How does smoking – the most popular form of cannabis administration – affect lung function? Coughing, a common symptom of cannabis smoking, signals an underlying irritation in lung tissue. However, it was not clear for a long time whether this reflected an acute but relatively benign problem, or if instead it hinted at a more deleterious risk under prolonged exposure.
In 1985, Dr. R. Morris examined sections of the lung tissue in corpses of cannabis smokers who had suddenly died. In his report he noted a high concentration of macrophage immune cells surrounding areas of infection and tissue scarring. But, as Dr. Nicolas Flamand and other researchers from Québec note, the study lacked enough information to determine if these cellular changes were due to marijuana alone, or to other constituents of smoke that are also present in drugs like tobacco. This observation is part of a comprehensive review on the effects of cannabinoids on the lungs that was published recently in the open access journal Frontiers in Pharmacology.
The authors inform us that later studies determined that cannabis and tobacco smoke indeed have different effects on lung function. The clearest evidence for this came from a 1991 study on primates, in which the animals were given marijuana or placebo cigarettes. The results replicated findings from previous human studies, showing that cannabis does incur specific dose-related forms of cellular damage, some of which are not observed in tobacco smokers. It was deduced that cannabinoids or other active compounds of cannabis must be responsible for these effects.
Studies of the effects of phytocannabinoids in lung cells are still at an early stage, with some evidence suggesting that THC may decrease cell viability and cause changes in gene expression related to the inflammatory response. More substantial findings for negative effects of THC come from studies on innate immune cells. Specifically, THC has been shown to impair animal macrophage activity in several ways (all crucial in the fight against bacteria, viruses and toxins), which are consistent with results from studies of human cannabis smokers. Additional evidence suggests that THC also impairs some aspects of learned immunity.
Recent discoveries of cannabinoid type 1 and 2 receptors in lung tissues and immune cells that are typically involved in lung immunity (including those that caught Dr. Morris’s attention thirty years ago) give strong evidence for an intervening role of the eCB system. Parallel to this line of research, authors have also turned their attention to the effects of endocannabinoids and their derivatives on cellular functions that could be relevant for lung functioning.
The evidence available suggests a prominent function of endocannabinoid derivatives in aspects of airway tissue permeability and activity of white blood cells. In the same context, the endocannabinoid 2-AG was found to recruit eosinophils, a type of white cell that is partially responsible for the inflammatory state that constricts air intake in asthma. While the impact of this in normal asthma conditions is still unclear, it is perhaps telling that two independent case reports found marijuana consumption to precede eosinophilic pneumonia.
Having established the cellular effects of cannabinoids, the next question pertained to how those substances affect the whole organism response to different types of pathogens. Several independent animal studies have shown that the direct administration of phytocannabinoids tends to impair pathogen clearance and, in some cases, increase mortality (see table below next paragraph).
A general anti-inflammatory response by cannabinoids seems to be behind this loss of function — an effect that in different circumstances could be actually helpful. For instance, a strong inflammatory response is a common but serious complication in acute lung injury, and several animal studies have now attested to the beneficial effects of cannabinoids in these cases (see table below).
Note: the inconsistencies in CBD effects are likely due to the differences in mode of administration between studies.
Taken together, these studies paint a complex picture of the role of cannabis in lung function. It is evident that cannabis smoking produces potentially deleterious effects that are not shared by tobacco. Further research is necessary to ascertain to what extent these findings generalize to humans. On the other hand, the anti-inflammatory effects of cannabinoids that increase lungs’ susceptibility to diseases could be helpful in certain conditions. The authors conclude their review by highlighting how the newly observed roles of cannabinoid derivatives call for medical investigation, as they suggest the possibility of modulating the eCB system in a more refined way, other than by using cannabinoids.