Cannabis Health Search



Cannabis contains THC. THC is a bronchial dilator, which means it works like a cough drop and opens up your lungs, which aids clearance of smoke and dirt. Nicotine does just the opposite; it makes your lungs bunch up and makes it harder to cough anything up.
 Scientists do not really know what it is that causes malignant lung cancer in tobacco. Many think it may be a substance known as Lead 210.

Of course, there are many other theories as to what does cause cancer, but if this is true, it is easy to see why no case of lung cancer resulting from marijuana use alone has ever been documented, because tobacco contains much more of this substance than cannabis.

Science & Research

Image shows just a few of the hundreds of chemicals found in a single tobacco cigarette

Cannabis and tobacco smoke are not equally carcinogenic

Robert Melamede:

Biology Department, 1420 Austin Bluffs Parkway, University of Colorado, Colorado Springs, 80918, USA

Bioenergetics Institute, 1420 Austin Bluffs Parkway, University of Colorado, Colorado Springs, 80918, USA
 More people are using the cannabis plant as modern basic and clinical science reaffirms and extends its medicinal uses. Concomitantly, concern and opposition to smoked medicine has occurred, in part due to the known carcinogenic consequences of smoking tobacco. Are these reactions justified? While chemically very similar, there are fundamental differences in the pharmacological properties between cannabis and tobacco smoke. Cannabis smoke contains cannabinoids whereas tobacco smoke contains nicotine. Available scientific data, that examines the carcinogenic properties of inhaling smoke and its biological consequences, suggests reasons why tobacco smoke, but not cannabis smoke, may result in lung cancer....please read more

Smoking Marijuana Does Not Cause Lung Cancer

Source: CounterPunch (US Web)
Column: Pot Shots
Copyright: 2005 CounterPunch
Author: Fred Gardner
Cited: International Cannabinoid Research Society
Cited: Center for Medicinal Cannabis Research
Cited: California Cannabis Research Medical Group
Bookmark: (Marijuana)
Bookmark: (Marijuana - Medicinal)
Bookmark: (Chronic Pain)
Bookmark: (GW Pharmaceuticals)

 Marijuana smoking -"even heavy longterm use"- does not cause cancer of the lung, upper airwaves, or esophagus, Donald Tashkin reported at this year's meeting of the International Cannabinoid Research Society.  Coming from Tashkin, this conclusion had extra significance for the assembled drug-company and university-based scientists ( most of whom get funding from the U.S.  National Institute on Drug Abuse ).  Over the years, Tashkin's lab at UCLA has produced irrefutable evidence of the damage that marijuana smoke wreaks on bronchial tissue.  With NIDA's support, Tashkin and colleagues have identified the potent carcinogens in marijuana smoke, biopsied and made photomicrographs of pre-malignant cells, and studied the molecular changes occurring within them.  It is Tashkin's research that the Drug Czar's office cites in ads linking marijuana to lung cancer.  Tashkin himself has long believed in a causal relationship, despite a study in which Stephen Sidney examined the files of 64,000 Kaiser patients and found that marijuana users didn't develop lung cancer at a higher rate or die earlier than non-users.  Of five smaller studies on the question, only two -involving a total of about 300 patients- concluded that marijuana smoking causes lung cancer.  Tashkin decided to settle the question by conducting a large, prospectively designed, population-based, case-controlled study.  "Our major hypothesis," he told the ICRS, "was that heavy, longterm use of marijuana will increase the risk of lung and upper-airwaves cancers."

The Los Angeles County Cancer Surveillance program provided Tashkin's team with the names of 1,209 L.A.  residents aged 59 or younger with cancer ( 611 lung, 403 oral/pharyngeal, 90 laryngeal, 108 esophageal ).  Interviewers collected extensive lifetime histories of marijuana, tobacco, alcohol and other drug use, and data on diet, occupational exposures, family history of cancer, and various "socio-demographic factors." Exposure to marijuana was measured in joint years ( joints per day x 365 ).  Controls were found based on age, gender and neighborhood.  Among them, 46% had never used marijuana, 31% had used less than one joint year, 12% had used 10-30 j-yrs, 2% had used 30-60 j-yrs, and 3% had used for more than 60 j-yrs.  Tashkin controlled for tobacco use and calculated the relative risk of marijuana use resulting in lung and upper airwaves cancers.  All the odds ratios turned out to be less than one ( one being equal to the control group's chances )! Compared with subjects who had used less than one joint year, the estimated odds ratios for lung cancer were .78; for 1-10 j-yrs, .74; for 10-30 j-yrs, .85 for 30-60 j-yrs; and 0.81 for more than 60 j-yrs.  The estimated odds ratios for oral/pharyngeal cancers were 0.92 for 1-10 j-yrs; 0.89 for 10-30 j-yrs; 0.81 for 30-60 j-yrs; and 1.0 for more than 60 j-yrs.  "Similar, though less precise results were obtained for the other cancer sites," Tashkin reported.  "We found absolutely no suggestion of a dose response." The data on tobacco use, as expected, revealed "a very potent effect and a clear dose-response relationship -a 21-fold greater risk of developing lung cancer if you smoke more than two packs a day." Similarly high odds obtained for oral/pharyngeal cancer, laryngeal cancer and esophageal cancer.  "So, in summary" Tashkin concluded, "we failed to observe a positive association of marijuana use and other potential confounders."

