Cannabis Facts

Health Risk Myths and Realities

Marijuana Overdose

No evidence exists that anyone has ever died of a marijuana overdose. Tests performed on mice have shown that the ratio of cannabinoids (the chemicals in marijuana that make you stoned) necessary for overdose to the amount necessary for intoxication is 40,000:1. For comparison’s sake, that ratio for alcohol is generally between 4:1 and 10:1. Alcohol overdoses kill about 5,000 yearly but marijuana overdoses kill no one as far as anyone can tell.

Brain Damage

Marijuana is psychoactive because it stimulates certain brain receptors, but it does not produce toxins that kill them (like alcohol), and it does not wear them out as other drugs may. There is no evidence that marijuana use is a cause of brain damage. Studies by Dr. Robert Heath claimed the contrary in experiments on monkeys, but Heath’s work has been sharply criticized by the Institute of Medicine and the National Academy of Sciences on three primary counts:

its insufficient sample size (only four monkeys),
its failure to control experimental bias, and its misidentification of normal monkey brain structure as “damaged”.

A far superior experiment by the National Center for Toxicological Research (NCTR) involving 64 rhesus monkeys that were exposed to daily or weekly doses of marijuana smoke for a year found no evidence of structural or neurochemical changes in the brains of rhesus monkeys. Studies performed on actual human populations will confirm these results, even for chronic marijuana users (up to 18 joints per day) after many years of use. In fact, following the publication of two 1977 JAMA studies, the American Medical Association (AMA) officially announced its support for the decriminalization of marijuana.

Contrary to a 1987 television commercial sponsored by the Partnership for a Drug-Free America (PDFA), marijuana does not “flatten” brain waves either. In the commercial, a normal human brain wave was compared to what was supposedly the (much flatter) brain wave of a 14-year-old high on marijuana. It was actually the brain wave of a coma patient. PDFA lied about the data, and had to pull the commercial off of the air when researchers complained to the television networks.

In reality, marijuana has the effect of slightly increasing alpha-wave activity. Alpha waves are generally associated with meditative and relaxed states which are, in turn, often associated with human creativity.

Memory

Marijuana does impair short-term memory, but only during intoxication. Although the authoritative studies on marijuana use seem to agree that there is no residual impairment following intoxication, persistent impairment of short-term memory has been noted in chronic marijuana smokers up to 6 and 12 weeks following abstinence.

Heart Problems

It is accepted in medical circles today that marijuana use causes no evident long-term cardiovascular problems for normal persons. However, marijuana-smoking does cause changes in the heart and body’s circulation characteristic of stress, which may complicate preexisting cardiovascular problems like hypertension, cerebrovascular disease, and coronary atherosclerosis. Marijuana’s effects upon blood pressure are complex and inconsistent.

Hormones

Chronic marijuana use has not been found to alter testosterone or other sex hormone levels, despite the conclusions of Dr. R.C. Kolodony’s 1974 study. Seven similar studies have been performed since then, the most recent by a Dr. Robert Block at the University of Iowa, and none have reproduced Kolodony’s results. In contrast, heavy alcohol use is known to lower these same testosterone levels.

Reproductive Damage

No trustworthy study has ever shown that marijuana use damages the reproductive system, or causes chromosome breakage. Dr. Gabriel Nahas reached the opposite conclusion in his experiments performed in the early 1980s, but did so in part using the in vitro (i.e., in test tubes and petrii dishes) cells of rhesus monkeys. His rather unjustified claim that these changes would also occur in human bodies in vivo (in the body) was criticized by his colleagues and, in 1983, he renounced his own results.

Studies of actual human populations have failed to demonstrate that marijuana adversely affects the reproductive system. Wu et al. found in 1988 a correlation between marijuana use and low sperm counts in human males. But this is misleading because (1) a decrease in sperm count has not been shown to have a negative effect on fertility, and (2) the sperm count returned to normal levels after marijuana use had ceased.

Claims that marijuana use may impair hormone production, menstrual cycles, or fertility in females are both unproven and unfounded.

