what can you do to clear out your lungs heavy marijuana use

Marijuana and the lung: hysteria or cause for concern?

Breathe 2018 xiv: 196-205; DOI: ten.1183/20734735.020418

Abstract

Increasing cannabis use and legalisation highlights the paucity of information we have on the safety of cannabis smoking for respiratory wellness. Unfortunately, concurrent utilise of tobacco among marijuana smokers makes it hard to untangle individual issue of marijuana smoking. Chronic cannabis simply smoking has been shown in large accomplice studies to reduce forced expiratory volume in i south/forced vital chapters via increasing forced vital capacity in chronic use contrary to the picture seen in tobacco smoking. The crusade of this is unclear and at that place are diverse proposed mechanisms including respiratory musculus training secondary to method of inhalation and acute anti-inflammatory consequence and bronchodilation of cannabis on the airways. While cannabis smoke has been shown to increase symptoms of chronic bronchitis, information technology has non been definitively shown to be associated with shortness of breath or irreversible airway changes. The evidence surrounding the development of lung cancer is less clear; however, preliminary evidence does not suggest association. Bullous lung illness associated with marijuana utilise has long been observed in clinical practice but published evidence is limited to a total of 57 published cases and only one cross-sectional study looking at radiological changes amidst chronic users which did non written report any increment in macroscopic emphysema. More than studies are required to elucidate these missing points to further guide risk stratification, clinical diagnosis and management.

Key points

• Cannabis smoking has increased and is likely to increase further with relaxation of legalisation and medicinal use of cannabinoids.

• Chronic marijuana smoking oftentimes produces symptoms like to those of chronic tobacco smoking such as cough, sputum product, shortness of breath and wheeze.

• Cessation of marijuana smoking is associated with a reduction in respiratory symptoms and no increased run a risk of chronic bronchitis.

• Spirometry changes seen in chronic marijuana smokers appear to differ from those in chronic tobacco smokers. In chronic marijuana smokers there is an increase in FVC as opposed to a definite decrease in FEV_one.

• Multiple case series have demonstrated peripheral bullae in marijuana smokers, but no observational studies have elucidated the risk.

• There is currently no clear clan betwixt cannabis smoking and lung cancer, although the inquiry is currently express.

Educational aims

• To update readers on legalisation of recreational and medicinal cannabis.

• To summarise the evidence base surrounding the respiratory effects of inhaled marijuana apply.

• To provide clinicians with an understanding of the main differences between cannabis and tobacco to be able to utilize this to patient teaching.

• To highlight mutual respiratory problems amongst cannabis users and the demand for recreational drug history taking.

Abstract

Chronic cannabis smoking develops a dissimilar respiratory picture compared to tobacco. The machinery backside this is unclear; however, given the increasing prevalence and legalisation it is important to keep in mind the differences in clinical practise. http://ow.ly/kcv930l1sG1

Cannabis is the near widely used illicit substance, and the second most widely smoked, in the world. Cannabis refers to products of the cannabis plant including marijuana (the flowers and tops of the plant; bud) and the resin (hash). Other terms in common utilise include "weed", "dope", "grass", "hemp", "ganga", "reefer", "spliff", "toke" and "blunt".

Although alcohol, caffeine and tobacco indulgence are more than widespread, illicit recreational drug apply polarises opinion more. Cannabis is seen as harmless on the one hand and as a gateway to hard drug use on the other. Dependence is associated with cannabis use disorder which is increasing in prevalence. Cannabis as a public health issue has risen upward the political agenda. With an aim to disrupt an illicit industry funding organised crime, Canada began regulating tetrahydrocannabinol (THC) content in July 2018 in an attempt to improve safety and protect the immature. Non surprisingly, there are vocal critics and cries for much more research [1].

As healthcare professionals, we deal with tobacco all the time but we also need to know about the respiratory effects of marijuana to be able to suggest our patients and colleagues. This brief review aims to summarise what is known and how concerned we should be, peculiarly with regards to the lungs.

The cannabis genus includes three species: Cannabis sativa, Cannabis indica and Cannabis ruderalis. Each species contains varying concentrations of the two major psychoactive compounds: delta-9-THC and cannabidiol [2]. The concentrations of psychoactive compounds in recreational marijuana too vary over time, with concentrations higher now than they were 50 years ago due to selective breeding. Positive psychoactive effects of cannabis include euphoria and relaxation [three]. Still, negative psychological side-effects range from anxiety to psychosis [3]. Normally available high authority cannabis, dubbed skunk (based on its distinct smell), is associated with a loftier risk of psychosis due to its loftier concentration of delta-9-THC [two, 3].

