Cannabis abuse/dependence linked to higher rates of bladder, kidney, and prostate cancer | Research

The takeaway

A large US claims database analysis found that men with cannabis abuse or dependence diagnoses had significantly elevated risks of bladder, kidney, and prostate cancer compared to matched controls.

Long-term cannabis users, especially those who smoke it, interested in cancer risk data.

4.21x higher risk of bladder cancer among those with cannabis abuse/dependence diagnoses

What the researchers found

After propensity matching on demographics, tobacco use, and cancer risk factors, cannabis abuse/dependence was associated with 4.21-fold increased risk of bladder cancer, 3.70-fold increased risk of kidney cancer, and 2.80-fold increased risk of prostate cancer.

Why it matters

Cannabis smoke contains many of the same carcinogens as tobacco smoke, yet the relationship between cannabis and urologic cancers has been poorly studied. This population-scale analysis provides the first large matched comparison for multiple urologic malignancies.

The numbers in context

Bladder cancer: 0.14% vs 0.03% (RR 4.21, 95% CI 2.70-6.57). Kidney cancer: 0.17% vs 0.05% (RR 3.70, 95% CI 2.52-5.43). Prostate cancer: 0.61% vs 0.22% (RR 2.80, 95% CI 2.19-3.58). No significant association for upper tract, testis, or penile cancer.

How the study worked

Researchers used the TriNetX database to identify US adults from 2004 to 2024 with or without cannabis abuse/dependence diagnoses. After excluding those with prior urologic cancers, 74,642 cannabis-diagnosed patients were matched against controls on demographics, tobacco use, nicotine dependence, substance-related disorders, and cancer-specific risk factors.

What this study cannot tell us

Claims-based diagnoses cannot distinguish smoking from other consumption methods. Cannabis abuse/dependence codes likely capture the heaviest users, so results may not apply to occasional use. Residual confounding from unmeasured lifestyle factors is possible. Rare cancers like testicular and penile cancer may lack statistical power to detect associations.

How to read the evidence

Large propensity-matched retrospective cohort from a national database, though limited by inability to assess consumption method or dose-response.

When this study was published

Published in 2025, using claims data from 2004 to 2024.

The bigger picture

While relative risks are notably elevated, absolute cancer rates remain low in both groups. The study matched on tobacco use and other substance disorders, but unmeasured confounders including cannabis consumption method and dose remain problematic. These findings add to a growing body of evidence that inhaled cannabis may carry cancer risks similar to tobacco.

Questions still open

Would the cancer associations hold for non-smoked cannabis consumption methods like edibles or vaporizers? Is there a dose-response relationship? Are specific cannabinoids protective or harmful, or is the risk driven by combustion byproducts?

Common questions

Does cannabis definitely cause these cancers?

This study found a statistical association, not proof of causation. While the risk ratios are large and the study controlled for tobacco use, claims data cannot rule out all confounding factors.

Were edible or vaporizer users included?

The study could not distinguish between consumption methods. Cannabis abuse/dependence diagnoses likely capture a mix, though smoking is the most common method among heavy users.

Why were testicular and penile cancers not significant?

These are relatively rare cancers, so the study may not have had enough cases to detect an association even if one exists.

Read the original research

A population-level analysis on the association of cannabis use and urologic cancers.

Urologic oncology, 43(10), 598.e11-598.e16

View on PubMed ↗Publisher’s paper ↗

Citation

Davis, Ryan J; Hershenhouse, Jacob; Gallagher, Tyler J; Sabharwal, Navin; Daneshvar, Michael A. (2025). A population-level analysis on the association of cannabis use and urologic cancers.. Urologic oncology, 43(10), 598.e11-598.e16. https://doi.org/10.1016/j.urolonc.2025.05.010