Pulmonary Fibrosis Medical cannabis is becoming more and more popular as a potential medical treatment for a variety of chronic health conditions. Medical marijuana for pulmonary fibrosis could Idiopathic pulmonary fibrosis (IPF), also known as diffuse interstitial pulmonary fibrosis, is an incurable disease with no known cause (i.e. an idiopathic condition). As its name suggests, it is characterised by diffuse fibrotic scarring of the lung tissue. This process leads to the healthy lung tissue being replaced with fibrotic tissue; as result, the lung loses its CBD Oil And Pulmonary Fibrosis Archivos de Bronconeumologia is a scientific journal that preferentially publishes prospective original research articles whose content is based upon results
Medical cannabis is becoming more and more popular as a potential medical treatment for a variety of chronic health conditions. Medical marijuana for pulmonary fibrosis could offer relief as well.
How and Why Marijuana Can Be an Effective Treatment for Pulmonary Fibrosis
Because there’s inflammation involved with pulmonary fibrosis, anti-inflammatory medications and treatments are usually effective. In one study, researchers found the THC in marijuana to have anti-inflammatory properties, which they feel accounts for the pulmonary function improvement in patients using cannabis.
Ingested or vaporized weed may offer potential benefits due to its immunosuppressant, anti-inflammatory and bronchodilation (airway-opening) properties.
In the 1970s, Donald Tashkin at the University of California Los Angeles performed studies that found both orally ingested and inhaled THC provide bronchodilation for several hours after it’s administered. Other studies found activating the CB1 receptor inhibits smooth muscle contraction of the lungs, which offers a potential acute bronchodilation mechanism linked with marijuana intake.
Cannabinoids provide anti-inflammatory qualities. Raw plant acidic cannabinoids (CBDA, THCA, etc.) provide greater anti-inflammatory properties than the raw plant’s non-acidic cannabinoids (CBD, THC, etc.). Researchers have found CBD to improve COPD symptoms. It also acts as an inflammatory agent and leads to reduced pulmonary inflammation and improved lung function in mice with inflammatory lung disease.
In addition to the anti-inflammatory benefits of marijuana for pulmonary fibrosis, the herb may also have an anti-anxiety effect. A researcher who performed clinical studies reports patients feeling relaxed and calm after using cannabis.
Studies like these show that marijuana may act as a way to reduce acute airway constriction attacks and become a viable preventative therapy for COPD patients. However, researchers need human trials to confirm these benefits.
What Side Effects and Symptoms of Pulmonary Fibrosis Can Medical Marijuana Treat?
According to the Lung Institute, marijuana and pulmonary fibrosis treatment could also help in:
- Improving sleep
- Reducing inflammation
- Reducing phlegm
- Supporting the immune system
- Easing pain
Just note that smoking cannabis presents one possible problem when using medical marijuana to treat pulmonary fibrosis. Smoking weed may harm patients with lung diseases, since there’s no “filter” on a joint or marijuana cigarette and individuals smoking it tend to inhale its smoke more deeply. This leaves smoke in their lungs for a more extended period than cigarettes.
Still, researchers found those who only smoke cannabis occasionally — a couple of joints a month — showed improved pulmonary function instead of reduced.
Best Strains of Marijuana for Pulmonary Fibrosis Symptoms and Treatment Side Effects
As with any treatment, finding the right medical cannabis strain for pulmonary fibrosis may take some trial and error. Just like not every treatment may be effective for your symptoms, not all strains will be, either. To help with this, below are some strains that are good for relieving the symptoms of pulmonary fibrosis:
- ACDC: Sativa
- Cannatonic: Hybrid
- Girl Scout Cookies: Indica with a strong sativa component
- Cookie Jar: Indica dominant with a sativa component
- Harlequin: Sativa
- White Widow: Hybrid
- Pennywise: Mostly-Indica strain with a high CBD count
- Sour Tsunami: Balanced High-CBD strain.
- OG Kush: Hybrid
Medical marijuana may also help alleviate the uncomfortable side effects of some of the medications used for pulmonary fibrosis, such as nausea and vomiting, headache, anxiety and more. For instance, Headband is good for nausea, Sour Diesel for a headache and Jack Herer for anxiety.
Best Methods of Marijuana Treatment for the Side Effects and Symptoms of Pulmonary Fibrosis
The benefit of cannabis and pulmonary fibrosis treatment, when compared with standard treatments, is the flexibility in delivery. These days, you can ingest cannabis in multiple ways, including:
CBD oil eliminates the THC chemical so you don’t get that “high” feeling — only relief from your symptoms.
Begin the Process of Securing Your Medical Marijuana for Pulmonary Fibrosis
Pulmonary fibrosis, like any other condition, can be distressing. But you can find some relief from its uncomfortable symptoms. Search for a medical marijuana doctor today so you can obtain your medical marijuana card and begin shopping around for your perfect strains by finding a cannabis dispensary. Once you book an appointment with a licensed cannabis doctor, you’ll be well on your way to experiencing the benefits medical marijuana can offer you.