There was time for only one question, said the moderator, and San Francisco oncologist Donald Abrams, M.D., was already at the microphone: "You don't see any positive correlation, but in at least one category [marijuana-only smokers and lung cancer], it almost looked like there was a negative correlation, i.e., a protective effect.  Could you comment on that?"

"Yes," said Tashkin.  "The odds ratios are less than one almost consistently, and in one category that relationship was significant, but I think that it would be difficult to extract from these data the conclusion that marijuana is protective against lung cancer.  But that is not an unreasonable hypothesis."

Abrams had results of his own to report at the ICRS meeting.  He and his colleagues at San Francisco General Hospital had conducted a randomized, placebo-controlled study involving 50 patients with HIV-related peripheral neuropathy.  Over the course of five days, patients recorded their pain levels in a diary after smoking either NIDA-supplied marijuana cigarettes or cigarettes from which the THC had been extracted.  About 25% didn't know or guessed wrong as to whether they were smoking the placebos, which suggests that the blinding worked.  Abrams requested that his results not be described in detail prior to publication in a peer-reviewed medical journal, but we can generalize: they exceeded expectations, and show marijuana providing pain relief comparable to Gabapentin, the most widely used treatment for a condition that afflicts some 30% of patients with HIV.

To a questioner who bemoaned the difficulty of "separating the high from the clinical benefits," Abrams replied: "I'm an oncologist as well as an AIDS doctor and I don't think that a drug that creates euphoria in patients with terminal diseases is having an adverse effect." His study was funded by the University of California's Center for Medicinal Cannabis Research.



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Blunt Smokers Link Dependence Potential To Nicotine

Article Date: 29 Sep 2006

 According to a study by researchers at National Development and Research Institutes, Inc. (NDRI) users of blunts (tobacco cigar shells filled with marijuana) do not understand or experience marijuana dependence in terms of conventional clinical criteria. Rather, they associate clinical symptoms with "harder" drugs such as heroin, crack, cocaine and nicotine. However, many suggested that blunts may have addictive potential because they contain tobacco (nicotine). This finding suggests that future studies on cannabis dependence should be designed to include blunts.

The results of this study have been published in a recent issue of the International Journal of Drug Policy. (Eloise Dunlap, Ellen Benoit, Stephen J. Sifaneck and Bruce D. Johnson. Social constructions of dependency by blunts smokers: Qualitative reports. The International Journal of Drug Policy 17(3) 2006:171-182.)

The NDRI study involved in-depth interviews with 92 users of blunts and cannabis in other forms (joints, pipes, bongs, etc.) in New York City. Respondents ranged in age from 14 to 62, and were racially diverse: 43% white, 40% Black and 15% Asian. Nineteen percent identified themselves as Latino/a, and 43% were female.

When asked if they think blunts are addictive, respondents were evenly divided between affirmative and negative responses. In explaining their answers, many cited the role of tobacco, without prompting. Of those who said they think blunts are addictive, 17% said it is most likely because tobacco, which contains the physically addictive ingredient nicotine, is present in the blunts cigar shell. Among those who said they do not think blunts are addictive, 15% qualified their answers by saying that the tobacco in blunts is addictive, but the marijuana in them is not.

For the most part, respondents did not assess the possibility of blunts dependence in terms that clearly correspond to official clinical criteria. Several users described smoking with increased frequency, but none of them reported developing tolerance, or smoking larger amounts to maintain desired effects.

A growing number of articles in peer-reviewed journals report survey findings that support official definitions of cannabis dependence, yet clinically significant dependence symptoms are relatively rare among cannabis users. Official criteria (such as those in the Diagnostic and Statistical Manual of the American Psychiatric Association - DSM) have been revised in recent years to recognize the subjective nature of cannabis dependence. However, the NDRI researchers argue that the diagnostic criteria may not be relevant to the actual experiences of marijuana/blunts users and that survey methods may not be the best way to capture those experiences.