The Immune System

Studies in which lab rats were injected with extremely large quantities of THC have found that marijuana (in such unrealistically huge quantities) does have an “immunosuppressive effect” in those lab rats, in that it temporarily shuts off certain cells in the liver called lymphocytes and macrophages. These macrophages are useful in fighting off bacterial, not viral, infections. But this is only for the duration of intoxication. There also exists some evidence that marijuana metabolites stay in the lungs for up to seven months after smoking has ceased, possibly affecting the immune system of the lungs (but not by turning the cells off). This said, doctors and researchers are still not sure that the immune system is actually negatively affected in realistic situations since there are no numbers to support the idea. In fact, three studies showed that THC may have actually stimulated the immune system in the people studied.

Birth Defects

Unlike alcohol, cocaine, and tobacco, studies show that there exists no evident link between prenatal use of marijuana and birth defects or fetal alcohol syndrome in humans. In fact, marijuana use during the third trimester has been found to have a positive impact on birthweight. It is known that Delta-9-THC does enter the placenta, so mothers are advised against consuming large quantities.

Cancer

Smoking marijuana has the potential to cause both bronchitis and cancer of the lungs, throat, and neck, but this is generally no different than inhaling any other burnt carbon-containing matter since they all increase the number of lesions (and therefore possible infections) in your airways. There are a couple of studies that claim on the basis of carcinogens that smoking marijuana is worse for your body than smoking a cigarette, but these are rather simplified. There are actually some very convincing reasons to believe that smoking cigarettes is relatively more dangerous to the body than smoking marijuana on more than one count: (1) It is accepted by a growing number of scientists today that all American cigarettes contain significant levels of polonium-210, the same sort of radiation given off by the plutonium of atom bombs (ionizing alpha radiation). It just so happens that the tobacco plant’s roots and leaves are especially good at absorbing radioactive elements from uranium-containing phosphate fertilizers that are required by U.S. law, and from naturally occurring radiation in the soil, air, and water. It is the opinion of C. Everette Koop that this radioactivity, not tar, accounts for at least 90% of all smoking-related lung cancer. Other estimates that have been made are, about 50% according to Dr. Joseph R. DiFranza of the Univ. of Mass. Medical Center and according to Dr. Edward Martell, a radiochemist with the National Center for Atmospheric Research, 95%. Dr. R.T. Ravenholt, former director of World Health Surveys at the Centers for Disease Control, agrees with the risk, asserting that “Americans are exposed to far more radiation from tobacco smoke than from any other source”. Supporting the radioactivity notion is the finding that (a) Relatively high levels of polonium-210 have been found in both cigarette smoke and the lungs of both smokers and nonsmokers alike [60]; (b) Smokers of low-tar-and-nicotine cigarettes die of lung cancer just as much as smokers of other cigarettes; and also, (c) Even the most potent carcinogen that has been found in cigarettes, benzopyrene, is only present in quantities sufficient to account for about 1% of the lung cancer cases that occur from smoking.

Why don’t you know any of this?

Because the tobacco industry is suppressing the information. (2) Tobacco smoke is theorized to work as a kind of “magnet” for airborne radioactive particles such as radon, causing them to deposit in your lungs instead of on walls, rugs, or draperies. (3) Tobacco, unlike marijuana, contains nicotine, which may harden arteries and cause many of the cases of heart disease associated with tobacco use. It also breaks down into cancer-promoting chemicals called N Nitrosamines when burned, and perhaps even when it is inside the body. (4) THC is a bronchial dilator, which means it works like a cough drop by opening up your lungs and therefore aiding in the clearance of smoke and dirt. Nicotine has the exact opposite effect. (5) Unlike the chemicals in marijuana, nicotine has a paralyzing effect on the tiny hairs along the body’s air passages. These hairs normally work to keep foreign matter out of the lungs. This means that carcinogenic tar from cigarette smoke is relatively much harder to purge from your lungs than is that from marijuana. And finally, (6) Marijuana users smoke significantly less than cigarette smokers do because of both marijuana’s psychoactive properties (this is called “auto-titration”) and nicotine’s high potential for physical addiction. It is important to note that the NCTR study found no signs of lung cancer in its autopsied rhesus monkeys who had smoked marijuana for one year.