What Is Pulmonary Fibrosis?
Pulmonary fibrosis (PF) is a health disorder that causes lung stiffness and scarring, making it hard to breathe. It may keep your body from getting the oxygen you need and can eventually result in heart failure, respiratory failure and other problems. Doctors and researchers discovered the first form of lung fibrosis during the 19th century. During this time, they took lung samples to try to understand the reason behind the scarring. PF didn’t show much improvement until the 20th century.
There’s no scarring in normal lungs — that means oxygen passes from the lungs easily and into the air sacs and bloodstream. This oxygenates the blood. With pulmonary fibrosis, your lungs don’t have elasticity and are stiff because of the scarring. The scarring makes it difficult for the oxygen to move around the air sacs, or alveoli, and reduces how much oxygen passes into your bloodstream.
The fibrosis also reduces the size of your lungs over time, which further worsens the condition. As your pulmonary fibrosis progresses, it may get harder and harder for you to breathe and you may need to rely on an oxygen device to help you.
A variety of factors can cause pulmonary fibrosis-related scarring. However, in most instances, physicians can’t figure out exactly what the cause of it is. When this occurs, it’s known as idiopathic pulmonary fibrosis. Researchers think a combination of lung irritant exposure and other factors may play a significant role in the condition. These may include:
- Certain chemicals
- Immune system activity
Scientists used to think inflammation caused pulmonary fibrosis. Now, they believe an irregular lung healing process could lead to scarring. Significant lung scarring formation eventually turns into pulmonary fibrosis.
Types of Pulmonary Fibrosis
There are two types of pulmonary fibrosis:
- Idiopathic Pulmonary Fibrosis (IPF)
When doctors can’t confirm the cause of the condition, they term it “idiopathic.” Since they don’t know what the disease’s underlying cause is, it can be hard for them to treat it. At present, there are a couple of medications the Food and Drug Administration (FDA) has approved to treat idiopathic pulmonary fibrosis (IPF). These are Ofev and Esbriet. They help slow the disease’s progression down and avoid exacerbations.
Respiratory failure is a concern for patients with IPF, but the condition may also lead to:
- Pulmonary hypertension
- Lung cancer
- Heart failure
- Familial Pulmonary Fibrosis (FPF)
People rarely get familial pulmonary fibrosis. Although it’s just as severe as idiopathic pulmonary fibrosis, doctors can often diagnose it much earlier to give the patient a better outcome. Physicians can also separate both types of pulmonary fibrosis into stages:
Doctors monitor the disease through staging, which helps them advise the patient and family about the progression of their PF, define the outcome and decide on a treatment approach.
Symptoms of Pulmonary Fibrosis
Pulmonary fibrosis symptoms may include:
- A dry cough
- Unexplained weight loss
- Dyspnea (shortness of breath)
- Clubbing (rounding and widening of the tips of toes and fingers)
- Aching joints and muscles
The severity of symptoms and course of pulmonary fibrosis can be considerably different for each person. While some may get sick fast with the condition, others may have moderate discomfort that gradually gets worse with time.
Then, there are those who have their symptoms become rapidly worse. This is called acute exacerbation and might include symptoms like shortness of breath, which could last for several weeks. If you have acute exacerbations, you doctor may place you on a mechanical ventilator. Your physician may also prescribe you corticosteroid medications or antibiotics to treat the acute exacerbation.
Effects of Pulmonary Fibrosis
Lung scarring associated with pulmonary fibrosis is not reversible. No treatments have proven effective in stopping the disease’s progression entirely, but some treatments might slow the advancement of the disease temporarily and improve symptoms.
Patients with idiopathic pulmonary fibrosis have a median survival rate of only two to three years, but there are those who do live much longer. The most common reason for death with PF is respiratory failure due to the progression of the condition. While there’s an overall poor prognosis for IPF, the clinical course of each patient differs from gradual progression of the condition to acute decompensation and death.
Several clinical variables associate with survival, but there’s no real approach to bring predictors together to define the disease’s stage or determine prognosis accurately.
When thinking of a person with lung disease like idiopathic pulmonary fibrosis, you can probably understand why a primary side effect would be physical exhaustion. However, what you may not realize is that mental exhaustion typically coincides with having chronic conditions like IPF.
Pulmonary fibrosis can make you feel mentally exhausted on top of taking a physical toll on your body. Asking for help can be difficult for you. Because of your declining lung function, you likely can’t do simple things like you once could. While your loved ones might offer you help, it may be a mental battle internally for you to accept it or ask for it.
You also need to consider your future needs. There will be things to think about such as:
- Needing help for basic tasks
- Transplant process
It all can become overwhelming. You may be worried about what your condition will do to your family and what it will put them through. Numerous things can cause mental exhaustion and fatigue relating directly to your IPF diagnosis and living with the condition.