In particular, surveys do not allow cannabis users to elaborate on the context of their use, particularly settings, which may influence the risk of dependence. The NDRI research team was able to gather such information through the in-depth interviews, but they also conducted field observations of more than 500 individuals during cannabis-smoking sessions in a number of settings.

These observations, combined with the interview responses, revealed a system of etiquette based on sharing. The sharing etiquette observed is more complex and involved than sharing norms of previous marijuana using subcultures. Blunt-smoking etiquette includes norms respecting appropriate times and places for smoking, limiting the number of hits one takes before passing a blunt, and contributing to the cost and effort of a blunts-smoking event. The rules are enforced by peer pressure, including the implicit threat of ejection from the group and an argot of demeaning labels for those who violate the norms of sharing.

 "Smoking in groups seems to involve conduct norms that discourage compulsive or excessive consumption," said Eloise Dunlap, Ph.D., principal investigator in the study. "If people associate blunts with group settings, they may be less likely to see blunts as potentially addictive." The vast majority (86%) of blunts smokers interviewed said they prefer to smoke in groups. The few who reported occasionally smoking blunts alone said that when they did so they tended to replicate the group practice of taking a few puffs and then putting the blunt out.

Although group conduct norms associated with blunts smoking can encourage more controlled use, the presence of tobacco in blunts may have a countervailing effect. The question of whether tobacco fosters dependence on blunts warrants further investigation and may yield data with significant implications for public-health and prevention messages.

Article adapted by CMMC from original press release.

This study is part of a larger investigation of marijuana/blunts use, subcultures and markets in New York City, funded by the federal National Institute on Drug Abuse (R01 DA13690).

Contact: Patrice Barron
National Development & Research Institutes


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Premiere British Medical Journal Pronounces Marijuana Safer Than Alcohol, Tobacco

December 1, 1998, London, England:

Moderate use of marijuana poses less of a risk to health than alcohol or tobacco, according to editors of the influential medical journal, The Lancet. Available medical evidence demonstrates that "moderate indulgence in cannabis has little ill-effect on health, and that decisions to ban or legalise [sic] cannabis should be based on other considerations," editors opined in the November 14 issue. They added, "It would be reasonable to judge cannabis less of a threat to health than alcohol or tobacco. Three years ago, the journal argued that "the smoking of cannabis, even long term, is not harmful to health."

The Lancet's latest statements came only days after a House of Lord's committee recommended amending federal law to allow physicians to prescribe marijuana as a medicine. NORML Executive Director R. Keith Stroup, Esq. praised The Lancet for conducting an apolitical assessment of marijuana's effects on health. "The Lancet's conclusions are reasonable based on the available scientific and medical literature," he said. "It is clear that marijuana prohibition causes far more harm to the user and society than the responsible use of marijuana itself.

An accompanying article by Australian professors Wayne Hall and Nadia Solowij in the same issue concluded the "most undesirable" effects of marijuana are: bronchial irritation, the risk of accidents while intoxicated, and possible "subtle" cognitive impairment and/or dependence with heavy, long term use. However, the researchers added that most marijuana smokers do not become regular users, and cease smoking the drug altogether by their mid to late twenties.

Although The Lancet's position received mainstream coverage internationally, no U.S. wire services have yet to report on the journal's findings. For more information, please contact either Allen St. Pierre or Paul Armentano of The NORML Foundation @ (202) 483-8751.


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Why Doesn't Smoking Marijuana Cause Cancer?

Original broadcast date: July 15, 1999

Haroon: There's such a big to-do about smoking and cancer, but people smoke marijuana and call that medicinal.

I was told that the heat from the smoke causes cancer among tobacco smokers. But then wouldn't smoking marijuana cause cancer, too?

Dr. Dean: Haroon, this is the big question about smoking. You'd think we'd know by now what part of it causes cancer, but we don't.

Some of the theories are tars, polonium, and, as you mentioned, the burning process.

The tars in cigarette smoke do contain known carcinogenic chemicals, but those chemicals don't really accumulate where lung cancer accumulates.

Polonium, which is radioactive, accumulates on tobacco leaves as a result of fertilizers. In a chronic smoker, polonium accumulates in the bronchial tree, which is also a location for cancer. If the fertilizer causes cancer, maybe non-fertilized tobacco would make a safe cigarette.

Burning vegetable matter also produces known carcinogens. But marijuana, which is certainly burning vegetable matter, doesn't seem to cause lung cancer.

