If you can refrain from inhaling either cannabis smoke or tobacco smoke, you should.
However, the intent of this post is to help clarify whether or not the biological consequences of smoking cannabis and tobacco are similar, in the context of free radical production, and the development of lung and colorectal cancers.
In order to adequately discuss this topic, it is essential that we dispel some common misconceptions about cannabis and tobacco smoke.
- Cannabis smoke contains four-fold more tars than tobacco smoke.
- Cannabis smoke has potentially higher levels of polycyclic aromatic hydrocarbons than tobacco smoke.
- Like tobacco smoke, cannabis smoke contains several known carcinogens and tumor promoters, including vinyl chlorides, phenols, aldehydes, nitrosamines, reactive oxygen species, and polycyclic aromatic hydrocarbons (PAHs)
- The PAHs Benzo[a]pyrene, and Benz[a]anthracene are highly pro-carcinogenic and are present in cannabis anywhere between 25-75% higher concentrations in cannabis smoke than tobacco smoke.
- Cannabis smoke has definite carcinogenic potential.
- Cannabis smoke – induced cellular damage was clearly demonstrated in-vitro through epidemiological analysis.
Ostensibly, it would appear that cannabis smoke could be more harmful in terms of oxidative stress, and the development of lung or colorectal cancers than tobacco smoke. However, it should be noted that,
“cannabis and tobacco smoke have similar properties chemically, their pharmacological activities differ greatly.”1
In other words, despite exhibiting a high carcinogenic potential, cannabis smoke, reacts differently biologically than tobacco smoke.
What does this mean in terms of the biological consequence of smoking cannabis or tobacco? It means that in spite of its carcinogenic potential, and demonstrable cellular damage, cannabis smoke does not necessarily have the same biological consequence as smoking tobacco.
In the article Cannabis and Tobacco Smoke Are Not Equally Carcinogenic, Robert Melamede writes that “recently, Hashibe et al carried out an epidemiological analysis of marijuana smoking and cancer. A connection between marijuana smoking and lung or colorectal cancer was not observed. These conclusions are reinforced by the recent work of Tashkin and coworkers who were unable to demonstrate a cannabis smoke and lung cancer link, despite clearly demonstrating cannabis smoke-induced cellular damage.”2
Here is why;
In the context of free-radical production, our body is a constant balance between oxidative stress and reduction.
A normal, healthy body maintains a healthy balance between oxidative stress and reduction through immunological response, and the anti-oxidant defense systems found within cells.
Free-radical production is thus a normal byproduct of cellular metabolism. However, coupled with aging, environmental, and behavioral factors, free – radical production is exacerbated and can lead to systemic, and chronic inflammation.
Free – radicals contribute to systemic, and chronic inflammation because they are inherently unstable molecules that seek stability by stealing electrons from other stable molecules.
This causes a chain reaction of free-radical formation that can cause damage to the body’s cells, proteins, and DNA. This process is a precursor for developing cancer.
Free-radicals attack the nucleic acids (RNA and DNA), thus affecting the function, growth, and repair of cells dependent on proper protein function.
This is relevant insofar as when we smoke either cannabis or tobacco, we are engaging in behaviors that contribute to systemic inflammation, cellular damage, inhibition or alteration of cellular mechanisms, and the introduction of pro-cancerous material into the body.
In doing so, we are adversely affecting the balance between oxidative stress and reduction by inhibiting , or altering our immunological responses and our cells anti-oxidant defenses.
Bottom line, inhaling smoke is bad for you.
However, that does not mean that the biological consequences of cannabis smoke and tobacco smoke are similar.
“Cannabis down-regulates immunologically – generated free – radical production by promoting a Th2 Immune Cytokine Profile.”3
This means that in spite of cannabis smoke being carcinogenic, a feature of cannabis, particularly THC, is that it promotes a Th2 dominant immunological profile. Th2 Cytokines are a subset of Helper T – Cells which help activate the Cytotoxic T – Cells that kill damaged cells. These play a vital role in the clearance of pathogens.
The significance of this is that while cannabis smoke does induce cellular damage, and is pro-carcinogenic, it does not necessarily progress from a pre-cancerous state.
In addition to mitigating immunologically – generated free – radical production,
“THC inhibits the enzyme necessary to activate some of the carcinogens found in smoke.”4
This enzyme is known as CYP1A1, and is a key enzyme that converts PAHs into ACTIVE carcinogens.
PAHs in tobacco smoke activate transcription of the CYP1A1 gene and increase pulmonary CYP1A1 activity several – fold.
What does this mean?
“The induction of CYP1A1 is time – and exposure – dependent and results in a marked increase in the conversion of smoked PAHs into carcinogens, and increase in DNA mutations in lung tissue, and an increased risk for developing cancer.“5
This is significant insofar as while both cannabis and tobacco are carcinogenic material, THC potentially mitigates some of the risk of cancer from smoking cannabis, while nicotine potentially increases the risk of cancer from smoking tobacco.
“Nicotine activates some CYP1A1 activities, potentially increasing the carcinogenic effects of tobacco smoke.”6
It is important to note that the epidemiological analysis conducted in the study being referenced for this article was conducted in – vitro. It was highly specific, and in a lab.
The parameters for the study must be respected, and themarijuanafacts.com is by no means suggesting what the clinical significance of this would be in a human body, nor what the long – term implications of smoking cannabis would be in regards to developing lung or colorectal cancers. That would require a longitudinal study and far more research.
The goal of this post was to be inquisitorial and informative, we are not endorsing cannabis or tobacco smoking, or making medical claims. We are seeking to advance the discourse on cannabis by providing original, sourced, and cited content.
Thanks for reading! If you enjoyed this post, or have a something to add, please leave a comment below.
- Melamede, Robert. “Cannabis and Tobacco Smoke Are Not Equally Carcinogenic.” Harm Reduction Journal2 (2005): 21. PMC. Web. 13 Apr. 2018.
- Roth, Michael D., Jose A. Marques-Magallanes, Michael Yuan, Weimin Sun, and Donald P. Tashkin. “Induction and Regulation of the Carcinogen-Metabolizing Enzyme CYP1A1 by Marijuana Smoke and Δ9-Tetrahydrocannabinol.”American Journal of Respiratory Cell and Molecular Biology, vol. 4, no. 3, 1 Mar. 2001, doi:https://doi.org/10.1165/ajrcmb.24.3.4252 , https://www.atsjournals.org/doi/full/10.1165/ajrcmb.24.3.4252#. Accessed 13 Apr. 2018.
- Berger, Abi. “Th1 and Th2 Responses: What Are They?” BMJ : British Medical Journal7258 (2000): 424. Print.
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