There’s also the risk of depression and anxiety. In a study, anxiety and depression symptoms were seen in around 25.9 percent and 21.4 percent of IPF patients. Anxiety and depression are quite common in idiopathic pulmonary fibrosis patients. While there are no substantial differences as far as hospitalization and survival rate, this study shows anxiety and depression can influence an idiopathic pulmonary fibrosis patient’s quality of life significantly.
Pulmonary Fibrosis Statistics
Statistics reported by the National Institutes of Health about pulmonary fibrosis include:
Current Treatments Available for Pulmonary Fibrosis and Their Side Effects
Each person who receives a pulmonary fibrosis diagnosis will experience the condition in their own way. There isn’t any expected or standard clinical course.
Some individuals remain stable for long periods of time while others experience a quick symptom progression. There are then those who suffer episodes of deterioration as time goes on that fluctuate between periods of worsening symptoms and stability. Because of this, doctors individualize PF treatment approaches based on medical history and symptoms.
Doctors prescribe a whole range of PF medications. Your doctor decides if you require medication to treat your pulmonary fibrosis case. Some medications your doctor could prescribe to treat your pulmonary fibrosis include:
Corticosteroids like prednisone decrease inflammation and suppress your immune system. Side effects may include:
- Weight gain
- Skin thinning
- Increased susceptibility to infection
- Glaucoma and cataracts
- Bruising easily
- Cyclophosphamide (Cytoxan)
Cytoxan is a chemo agent that suppresses inflammation. Doctors commonly prescribe it to treat different types of PF. While patients usually take cyclophosphamide in pill form, you can receive it intravenously. Side effects may include:
- Stomach upset or pain
- Nausea or vomiting
- Temporary hair loss
- Loss of appetite
- Missed menstrual periods
- Skin color changes (darkening)
- Mycophenolate Mofetil
Myfortic and Cellcept are two types of mycophenolate mofetil medications. They modulate your immune system. Doctors may prescribe them by themselves or with corticosteroids. Side effects may include:
- Stomach pain
- Nausea or vomiting
- Sleep problems
- Tingling or numbness feeling
- Swelling of your feet or hands
- Nintedanib (Ofev)
This is an anti-fibrotic that doctors use to treat IPF. It helps slow lung function decline in those who have mild-to-moderate cases of idiopathic pulmonary fibrosis. You take it twice a day orally. Side effects may include:
- Nausea or vomiting
- Abdominal or stomach pain
- Liver enzyme elevation
- Liver problems
- A headache
- Weight loss
- Decreased appetite
These are only some of the many different medications prescribed to patients with pulmonary fibrosis. Be sure to talk with your doctor to see which of these or other medicines might help treat your PF.
The medical research community continues to aggressively investigate new treatments for all types of pulmonary fibrosis. You can reach out to your doctor to see if you can join a study testing experimental treatment options. Clinical trials for pulmonary fibrosis can include studies of anti-fibrotic therapies, stem cell therapies, growth factor inhibitor proteins and genetic research.
You can search for clinical trials for pulmonary fibrosis at the National Institutes of Health (NIH) website.
Idiopathic pulmonary fibrosis, the endocannabinoid system and cannabinoids
Dr. Raquel Peyraube is a doctor in medicine and a specialist in the problematic use of drugs. She has trained in psychiatry, toxicology and psychoanalytical psychotherapy and in subjects such as childhood, adolescence and social exclusion. She has 28 years’ experience in the field. Throughout her career, she has made contributions in training, prevention, treatment and damage reduction, including innovating theoretical and methodological developments with emphasis on ethical issues. As a former clinical director of ICEERS, she is now an ad hoc consultant of the Uruguayan National Drugs Secretariat giving advice on reform of the public drugs policy and of the Institute of Cannabis Regulation and Control. She is a clinical researcher and a member of research teams for monitoring the law in Uruguay. She sits on several international scientific committees and is an active member of the IACM (International Association for Cannabinoid Medicines). She currently works on the development of clinical trials, medical education on medicinal cannabis, and dissemination of information and advice for reform of drugs policies in various countries.
Idiopathic pulmonary fibrosis (IPF), also known as diffuse interstitial pulmonary fibrosis, is an incurable disease with no known cause (i.e. an idiopathic condition). As its name suggests, it is characterised by diffuse fibrotic scarring of the lung tissue. This process leads to the healthy lung tissue being replaced with fibrotic tissue; as result, the lung loses its elasticity, becoming rigid. Progress of the fibrotic process gradually impairs respiratory function to the point where it is severely compromised, as the tissue is not fit to perform the gas exchange (delivery of oxygen and elimination of carbon dioxide) involved in the respiratory function.
IPF is a very uncommon disease. It is estimated that it affects around 5 million people throughout the world and it is slightly more prevalent among men than women. Onset usually occurs between 55 and 66 years of age, although it can start earlier in some cases. Some forms of the disease are familial.
