Addiction & recovery
Mack A, Joy J. Marijuana as Medicine? The Science Beyond the Controversy. The most heated arguments over medical marijuana do not concern its ability to alleviate patients' symptoms but rather its potential danger to individual users and to society.
This chapter first examines the scientific evidence that marijuana causes physical and psychological injury to individual users. Then it considers the potential social harms that could result from legalizing marijuana for medical uses. More detailed information and complete references for studies described below can be found in Chapter 3 of the IOM report, Marijuana and Medicine: Assessing the Science Base. Given the well-known consequences of tobacco smoking, it seems logical to suspect that marijuana could be equally detrimental to physical health.
Although free of nicotine, marijuana smoke certainly pollutes the lungs. And since tobacco smoking has been linked to respiratory injury, cancer, emphysema, heart disease, complications of pregnancy, low birth weight, and other ills, it makes sense to worry whether smoking marijuana might prove equally harmful. Scientists have compared marijuana and tobacco smoking on the basis of many different factors but have failed to find consis tent evidence that either substance poses a greater health risk than the other.
On the one hand, marijuana ts have been shown to deliver at least four times as much tar to the lungs as tobacco cigarettes of equivalent weight. This difference is due to the lack of filters on ts and because marijuana smokers typically inhale a larger volume of smoke and take it more deeply into the lungs than tobacco smokers do. Marijuana smokers also tend to hold smoke in for a time before exhaling, exposing the lungs to even greater levels of cancer-causing agents.
On the other hand, because they are packed more tightly, commercial cigarettes produce more smoke than hand-rolled ts. The harmful effects of marijuana, plus the fact that most tobacco users typically smoke more cigarettes per day than their marijuana-using counterparts, means that over the course of a day most tobacco users take far more smoke into their lungs than people who smoke marijuana exclusively. Thus it is impossible to make precise comparisons between the damage to one's health caused by smoking marijuana versus the damage caused by smoking tobacco.
And since an estimated 70 percent of marijuana users also smoke tobacco, it is difficult to conduct epidemiological studies that isolate the effects of marijuana smoking. Not surprisingly, clinical studies suggest that people who smoke marijuana are more likely to develop respiratory illnesses than are nonsmokers. A survey of outpatient medical visits at a large health maintenance organization HMO found that marijuana users were more likely to seek help for respiratory illnesses than people who smoked neither marijuana or tobacco.
One possible explanation for this finding is that the people who continued smoking for a long time had not been troubled by respiratory problems such as shortness of breath, while those who did develop uncomfortable symptoms quit smoking relatively quickly.
Unfortunately, the marijuana smokers who responded to this survey were not asked if they also used cocaine, which is known to intensify respiratory symptoms. It is also likely that some participants underreported their use of tobacco, alcohol, and marijuana.
A study of volunteers compared the incidence of chronic bronchitis symptoms excessive cough, sputum production, and wheezing among habitual marijuana smokers, tobacco smokers, and nonsmokers. Smokers—even those who did not smoke tobacco—had episodes of acute bronchitis more than five times as often as nonsmokers. Marijuana smokers also performed worse on lung function tests than did nonsmokers. The average marijuana smoker in this study consumed three to four ts per day; the tobacco users smoked an average of 20 cigarettes per day.
In this study of habitual marijuana smokers, participants who smoked both marijuana and tobacco reported no more symptoms of chronic bronchitis overall than those who smoked tobacco alone, an indication that smoking marijuana does not increase the harms caused by smoking tobacco. Another study did show evidence of such an interaction, but it was conducted on people who smoked considerably less marijuana and tobacco than those who participated in the ly described study.
Health effects of cannabis
Researchers have found that, in general, the interactive effects of toxic substances tend to be easiest to detect at low exposure levels. This may explain why the lighter smokers in the second study showed s of increased respiratory damage when they used both marijuana and tobacco, while the heavier smokers in the first study did not.
In any case, both studies indicate that marijuana smoke reduces respiratory function. Habitual smoking of either marijuana or tobacco damages the lining of the bronchial airways. After continuous exposure to smoke, the delicate tissues along these passageways become red and swollen. Smoking also transforms the cells of the bronchial airways.
These passages are normally lined with ciliated cells, whose hairlike projections move rapidly to sweep mucus toward the mouth. Bronchial injury, a more sensitive measure of damage than the symptoms of chronic bronchitis, is even greater among people who smoke both marijuana and tobacco. The damage extends to the interiors of bronchial cells, which develop a variety of abnormalities. Some of these changes, which are known to be precursors of cancer, have also been discovered in the respiratory tracts of marijuana and hashish smokers who did not use tobacco.
Another form of respiratory injury caused by tobacco smoke is a condition known as chronic obstructive pulmonary disease COPDa slow, progressive loss of elasticity in the passages that deliver air to the lungs. People with COPD become short of breath and exhibit symptoms of chronic bronchitis.
Attempts to determine whether marijuana smoke also provokes COPD have produced conflicting. For example, one group reported that smoking as little as a single t per day ificantly impaired small airway function, 3 while another failed to detect similar damage even in people who smoked four ts a day for more than 10 years. While many tobacco smokers accept coughing and shortness of breath as part of the price they pay for the pleasure of smoking, fear of cancer sometimes persuades them to quit. And then there are people who get little pleasure out of smoking but continue smoking to calm their nerves, that is, to avoid feeling anxious and irritable—the withdrawal symptoms of nicotine addiction.
