study. A total of 506 boys were followed longitudinally: 257 scored at or above the 70th percentile of a multi-informant conduct problem score, and 249 scored below the 70th percentile. This study found no link between cannabis use and self-reported asthma symptoms. The limitations of this study include a lack of generalizability to the general population, given the selection criteria for conduct problems, a lack of inclusion of women in their study, and the fact that health outcomes were based on self-report and biased to those who had sought care for health problems.
Weekes et al. (2011) studied a cohort of 110 black urban adolescents with asthma. In this study, the investigators found that 16 percent of the adolescents smoked cannabis, but there was no association between cannabis use and asthma concern or asthma severity or asthma symptoms. The limitations of this study include the reliance on the self-report of cannabis use, which the study authors speculated may be underreported in black adolescents when compared to whites, and a lack of data on asthma medication adherence.
Discussion of Findings
The committee did not find evidence for an association between cannabis use and either asthma risk or asthma exacerbations, and current studies failed to control for other important confounders, including adherence to asthma medications.
The evidence linking cannabis use with asthma risk or exacerbation is limited by the scope and sample size of available studies and by the use of more standardized approaches to measure asthma prevalence or exacerbations of asthma. Few studies have examined the link between cannabis and asthma, and no clear evidence exists of a link between asthma or asthma exacerbation and cannabis use. However, asthma symptoms such as wheeze appear to be common among cannabis users.
CONCLUSION 7-4 There is no or insufficient evidence to support or refute a statistical association between cannabis smoking and asthma development or asthma exacerbation.
The effects of cannabis smoke on respiratory health remain poorly quantified. Further research is needed to better elucidate the influence of exposure levels to cannabis smoke on respiratory outcomes, the chronicity of cannabis smoking, the effects of an underlying predisposition to respiratory disease, and possible interaction effects with tobacco smoke to promote airway inflammation, worsen respiratory symptoms, accelerate lung function decline, or increase exacerbation of COPD and asthma. Previous studies have not been able to adequately separate cannabis smoke effects from tobacco smoke effects, and this has meant that some important questions remain unanswered. It is unknown whether or not:
Long-term cannabis smoking, above and beyond that of tobacco smoking, leads to a more rapid decline in lung function and to the development of chronic bronchitis or COPD.
To address the research gaps relevant to respiratory disease, the committee suggests the following:
Design better observational studies with both self-reported and quantitative measures of cannabis smoking and systematic approaches to measure the duration and dose to determine if long-term exposure to cannabis smoke, above and beyond exposure to tobacco smoke, leads to the development of chronic bronchitis or COPD or to a higher rate of COPD exacerbation.
Design longitudinal studies to determine if long-term cannabis smoking is associated with the development of allergic disease and risk of asthma.
Conduct clinical trials of alternative inhaled delivery methods versus cannabis smoking to determine if they reduce respiratory symptoms.
This chapter summarizes all of the respiratory disease literature that has been published since 1999 and deemed to be good or fair by the committee. Overall, the risks of respiratory complications of cannabis smoking appear to be relatively small and to be far lower than those of tobacco smoking. While heavy cannabis users may be at a higher risk for developing chronic bronchitis and COPD or at an increased risk of exacerbating COPD and asthma, current studies do not provide sufficient evidence for a link. Limitations of reviewed studies are that it is difficult to separate the effects of cannabis smoking from those of tobacco smoking from current available data; that exposures have generally been measured by self-report of cannabis smoking; and that there is a lack of cohort studies of regular or daily cannabis users, of adequate controls for environmental factors, and of generalizability of findings. The committee has formed a number of research conclusions related to these health endpoints (see Box 7-1); however, it is important that each of these conclusions be interpreted within the context of the limitations discussed in the Discussion of Findings sections.
Summary of Chapter Conclusions .
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High CBG Formula To Fight Bronchitis? | CBG Oil For Bronchitis
CBG or Cannabigerol is a non-toxic and non-psychoactive cannabinoid produced when the cannabigerolic acid molecule, CBGA is oxidized. It is one of more than 100 cannabinoids found in the cannabis plant that includes Cannabidiol, THC, and CBC. Not only is CBG non-psychoactive, but it also interferes and acts against the mind-altering properties of THC. It is also effective against a variety of physical and mental issues we face that include pain, bacteria, seizures, inflammation, sleep problems, mood issues, and appetite. It is also highly effective against bronchitis. In fact, It is the most natural and safest way to cure bronchitis and enables you to live a happier, more healthy, and satisfying life with ease. But, before seeing how CBG affects bronchitis, let us take a quick look at the causes, symptoms, and diagnosis of bronchitis
What Is Bronchitis?
Bronchitis is an inflammation of the lining of the bronchial tubes or airways responsible to carry air in and out of the lungs. This is primarily because of the infection caused in the bronchial tubes that leaves you with a persistent cough and mucus. So, if you recover in a couple of weeks from cold or flu, then it’s fine but if the problem prevails for more than a few weeks, chances are you might be suffering from bronchitis. Sometimes, referred to as a common cold, bronchitis is divided into two types based on the duration it affects a person. The more common one that lasts for a few weeks is called acute bronchitis.
The symptoms of acute bronchitis do not cause any major problems. The other type is a more severe one and is called chronic bronchitis, COPD or chronic obstructive pulmonary disease. It keeps coming back again and again and does not go away at all. So, even though acute and chronic bronchitis has the same symptoms, they are different illnesses that last for different lengths of time.
What causes bronchitis?