You can see how difficult it is.

Burning materials, even the ones produced when we barbecue, create substances that cause cancer in laboratory animals. Those substances are more abundant in marijuana and hashish smoke than in tobacco smoke.

However, a cigarette smoker smokes 20 or 30 cigarettes a day; a marijuana smoker smokes one or two at the most. The quantity might be the difference between cancer and no cancer.

One of the main reasons we can't pinpoint what part of smoking causes cancer is that cigarette companies have a big secret. An incredible loophole in the law allows them not to disclose about 500 of the ingredients in cigarettes. Maybe the burning of one of those ingredients causes lung cancer. But we can't test it, because we don't know what it is.

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Marijuana Smoking Found Non-Carcinogenic

By Neil Osterweil, Senior Associate Editor, MedPage Today
Published: May 24, 2006
Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco 

 SAN DIEGO, May 24 — Smoking marijuana does not appear to increase the risk of lung cancer or head-and-neck malignancies, even among heavy users, researchers reported here.

"We expected that we would find that a history of heavy marijuana use, more than 500 to 1,000 uses, would increase the risk of cancer from several years to decades after exposure to marijuana, said Donald Tashkin, M.D., of the University of California in Los Angeles.

But in fact, they reported at the American Thoracic Society meeting here, marijuana use was associated with cancer risk ratios below 1.0, indicating that a history of pot smoking had no effect on the risk for respiratory cancers.

Dr. Tashkin was quick to point out, however, that marijuana does not appear to have a protective effect against cancer. "If it did, there would be a dose-dependent effect, with people who smoked more having a lower risk," he said. "We didn't see that."

Studies have shown that marijuana contains many compounds that when burned, produce about 50% higher concentrations of some carcinogenic chemicals than tobacco cigarettes.

In addition, heavy, habitual marijuana use can produce accelerated malignant change in lung explants, and evidence on bronchial biopsies of pre-malignant histopathologic and molecular changes, Dr. Tashkin said.

The investigators had also previously shown that smoking one marijuana cigarette leads to the deposition in the lungs of four times as much tar as smoking a tobacco cigarette containing the same amount of plant material. Marijuana cigarettes are not filtered and are more loosely packed than tobacco, so there's less filtration of the tar. In addition, pot smokers hold the smoke in their lungs about four times longer than tobacco smokers do, Dr. Tashkin pointed out.

He and his colleagues, led by epidemiologist Hal Morgenstern, Ph.D., of the University of Michigan in Ann Arbor, conducted a study to look at possible associations between marijuana use and the risk of respiratory cancers among middle-age adults in the Los Angeles area.

For the population-based case-control study, they identified cancer cases among people from the ages of 18 to 59, using the Los Angeles County Cancer Surveillance Program registry.

They identified 611 people with lung cancer, 601 with cancers of the head and neck, and 1,040 controls matched by age, gender and neighborhood (as a surrogate for socioeconomic status).

They conducted extensive personal interviews to determine lifetime marijuana use, measured in joint-years, with one joint-year equivalent to 365 marijuana cigarettes. The interviewers also asked participants about tobacco use, alcohol consumption, use of other drugs, socioeconomic status, diet, occupation, and family history of cancer.

The investigators also used logistic regression to estimate the effect of marijuana use on lung cancer risk, adjusting for age, gender, race/ethnicity, education, and cumulative tobacco smoking and alcohol use.

They found that the heaviest users in the study had smoked more than 60 joint years worth of marijuana, or more than 22,000 joints in their lifetime. Moderately heavy users smoked between 11,000 and 22,000 joints.

"That's an enormous amount of marijuana," Dr. Tashkin said.

Despite the heavy use, "in no category was there any increased risk, nor was there any suggestion that smoking more led to a higher odds ratio," he continued. "There was no dose-response—not even a suggestion of a dose response—and in all types of cancer except one, oral cancer, the odds ratios were less than one."

The confidence intervals around the odds ratios were wide however, and the odds ratios did not show a dose response.

In contrast, tobacco smoking was associated with increased risk for all cancers, and there was a "powerful" dose-response relationship. People who smoked more than two packs of cigarettes per day had a 21-fold risk for cancer, as opposed to a less than onefold risk for marijuana, Dr. Tashkin said.

"When we restricted the analysis to those who didn't smoke any tobacco we found the same results, and when we looked for interaction between tobacco and smoking—would marijuana increase the risk, potentiate the carcinogenic effect of tobacco—we didn't find that, nor did we find a protective effect against the effect of tobacco, which is very important, because the majority of marijuana smokers also smoke tobacco," he commented.