Whether marijuana users should be similarly concerned remains to be conclusively proven. However, cellular, genetic, and clinical studies all suggest that marijuana smoke is an important risk factor in the development of respiratory cancer. Many of the same carcinogenic, or cancer-causing, compounds present in tobacco smoke are also found in burning marijuana. In particular, unfiltered smoke from ts contains higher concentrations of a class of chemicals called polycyclic aromatic hydrocarbons PAHs than does smoke from tobacco cigarettes. Since marijuana users generally inhale more deeply than tobacco smokers, they may be exposing their lungs to even higher levels of these dangerous substances.
Preliminary research also suggests that marijuana smokers' lung cells contain higher levels of an enzyme that converts PAHs into a cancer-causing form. Thus, it is not surprising that several studies implicate marijuana smoking as a risk factor for lung cancer as well as for mouth and throat cancer. Several reports have suggested that marijuana smokers are at greater risk than nonsmokers of developing cancers in tissues that come into contact with smoke, such as the lungs, mouth, larynx, pharynx, and esophagus.
However, these conclusions were based on series of case reports of patients with these cancers rather than from controlled studies. Thus, the increased frequency of cancers among marijuana smokers cannot be attributed to marijuana alone but may also result from other factors, such as tobacco smoking.
To date, only one large-scale study 5 has sought to determine the frequency with which marijuana smokers develop cancer. It included some 65, men and women HMO clients between the ages of 15 and Among these people, 1, cases of cancer were found, but marijuana use—defined as taking the drug on six or more occasions—appeared to increase only the risk of prostate cancer in men who did not smoke tobacco.
No association was found between marijuana use and any other type of cancer, including cancers normally linked to tobacco smoking. However, this study was limited by the fact that many of its participants were younger than the average ages when many cancers appear as well as by the short duration of their marijuana use. Lung cancer, for example, usually develops only after a long exposure to smoking; relatively few marijuana users persist in the habit for more than a few years, and most also smoke tobacco.
Researchers should soon be better able to pursue the question of marijuana's carcinogenicity.
More than 30 years have elapsed since the start of widespread marijuana use among young people in the United States, who now constitute a sufficiently large population to support meaningful epidemiological studies. On the other hand, such surveys are difficult to conduct, since far fewer people have smoked marijuana exclusively than have smoked tobacco alone and also because marijuana smokers are likely to underreport their use of the illegal drug.
In contrast to human studies, research on the effects of marijuana smoke at the cellular level provides strong evidence that it contains abundant carcinogens. Exposure to marijuana smoke has been shown to cause chromosomal changes that precede cancer—and in some cases outright malignancies—in isolated human and animal lung cells. Similar alterations have been detected in the actual lung cells of marijuana smokers and at even higher levels among those who also smoked tobacco.
An especially convincing study evaluated changes in blood cells taken from pregnant women who were exclusive smokers of marijuana and also from their babies after they were born. In studies the same group of investigators had found similar changes in the DNA of tobacco smokers, indicating that the substances responsible for this damage are present in both marijuana smoke and tobacco smoke.
Marijuana smoking has also been associated with increased mortality among men with AIDS. This finding is especially important since such patients comprise the largest group of medical marijuana users in the United States. Several factors may contribute to this trend, which is still largely unexplained.
It may be that people who use marijuana also tend to engage in risky sexual behavior or intravenous drug use, either of which puts them at higher risk for developing AIDS, but it is also likely that smoking marijuana adds to the burden that HIV places on the immune system. HIV-seropositive individuals who use marijuana regularly appear to be at increased risk of opportunistic infections and Kaposi's sarcoma; for those who smoke more than one-half pack of cigarettes per day, the risk is somewhat lower.
If smoking marijuana indeed makes AIDS patients sicker, it remains to be determined whether smoke, cannabinoids, or both are to blame see Chapter 5. The vast majority of studies on the physiological consequences of marijuana use have focused on smoking.
However, a few researchers have directly evaluated the effects of cannabinoids on isolated cells, experimental animals, and human subjects.
Most such studies have examined one of three areas of po tential damage: the immune system, the cardiovascular system, and reproductive and fetal health. As discussed in the last chapter, several biological studies suggest that cannabinoids can depress the immune system's response to infection.
Not all studies of this nature implicate cannabinoids as immune suppressants. In fact, some immune functions have been found to increase in response to cannabinoids. Such are not necessarily contradictory because many physiological processes contribute to immunity. That is particularly true of studies that test the effects of pure cannabinoids such as THC, since marijuana contains a variety of chemicals that may affect immune activity.
Although it demands equally cautious interpretation as studies on individual immune cells, research on disease resistance in animals exposed to cannabinoids more closely tracks the overall impact of cannabinoids on the immune system. Mice infected with pneumonia-causing bacteria died of septic shock when they were injected with THC before and after infection; those that did not receive THC developed immunity to the bacterium and survived.
This response was found to vary depending on the amount of THC the mice received and whether it was injected before or after they were infected with the bacteria. Similarly, two doses of THC given before and after infection with the herpes simplex virus appeared to hasten the death of immunodeficient mice, although a single dose of THC prior to infection did not.
Both experiments suggest that the timing of THC exposure relative to infection determines whether THC suppresses the immune response. Even if cannabinoids themselves cause little or no harm to the immune system, there is good reason to believe that smoking marijuana does.
Marijuana smoke been linked to increased mortality in people with AIDS and it also appears to injure an important class of immune cells in the lungs.