The virus that is responsible to cause cold or flu is the same virus that causes bronchitis. It can also be caused due to bacteria. When a virus or bacteria attacks your body, the body’s first reaction is fighting off these germs. This leads to inflammation of the bronchial tubes and the production of more mucus which decreases the openings for air to flow making it harder to breathe. Other causes of bronchitis include a weaker immune system, persistent cold, smoking or living with someone who smokes, pollution, or if you work or live in an area that has too much dust or has industries that release chemical fumes. These causes make it a common problem amongst people who work in coal mines or around farm animals.
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How does it feel when you have bronchitis?
A cough is one of the most common indicators of bronchitis. Also, since bronchitis is related to the inflammation of the bronchial tubes that pass air to and from the lungs, it leads to breathing problems too. Some of the other common symptoms of bronchitis are:
- Chest congestion involving the feeling of a clogged or full chest
- Clear, white, yellow, or a green cough with a lot of mucus persistent for a longer time
- Breath Shortness
- Whistling or Wheezing sound while breathing
- Body aches and chills
- Feeling extremely tired or exhausted
- Runny and stuffy nose
- A sore throat
How Bronchitis Is Diagnosed?
Bronchitis is easily diagnosable and if you consult a doctor with the symptoms mentioned above, he will be able to tell you whether you have bronchitis or not based on a physical examination. He will also inquire about the primary symptoms that include the duration of a cough, and the type of mucus that accompanies it.
He may also check your lungs for sounds like wheezing. If he is unsure, he can order blood tests, do a lung function test with a spirometer to test for emphysema and asthma, or do a chest X-ray. If you experience a whooping cough that makes it hard to breathe, the doctor might even ask you to take a nasal swab for a clearer diagnosis.
Pharmaceutical Treatment For Bronchitis || CBG Oil For Bronchitis
If you are suffering from acute bronchitis, it will go away on its own within a couple of weeks if you take a few preventive measures without any treatment. But, if it does not go away, then the doctor may prescribe pharmaceutical drugs as per your symptoms. These drugs may contain (NSAIDs) nonsteroidal anti-inflammatory drugs like ibuprofen and naproxen to relieve pain, reduce inflammation and control fever, analgesic drugs like acetaminophen and oxycodone to relieve pain, and simple cough medicines like guaifenesin. All these medicines mentioned do not treat bronchitis but work on reducing the symptoms to a level where you don’t face any issues. But, chronic consumption of these drugs is known to have serious side effects which include drowsiness, sleep interference, nausea, vomiting, and even addiction. So, there are various preventive measures and better natural options like CBG that have no side effects to get relief from Bronchitis. Take a look.
How does CBG Oil help With Bronchitis? Using CBG Oil For Bronchitis
Some of the best ways to reduce the effect of the symptoms of Bronchitis include drinking lots of water, getting plenty of rest, and using a humidifier to loosen up the mucus. If you follow these three things and inculcate cannabinoids like CBG oil in your daily life, you are sure to get relief from Bronchitis. CBG is extremely effective against the symptoms of Bronchitis due to its anti-inflammatory and analgesic properties that provide relief against pain and the inflammation caused in the bronchial tubes. CBG is also effective against bronchitis caused by bacteria since it is an antibacterial agent and stops bacteria from regenerating. So, if you are suffering from bronchitis and need a safe, completely organic, and vegan supplement to treat bronchitis, Cannabidiol and CBG is the perfect solution to lead a relaxed and stress-free life. CBG is also a very effective pain management cannabinoid that is helpful in reducing any chronic pain.
CBD CBG Review
Every morning I wake up and instantly start sneezing. That’s when I reach for my Thoughtcl0ud CBD high CBG formula. Within a few minutes, my sneezing subsides because this formula reduces the inflammation in my sinuses. I also love this formula for my old running injuries. I love mixing it into homemade body oils and feeling the pain in my sore ankles vanish! A few drops in an Epsom salt bath is also complete magic! (sic)
I wanted to try CBG CBD oil to help with inflammation and occasional allergies. I never thought I would love as much as I did. It helps me sleep as well as help with inflammation. I did not experience any negative side effects. I highly recommend it! (sic)
Final Words On CBD CBG Oil for Bronchitis
Bronchitis can be caused due to various factors. So, keeping yourself safe from these is the first thing you need to avoid this untreatable and irritating disease. Inculcate a healthy lifestyle, avoid smoking cigarettes, go vegan, get the pertussis vaccine and pertussis vaccine, keep yourself clean, wash your hands often and wear a mask if you are around allergic to things that bother your lungs like paint fumes. If still, you get bronchitis, use plant-based cannabinoids like CBG for bronchitis to slow down and reduce the intensity of your symptoms significantly within a few weeks.
Acute and subacute bronchial effects of oral cannabinoids
The bronchodilating activity of oral cannabinoids was evaluated in three double-blind experiments that involved the study of dose-response and interactive relationships and the potential development of tolerance. Data indicated that delta 8-tetrahydrocannabinol (delta 8-THC), cannabinol (CBN), and cannabidiol (CBD) in maximal doses of 75 mg, 1200 mg, and 1200 mg, respectively, did not induce significant dose-related physiologic effects in experienced marijuana smokers. delta 8-THC (75 mg) was, however, associated with bronchodilation, tachycardia, and peak highs less than that after delta 9-tetrahydrocannabinol (delta 9-THC). The combinations of CBN and CBD with low-dose delta 9-THC (5 mg) did not induce significant bronchodilation but did exert interactive effects on heart rate and “high.” A 20-day study of daily delta 9-THC (20 mg), CBN (600 mg), and CBD (1200 mg) did not indicate tolerance or reverse tolerance to any drug. We conclude that delta 9-THC and, to a lesser extent, delta 8-THC, have acute bronchodilator activity but that CBN, CBD, and their combinations do not provide effective bronchodilation. The daily use of delta 9-THC was not associated with clinical tolerance.
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