Smoking cigarettes and smoking marijuana negatively affect different areas of the body, and therefore cause different problems. But everything considered, marijuana-only smokers who average 3 – 4 joints per day show similar symptoms to cigarette smokers who polish off 20 in a day. Although one well-done study tells us that frequent marijuana smokers have a 19% greater risk of respiratory diseases than people who smoke nothing at all [66], it seems that neck and throat cancers are much more likely to result than lung cancer or emphysema. This is because, unlike tobacco, marijuana does not penetrate deeply into the lung. In order to minimize the risk of acquiring neck or throat cancer from marijuana smoke, it is best to (1) avoid as much as possible cigarette-smoking and heavy drinking while smoking marijuana, and (2) eat plenty of vegetables (such as carrots, broccoli, squash, and sprouts) or vitamin supplements of beta carotene, vitamins A, C and E, and selenium. These are believed to impede cancer’s progress.

In addition, there are actually things that can be done to reduce and even entirely eliminate the bodily harm that may potentially result from smoking marijuana. This is possible because all of the principle psychoactive ingredients of marijuana (THC and the cannabinoids) are neither mutagenic (gene-mutating) nor carcinogenic (cancer-causing).

Legalizing marijuana would make (better) water bongs and marijuana foods, drinks, and pills both less expensive and more accessible. Smoking marijuana through a water-filled bong will cool the smoke and there is reason to believe that it will filter some of the carcinogens. Eating or drinking marijuana effectively eliminates all negative effects. In addition, it is conceivable that an aerosol contraption or vaporizer, commonly called a tilt pipe, could easily be constructed that would surpass joints in efficiency, match them in onset and control of effects, and yet would be effectively harmless to the body.

Fat Cells

One of the more ridiculous myths being circulated is that marijuana stays in your fat cells and can keep you high for months. Even though they may have similar names, the psychoactive THC (Delta-9-THC) is different from the metabolites (for instance, 11-OH-THC and 11-nor) that your body breaks it down into in that the latter will not get you stoned. It is the metabolites that stay in your fatty cells and show up on drug tests. Your body is depleted of Delta-9-THC only hours after ingestion.

Other MJ Myths and Realities

Amotivational Syndrome

Amotivational syndrome is defined as a condition in which a person loses ambition or motivation to complete tasks that he would normally like to have completed. Claims made in the 60’s that marijuana use resulted in amotivational syndrome were predominantly founded on stereotypes. But more recently, the carefully-designed NCTR study has actually confirmed these suspicions under certain conditions. It found that marijuana use may consistently produce something akin to amotivational syndrome in adolescent monkeys. It did not however prove that marijuana makes adolescents apathetic or depressed. A full recovery to normal motivation levels was typically observed to occur between two to three months following cessation of exposure. For unknown reasons, one monkey was observed to never fully recover. Surprisingly, the willingness to work appeared to be equally affected in both the daily and weekend rhesus smokers in the study. Other studies have failed to prove amotivational syndrome in adults, so there is much reason to believe that this effect only occurs during adolescent use.

Marijuana Potency

Marijuana is not significantly more potent today than it has been in the past. It is generally agreed that this myth was the result of bad data. The researchers making the claims used as their baseline the THC content of marijuana seized by police in the early 1970’s, which had deteriorated since then because of poor storage conditions. In reality, it seems that domestic marijuana’s average potency probably doubled in the 70’s with the advent of sinsemilla, but has remained more or less constant since then. Scare tactics claiming that marijuana potency has increased are rather irrelevant anyways since marijuana users typically stop smoking when the desired effect is achieved (once again, “auto-titration”). Contrary to one of DARE’s allegations, it is generally agreed that marijuana does not create a tolerance, withdrawal symptoms, or physical dependence in the user. Lester Grinspoon adds, “there are many who assert that there is nevertheless drug dependence because of [marijuana’s] capacity to generate psychic dependency. However it is not at all clear that this type of dependency is essentially any different from that which a man may develop with respect to his trousers, his automobile, or his wife”.