The cause or causes of the disease are still unknown. Nor is it known why some people are affected and others are not, even when exposed to the same factors that have been postulated as being possible triggers of its genesis. Nonetheless, some information is available and certain hypotheses have been put forward regarding its etiopathogenesis. Multiple causes have been postulated, ranging from genetic components, environmental pollutants, infection, exposure to certain medicines and tobacco smoke.
Symptoms include progressive respiratory difficulty as the disease advances. Blood oxygenation levels gradually fall, initially in common activities and then even with the most minimal movements. This evolution is generally rapid, taking between some months and some years, but in some cases, it is much slower.
Other symptoms include a (generally dry) cough, fatigue and fever. When oxygenation levels fall, cyanosis appears (i.e. a bluish discolouration of lips and nails). As in other pulmonary conditions, clubbing of the fingers may occur.
Pulmonary fibrosis with the loss of the fine lung vasculature eventually affects the heart as the result of an increase in pressure in the pulmonary arteries which the heart must overcome to pump blood to the lung for oxygenation.
Treatment is oriented towards relieving the symptoms and trying to delay evolution of the disease. Basically, two drugs are used which have been approved for treating IPF: pirfenidone and nintedanib. As the disease advances, patients will require an oxygen supply at home and portable devices to provide oxygen wherever they go. Respiratory rehabilitation and physiotherapy can help relieve the symptoms for a time. A lung transplant may be considered in some cases.
A study was presented at the ICRS conference in Montreal in June 2017, which I consider to be particularly important given the present state of our knowledge and the therapeutic possibilities for treating IPF. At present, we have little to offer such patients, who have a very delicate prognosis.
I found the study especially interesting as I have had two consultations regarding this disease. Patients quite often consult their physicians about the possibility of using additional cannabis-based treatments when their prognosis is unpromising and when treatment has proved either ineffective or has many adverse side effects.
My clinical reasoning had already led me to consider using cannabidiol, given its powerful anti-inflammatory action, despite the fact that assessments of anti-inflammatory treatment have not shown it to reduce the fibrotic response in this pathology (this is probably because the mechanism whereby the fibrosis is activated does not appear to be a response to a triggering inflammatory process).
One group of American researchers have proposed the CB1 receptor as a therapeutic target for treating IPF in association with another therapeutic target to try to improve antifibrotic effectiveness (Cinar R et al 1 ). Endocannabinoids acting by way of the CB1 receptor are known to promote fibrosis at a hepatic, cardiac and renal level and in radiation-induced pulmonary fibrosis. Given that the role of these compounds in IPF is unclear, the authors tried to identify its role in the complex and multifactorial pathogenesis of this disease, and hypothesised that it might be possible to improve the therapeutic effectiveness by addressing several of the mechanisms involved.
Inducible nitrous oxide synthase (iNOS) activity is increased in IPF and this increase correlates with the progress of the disease. Inhibitors of this enzyme have shown to have an antifibrotic effect in animal models (mice).
In their research, the authors assessed endocannabinoid activity and the activity of the CB1 receptor and iNOS, both in humans and in the animal model equivalent. They also assessed the therapeutic potential in mice of an orally administered synthetic molecule that inhibits both the CB1 receptor and iNOS. The study was conducted on human and animal lung samples. The researchers found that anandamide increased both in patients with IPF and in animals in which pulmonary fibrosis was induced, and that this increase was accompanied by a worsening of the pulmonary function (measured using tests of pulmonary function). In the animal lungs, this increase was correlated with a worsening of the pulmonary function. The findings confirmed a reduction in the expression of FAAH (Fatty Acid Amine Hydrolase), an enzyme that degrades anandamide, which evidently contributes even more to raising these levels. They also found a significant and mutually independent elevation in levels of CB1 and iNOS in patients with severe IPF. Likewise, CB1 activation in macrophages (active cells in inflammatory processes) was associated with a proinflammatory and profibrotic state, and an increased expression of interferon regulatory factor 5.
Simultaneous blocking of the CB1 receptor at a pulmonary level and of iNOS with the experimental molecule administered dramatically improved animal survival rates. The authors conclude that simultaneous blocking of the two increases the therapeutic antifibrotic effectiveness.
However, as already stated, treatments with anti-inflammatories in IPF patients have not given the results that would be expected of a fibrosis secondary to an inflammatory process. In other words, if the fibrosis were the result of an inflammatory process, as commonly occurs, inhibiting the inflammatory response with anti-inflammatories should improve the fibrosis.
Obviously, there is much that much remains to be clarified about the mechanism involved in IPF, but the results of this study open a window of hope to patients, in that it appears that simultaneous blocking of iNOS and CB1 might improve the effectiveness of antifibrotic treatment. We might therefore be on the threshold of a treatment for these patients, which although not curing them, would at least slow the evolution of the disease significantly as compared to the treatments currently available.
