Does cannabis use disorder increase the risk of head and neck cancer?

By Dr. Liji Thomas, MDReviewed by Benedette Cuffari, M.Sc.Aug 12 2024

A recent study published in JAMA Otolaryngology Head & Neck Surgery determines whether cannabis use disorder (CUD) increases the risk of head and neck cancer (HNC).

Study: Cannabis Use and Head and Neck Cancer. Image Credit: Andry Jeymsss / Shutterstock.com

What is HNC?

HNC is the sixth leading cause of cancer throughout the world. In 2020, over 870,000 HNC cases were reported globally, 440,000 of which resulted in death. In the United States, HNC is responsible for about 3% of all cancers and over 1.5% of cancer-related deaths.

HNC can be further categorized based on the different tissues affected, some of which include the oral cavity, pharynx, larynx, and adjacent salivary glands. HNC has historically been caused by tobacco use and drinking; however, a significant proportion of HNC cases are also caused by human papillomavirus (HPV) infection.

Cannabis risk

Throughout both the U.S. and the rest of the world, cannabis is the most commonly used illicit substance. Cannabis is most commonly consumed through inhalation for both recreational and medical purposes, the latter of which may include amelioration of nausea, cancer pain, and anorexia.

Despite its potential therapeutic effects for these conditions, cannabis use remains controversial, as it may increase the risk of developing psychotic disorders and cognitive defects. Furthermore, the smoke content of cannabis contains carcinogens similar to those found in cannabis, such as polycyclic aromatic hydrocarbons (PAHs) and nitrosamines. Tetrahydrocannabinol (THC), which is the primary psychoactive component in cannabis, also promotes the conversion of PAHs to carcinogens.  

About the study

The current study used medical records from TriNetX, a 20-year database comprising 64 healthcare organizations. Adults with and without CUD with no history of HNC and a recorded outpatient clinic visit were included in the study.

After demographic, alcohol disorder, and tobacco use matching, the relative risks of HNC and its incidence at various sites in the two groups were estimated. Age-stratified analysis in those below 60 years as compared to older patients was also performed.

What did the study show?

The CUD group comprised 116,076 people, about 45% of whom were women and 60% were White with a mean age of 46.4 years. About 19% of patients with CUD reported tobacco use, whereas 22.6% reported alcohol use.

The control group without a history of CUD comprised 115,865 individuals, 74.9% of whom were White and 54.5% were women with an average age of 60.8 years. About 2.4% and 2.5% of these individuals reported alcohol and tobacco use, respectively.

As compared to controls, people with CUD were at a 3.5-fold increased risk of HNC. The risk of oral, salivary, and nasopharyngeal HNC was 2.5-fold greater in the CUD cohort, whereas the oropharyngeal cancer rate was nearly five-fold that of controls. The incidence of laryngeal cancer was also 8.4-fold greater in the CUD group than controls.

This increased risk was consistently observed in older and younger age patients for cancers reported one or more years after the first outpatient visit. Although the risk of any HNC remained significant five or more years after the first outpatient visit, it was no longer significant for HNC subsites. This loss of strength for associations with HNC at five or more years from the reporting of CUD may be due to low sample sizes, other confounding factors, and variations in cannabis use.

Conclusions

The study findings suggest that CUD is a significant risk factor for HNC, as well as cancers affecting various tissues within the head and neck in U.S. adults. Propensity score matching was performed for alcohol and tobacco use; however, these results should be interpreted with caution due to the inability to completely control for these demographic factors and HPV status.

Although cannabis consumption rates were not provided, the utilization of data from patients with a diagnosis of CUD indicates that these individuals had substantial cannabis exposure that was sufficient to cause physical and/or emotional symptoms requiring hospitalization.

We can estimate that the association of cannabis use seen in this study with risk of developing HNC was slightly less than that of alcohol and tobacco use.”

Cannabis smoke may promote inflammation, especially since it is unfiltered, deep inhalations are taken, and cannabis burns at higher temperatures. In addition to inflammatory injury, oxidative stress and suppression of antitumor immunity may also contribute to the increased risk of HNC among patients with CUD.

Further research is needed to validate the increased risk of HNC in patients with CUD and explore underlying mechanisms that may contribute to this association.