Most tobacco smokers consume more than 10 cigarettes per day and some consume 40 or more. Regular marijuana smokers seldom consume more than 3-5 cigarettes per day and most consume far fewer. Thus, the amount of irritant material inhaled almost never approaches that of tobacco users.
Frequent marijuana smokers experience adverse respiratory symptoms from smoking, including chronic cough, chronic phlegm, and wheezing. However, the only prospective clinical study shows no increased risk of crippling pulmonary disease (chronic bronchitis and emphysema).
Since 1982, UCLA researchers have evaluated pulmonary function and bronchial cell characteristics in marijuana-only smokers, tobacco-only smokers, smokers of both, and non-smokers. Although they have found changes in marijuana-only smokers, the changes are much less pronounced than those found in tobacco smokers.
The nature of the marijuana-induced changes were also different, occuring primarily in the lung's large airways-not the small peripheral airways affected by tobacco smoke. Since it is small-airway inflamation that causes chronic bronchitis and emphysema, marijuana smokers may not develop these diseases.
In an epidemiological survey, approximately 1200 subjects gave information on smoking and pulmonary function at 2-year intervals. A large percentage of the subjects underwent pulmonary function testing. Although a small group who reported previous marijuana smoking had significant pulmonary abnormalities, curent marijuana smokers had no significant reduction in any pulmonary functions.
There are no epidemiological or aggregate clinical data suggesting that marijuana-only smokers develop lung cancer. However, since some bronchial cell changes appear to be pre-cancerous, an increased risk of cancer among frequent marijuana smokers is possible.
Since the pulmonary risks associated with marijuana are related to smoking, the danger is eliminated with other routes of administration. For committed smokers, pulmonary risk might be reduced with higher-potency products, which produce desired psychoactive effects with less inhalation of irritants. Smokers could also be encouraged to abandon deep inhalation and breath-holding, which increase drug delivery only slightly.
Finally, pulmonary risk might be reduced if marijuana were smoked in water pipes rather than cigarettes.
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."
BOSTON, Jan. 30, 1997 (UPI) - The U.S. federal government has failed to make public its own 1994 study that undercuts its position that marijuana is carcinogenic - a $2 million study by the National Toxicology Program.
The program's deputy director, John Bucher says the study "found absolutely no evidence of cancer." In fact, animals that received THC had fewer cancers. Bucher denies his agency had been pressured to shelve the report, saying the delay in making it public was due to a personnel shortage.
The Boston Globe reported Thursday (1-30-97) that the study indicates not only that the main ingredient in marijuana, THC, does not cause cancer, but also that it may even protect against malignancies, laboratory tests on animals show.
The report comes on the heels of an editorial in the prestigious New England Journal of Medicine that favours the controlled medical use of marijuana, and calls current federal policy "misguided, heavy-handed and inhumane." The Clinton administration has said that doctors prescribing marijuana could be prosecuted for a federal crime.
Marijuana has been reported to ease the pain, nausea and vomiting in advanced stages of cancer, AIDS and other serious illnesses, but the federal government claims other treatments have been deemed safer than what it calls "a psychoactive, burning carcinogen."
However, The Boston Globe says the government's claim appears to be undercut by its own $2 million study.