At the same time, CBD has been shown to modulate the levels of anandamide to a greater or lesser degree in different pathological processes. Despite the lack of scientific evidence of its potential beneficial effect in IPF, it is reasonable to wonder whether because of its mechanisms of action, CBD might also have this simultaneous twin action at a pulmonary level and particularly in IPF: downregulation of CB1 receptors because of its action as a CB1 antagonist, combined with its action in reducing the expression of proinflammatory enzymes, including precisely iNOS through NFκB antagonism (a core potentiating factor of the kappa light chains of activated B cells) through activation of the PPAR-γ receptors.
In view of safety levels in the use of CBD (when properly medicated and indicated, it has a low rate of adverse effect, generally ranging from slight to moderate). Depending on the absence or availability of effective treatments, I consider that doses of cannabidiol of between 100 and 300 mg per day might be added to patients’ current treatments, depending on their tolerance and their financial possibilities.
Given the absence of legal regulation for such products in most countries, their medicinal use is also unsubsidised. Unfortunately, this means that economic factors have a bearing on patients’ ability to access products of pharmaceutical quality in sufficient doses to treat their conditions.
1. Cinar R, Gochuico BR, Iyer M, Yokoyama T, Park JK, Coffey NJ, Jourdan T, Gahl WA and Kunos G. Laboratorio de Estudios Fisiológicos de NIAAA y Medical Genetic Branch de NHGRI
CBD Oil And Pulmonary Fibrosis
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- Palabras clave
- Palabras clave
- Epidemiological data
- Pharmacological data
- Health effects of using marijuana
- Effects on lung function and its role in chronic obstructive pulmonary disease
- Respiratory symptoms
- Lung cancer
- Bullous disease, pneumothorax and pneumomediastinum, barotrauma
- Risks of respiratory infection
- Legalization of marijuana use and public health risks
- Conflict of interests
José Miguel Chatkin a , Gustavo Zabert b , Ignacio Zabert b , Gustavo Chatkin a , Carlos Andrés Jiménez-Ruiz c ,
, Jose Ignacio de Granda-Orive d , Daniel Buljubasich e , Segismundo Solano Reina f , Ana Figueiredo g , Sofia Ravara h , i , j , Juan Antonio Riesco Miranda k , Christina Gratziou l , en representación del Grupo de trabajo de tabaquismo ERS/ALAT/SEPAR/SBP/SPP
Marijuana is the most widely used illegal drug in the world, with a prevalence of 2.5%–5%, and the second most commonly smoked substance after tobacco. The components of smoke from combustion of marijuana are similar to those produced by the combustion of tobacco, but they differ in terms of psychoactive components and use. Inhalation of cannabis smoke affects the respiratory tract, so the available evidence must be updated in order to provide pulmonologists with the latest scientific information.
In this article, we review the impact of cannabis consumption on the lungs, taking into account that the respiratory route is the most popular route of cannabis consumption.
La marihuana es la droga ilícita más consumida en el mundo con prevalencia de 2,5 a 5% y la segunda sustancia fumada después del tabaco. Los componentes del humo por la combustión de esta sustancia son similares a los producidos en la combustión del tabaco, pero difieren en la sustancia psicoactiva y en la práctica de fumar. La inhalación del humo de cannabis produce consecuencias sobre el aparato respiratorio. Por ello se hace necesario actualizar la evidencia disponible para ofrecer información científica al neumólogo.
En este artículo se revisa el impacto del consumo de cannabis en los pulmones, teniendo en cuenta que la ruta más popular de la ingestión de cannabis es a través de las vías respiratorias.
Cannabis, better known as marijuana, is a dioecious herbaceous plant. 1,2 Marijuana is the name given to the different species of the Cannabis genus, of which Cannabis sativa is the most widespread. All species contain terpenophenolic organic compounds called phytocannabinoids. The most well-known cannabinoids are delta-9-tetrahydrocannabinol (THC), cannabinol (CBN), and cannabidiol (CBD). These compounds affect the neurocognitive system by stimulating a series of specific cannabinoid (CB) receptors in the body, the most widely investigated of which are CB1 and CB2. 3–6 The major psychoactive cannabinoid is THC; it has relaxing, analgesic effects but it also causes alteration of the senses, fatigue and appetite stimulation. The next most psychoactive compounds are CBN, a metabolite of THC that has similar effects, and CBD, which has antiepileptic and antiemetic effects, and also affects sleep. 7–10,6
The aim of this review is to analyze the available literature, focusing on the consequences of regular and continuous use of this substance on the respiratory tract. In this article we will not analyze in depth the political implications of legalization for medicinal or recreational purposes, or other effects on other organs and systems.