Pharmacology

The loftier number of cannabinoids recognised (perhaps over 90) means that cannabis pharmacology is necessarily complex; and a full discussion is non warranted hither.

Traditional CB1 receptors, belonging to the G-protein coupled family, were identified in 1988 and cloned in 1990. The concept of an endogenous cannabinoid system was developed after the discovery of an endogenous arachidonic acid metabolite ligand (N-arachidonylethanolamide (anadamide) and after a much more selective agonist 2-arachidonylglycerol). delta-nine-THC and synthetic derivatives are CB1 agonists. The CB2 receptor subtype was originally described in differentiated myeloid cells and shows 44% amino acid homology with CB1 but a distinct, though like, binding profile. Five classes of cannabinoid compounds show activeness at CB1 and CB2 receptors with minor selectivity for the agonists delta-ix-THC and cannabidiol but major selectivity (>1000-fold) and nanomolar affinity shown past antagonists [four]. Other cannabinoid receptor subtypes accept been postulated simply not confirmed [5].

Cannabis apply is increasing

Recent data from the 2016 Crime Survey for England and Wales on drug misuse suggest that around 2.1 million adults accept used cannabis in the by year [half-dozen]. In addition, 1-third of those surveyed thought it was adequate for people of their own age to employ cannabis occasionally. These figures are unsurprising given the global shift in attitudes towards cannabis and the growing number of countries relaxing legislation on both medical and recreational marijuana use (table 1).

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Table one

Increasing legalisation of cannabis

Epidemiology

While we know that marijuana use is increasing, legality remains a major problem for epidemiological studies. In the Great britain, it is a class B drug meaning it is illegal for Great britain residents to possess cannabis in whatsoever form.

Cannabis tin be smoked in a variety of ways, usually without a filter and burned at a college temperature, and with users generally holding their breath for longer periods of fourth dimension, compared to tobacco smokers [two]. Joints tin be made using only cannabis leaves or tin be mixed with tobacco in spliffs. Many cannabis users also concurrently smoke tobacco cigarettes. Routes of administration vary by geographical region also, with European countries mostly smoking spliffs while the Americans largely smoke cannabis only joints [seven]. Bated from joint smoking, users may as well use h2o bongs, pipes and, more than recently, vaporisers [vii, 8].

It follows that the long-term health effects of marijuana smoking are less understood compared to traditional cigarette smoking.

Chronic respiratory effects

Tobacco smoking is well known to increase the risk of chronic bronchitis, emphysema and pocket-size airways illness (all components of chronic obstructive pulmonary affliction; COPD), too as the development of diverse forms of lung cancer. Information technology might be expected that chronic cannabis smoking would have similar sequelae considering that the contents and properties of tobacco and cannabis smoke are like [ii]. Nonetheless, observational studies tell a different story.

Symptoms

Respiratory symptoms such as cough, sputum production and wheeze are increased in current cannabis users [2, 9, 10]. Chiefly, associations with shortness of breath were not plant in larger studies [9, x]. This suggests that cannabis fume causes chronic bronchitis in current smokers just not shortness of breath or irreversible airway damage.

This is supported by studies examining the effect of quitting marijuana smoking. They show a pregnant reduction in morn cough, sputum production and wheeze compared to those who continue to smoke [2, 10]. Quitters besides had no increased gamble for developing chronic bronchitis compared with nonsmokers at follow-upwardly x years subsequently [2, x].

Vaping cannabis is increasingly popular among young adults [eight]. While we don't know the long-term respiratory health effects of e-cigarette utilise, for either tobacco or cannabis, it has been suggested that vaping may reduce the symptoms associated with smoking [viii].

Lung function

COPD is conventionally diagnosed when a patient has an irreversible reduced forced expiratory volume in 1 s (FEV₁) compared with forced vital capacity (FVC) on spirometry. Several big, recently published observational studies (table ii) take reported that long-term marijuana just users accept an increment in their FVC with little or no change in FEV₁, fifty-fifty after 20 joint-years of smoking (1 joint-year is equivalent to 365 joints per twelvemonth) [ii, 27, 29]. A reduced FEV_i/FVC ratio due to increased FVC clearly differs from the classical spirometric changes seen in tobacco smoking. The crusade of this increase in FVC is unclear. Respiratory muscle training by the breath-property techniques used during marijuana smoking has been proposed every bit a cause; nonetheless, at that place is little evidence that grooming can increment FVC [ii, xxx]. Additional lung function measurements accept only been examined in smaller studies [two]. Very small changes in full lung capacity have been reported in several studies. Small effects on specific airways conductance and resistance have been interpreted as consequent with fundamental airways inflammation. The transfer factor of the lung for carbon monoxide has been reported to be reduced only in smokers of cannabis and tobacco. Interestingly marijuana use within 0–4 days of lung function measurement showed a 13% reduction in exhaled nitrous oxide, though the clinical manifestation of this acute upshot is unknown [29].