It's possible that tetrahydrocannabinol (THC) in marijuana smoke may encourage apoptosis, or programmed cell death, causing cells to die off before they have a chance to undergo malignant transformation, he said.

Dr. Tashkin also noted that "it's never a good idea to take anything into your lungs, including marijuana smoke.

Primary source: 2006 American Thoracic Society Annual Meeting
Source reference:
Tashkin DP et al. "Marijuana Use and Lung Cancer: Results of a Case-Control Study." Presented in a briefing May 23 and in an oral session May 24, 2006.
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Cannabis Smoke and Cancer: Assessing the Risk

by Paul Armentano
Senior Policy Analyst
NORML | NORML Foundation

Presumptions regarding cannabis use as a risk factor for the development of certain types of cancer, particularly lung cancer, warrant critical examination. Epidemiologic studies over the past several decades have established causation between alcohol consumption and cancers of the oral cavity, pharynx, larynx, esophagus, liver, colon and rectum, among others. Tobacco use, particularly cigarette smoking, has also been determined to cause similar upper aerodigestive tract (UAT) cancers, as well as cancers of the pancreas, kidneys and bladder, and is implicated with cancers of the stomach and liver, among others.

To date, similar epidemiologic and/or clinical studies on the use of cannabis and cancer are few and not definitive. However, the public and policy-makers should interpret the ambiguity of these results with caution – neither construing them at this time as an endorsement of cannabis’ safety nor as an indictment of its potential health hazards.

(References: Alcohol and cancer. The Lancet. 2006. | Tobacco use and cancer: an epidemiological perspective for geneticists. Oncogene. 2002)

Cannabis Smoke Versus Tobacco Smoke

Cannabis smoke contains many of the same carcinogens as tobacco smoke, including greater concentrations of certain aromatic hydrocarbons such as benzopyrene, prompting fears that chronic marijuana inhalation may be a risk factor for tobacco-use related cancers. However, marijuana smoke also contains cannabinoids such as THC (delta-9-tetrahydrocannabinol) and CBD (cannabidiol), which are non-carcinogenic and demonstrate anti-cancer properties in vivo and in vitro.

By contrast, nicotine promotes the development of cancer cells and their blood supply. In addition, cannabinoids stimulate other biological activities and responses that may mitigate the carcinogenic effects of smoke, such as down-regulating the inflammatory arm of the immune system that is responsible for producing potentially carcinogenic free radicals (unstable atoms that are believed to accelerate the progression of cancer).

Cannabis smoke – unlike tobacco smoke – has not been definitively linked to cancer in humans, including those cancers associated with tobacco use. However, certain cellular abnormalities in the lungs have been identified more frequently in long-term smokers of cannabis compared to non-smokers.

Chronic exposure to cannabis smoke has also been associated with the development of pre-cancerous changes in bronchial and epithelium cells in similar rates to tobacco smokers.

Cellular abnormalities were most present in individuals who smoked both tobacco and marijuana, implying that cannabis and tobacco smoke may have an additive adverse effect on airway tissue.

The results suggest that long-term exposure to cannabis smoke, particularly when combined with tobacco smoking, is capable of damaging the bronchial system in ways that could one day lead to respiratory cancers. However, to date, no epidemiologic studies of cannabis-only smokers have yet to reveal such a finding. Larger, better-controlled studies are warranted.

Cannabis consumers who desire the rapid onset of action associated with inhalation but who are concerned about the potential harms of noxious smoke can dramatically cut down on their intake of carcinogenic compounds by engaging in vaporization rather than smoking.

Cannabis vaporization limits respiratory toxins by heating cannabis to a temperature where cannabinoid vapors form (typically around 180-190 degrees Celsius), but below the point of combustion where noxious smoke and associated toxins (i.e., carcinogenic hydrocarbons) are produced (near 230 degrees Celsius).

Because vaporization can deliver doses of cannabinoids while reducing the users intake of carcinogenic smoke, it is considered to be a preferred and likely safer method of cannabis administration than smoking marijuana cigarettes or inhaling from a water pipe. According to the findings of a recent clinical trial, use of the Volcano vaporizing device delivered set doses of THC to subjects in a reproducible manner while suppressing the intake of respiratory toxins.

"Our results show that with the Volcano, a safe and effective cannabinoid delivery system seems to be available to patients," investigators at Leiden University's Institute of Biology (the Netherlands) concluded.

"The final pulmonal uptake of THC is comparable to the smoking of cannabis, while avoiding the respiratory disadvantages of smoking."