Cannabis is currently the most widely used illicit drug worldwide, and is taken by 120–250 million individuals, 2.6%–5.0% of the world’s adult population. 11,12 The highest prevalences are reported in North America (10.8%) and Oceania (10.9%), but it is used in most countries. 13 Prevalence data in South America show particularly alarming rates in Uruguay (8.3%) and Brazil (8.8%). The highest rates of use in Central America and the Caribbean are in Bermuda (10.9%), Belize (8.45%), and Barbados (8.3%), although figures are probably significantly underreported. 11
This drug can be consumed in different forms and via different routes, the most popular being smoking marijuana grass or cannabis resin hashish, but it is also inhaled via vaporizers, ingested or applied to the skin or mucous membranes. Marijuana is consumed by replacing the tobacco in cigarettes or by wrapping it manually in cigarette papers, in pipes, water pipes, or more recently, in vaporizers. 7,14 Marijuana is smoked in longer inhalations than tobacco, the volume inhaled is greater, and the inspiration is held for several seconds. This leads marijuana consumers to retain 3 and 5 times more tar and carbon monoxide, respectively, than amounts inhaled when smoking tobacco. 7 When tobacco and cannabis smoking are compared, it is important to remember that, in addition to the different inhalation techniques described above, tobacco cigarettes are generally smoked more frequently and at shorter intervals, due to the pharmacology of the psychoactive components: the half-life of nicotine is approximately 2 h, while cannabinoids are deposited in fat and can be detected in the body for several days or weeks. Thus, with the exception of time of use, calculations of exposure in terms of amount consumed or accumulated consumption in pack-years for tobacco or number of marijuana cigarettes per year for cannabis cannot be used to estimate the effects on health. 16
THC is a small lipophilic molecule, rapidly absorbed in the lung: within 4–10 min, it reaches a peak blood concentration 17 that will depend on the THC content of the plant. Psychotropic effects appear in a few seconds or minutes, and last up to 2–3 h. However, bioavailability varies between 2% and 56%, depending on the depth and duration of the inhalation and apnea time. 18
Except for nicotine and cannabinoids, which occur exclusively in each plant, the components of tobacco and cannabis smoke are similar. 17,19
Health Effects of Using Marijuana
A study in primates exposed to different doses of marijuana smoke, placebo cigarettes, or common tobacco smoke revealed epithelial hyperplasia in all groups, but a higher incidence and severity of bronchiolitis, alveolar cell hyperplasia with atypia and fibrosis was observed in subjects exposed to marijuana smoke. The authors concluded that endocannabinoids may be responsible for these effects. 20
For this reason, the damage that marijuana consumption can cause to the respiratory system merits in-depth analysis, not only due to the health implications deriving from the high prevalence of illegal consumption, but because its medicinal and recreational use is now proposed in several countries. 9,11,21
Most studies have methodological limitations, due in part to the information bias imposed by the consumption of illegal drugs, but also by the limited number of consumers, particularly heavy users, included in the analyses, and the difficulty in quantifying consumption. 1 As marijuana is usually smoked without a filter, the concentration of particles in the airways is 4 times higher than with tobacco smoke. This manner of smoking also generates higher temperatures, modifying biochemical processes and producing many substances. 17 In addition, cannabis and tobacco are often mixed, not only due to overlapping addictions, but also because the mix increases the supply of THC, producing greater psychoactive effects than when cannabis is smoked alone. 3,22,23
Effects on Lung Function and its Role in Chronic Obstructive Pulmonary Disease
In 1973, some studies described acute bronchodilation in normal subjects and in asthmatics after smoking marijuana with controlled doses of THC in aerosol and orally. 24,25 A suggested mechanism for this phenomenon is stimulation of CB1 receptors in the postganglionic axons of the parasympathetic nerves in the airways, inhibiting the release of acetylcholine and preventing contraction of the bronchial muscles. In contrast, acute exposure to tobacco cigarette smoke is known to induce acute bronchospasm by activation of the cholinergic airway reflexes. 26,27
In 1997, Tashkin et al. 28 found in a cohort with an 8-year follow-up that, unlike tobacco, smoking marijuana (3 marijuana cigarettes per day) did not accelerate FEV1 decline. However, the authors referred to a low follow-up rate of 65% as one of the limitations of the study.
Ten years later, in 2007, Tetrault et al. 29 reported the acute bronchodilator effects of marijuana use: increased FEV1, peak flow and airway resistance (Raw); and decreased specific airways conductance (sGAW).
In 2012, Pletcher et al. 30 evaluated the association between exposure to marijuana and lung function in a cohort study with a follow-up of more than 20 years. The authors found that in marijuana users, lower exposure was associated with improvements in FEV1 and FVC, but that this effect was lost and FEV1 worsened when exposure was higher, while in tobacco smokers, lung function decline measured by FEV1 and FVC was linearly related with exposure.
More recently, Tashkin 31 confirmed that comparing lung function between marijuana smokers and non-smokers produces heterogeneous results. Some studies found no differences in lung function, others reported a real increase in FVC and/or FEV1, and others reported a decrease in the FEV1/FVC ratio. Macleod et al., 32 in a cross-sectional study of 500 cases, found that smokers of marijuana and tobacco showed lower lung function values than smokers of tobacco alone, and that the prevalence of chronic obstructive pulmonary disease (COPD) increased by 0.3% for each marijuana cigarette-year unit.