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Table two

Summary of observational studies on marijuana exposure and lung function

Acute airway effects of cannabis

Experimentally, the astute bronchodilator effect of inhaled cannabis is well described as an effect of THC [2]. However, since cannabinoids can have partial agonist, or even adversary, effects little is known about differences in airway furnishings from different strains of cannabis containing varying concentrations of cannabinols.

We do not know why cannabis smoking does non produce COPD. Possible explanations include a persistent bronchodilator consequence (offsetting airway narrowing) or anti-inflammatory or immunomodulatory effects of THC [two].

Bullous lung illness

Bullous lung disease, usually presenting with pneumothorax, is widely recognised as a possible result of marijuana smoking. Nonetheless, while well-established anecdotally, at that place is actually a paucity of relevant information [two]. As of 2018, there have been 7 case series and 11 case reports published. A total of only 57 individual cases were described. Concurrent tobacco smoking was recorded in all but four of the cases. Patient details are summarised in tabular array iii. The majority were heavy marijuana users, up to 149 joint-years. Most of the cases had predominantly upper lobe interest with added peripheral emphysema and most presented with pneumothorax, presumably due to rupture of a bulla. They are therefore not representative of the general marijuana smoking population. We have found only a single cross-exclusive study (n=339) looking at radiological changes amongst marijuana smokers in New Zealand [23]. Interestingly they reported an increment in macroscopic emphysema in tobacco smokers compared with nonsmokers but not in cannabis simply smokers. Depression-density lung regions on loftier-resolution computed tomography in cannabis smokers were interpreted as hyperinflation rather than microscopic emphysema. This is in contrast to a case serial of 10 patients which found asymmetrical bullous changes on CT among chronic marijuana smokers but with normal spirometry and chest radiographs [37]. A report looking at smoking status and the presence of emphysematous computed tomography changes of spontaneous pneumothorax patients found no difference in emphysema prevalence among tobacco smokers and tobacco plus cannabis smokers (at that place were no cannabis only smokers); however, concurrent smokers were significantly younger [49]. While the authors have suggested that cannabis added to tobacco leads to emphysema at a younger age, there are too many confounders such as the subject population, to come to a definitive conclusion.

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Table 3

Summary of cannabis-associated bullous lung disease case reports

Various mechanisms have been proposed to explicate an observed association [ii, 23]; the chief i relating to breath-holding techniques employed during smoking, resembling a Valsalva manoeuvre. It is suggested that this could precipitate barotrauma increasing bulla formation and predisposing to pneumothorax. There is currently no direct show for this hypothesis.

Information technology is possible that the lack of published data on bullous lung disease in marijuana smokers relates to its widespread recognition and familiarity. However, information technology is hard to describe any firm conclusions on an association, its frequency, other epidemiological characteristics, mechanisms, etc. More studies, preferably prospective serial, are required to gather epidemiological data. It falls to health professionals to recognise possible cerebral bias, and to fully investigate pneumothorax and bullous affliction rather than but relating it to drug history.

Lung cancer

The clear clan of tobacco smoking and lung cancer and the like carcinogens nowadays in burning cannabis institute material have long raised the possibility of an association of marijuana utilize and lung cancer. Furthermore, premalignant changes in bronchial biopsies from marijuana smokers accept been shown histologically [ii]. However, as with chronic lung disease, at that place is currently little evidence of a definite link. A Swedish accomplice report of virtually 50 000 regular army conscripts reported a two-fold increased risk of lung cancer among marijuana smokers, compared with nonsmokers subsequently 40 years. Unfortunately, and critically, smoking history was only assessed at the fourth dimension of conscription and there was no data on smoking status earlier conscription or in the 40 years afterwards [50]. A pooled analysis of vi example–command studies found no increased hazard of cannabis compared to non-habitual smokers [51]. Other epidemiological studies investigating cancer run a risk suffered from methodological limitations including pocket-size sample sizes or curt follow-upwards [2].