(References: On the carcinogenicity of marijuana smoke. Recent Advances in Phytochemistry. 1975. **Author’s Note: More recent studies on higher potency marijuana and/or sinsemilla have not been conducted and could potentially yield different results. | Cannabinoids and cancer: causation, remediation, and palliation. Lancet Oncology. 2005 | Cannabinoids: potential anticancer agents. Nature Reviews Cancer. 2003. | Nicotine exposure and bronchial epithelial cell nicotinic acetylcholine receptor expression in the pathogenesis of lung cancer. Journal of Clinical Investigation. 2003 | Cannabis and tobacco smoke are not equally carcinogenic. Harm Reduction Journal. 2005 | Ibid. | National Academy of Sciences, Institute of Medicine. Marijuana and Medicine: Assessing the Science Base. National Academy Press. 1999 | Tracheobronchial histopathology in habitual smokers of cocaine, marijuana and/or tobacco. Chest. 1997 | Histopathologic and molecular alterations in bronchial epithelium in habitual smokers of marijuana, cocaine and/or tobacco. Journal of the National Cancer Institute. 1998 | See footnotes 10 and 11 | Cannabis vaporizer combines efficient delivery of THC with effective suppression of pyrolytic compounds. Journal of Cannabis Therapeutics. 2004 | Hazekamp et al. 2006. Evaluation of a vaporizing device (Volcano) for pulmonary administration of tetrahydrocannabinol. Journal of Pharmaceutical Sciences 95: 1308-1317.) | Vaporization as a smokeless cannabis delivery system: a pilot study.
Clinical Pharmacology & Therapeutics. 2007.

Head, Neck and Lung Cancers

While a handful of anecdotal reports and one small case-control study associate heavy marijuana use among younger adults with increased incidents of head, neck and lung cancers, no large scale population studies have replicated these results. Investigators at John Hopkins University in Baltimore reported that neither "lifetime use" nor "ever use" of cannabis were associated with head, neck or lung cancer in younger adults in a large, hospital-based case-control study of 164 oral cancer patients and 526 controls. Researchers concluded, "The balance of evidence from this, the largest case-control study addressing marijuana use and cancer to date, does not favor the idea that marijuana as commonly used in the community is a major causal factor for head, neck or lung cancer in young adults."

More recently, the results of a 2004 population-based case-control study of 407 individuals diagnosed with oral squamous cell carcinoma and 615 healthy controls found "no association" between cannabis use and incidents of oral cancer, regardless of how long, how much or how often individuals had used it. A second 2004 case-control study of 116 oral cancer patients and 207 matched controls also failed to identify any association between self-reported cannabis use and oral cancers in adults age 45 years old or younger, although only 10 percent of patients in the study identified themselves as heavy users of cannabis.

A 1997 retrospective cohort study examining the relationship of marijuana use to cancer incidence in 65,171 men and women 15 to 49 years of age in California found that cannabis use was not associated with increased risks of developing tobacco-use related cancers of the lung and upper aerodigestive tract, and in fact, no cases of lung cancer were identified among men and women who used marijuana but did not smoke tobacco.

Critics charge that volunteers in the study were relatively young and that the follow up period was fairly short, arguing that "such a study could not have been expected to detect any relationship between marijuana and lung cancer if the lag period were comparable to that seen with tobacco," which typically occurs after at least 20 years of smoking cigarettes and/or among adults over age 60. The study’s author responds: "[I]n contrast to users of tobacco and alcohol, most cannabis users generally quit using cannabis relatively early in their adult lives. … Therefore, even diseases that might be related to long-term use of cannabis (e.g. lung cancer) are unlikely to have a sizeable public health impact because most people who try cannabis do not become long-term users."

Government reviews investigating a possible link between cannabis use and lung cancer have also failed to find a definitive causal connection between the two. A 1998 report by the British House of Lords Science and Technology Committee concluded, "There is as yet no epidemiological evidence for an increase risk of lung cancer" in cannabis smokers, though authors did concede that studies have revealed cellular changes in the airways of cannabis smokers that could potentially be pre-cancerous.

An 18-month study by the US National Academy of Science Institute of Medicine also concluded, "There is no conclusive evidence that marijuana causes cancer in humans, including cancers generally related to tobacco use," but added that cellular studies and a handful of poorly controlled case studies suggest that cannabis smoke may be "an important risk factor" for the development of upper aerodigestive or lung cancers.

A 2002 Canadian Senate review further commented that among the small number of case studies present in the literature: "[N]one compare the prevalence of cancer with a control group or evaluates the use of cannabis in a standardized way. Interpretation is also limited by the fact the patients smoked tobacco and drank alcohol."

