Both Tobacco and Cannabis Smoking Activated the Same Inflammatory Immune Pathway in Young Adults | Research

The takeaway

Cannabis and tobacco smoking both increased GPR15 expression on helper T cells, which in turn drove pro-inflammatory cytokine ratios — accounting for about half of smoking's inflammatory effect.

Cannabis smokers curious about whether smoking (vs other methods) specifically drives inflammation.

~50%
Of smoking's inflammatory effect was mediated through GPR15 on T cells

What the researchers found

In a cohort of 62 primarily African American young adults, researchers measured a specific immune marker: GPR15 expression on helper T cells. Both tobacco and cannabis smoking were strongly associated with increased GPR15 expression (p < 0.001), and that increase was in turn strongly associated with a shift toward pro-inflammatory cytokine ratios.

The key finding was the mediation analysis: increased GPR15 expression accounted for roughly half of the relationship between smoking (either substance) and pro-inflammatory immune markers. In other words, GPR15 appeared to be a major pathway through which both tobacco and cannabis drive systemic inflammation.

This was notable because cannabis and tobacco smoke have different active compounds (THC/cannabinoids vs nicotine) but share the combustion products — tar, carbon monoxide, particulate matter. The shared GPR15 pathway suggests it's the smoke itself, not the specific drug, driving much of the inflammatory response.

Why it matters

This study bridged cannabis and tobacco research by showing they share an inflammatory mechanism. The implication is direct: if you smoke cannabis, your immune system responds to the combustion much like it responds to tobacco smoke. The active ingredient may be different, but the inflammatory damage from inhaling burned plant matter is similar.

This matters for the "cannabis is safer than tobacco" narrative. For the specific dimension of systemic inflammation via inhaled smoke, they appear to be comparably harmful. Vaporizing or edibles would avoid this pathway entirely.

The numbers in context

• Both tobacco and cannabis: strongly associated with increased GPR15 (p < 0.001)

• GPR15 accounted for ~50% of smoking's effect on pro-inflammatory cytokine ratios

• Sample: 62 young adults, primarily African American, aged 27-35

• Measured: CRP + 17 cytokines alongside GPR15 T cell expression

How the study worked

Cross-sectional study of 62 primarily African American young adults (aged 27-35). Measured GPR15+CD3+CD4+ helper T cells via flow cytometry. Serum assays for CRP and 17 cytokines. Smoking quantified via cotinine (tobacco) and THC (cannabis) serum biomarkers. Correlational analyses and linear regression with mediation analysis.

Who was studied

N=62 primarily African American young adults aged 27-35 years

What this study cannot tell us

Small sample size (n=62) limits statistical power and generalizability. Cross-sectional design cannot establish causation. Primarily African American sample may not represent other populations. Cannot fully separate cannabis and tobacco effects since many participants used both. Serum THC measures recent use but not chronic exposure patterns.

How to read the evidence

Small cross-sectional study with novel biomarker analysis. Compelling mechanistic finding but limited by sample size and design.

When this study was published

Published in 2021. GPR15 as a smoking biomarker is a relatively new area of research.

The bigger picture

This study added molecular evidence to the common-sense observation that inhaling smoke is inflammatory regardless of what you're smoking. As cannabis legalization expands, the delivery method question becomes increasingly important for harm reduction. The inflammatory pathway identified here — GPR15 on helper T cells — provides a measurable biomarker for tracking whether alternative delivery methods actually reduce immune harm.

Replication

Not stated in abstract.

Funding

Not reported in abstract.

Conflicts of interest

Not reported in abstract.

Questions still open

Does vaporizing cannabis avoid the GPR15-mediated inflammatory response?
Is the inflammatory effect reversible after smoking cessation?
Do edible cannabis products have any comparable immune effects?

Common questions

Does smoking cannabis cause inflammation like tobacco?

Yes, through the same pathway. Both activated GPR15 on helper T cells, driving pro-inflammatory immune responses. The shared factor appears to be combustion products, not the drug itself.

Would vaping or edibles avoid this?

Likely. The inflammatory pathway identified here was driven by smoke inhalation. Non-combustion methods should bypass it, though this study didn't test that directly.

Read the original research

Inflammatory biomarker relationships with helper T cell GPR15 expression and cannabis and tobacco smoking.

Journal of psychosomatic research, 141, 110326

The Journal of Psychosomatic Research is a well-regarded journal focusing on the relationship between psychological and physical health.

View on PubMed ↗Publisher’s paper ↗

Citation

Andersen, Allan M; Lei, Man-Kit; Beach, Steven R H; Philibert, Robert A. (2021). Inflammatory biomarker relationships with helper T cell GPR15 expression and cannabis and tobacco smoking.. Journal of psychosomatic research, 141, 110326. https://doi.org/10.1016/j.jpsychores.2020.110326