One reason marijuana smoke is a suspected carcinogen is that marijuana smoke contains polycyclic aromatic hydrocarbons (PAH), which are known carcinogens. A marijuana cigarette typically delivers nanogram quantities of PAHs and microgram quantities of cannabinoids, a unique class of cyclic hydrocarbons. Marijuana smoke is presumed carcinogenic not only because it contains PAHs, but also because cannabinoids, in their own right, modulate cytochrome (CYP1) enzymes required for PAH activation and detoxification.
Until quite recently, PAH-related carcinogenicity was attributed to CYP1 involvement with PAH-related DNA damage in vitro, whereas in vivo experiments now suggest a crucial role for CYP1 enzymes in the detoxification rather than metabolic activation of PAHs (Nebert et al. 2004). As competitive substrates for CYP1 enzymes, concomitantly administered hydrocarbons have been shown to prevent the development of tumors that otherwise results from the administration of a single hydrocarbon (Conney 2003). In the same respect, cannabinoids may competitively inhibit the activation of otherwise carcinogenic hydrocarbons (i.e., PAHs). Cannabinoids may also exert anti-carcinogenic effects unrelated to their hydrocarbon structure. Like anti-carcinogenic polyphenols (Ciolino et al. 1998), cannabinoids have been shown to increase levels of CYP1A1 messenger RNA while reducing CYP1A1 enzyme activity through aryl hydrocarbon receptor ligation. Spiking tobacco tar with THC, the primary cannabinoid in marijuana smoke, was shown to markedly reduce CYP1A1 activity (Roth et al. 2001).
Another reason marijuana smoke is a suspected carcinogen is that cannabinoid administration promotes cancer in laboratory mice under certain conditions. High systemic doses of cannabinoids have been shown to promote cancer via COX-2 elevation (Gardner et al. 2003) and immunosuppression (Zhu et al. 2000) favoring tumors devoid of cannabinoid receptors (McKallip et al. 2005); overwhelmingly, however, most in vivo studies have demonstrated that cannabinoids  administered either locally or systemically over a range of doses  inhibit cancer (Munson et al. 1975, Kaplan 1984, Chan et al. 1996, Blazquez et al. 2003, Blazquez et al. 2004, Bilfuco et al. 2001, Bilfuco et al. 2004, Casanova et al. 2003, Duntsch et al. 2005, Grimaldi et al. 2006, Kogan at al. 2004, Massi et al. 2004, McKallip et al. 2002, Portella et al. 2003, Recht et al. 2001, Sanchez et al. 2001).
A third reason marijuana smoke is a suspected carcinogen is the presence of lesions in the bronchial epithelium of marijuana smokers. Smoking marijuana produces epithelial changes such as squamous metaplasia (SM) and other lesions commonly associated with respiratory exposure to smoke in general (Barskey et al. 1998). On the one hand, SM not only follows exposure to potent carcinogens in laboratory strains of mice, but it also precedes the development of squamous cell carcinoma of lungs (SCCL) in humans. One the other hand, the multiplicity of SM lesions was higher among SCCL-resistant mice (e.g., C57BL/6J = 5.0 - 6.0) than it was among SCCL-susceptible mice (e.g., NIH Swiss = 2.1 - 4.9: Wang et al. 2004); in humans preneoplastic lesions such as SM are generally reversible and often regress spontaneously (Winterhalder et al. 2004).
As it turns out, bronchial lesions may have little, if any at all, predictive value. In fact, according to recent findings, "Distribution and outcome of preneoplastic lesions have been found to be unrelated to various risk factors such as smoking... The 54% regression rate of all preneoplastic lesions, 26% to 39% progression rate to CIS/SCC of individuals with lower-grade dysplasia or severe dysplasia with no significant difference in progression rate and time to progression combined with nonstepwise histologic changes unrelated to the initial histologic grading indicate that one cannot differentiate the potentially more malignant preneoplastic lesions among the many preneoplastic lesions present in the bronchial mucosa. The initial WHO classification of any preneoplastic lesion cannot be reliably used for accurate risk assessment of field carcinogenesis" (Breuer et al. 2005).
A fourth reason marijuana smoke is a suspected carcinogen is that marijuana tar, much like that from tobacco, was shown to produce benign tumors when painted on the skin of animals (Cottrell et al. 1973); however, tar from tobacco smoke was shown to cause frank malignancies when painted on the skin of animals, whereas that from marijuana smoke was not (Cottrell et al. 1973). Along these lines, subsequent research has failed to establish the carcinogenicity of marijuana smoke in animals. In one study, prolonged exposure to marijuana smoke failed to cause precancerous or carcinogenic effects in monkeys (Talaska et al. 1992). In another study, interestingly enough, exposure to marijuana smoke actually retarded the growth of implanted murine sarcoma (Watson 1989). This inhibition was not related to the cannabinoid content of the smoke.
The true neoplastic effects of marijuana smoke might emerge from administration of marijuana-derived chemicals directly to cancers pre-existing in (pulmonary) tissues with the highest exposure to marijuana smoke. Thus far, in vivo studies on the neoplastic properties of cannabinoids have, unfortunately, been conducted with BALB/cJ and C57BL/6J murine strains, which are not susceptible to SCCL. Animal research on smoke-related cancer is problematic because, for example, there has yet to be an animal model in which tobacco smoke exposure causes SCCL.
In evaluating the carcinogenicity of any type of smoke, one must remember that it was epidemiology, rather than animal research, that first incriminated tobacco smoke as a carcinogen 70 years ago. More recently, epidemiologic studies  especially those that included a large number of cases and/or randomly selected controls  tend to suggest, if anything, an inverse association between marijuana use and cancers (Morgenstern et al. 2006; Rosenblatt et al. 2004; Ford et al. 2001; Zhu et al. 2002). Marijuana smoke may ultimately prove to be as carcinogenic in humans as some experts claim it to be animals, but it is animal research that serves to elucidate epidemiology, rather than vice versa.
Further reading(s):
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Comments
Good point about smoking less, though it should also be said that marijuana doesn't have additives like tar.
by WarSpite on January 17th, 2004
good to know. i do both
by Ali Bulut on January 20th, 2004
Most marijuana smokers hold the smoke in their lungs longer than tobacco smokers, causing more damage with less usage.
by James Edwards on November 12th, 2004
A study done in 2005 shows that smoking marijuana is FAR less damaging than tobacco smoke
by Anonymous on February 3rd, 2006
the amount of time you hold the smoke is irrelavent it does not multiply the amount of smoke you inhale the longer you hold it besides tell me how marijuana is more harmful to you than cigarettes marijuana only contains aproximatly 400 chemicals and no carcinogens (cancer causing chemicals) and cigarettes contain over 4000 chemicals 40 of which are carcinogens (cancer causing chemicals) so even if i was true about how long you hold marijuana smoke you would have to hold it ten times longer than a cigarette then you still would not run the risk of developing cancer like you would be subjected to by smoking cigarettes....... please comment i would love to hear your reasoning
by big_J019 on April 23rd, 2010
well if u do marijuana out of a vaporizer you are not inhaling any smoke, so it ain't harmful.
by vic107 on July 13th, 2010