MR1 presents small‑molecule metabolites to mucosal‑associated invariant T (MAIT) cells, a highly abundant T‑cell population enriched at mucosal barrier sites such as the lung. Air pollution is a pervasive environmental exposure, yet the specific chemical components that influence MAIT cell function remain largely unknown. Using integrated computational, cellular, and biochemical approaches, we identified a set of pollution‑derived phenylpropanoid and furanoid aldehydes that bind MR1. Some of these compounds altered MR1 surface expression and suppressed MAIT cell activation in vitro and ex vivo. Structural analyses revealed that these non‑stimulatory ligands for a Schiff base with the key MR1-Lys43 residue and adopt binding poses within MR1 that resembles the inhibitory ligands, consistent with a shared mode of MAIT cell modulation. Together, our findings uncover a previously unrecognised class of air‑pollution‑derived MR1 ligands and suggest that chemical exposures at mucosal surfaces may directly shape MAIT cell immunity.