The few studies that analyzed carbon monoxide diffusing capacity in marijuana users found no significant changes. When airway resistance was evaluated by plethysmography in marijuana smokers, only a modest increase in airway resistance was found, suggesting central airway obstruction. 33
In the NHANES Nutrition Survey of 2009–2010, data were collected on accumulated use of marijuana. An association was observed between airway obstruction and high consumption but not with mild to moderate consumption, with a cutoff point of 20 marijuana cigarettes-year. 33 Although the mechanism for these findings has not been clarified, a proposed hypothesis is that they are a result of stretching the lungs during the deep and repeated inhalations associated with the usual technique of smoking marijuana. 15
Aldington et al., 34 in a study that used chest high-resolution computed tomography, found that marijuana smokers had lower apical lung density than non-smokers and tobacco smokers, but only the latter group showed macroscopic emphysema.
Another study found that the consumption of more than 50 marijuana cigarettes was associated with a higher risk of COPD when smoked in a mixture with tobacco (OR 2.90, 95% CI, 1.53–5.51). The authors found no association between marijuana and COPD, but underline that the power of the study was insufficient to test this hypothesis. 35 Aldington et al., 34 mentioned above, described an association between tobacco and cannabis consumption and a reduced FEV1/FVC ratio, and although this association was statistically marginal for marijuana, they estimated an exposure/lung effect ratio of 1:2.5–5 between marijuana cigarettes-year in the case of cannabis and pack-years for cigarettes.
The consumption of marijuana and THC reduces sleep latency, causes sleepiness, 4 increases stage 4 sleep and decreases time of REM sleep, while abstinence is associated with insomnia, reduced slow wave sleep, and REM sleep rebound. 38,39 Similar effects have been observed in neonates of mothers who used marijuana during pregnancy. 40
Most studies indicate an increase in respiratory symptoms, such as cough, dyspnea, sputum, and worsening asthma in habitual marijuana smokers, with or without the concomitant use of tobacco, compared to non-smokers. 4 Marijuana use has also been associated with hoarseness and pharyngitis. 41
Marijuana users attend emergency departments more frequently with respiratory complaints, particularly exacerbations of bronchial asthma. 29,42
The NHANES III study 43 reported that smoking marijuana and tobacco increased respiratory symptoms even after adjusting for age, sex, smoking habit, and asthma. The association was maintained for chronic cough (OR=2.00 95% CI 1.32–3.01), chronic expectoration (OR=1.89 95% CI 1.35–2.66), and wheezing (OR=2.98 95% CI 2.05–4.34), but not for dyspnea. One of the most striking observations of this study was that the rates of respiratory symptoms reported by marijuana users were comparable to those of tobacco smokers who were 10 years older, an observation that has been echoed in other studies. 29,31,44–46
Tashkin et al. 46 followed up a group of tobacco smokers for 10 years, and found a reduction or resolution of respiratory symptoms in participants who gave up marijuana use, while those who continued to use the drug showed a progressive increase in symptoms.
The first studies to describe an association between carcinogenic substances and mutagenic changes and marijuana use were published in the 1970s. 47 Polycyclic aromatic hydrocarbons (PAH), such as benzopyrenes and phenols, are produced in marijuana smoke, suggesting that the consumption of marijuana may also be a risk factor for cancer, particularly of the lung.
Squamous metaplasia and tumor progression markers have been observed in bronchial biopsies of marijuana smokers, and changes in the expression of genes involved in the development of cancer were observed in experimental animal models. 48
Epidemiological studies that attempt to measure the association between marijuana and cancer have limitations. The main methodological drawbacks of these studies are that marijuana smokers are usually also concomitant tobacco users, sample sizes are generally small, participants are young, and data are biased, as marijuana is an illicit drug. 49 These factors might, at least in part, explain the contradictory results from the various studies.
An analysis investigating the marijuana use and its association with head and neck cancer found an OR of 2.6, 95% CI 1.1–6.6, but other studies did not obtain these results. 50,51
In California, a retrospective cohort study of 64,855 individuals aged 15–49 years examined the association of self-reported marijuana use with cases of cancer over a mean follow-up of 8.6 years. Marijuana use was not associated with an increased risk of cancer, after adjusting for tobacco and alcohol consumption, socioeconomic level, and sex. An important limitation of this study is that participants were young and the follow-up period was relatively short. Thus, during the observation period, most of the cohort had not yet reached the age at which the incidence of cancer is relevant. 51
In 2006, Mehra et al. 52 published a similar review in which they found no association between marijuana smoking and lung cancer, but the authors point out the same limitations mentioned above. In 2008, Berthiller et al. 53 reported an association between cannabis use, describing 430 cases of lung cancer compared to 778 controls in a case control study. The results remained statistically significant after adjustment for the consumption of tobacco in pack-years, OR=2.3, 95% CI: 1.5–3.6. In 2013, Callaghan et al. 54 questioned 49,321 men about their consumption of tobacco and marijuana during their military service when they were aged 18–20 years old. The cohort was followed for a further 40 years. They found a positive association between lung cancer and marijuana smoking when lifetime consumption was greater than 50 marijuana cigarettes, with a 2-fold increase in risk (HR 2.12, 95% CI 1.08–4.14) even after adjustment for tobacco and alcohol use, other respiratory diseases, and socioeconomic status.
