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Editorials

Comparing cannabis with tobacco

BMJ 2003; 326 doi: https://doi.org/10.1136/bmj.326.7396.942 (Published 03 May 2003) Cite this as: BMJ 2003;326:942

A Science Based Evaluation of Cannabis and Cancer

While there can be little doubt that smoking anything is likely to be

detrimental to the health of one’s respiratory system, scientific data
does not support the extension of the biological consequences
resulting from tobacco smoke to marijuana smoke(1). Two
complementary pieces of information support the position that the
effects of the two, tobacco and marijuana, are different.

The irritant
properties of all smoke will naturally tend to promote a pro-
inflammatory immune response with the corresponding production
of potentially carcinogenic free radicals. However, cannabis
promotes immune deviation to an anti-inflammatory Th2 response
via immune-system specific CB2 receptors(2). Thus, the natural
pharmacological properties of marijuana’s cannabinoids, that are
not present in tobacco smoke, would minimize potential irritant
initiated carcinogenesis.

In contrast, the nicotine present in
tobacco smoke, but lacking in cannabis smoke, specifically
activates nicotine receptors in respiratory pathways that in turn
protect these cells from apoptosis normally promoted by genotoxic
agents found in smoke(3). Thus, the pharmacological activities of
tobacco smoke would tend to amplify its carcinogenic potential by
inhibiting the death of genetically damaged cells. Together these
observations support the epidemiological study of the Kaiser
Foundation that did not find cannabis smoking to be associated
with cancer incidence(4). Additionally, the demonstrated cancer
killing activities of cannabinoids has been ignored. Cannabinoids
have been shown to kill some leukemia and lymphoma(5), breast
and prostate (6), pheochromocytoma(7), glioma(8) and skin
cancer(9) cells in cell culture and in animals.

1. Henry JA, Oldfield WL, Kon OM. Comparing cannabis with
tobacco. BMJ. 2003;326:942-943.

2. Yuan M, Kiertscher SM, Cheng Q, Zoumalan R, Tashkin DP,
Roth MD. Delta 9-Tetrahydrocannabinol regulates Th1/Th2
cytokine balance in activated human T cells. J Neuroimmunol.
2002;133:124-131.

3. West KA, Brognard J, Clark AS, Linnoila IR, Yang X, Swain SM,
Harris C, Belinsky S, Dennis PA. Rapid Akt activation by nicotine
and a tobacco carcinogen modulates the phenotype of normal
human airway epithelial cells. J Clin Invest. 2003;111:81-90.

4. Sidney S, Beck JE, Tekawa IS, Quesenberry CP, Friedman GD.
Marijuana use and mortality. Am J Public Health. 1997;87:585-
590.

5. McKallip RJ, Lombard C, Fisher M, Martin BR, Ryu S, Grant S,
Nagarkatti PS, Nagarkatti M. Targeting CB2 cannabinoid receptors
as a novel therapy to treat malignant lymphoblastic disease.
Blood. 2002;100:627-634.

6. Melck D, De Petrocellis L, Orlando P, Bisogno T, Laezza C,
Bifulco M, Di Marzo V. Suppression of nerve growth factor Trk
receptors and prolactin receptors by endocannabinoids leads to
inhibition of human breast and prostate cancer cell proliferation.
Endocrinology. 2000;141:118-126.

7. Sarker KP, Obara S, Nakata M, Kitajima I, Maruyama I.
Anandamide induces apoptosis of PC-12 cells: involvement of
superoxide and caspase-3. FEBS Lett. 2000;472:39-44.

8. Sanchez C, Galve-Roperh I, Canova C, Brachet P, Guzman M.
Delta9-tetrahydrocannabinol induces apoptosis in C6 glioma cells.
FEBS Lett. 1998;436:6-10.

9. Casanova ML, Blazquez C, Martinez-Palacio J, Villanueva C,
Fernandez-Acenero MJ, Huffman JW, Jorcano JL, Guzman M.
Inhibition of skin tumor growth and angiogenesis in vivo by
activation of cannabinoid receptors. J Clin Invest. 2003;111:43-50.

Competing interests:  
None declared

Competing interests: No competing interests

23 May 2003
Robert Melamede
UCCS
80933-7150