Nosotros practice non know why cannabis smoking does non appear to be carcinogenic. Diverse factors might contribute, e.k. potential anti-inflammatory and anti-neoplastic properties of THC and other cannabinoids [52].

Pneumonia

Cannabis has been shown to have immunosuppressive effects on alveolar macrophages and to cause loss of ciliated bronchial epithelium [53]. An increased incidence of pneumonia in cannabis users might exist expected. One cross-sectional study surveyed current marijuana users regarding a diagnosis of pneumonia within the previous 12 months and found no increased risk compared to nonsmokers [9]. Otherwise, we have found just isolated case series and studies on immunocompromised patients [53]. Such cases include invasive aspergillosis from spores which were found in contaminated leaves andPseudomonas associated with bell smoking [54, 55].

Interstitial lung illness

Reports of cannabis-associated interstitial lung disease are few and far between. There are occasional reports of eosinophilic pneumonia (equally with smoking generally) and a case of pneumoconiosis associated with talc-adulterated marijuana [52].

Medical use of cannabis

Medical utilise of cannabis past mouth/orally dates back to 2737 BC in China [56]. Raw herbal cannabis, cannabis oil extracts including products prepared in a chemist's shop (magistral preparations), and cannabinoids are all used. There has been increasing recent involvement with wide acceptance and dominance of use of herbal preparations in many European countries and even more widespread authority of oral cannabinoid medications in most European countries and the Us and Canada (tabular array 4). The nigh accepted indications include chronic pain, spasticity in multiple sclerosis, sure rare epilepsy syndromes, and chemotherapy-induced nausea and airsickness [57]. There has also been experimental bear witness in the anti-neoplastic issue of cannabinoids [19], likewise as in palliative intendance. Information technology has been recommended in a large variety of other conditions and for improving slumber quality including in obstructive sleep apnoea, although with express evidence [58].

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Table four

Licensed cannabinoid medication

Conclusions

The long-term respiratory effects of cannabis differ from traditional tobacco smoking; nevertheless, we practice non know why and this may be a fruitful area for enquiry. We need to know more near cannabis pharmacology and anti-inflammatory and anti-cancer effects equally well as endocannabinoids. Cannabis employ has been increasing and is probable to increment more merely this should non foster hysteria. Chronic cannabis use is associated with chronic bronchitis but an increase in FVC with no modify in FEV_ane and not with COPD. The clinical implications and causes of these spirometric changes are currently unknown. Larger prospective longitudinal studies are needed, in particular comparing spirometric changes with bullous/emphysematous changes on loftier-resolution computed tomography scans. Monitoring symptoms amid cannabis users, peculiarly breathlessness, is paramount. Reducing or eliminating cannabis smoking benefits patients suffering from symptoms of cough and phlegm.

Detailed inhalational drug history taking should be part of the standard cess of patients in both primary and secondary care. This could support ameliorate epidemiological data collection and likewise foster meliorate patient communication about respiratory and psychological health risks. No medicinal part for cannabinoids has been established as regards the lungs and more than research is needed relating to rubber.

Self-evaluation questions

• one. Which of the following countries take legalised marijuana?

  • a) Republic of austria

  • b) Japan

  • c) Romania

  • d) Thailand

  • due east) Uruguay

• two. Which of the following statements on the pharmacology of cannabis is truthful?

  • a) All strains of cannabis incorporate the same concentrations of compounds

  • b) THC is the but psychoactive compound in cannabis

  • c) The endogenous agonist of the CB1 receptor is cannabidiol

  • d) Cannabis has been shown to accept an acute bronchodilator effect

  • due east) The currently used measure of joint-years takes into business relationship varying sizes of joints

• 3. Which of these is not associated with chronic cannabis smoking?

  • a) A decrease in FEV₁/FVC to <70% pred

  • b) An increase in FVC

  • c) Increased airway resistance and increased airway conductance

  • d) FVC and FEV_one have a non-linear association with lifetime cannabis exposure

  • e) Erstwhile cannabis smokers accept been shown to have a decreased FEV₁/FVC ratio

• 4. What type of bullae distribution is most commonly seen amidst cannabis-associated bullous lung disease?

  • a) Mediastinal

  • b) Apical

  • c) Basal

  • d) Paraseptal

  • eastward) Lingular

Suggested answers

1. e.

2. d.

3. c.

four. b.

Footnotes

• Conflict of interest: None declared.

• Copyright ©ERS 2018

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Source: https://breathe.ersjournals.com/content/14/3/196

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