Driving

Driving in any inebriated state is adding complication to what already amounts to a constant life-threatening situation. That said, the National Highway Transportation Safety Administration (NHTSA) summarized all of its studies by saying that there was “no indication that marijuana by itself was a cause of fatal accidents,” and that alcohol was by far the “dominant problem” in drug-related accidents. The Victorian Institute of Forensic Pathology and Monash University’s Department of Forensic Medicine in Melbourne, Australia have found that drivers who use cannabis are actually less likely to cause fatal accidents than drug-free drivers, and are no more likely than other drivers to be killed or seriously injured in road accidents. One experiment tested marijuana-intoxicated drivers on both a closed course and on a crowded city street. It found that the elements of driving most affected were concentration and judgment. An experiment involving a driving simulator that tested actual driving ability according to how many mistakes are incurred by sober, drunk, and high subjects found that marijuana, unlike alcohol, does not significantly affect driving ability. It was found that these results hold true for even higher doses (within reason) and inexperienced marijuana users. In fact, the only significant difference reported by the stoned subjects was an altered perception of time, which effectively made them drive relatively slower. A similar study found that marijuana additionally impairs the driver’s ability to attend to peripheral stimuli. One theory attempting to explain these surprising findings states that marijuana users, in instances requiring seriousness, are in fact able to willingly “bring themselves down,” such that they are no longer high. Studies that in the past have shown that marjuana-intoxicated drivers cause significantly more accidents than sober drivers are typically unreliable on one or more of the following counts: (1) They use drug tests to determine whether or not a person is high, and drug tests in use only indicate use over the past 30 days; (2) Some studies have not corrected for alcohol use, or do not provide a control group; and (3) In many studies there were relatively more stoned drivers killed, but it was not their fault. And when the police “culpability scores” were tallied and factored in, marijuana was generally not to blame for the accidents. It must be emphasized however that one study shows that daily marijuana smokers tend to have a 30% higher risk of injuries than non-users [66]. In fact, accidents resulting from intoxication are thought to be “the number one hazard of marijuana use”.

The Gateway Effect

Marijuana use has not been found to act as a gateway drug to the use of harder drugs. Studies show that when the Dutch partially legalized marijuana in the 70’s, heroin and cocaine use substantially declined, despite a slight increase in marijuana use. If the stepping stone theory were true, use should have gone up rather than down. In reality, it appears that marijuana use tends to substitute for the use of relatively more dangerous hard drugs like cocaine and heroin, rather than lead to their use. Thus, oftentimes strict marijuana laws themselves are the most significant factor involved in moving on to harder drugs like cocaine. Such is the case in Nevada and Arizona, the states toughest on marijuana use. A recent study by Columbia University’s Center on Addiction and Substance Abuse attempts to show, like many past studies have, that marijuana users are more likely to use heroin or cocaine. But what the study actually does show is that a large number of heroin or cocaine users have used marijuana, not the reverse. What is not mentioned is that just as many or even more had probably also drank alcohol, smoked cigarettes, had sex, or eaten sandwiches prior to their hard drug use. In fact, a National High School survey tells us that in 1990, 40.7% of all high school students had tried marijuana or hashish at least once, whereas only 9.4% and 1.3% had ever used cocaine and heroin, respectively. Thus, at maximum, only 23% of marijuana users go on to use cocaine, and only 3% go on to use heroin. Thus, the stepping stone theory fails on even empirical grounds.

Marijuana and Crime

DARE literature would have you believe that there exists a strong correlation between marijuana use and juvenile and young adult crime. And a recent study attempts to present a link between marijuana use and violence by stating that 2/3 of all students who admit to taking a gun to school at least once had smoked marijuana. In fact, DEA head Thomas Constantine recently stated in a Washington Times interview that “Many times people talk about the nonviolent drug offender. That is a rare species. There is not some sterile drug type not involved in violence who is contributing some good to the community; that is ridiculous. They are contributing nothing but evil.” But these allegations are unsupported by research because test results show that changes in personality resulting from marijuana use, even though they are not relatively significant, include among other things a lessening of aggressive trends. And large population studies such as the La Guardia report have found that, if anything, marijuana use inhibits antisocial activity such as violence. The drug-inspired violence myth, including a comprehensive history of its conception, is discussed at great length in Lester Grinspoon’s book, where it is shown to be based largely on a distorted Persian story that is hundreds of years old. The problem inherent in drawing conclusions based on correlations such as the 2/3 statistic above is that causality cannot be inferred from correlation. In other words, there is no way of determining whether marijuana use contributed in some way to the existence of certain traits of marijuana users, i.e. bringing a gun to school, or, as seems entirely more likely, people with such traits are drawn to marijuana use. One study found that chronic marijuana users had significantly higher WAIS IQ scores (113.08) than both moderate users (102.15) and nonusers (103.26). It is simply impossible to make sense of such statistics as presented.

