Finally, the proteomic study of 50,553 participants revealed that air pollution interacts with key plasma proteins—including CDHR5, TNFRSF13C, ICAM5, and HSD11B1—to modulate depression risk through neuroinflammatory, endocrine (steroid biosynthesis), and metabolic (lipid digestion) pathways, with drug–protein interactions implicating antipsychotics (risperidone) and hormones (progesterone) as potential modifiers of pollution-induced depression [50]. This evidence concerns the gene TNFRSF13C and depressive symptom measurement.