A recently published study JAMA Otorhinolaryngology determines whether cannabis use disorder (CUD) increases the risk of head and neck cancer (HNC).

Study: Cannabis use and head and neck cancer. Photo credit: Andry Jeymsss / Shutterstock.com

What is HNC?

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

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

Cannabis risk

Cannabis is the most commonly consumed illegal substance in both the United States and the rest of the world. Cannabis is most commonly consumed through inhalation for both recreational and medicinal purposes. The latter can relieve nausea, cancer pain, and anorexia.

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

About the study

The current study used medical records from TriNetX, a 20-year database of 64 healthcare organizations. The study included adults with and without CUD, with no history of HNC, and with a documented outpatient clinic visit.

After matching demographic characteristics and alcohol and tobacco dependence criteria, the relative risks for HNC and its incidence at different sites were estimated in the two groups. In addition, an age-stratified analysis of those under 60 years of age was compared with older patients.

What did the study show?

The CUD group included 116,076 individuals, approximately 45% of whom were female and 60% white, with a mean age of 46.4 years. Approximately 19% of patients with CUD reported tobacco use, while 22.6% consumed alcohol.

The control group without a history of CUD included 115,865 individuals, of whom 74.9% were white and 54.5% were female, with a mean age of 60.8 years. Approximately 2.4% and 2.5% of these individuals reported using alcohol and tobacco, respectively.

Compared with controls, people with CUD had a 3.5-fold increased risk of HNC. The risk of oral, salivary and nasopharyngeal HNC was 2.5-fold higher in the CUD cohort, while the rate of oropharyngeal cancer was almost five times higher than in the control group. The incidence of laryngeal cancer was also 8.4 times higher in the CUD group than in the control group.

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

Conclusions

The results of the study suggest that CUD is a significant risk factor for HNC as well as cancers affecting various tissues in the head and neck region in US adults. Propensity score matching was performed for alcohol and tobacco use. However, these results should be interpreted with caution because these demographic factors and HPV status cannot be fully controlled.

Although no data were provided on cannabis use rates, analysis of data from patients diagnosed with CUD indicates that these individuals had significant exposure to cannabis, sufficient to produce physical and/or emotional symptoms requiring hospitalization.

We can assume that the association found in this study between cannabis use and the risk of developing HNC was somewhat lower than that found between alcohol and tobacco use..”

Cannabis smoke may promote inflammation, particularly because it is unfiltered, deeply inhaled, and cannabis burns at higher temperatures. In addition to inflammatory damage, oxidative stress and suppression of antitumor immunity may also contribute to the increased risk of HNC in patients with CUD.

Further studies are needed to confirm the increased risk of HNC in patients with CUD and to explore the underlying mechanisms that may contribute to this association.