L'ESTEREL, Quebec -- Heavy marijuana smokers show less evidence of lung injury than heavy tobacco smokers, and it may be cannabinoids that are protecting them from developing a condition like emphysema.
That's according to the principal investigator of a study done at the University of California at Los Angeles (UCLA).
Speaking at the third annual meeting of the International Cannabis Research Society here, Dr. Donald Tashkin, a pulmonologist and UCLA professor of medicine, concluded heavy marijuana use did not cause the same degree of lung injury as tobacco smoke.
"My own feeling is that marijuana smokers probably will not develop emphysema as a consequence of smoking marijuana," he said, but cautioned that does not rule out the development of other conditions like respiratory carcinoma.
"It may be that the THC (delta-9-tetrahydrocannabinol) in marijuana could have different effects on inflammatory cells, which may mediate injury in the lung."
His study, which aimed to measure the pulmonary effects of habitual marijuana use, followed nine tobacco smokers, 10 marijuana smokers, 10 nonsmokers and four smokers of both marijuana and tobacco. He gave both quantitative and qualitative explanations for his finding.
Marijuana users in the study smoked three or four joints daily for 15 years on average, while tobacco smokers in the study smoked 25 cigarettes daily over a period of 20 years, indicating a marked difference in exposure to smoke.
"There is a seven-fold difference in the amount of smoke to which marijuana and tobacco smokers are exposed," he said.
"It's the quantitative difference in smoke exposure that might explain the difference in the degree of lung injury as assessed by these physiologic indices."
Moreover, the phagocytes gathered from the lungs of marijuana smokers do not have the same properties as those gathered from the lungs of tobacco smokers.
"We have previously shown that the macrophages that are harvested from the rinse-out of the lungs of marijuana smokers seem not to be activated," he said. "They do not release toxic oxygen species, either under basal conditions or under stimulated conditions nearly to the extent that tobacco macrophages do. If anything, basal secretion of superoxide seems to be reduced in the marijuana smokers."
Dr. Tashkin measured the clearance of the molecule diethylene triamine penta-acetate (DTPA) from the lung, believed to be a more sensitive indicator of lung injury than measuring the lung's diffusing capacity.
If DTPA clearance is accelerated, then it implies an increase in the leakiness of the alveolar epithelial membrane, which implies injury to the membrane, he said.
Dr. Tashkin noted DTPA clearance is accelerated in tobacco smoke-related lung injury.
Initially, the chronic effects of marijuana smoke were measured in comparison to those of tobacco smoke: DTPA clearance was measured at about 12 hours after the last marijuana or tobacco cigarette smoked.
To determine the acute effects of marijuana and tobacco smoking, Dr. Tashkin restudied these smokers a week or two later, giving them a single joint of marijuana or a single tobacco cigarette or both, and then measuring DTPA clearance 15 minutes subsequently.
"What we found was the clearance of DTPA was abnormally rapid from the lung in the tobacco smokers," he said. "It was about twice the rate of non-smokers. In the marijuana smokers, there was a tendency toward a much less rapid rate of clearance. There was no acute effect in either tobacco or marijuana, and there was no added effect of marijuana or tobacco."
As with the lungs to tobacco smokers, when the lungs of marijuana smokers are "washed out", a marked increase in the number of alveolar macrophages is witnessed.
But whereas tobacco smoke has a concomitant effect of activating the macrophages, leading to the subsequent release of certain toxic substances, marijuana smoke fails to activate the macrophages, Dr. Tashkin said. He noted this difference could be attributed to differential regulation of cytokins.
"It may be that the macrophages from marijuana smokers release certain suppressive cytokins, like transforming growth factor-beta, which is known to suppress the inflammatory activity of nearly all of the site populations," he said. "That's our hypothesis, which we are currently exploring."
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