What asthma is
Asthma is a chronic inflammatory condition of the airways characterised by variable and reversible airflow obstruction, bronchial hyperresponsiveness, and underlying inflammation. Common symptoms include wheeze, shortness of breath, chest tightness, and cough, which vary over time and in intensity. In the UK, an estimated 5.4 million people receive treatment for asthma.
Standard management follows the British Thoracic Society (BTS) and Scottish Intercollegiate Guidelines Network (SIGN) stepped approach, starting with short-acting beta-2 agonists (such as salbutamol) for symptom relief, adding inhaled corticosteroids for maintenance control, and escalating through long-acting beta-2 agonists, leukotriene receptor antagonists, and, for severe cases, biologic therapies. The goal of treatment is to achieve symptom control and reduce the risk of exacerbations and fixed airway obstruction.
Cannabis research on Asthma
One is directly relevant: a 1974 double-blind crossover study by Tashkin and colleagues. The other is a general review of cannabis use and medication management in HIV patients that does not address respiratory physiology.
The key study: Tashkin et al., 1974
Tashkin, Shapiro, and Frank conducted a double-blind, placebo-controlled crossover study of the acute effects of smoked marijuana and oral THC on airway function in 10 subjects with stable bronchial asthma (human double-blind crossover trial, n=10). The study tested smoked 2 per cent natural marijuana (7 mg per kg) and 15 mg oral delta-9-tetrahydrocannabinol (THC) compared with placebo. Airway resistance and specific airway conductance (SGaw) were measured by whole-body plethysmography.
After smoked marijuana, specific airway conductance increased immediately and remained significantly elevated at 33 to 48 per cent above initial control values for at least 2 hours. Placebo produced no change. The peak bronchodilator effect of 1,250 micrograms of isoproterenol (a standard short-acting beta-agonist) was more pronounced than that of marijuana, but the effect of marijuana lasted longer.
After oral ingestion of 15 mg THC, specific airway conductance was significantly elevated at 1 and 2 hours, and airway resistance was significantly reduced at 1 to 4 hours. Placebo produced no change. Both smoked marijuana and oral THC caused significant bronchodilation of at least 2 hours’ duration in asthmatic subjects.
This is a well-designed acute physiology study. It measured airway function precisely in a controlled setting. It established that THC, whether smoked or ingested, produces measurable bronchodilation in people with asthma. It did not test whether cannabinoids can be used as an ongoing asthma treatment, did not follow patients beyond a few hours, and did not evaluate clinical outcomes such as symptom control, exacerbation rates, or quality of life.
Historical context and limitations
The 1974 Tashkin study is now over 50 years old. It tested a single acute dose in 10 subjects. No modern replication with standardised cannabis preparations, vaporised delivery, or a larger sample exists in the published literature. The study is frequently cited but has not led to the development of cannabinoid-based asthma treatments.
A 1977 study by Tashkin and colleagues tested aerosolised delta-9-THC in healthy and asthmatic subjects and found significant bronchodilation in three of five asthmatic subjects, but cough, chest discomfort, and moderate to severe bronchoconstriction in the other two (human experimental study, PMID 319717). The inconsistency of response — bronchodilation in some, bronchoconstriction in others — is a significant safety concern for an airway-compromised population.
A 1980 review noted that short-term marijuana smoking produces bronchodilation but that long-term respiratory effects appear comparable to those of heavy cigarette use (PMID 7375399). The review predates vaporiser technology, which reduces but does not eliminate the respiratory risks of inhaled cannabis.
The smoking problem
The 1974 study’s positive bronchodilation finding was obtained with smoked marijuana. Smoking cannabis involves the inhalation of combustion products including carbon monoxide, tar, polycyclic aromatic hydrocarbons, and particulate matter. These are airway irritants and carcinogens. Chronic cannabis smoking is associated with bronchitis symptoms, airway inflammation, and increased sputum production. The acute bronchodilator effect of THC does not cancel the chronic airway damage caused by inhaling smoke. For people with asthma, whose airways are already inflamed and hyperresponsive, smoking any substance is a recognised asthma trigger and is contraindicated in standard clinical guidance.
No study has tested whether non-smoked cannabinoid delivery — such as oral THC, sublingual oils, or vaporised cannabis — can produce clinically meaningful improvement in asthma control over weeks or months of regular use. The 1974 study showed that oral THC produced bronchodilation lasting 2 to 4 hours, which provides a rationale for non-smoked delivery, but this single acute observation has not been developed into a treatment protocol.
