Cannabis smoke caused more damage to placental cells than THC alone, suggesting combustion byproducts add their own risks

Cannabis smoke extract (CaSE) reduced markers of placental cell maturation (hCG protein and syncytin-1 gene expression) and caused dose-dependent mitochondrial dysfunction. Lower concentrations elevated reactive oxygen species while higher concentrations disrupted mitochondrial respiration. Blocking the CB1 receptor rescued the effects of pure THC but not of cannabis smoke extract.

In vitro study using human trophoblast cells exposed to cannabis smoke extract versus pure THC. Researchers measured markers of cell differentiation, reactive oxygen species, mitochondrial membrane potential and respiration, antioxidant gene expression, and the effect of CB1 receptor blockade.

Smoking remains the most common way pregnant people consume cannabis, yet most research focuses on THC alone. This study demonstrates that combustion byproducts create additional harm to placental cells that cannot be blocked by targeting cannabinoid receptors.

Public health messaging about cannabis in pregnancy typically focuses on THC. This research suggests how cannabis is consumed may matter as much as whether it is consumed, with smoking introducing combustion-related toxicity that pure cannabinoid exposure does not.

In vitro study using cell cultures, not a living placenta. Cannabis smoke extract preparation may not perfectly replicate real-world smoking. Single cell type studied. No comparison with vaporized or edible cannabis.