More recent reviews of the subject published in the journals Alcohol and Lancet Oncology reach similar conclusions. A review of two cohort studies and 14 case-control studies assessing the association of marijuana and cancer risk by Hashibe and colleagues concluded, "[R]esults of cohort studies have not revealed an increased risk of tobacco related cancers among marijuana smokers." Authors did highlight a pair of African case control studies citing marijuana use as a possible elevated risk factor for lung cancer, though they added that investigators failed to assess either the durations of cannabis use or quantify the amount of tobacco used by subjects in conjunction with marijuana.

A second 2005 review by Hall and colleagues conclude, "There is a conspicuous lack of evidence on the association between cannabis smoking and lung cancers," and recommends the subject receive additional study.

A large US case-control study funded by the US National Institutes of Health assessing the effects of marijuana smoking on the risks of lung cancer and upper aerodigestive tract cancers among 2,400 Los Angeles County residents less than 60 years of age is ongoing. Preliminary data from the study, presented by investigators at the 2005 annual conference of the International Cannabinoid Research Society (ICRS), report that those who self-reported using moderate levels of cannabis had no greater odds of suffering from lung or UAT cancers than controls.

(References: Marijuana use and increased risk of squamous cell carcinoma of the head and neck. Cancer Epidemiology Biomarkers & Prevention. 1999 | Marijuana use is not associated with head, neck or lung cancer in adults younger than 55 years: Results of a case cohort study. In: National Institute on Drug Abuse (Eds) Workshop on Clinical Consequences of Marijuana: Program Book. National Institutes of Health. 2001 | Marijuana use and risk of squamous cell carcinoma. Cancer Research. 2004 | An analysis of risk factors for oral cancer in young people: a case-control study. Oral Oncology. 2004 | Marijuana use and cancer incidence. Cancer, Causes & Controls. 1997 | Leslie Iversen. The Science of Marijuana. Oxford University Press. 2000 | Comparing cannabis with tobacco – again. British Medical Journal. 2003 | House of Lords Science and Technology Committee. Ninth Report. 1998 | National Academy of Sciences, Institute of Medicine. Marijuana and Medicine: Assessing the Science Base. National Academy Press. 1999 | Report of the Special Senate Committee on Illegal Drugs. Cannabis: Our Position for a Canadian Public Policy. 2002 | Epidemiologic review of marijuana use and cancer risk. Alcohol. 2005 | Cannabinoids and cancer: causation, remediation, and palliation. Lancet Oncology. 2005 | Ongoing case-control study of marijuana use and cancer. In: National Institute on Drug Abuse (Eds) Workshop on Clinical Consequences of Marijuana: Program Book. National Institutes of Health. 2001 | Marijuana Use and the Risk of Lung and Upper Aerodigestive Tract Cancers: Results of a Population-Based Case-Control Study. Cancer Epidemiology Biomarkers & Prevention. 2006.

Childhood Cancers

Acute myeloid leukemia (AML) comprises approximately 16 percent of leukemias diagnosed in individuals younger than 15 years of age. A 1989 study suggested that prenatal exposure to marijuana increased the risk of childhood leukemia. However, a more recent 2006 study – the largest epidemiological study of childhood AML to date in the US – rebuts this premise.

"Overall, no positive associations between parental marijuana use and childhood AML were observed," investigators at the University of North Carolina at Chapel Hill found. They concluded:

"The previously reported positive association between maternal marijuana use before or during pregnancy and childhood AML was not confirmed in this study. Parental marijuana use is unlikely as a strong risk factor for childhood AML."

Investigators also noted evidence of an "inverse association" between cannabis use and a decreased risk of childhood AML, though they suggested that this result was likely due to "recall bias" (e.g., case mothers may have been less likely than control mothers to report having used marijuana before or during pregnancy) rather than any potential protective effects of cannabis. At least one prior large, population-based case-control study also reports an inverse association between marijuana use and a reduced risk of cancer. That study, published in the American Journal of Epidemiology in 1999, reported that lifetime use of cannabis was associated with a reduced risk of adult, non-Hodgkin’s lymphoma. "Marijuana was the only recreational drug that remained associated with a reduced risk for non-Hodgkin’s lymphoma after adjusting for potential cofounding factors, investigators determined. (A second study on marijuana use and non-Hodgkin’s lymphoma found no association between cannabis use and onset of the disease.)