Compounds studied for Asthma
THC is the only cannabinoid with direct human evidence of bronchodilator effect in asthmatic subjects. The 1974 Tashkin study demonstrated that both smoked marijuana and oral THC produce acute, measurable bronchodilation in people with stable asthma. The oral THC result indicates that the bronchodilator effect is a pharmacological property of THC and not simply a non-specific effect of deep inhalation. This is a finding of physiological interest. It does not establish that THC is a safe or effective asthma treatment, and the delivery method matters critically — smoking THC is harmful to asthmatic airways even if it produces short-term bronchodilation.
CBD has anti-inflammatory properties demonstrated in preclinical models of airway inflammation, but no human study has tested CBD for asthma or any respiratory condition. The relevance of preclinical anti-inflammatory data to clinical asthma outcomes is unknown.
Caryophyllene is a CB2 receptor agonist with anti-inflammatory properties shown in preclinical models. CB2 receptors are present on immune cells involved in airway inflammation. No human asthma study of caryophyllene exists.
Pinene is a monoterpene found in some cannabis varieties and has been noted anecdotally as a bronchodilator in traditional herbal medicine, but there is no controlled human study testing pinene for asthma or any respiratory condition.
Eucalyptol is a monoterpene oxide found in certain cannabis varieties and has been studied outside of cannabis research for its expectorant and airway-cooling effects. No human asthma study of eucalyptol as a cannabis-derived compound exists.
Limits of the evidence for Asthma
The evidence that cannabinoids produce acute bronchodilation in people with asthma comes from one study conducted in 1974 involving 10 subjects and a single acute dose. That study has never been replicated in a modern clinical trial using standardised cannabis preparations, vaporised delivery, or adequate sample sizes.
The acute bronchodilator effect demonstrated in 1974 is a short-term physiological observation limited to a few hours. It does not establish that regular cannabinoid use improves asthma control, reduces exacerbations, replaces or augments standard inhaler therapy, or is safe for the asthmatic airway over weeks, months, or years.
The delivery route is the central unresolved problem. Smoking cannabis — the delivery method used in the positive 1974 result and the most common route of recreational cannabis use — involves inhaling combustion products that are harmful to airways. Chronic cannabis smoking is associated with airway inflammation, bronchitis symptoms, and impaired respiratory function. The 1980 review that documented both acute bronchodilation and chronic respiratory harm from cannabis smoking described exactly this tension. For people with asthma, smoking any substance is clinically contraindicated.
Non-smoked delivery (oral, sublingual, vaporised) avoids combustion products but has not been studied for asthma in any clinical trial. Oral THC produced bronchodilation lasting 2 to 4 hours in the 1974 study, but the psychoactive effects of an oral THC dose sufficient to produce bronchodilation are a barrier to clinical use.
The 1977 aerosolised THC study, which found bronchodilation in three subjects but bronchoconstriction in two, is a reminder that individual responses vary and that a cannabinoid delivered to the airway can trigger bronchospasm, which in an asthmatic person is a potentially serious adverse event.
There is no cannabinoid-based product licensed for asthma. Standard asthma treatments — inhaled corticosteroids and beta-agonists — have a large, high-quality evidence base. No cannabinoid preparation has been compared against standard asthma treatment in a controlled trial.
Related conditions
- Anxiety disorders ; CBD laboratory studies and THC dose effects
- Inflammatory bowel disease ; small Crohn’s and ulcerative colitis trials
- Sleep disorders ; negative CBN trials and modest THC findings
- Chronic pain (NICE context) ; the evidence behind NICE guideline NG144
Read next
- THC ; acute bronchodilation documented in early human research
- CBD ; anti-inflammatory properties examined preclinically
- Browse the cannabinoid reference
- Browse the terpene reference
Sources
1. Tashkin DP, Shapiro BJ, Frank IM. Acute effects of smoked marijuana and oral delta-9-tetrahydrocannabinol on specific airway conductance in asthmatic subjects. American Review of Respiratory Disease. 1974;109:420-428. Study record
2. Tashkin DP, Soares JR, Hepler RS, Shapiro BJ, Rachelefsky GS. Bronchial effects of aerosolized delta 9-tetrahydrocannabinol in healthy and asthmatic subjects. American Review of Respiratory Disease. 1977;115(1):57-65. PMID: 319717. Study record
3. Tashkin DP. Marijuana and the lung. Chest. 1980;77(2 Suppl):304-306. PMID: 7375399. Study record
4. Tetrahydrocannabinol as a bronchodilator. Why bother. Chest. 1977;71(5):557-558. PMID: 852329. Study record