To overcome methodological difficulties, in 2015 the International Lung Cancer Consortium 49 investigated the association of marijuana smoking and lung cancer in 2159 cases and 2985 controls in pooled data from 6 studies. The results were inconclusive, but a higher risk was observed in cannabis user than in individuals who had never smoked tobacco.
Nevertheless, another case control study examined 1212 cases of cancer, 611 of which were lung cancer, and 1040 control cases with a comprehensive history of drug, tobacco and alcohol use, occupational exposure, diet, and family history of cancer over a 5-year period. Results showed an association that was lost in the adjusted analysis. The authors acknowledged limitations in this study, but concluded that the association between marijuana and lung cancer is not strong. 50
In conclusion, available evidence suggests that the use of marijuana at high doses, and perhaps moderate doses, may be a risk factor for lung cancer, a hypothesis that appears to be plausible. 48,55 A recent systematic review reached similar conclusions. 56
Bullous Disease, Pneumothorax and Pneumomediastinum, Barotrauma
Cases have been reported of bullous disease, 57,58 emphysema, 59 pneumothorax, and pneumomediastinum 60 associated with the use of marijuana in young patients. 44,57,61–63 However, as these studies are generally only case series, no association or causal relationship could be established. 44
Marijuana smoking techniques might explain these events. 60–63 “Shotgunning”, exhaling smoke into the mouth of another person, is another practice that could be related with these cases. 64 Lastly, some authors suggest the existence of inflammatory mechanisms in the bullae of marijuana smokers. 65
Risks of Respiratory Infection
Marijuana smoke damages the epithelium, with loss of ciliated cells and hyperplasia of mucus-secreting goblet cells. These changes cause reduced mucociliary clearance, with mucus accumulation and bacterial colonization increasing the risk of infections in the respiratory tract. 66 THC also alters the bactericidal and fungicidal activity of the alveolar macrophages. 3
Cannabinoids affect the functioning of immune cells, such as B and T lymphocytes and NK cells, 27,67 and can also alter the expression of many cytokines.
Marijuana contaminated with Aspergillus fumigatus 68 and Gram-negative bacteria 69 has also been encountered, possibly explaining some very severe cases of aspergillosis in marijuana smokers with immune deficiency due to HIV-AIDS, chronic granulomatous disease, bone marrow transplant, kidney transplant and cancer treated with chemotherapy. 70,71
The spread of tuberculosis by sharing marijuana cigarettes or water pipes has also been described. 72,73
Marijuana is an independent risk factor for opportunistic lung infections in HIV-Aids. However, neither marijuana nor other psychoactive drugs were identified as a risk factor for accelerating immunodeficiency in a multicenter cohort study. 74
Legalization of Marijuana use and Public heAlth Risks
Without going into the possible political and strategic considerations for the control of drug trafficking, the legalization of cannabis for recreational use can be expected to contribute to an increase in social tolerance and a normalization of consumption. 1,4,9,10,75 This drug will not only be more accessible, but also more affordable for the entire population. 76
To date, the available studies and observations on the effects of policies legalizing the use of marijuana do not provide sufficient evidence to judge the benefit and/or harm of such actions. Very few countries have agreed to implemented such policies, so this would be a good moment to propose global strategies for the control of these substances, similar to the FCTC 77 and MPOWER. 78
Evidence shows that active inhalation of marijuana smoke is associated with respiratory diseases and in particular with COPD and cancer when smoked concomitantly with tobacco. The composition of marijuana smoke is similar to that of tobacco smoke, so the increasing consumption of cannabis by inhalation in the last few decades should alert the scientific community to the possible impact on lung health. 79–85
The available evidence is still inconclusive, and many aspects need confirmation or further studies. However, in their daily practice, physicians, and in particular respiratory medicine experts must address the use of marijuana, especially among young people. Individuals must be informed that the recreational use of this substance is not free of risks to health in general and the respiratory tract in particular. 6 The available evidence tends to be limited by imprecise methods of determining exposure to marijuana smoke and recording data, and by the fact that in most countries consumption is still illegal, impeding the collection of accurate information. 86 We need new studies that carefully take into account these shortcomings, as well as more basic research in animal models exploring the effects of marijuana on the respiratory tract.
While the medicinal use of cannabis derivatives with proven scientific evidence and products currently under development is acceptable, the usual procedures for the evaluation of any drug must be followed, and recreational uses must be considered separately.