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References

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[2] Cotts, Cynthia, “Hard Sell in the Drug War.” The Nation. March 9, 1992. p 300 – 302.

[3] Nadelmann, Ethan A. “Drug Prohibition in the United States: Costs, Consequences, and Alternatives,” Science, Vol 245: 943, 1 September 1989.

[4] Heath, R.G., A.T. Fitzjarrell, C.J. Fontana, and R.E. Garey. “Cannabis sativa: Effects on brain function and ultrastructure in Rhesus monkeys,” Biological Psychiatry. 15:657-690, 1980.

[5] Marijuana and Health, Institute of Medicine, National Academy of Sciences, 1982.

[6] Slikker, William Jr. et al. “Behavioral, Neurochemical, and Neurohistological Effects of Chronic Marijuana Smoke Exposure in the Nonhuman Primate” in “Marijuana Cannabinoids Neurobiology and Neurophysiology,” Laura Murphy, Andrzej Bartke ed. Boca Raton, FL: CRC Press, 1992.

[7] Matsuda, L.A., S.J. Lolait, M.J. Brownstein, A.C. Young, and T.I. Bonner. “Structure of a Cannabinoid Receptor,” Nature, 346 (issue 6824): 561-564. August, 1990.

[8] Co, B.T., D.W. Goodwin, M. Gado, M. Mikhael, and S.Y. Hill. “Absence of cerebral atrophy in chronic cannabis users,” Journal of the American Medical Association, 237: 1229-1230, 1977.

[9] Kuehnle, J., J.H. Mendelson, K.R. Davis, and P.F.J. New. “Computed topographic examination of heavy marijuana smokers,” Journal of the American Medical Association, 237: 1231-1232, 1977.

[10] Lancaster, Cattell. Mayor’s Committee on Marijuana. The Marijuana Problem in the City of New York. 1944.

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[14] Block, Robert, M.D. Drug and Alcohol Dependence, 28: 121-8, 1991.

[15] Hollister, Leo E. “Marijuana and Immunity”, Journal of Psychoactive Drugs, 24 (issue 2):159-164, April, June, 1992. pub. Haight-Ashbury Publications in association with the Haight-Ashbury Free Medical Clinic, San Francisco, CA.

[16] Kaklamani, et al. “Hashish smoking and T- lymphocytes,” 1978.

[17] Kalofoutis et al. “The significance of lymphocyte lipid changes after smoking hashish,” 1978.

[18] Wallace, J.M., D.P. Tashkin, J.S. Oishi, R.G. Barbers. “Peripheral Blood Lymphocyte Subpopulations and Mitogen Responsiveness in Tobacco and Marijuana Smokers,” Journal of Psychoactive Drugs, 1988.

[20] Kaplan, John. Marijuana, The New Prohibition, New York, World Publishing Co., 1969.

[21] Health Consequences of Smoking: Nicotine Addiction, Surgeon General’s Report, 1988.

[22] Winters, T.H., and J.R. Franza. “Radioactivity in Cigarette Smoke.” New England Journal of Medicine, 1982: 306 (6): 364-365.

[23] Mikuriya, Tod H., M.D., and Michael R. Aldrich, Ph.D. “Cannabis 1988, Old Drug New Dangers, The Potency Question” , Journal of Psychoactive Drugs. Vol. 20, Issue 1: 47-55. pub. Haight-Ashbury Publications in association with the Haight-Ashbury Free Medical Clinic San Francisco, Calif.: January March, 1988.

[24] Dennis, Richard J. “The Economics of Legalizing Drugs,” The Atlantic Monthly, Vol. 266, No. 5, Nov 1990, p. 130.

[25] Data supplied by the U.S. Department of Health and Human Services, Public Health Service, Alcohol, Drug Abuse, and Mental Health Administration. Revised January, 1991. For more information contact the National Clearinghouse for Alcohol and Drug Info., P.O. Box 2345, Rockville, Maryland 20847 / (800) 729-6686.

