Synthetic cannabinoids induce acute lung inflammation via cannabinoid receptor 1 activation

• Published in: ERJ open research Vol. 6; no. 3; p. 121
• Main Authors: Zawatsky, Charles N., Abdalla, Jasmina, Cinar, Resat
• Format: Journal Article
• Language: English
• Published: European Respiratory Society 01.07.2020
• Subjects: Original Research Letters
• ISSN: 2312-0541; 2312-0541
• DOI: 10.1183/23120541.00121-2020

Synthetic cannabinoid (SC) use has persisted in the United States despite schedule-1 placement under the Synthetic Drug Abuse Prevention Act of 2012 [1]. Analysis of the National Poison Data System indicates that hospitalisations caused by SC use increased significantly between 2010 and 2015 [2]. Moreover, there is a trend of the increasing use of such compounds among adolescents [3]. SCs are often 30–100-fold more potent than Δ 9 -tetrahydrocannabinol (THC), the major psychoactive ingredient of cannabis, in activating Cannabinoid receptor 1 (CB 1 R). Users are attracted to SCs because of the cheaper, novel and stronger highs such substances offer compared to cannabis, and because the compounds are not screened for in typical drug tests [1, 2]. Among those hospitalised for SC use, some patients exhibited respiratory failure [4–7], pulmonary infiltrates [5, 7], alveolar damage or haemorrhage [5–7] and histopathologic features similar to organising pneumonia [4–6]. The mechanism by which SCs damage pulmonary tissue has yet to be elucidated – whether by SC binding at CB 1 R, CB 2 R or another receptor, and what downstream effects such binding elicits. Solving this conundrum is the first step in optimising treatment for patients presenting with SC-related respiratory distress. Synthetic cannabinoids (SCs) induce a pro-inflammatory condition by activating cannabinoid receptor 1 (CB 1 R) in the lungs of mice, which raises a potential therapeutic use of CB 1 R antagonists in SC-induced lung disease resulting in hospitalisation https://bit.ly/31bWw4Q