A review of the literature reveals two additional case-control studies suggesting an increased risk of certain childhood cancers in offspring of mothers who reported using cannabis. However, neither study was a planned investigation of the potential association between maternal cannabis use and childhood cancers; rather, marijuana use was one of several possible confounding variables measured, making it impossible for investigators to ascribe causation. To date, neither of these findings has been replicated.

(References: Maternal drug use and risk of childhood nonlymphoblastic leukemia among offspring. 1989. Cancer | Parental marijuana use and risk of childhood acute myeloid leukemia: a report from the Children’s Cancer Group. Paediatric and Perinatal Epidemiology. 2006 | Case-Control study of non-Hodgkin’s Lymphoma among women and heterosexual men in the San Francisco Bay area, California. American Journal of Epidemiology. 1999 | Alcohol, tobacco and recreational drug use and the risk of non-Hodgkin’s lymphoma. British Journal of Cancer. 1997 | Parents’ use of cocaine and marijuana and increased risk of rhabdomyosarcoma in their children. Cancer Causes and Control. 1993 | Gestational and familial risks factors for childhood astrocytoma: results of a case-control study. Cancer Research. 1990)

Other Cancers

Sidney and colleagues, in their 1997 retrospective cohort study of 65,171 men and women, determined that "ever" and "current use" of cannabis was not associated with an increased risk of tobacco-use related cancers or cancers of the colon, lung, skin, prostate, breast and cervix. "Compared with nonusers/experimenters (lifetime use of less than seven times), … marijuana use [was] not associated with increased risk of cancer … in analyses adjusted for sociodemographic factors, cigarette smoking, and alcohol use," investigators determined. A 2005 review of case studies by Hashibe and colleagues also failed to note evidence of a strong association between cannabis use and either anal or penile cancer.

A second cohort study by University of Hawaii researchers investigating the risk for malignant primary onset glioma (brain cancer) associated with cigarette smoking and other lifestyle behaviors did report an increased incidence risk for individuals who smoked cannabis at least once per month, after adjustment for sex, race, education, smoking status, alcohol consumption, and coffee intake. However, no dose-response relation was observed -- by contrast, drinkers of >7 cups of coffee per day had a 70 percent increased risk for glioma – and cannabis was only incidentally assessed as a potential confounding factor

The above finding is curious in light of several recent preclinical studies demonstrating that the administration of cannabinoids selectively inhibit the growth of glioma cells in a dose dependent manner. Among these, an Italian research team, writing in the 2004 issue of the Journal of Pharmacology and Experimental Therapeutics demonstrated that the administration of the non-psychoactive cannabinoid cannabidiol (CBD) to nude mice significantly inhibited the growth of subcutaneously implanted U87 human glioma cells. Authors wrote, "In conclusion, … CBD was able to produce a significant antitumor activity both in vitro and in vivo, thus suggesting a possible application of CBD as an antineoplastic agent (an agent that inhibits the growth of malignant cells.)" More recently, investigators at the California Pacific Medical Center Research Institute reported that the administration of THC on human glioblastoma multiforme cell lines decreased the proliferation of malignant cells and induced apoptosis (programmed cell death) more rapidly than did the administration of an alternative synthetic cannabis receptor agonist.

Finally, a team of investigators from Stanford University and the Medical College of Georgia recently reported an association between marijuana exposure and bladder cancer in a pilot study of Vietnam-era veterans aged less than 60 years old. However, 77 percent of the cancer patients in the study reported smoking both tobacco and marijuana, and only six subjects (11 percent) admitted to having used marijuana and not tobacco. A 2006 case report published in the journal Urology also suggests heavy cannabis use (up to five cigarettes daily for more than 30 years) as a potential risk factor in a 45-year-old man with transitional cell carcinoma. Follow-up, large-scale epidemiological studies may be warranted in this area.

(References: Marijuana use and cancer incidence. Cancer, Causes & Controls. 1997 | Epidemiologic review of marijuana use and cancer risk. Alcohol. 2005 | The risk for malignant primary adult-onset glioma in a large, multiethnic, managed-care cohort: cigarette smoking and other lifestyle behaviors. Journal of Neurooncology. 2004 | Anti-tumor effects of cannabidiol, a non-psychotropic cannabinoid, on human glioma cell lines. Journal of Pharmacology and Experimental Therapeutics. 2003 | Cannabinoids selectively inhibit proliferation and induce cell death of cultured human glioblastoma multiforme cells. Journal of Neurooncology. 2005 | Association between marijuana use and transitional cell carcinoma. Urology. 2006 | Transitional cell carcinoma associated with marijuana: case report and review of the literature. Urology. 2006.)


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