[28] the name of the DARE pamphlet is “Facts About Marijuana; Marijuana: Drug of Deception”

[29] Nationally-televised speech in 1990

[30] Singer, Jerome L. “Ongoing Thought: The Normative Baseline for Alternate States of Consciousness,” Alternate States of Consciousness.

[32] The NHTSA report, “The Incidence and Role of Drugs in Fatally Injured Drivers,” by K.W. Terhune, et al. of the Calspan Corp. Accident Research Group in Buffalo, NY (Report # DOT-HS-808-065) is available from the National Technical Information Service, Springfield VA 22161.

[33] Bruer, Mark. Age, March 23, 1994, p. 3 [Melbourne, Australia; this report is also published in the university’s

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[34] Halpern. “Emotional Reactions and General Personality Structure,” The Marihuana Problem, pp. 130 – 131.

[35] Martell, Edward. Proceedings of the National Academy of Science, Biophysics, and Biological Science, March 1983.

[36] Hoffmann, Dietrich, Gunter Rathkamp, and Ernest L. Wynder. “Comparison of the Yields of Several Selected Components in the Smoke From Different Tobacco Products,” Journal of the National Cancer Institute, Vol. 31, No. 3, 1963, p. 627-635

[37] Hofmann, D., J.D. Adams, K.D. Brunnemann, and D.D. Hecht. “Formation, occurrence and carcinogenesity of N-nitrosamines in tobacco products,” Am. Chem. Soc. Symp. Ser., 174:247-273, 1981.

[39] Hammond, E.C., L. Garfinkel, H. Seidman, and E.A. Lew. “Some Recent findings concerning cigarette smoking,” In: Origins of Human Cancer. New York: Cold Spring Harbor Laboratory, 1977. p. 101-112.

[40] Starks, Michael, “Marijuana Chemistry Genetics, Processing, and Potency’,” Ronin Inc., 1990.

[41] Murphy, Laura, and Andrzej Bartke. “Marijuana Cannabinoid Neurobiology and Neurophysiology,” CRC Press Boca Raton, FL, 1992.

[42] Mendelson, Dr. Jack H., “Behavioral and Biological Concomitants of Chronic Marijuana Use,” 1974.

[43] “Marihuana A Signal of Misunderstanding,” U.S. Government Printing Office Washington, 1972.

[44] Wu, Tzu Chin, Donald P. Tashkin, Behnam Djahed, and Jed E. Rose. “Pulmonary Hazards of Smoking Marijuana as Compared with Tobacco,” New England Journal of Medicine, 318 (issue 6): 347-351, 1988.

[45] Slikker, William Jr, H.C. Cunny, J.R. Bailey, and M.G. Paule. “Placental Transfer and Fetal Disposition of Delta-9-Tetrahydrocannabinol (THC) During Late Pregnancy in the Rhesus Monkey,” pp. 97-102.

[46] Lyman, W.D., J.R. Sonett, C.F. Brosnan, R. Elkin, and M.B. Bornstein. “Delta-9-tetrahydrocannabinol A Novel Treatment for Experimental Autoimmune Encephalitis” by in Journal of Neuroimmunology, 23: 73-81. 1989.

[47] Cabral, Guy A., Amy L. Stinnet, John Bailey, Syed F. Ali, Merle G. Paul, Andrew C. Scallet, and William Slikker, Jr. “Chronic Marijuana Smoke Alters Alveolar Macrophage Morphology and Protein Expression,” 1991.

[48] Ponte, Lowell. “Radioactivity: The New-Found Danger in Cigarettes,” Reader’s Digest, March 1986, pp. 123-127.

[49] Litwak, Mark. “Would You Still Rather Fight Than Switch?” Whole Life Times, Mid-April/May, 1985, p. 11.

[50] Crancer, A., et al. “Comparison of the Effects of Marihuana and Alcohol on Simulated Driving Performance,” Science, 164:851-854, 1969.

[51] Caldwell, D.F., et al. “Auditory and Visual Threshold Effects of Marihuana in Man,” Perceptive and Motor Skills, 29:758-759, 1969.

[52] Klonoff, H. (1974). “Effects of marihuana on driving in a restricted area and on city streets: Driving performance and physiological changes.” In L. L. Miller (Ed.), Marijuana, Effects on human behavior (pp. 359-397). New York: Academic Press.

[57] Westlake, Tracy M., Allyn C. Howlett, Syed F. Ali, Merle G. Paule, Andrew C. Scallet, William Slikker, Jr. “Chronic Exposure to Delta-9-Tetrahydrocannabinol Fails to Irreversibly Alter Brain Cannabinoid Receptors,” Brain Research, 544: 145-149, 1991.

[58] Ali, Syed F., Glenn D. Newport, Andrew C. Scallet, Merle G. Paule, John R. Bailey, William Slikker, Jr. “Chronic Marijuana Smoke Exposure in the Rhesus Monkey IV Neurochemical Effects and Comparison to Acute and Chronic Exposure to Delta-9-Tetrahydrocannabinol (THC) in Rats” Pharmacology, Biochemistry & Behavior, 40: 677-682. 1991.

[59] Radford EP Jr, and V.R. Hunt. “Polonium-210: a volatile radioelement in cigarettes.” Science. 1964; 143:247-9.

[60] Little JB, E.P. Radford Jr, H.L. McCombs, V.R. Hunt. “Distribution of polonium-210 in pulmonary tissues of cigarette smokers.” New England Journal of Medicine. 1965, 273:1343-51.

[66] Polen, Michael. “Health Care Use by Frequent Marijuana Smokers Who Do Not Smoke Tobacco,” West J Med 1993: 158.

[67] Gieringer, Dale. “Marijuana, Driving and Accident Safety,” Journal of Psychoactive Drugs, Jan-Mar, 1988.

[68] Weil, Andrew, and Winifred Rosen, From Chocolate to Morphine: Everything You Need to Know About Mind-Altering Drugs. Boston: Houghton Mifflin, 1993.

[69] Cozzi, Nicholas. “Effects of Water Filtration on Marijuana Smoke: A Literature Review.” MAPS Newsletter IV #2 (Multidisciplinary Association for Psychedelic Studies, 1993). Reprints available from California NORML.

[70] “Cannabis and Memory Loss,” (editorial) British Journal of Addiction, 86:249-252 (1991).

[71] Muskowitz, H., Hulbert, S., & McGlothlin, W.H. (1976). “Marihuana: Effects on simulated driving performance.” Accident Analysis and Prevention, 8(1), p. 45 – 50.

[72] Astley, Susan, Dr. “Analysis of Facial Shape in Children Gestationally Exposed to Marijuana, Alcohol, and/or Cocaine,” Pediatrics, 89 #1: 67 – 77 (June 1992).

[73] Day, Nancy, et. al. “Prenatal Marijuana Use and Neonatal Outcome,” Neurotoxicology and Teratology, 13: 329-334 (1992).

[74] Tashkin, Donald, et. al. “Effects of Habitual Use of Marijuana and/or Cocaine on the Lung,” in C. Nora Chiang and Richard L. Hawks, ed., Research findings on Smoking of Abused Substances, NIDA Research Monograph 99 (US Dept of Health and Human Services, 1990).

Suggested Reading

[61] Grinspoon, Lester. Marihuana Reconsidered. Cambridge: Harvard University Press, 1971.

[62] Herer, Jack. The Emperor Wears No Clothes. Van Nuys, CA: Hemp Publishing, 1990.

[63] Hendin, Herbert. Living High: Daily Marijuana Use Among Adults. New York: Human Sciences Press, 1987.

[64] Himmelstein, Jerome L. The Strange Career of Marihuana: Politics and Ideology of Drug Control in America. Westport, Conn.: Greenwood Press, 1983.

[65] Dale Gieringer, Ph.D from California’s NORML. “Health Tips for Marijuana Smokers,” Feb. 1994 edition. To receive this very comprehensive 32-page compilation of reports, send a $5 donation to California NORML, 2215-R Market St. #278, San Francisco, CA 94114 or call (415) 563-5858 and ask for the paper by name. The packet includes detailed instructions on how to construct a vaporizer.