Inhaled particulate matter (PM10 and PM2.5) contributes to inflammatory responses, oxidative stress, and immune dysregulation, increasing susceptibility to respiratory diseases like tuberculosis by inducing inflammatory gene expression (e.g., TNF-α, IL-1β), suppressing anti-tuberculosis immune responses, and altering the lung microenvironment and immune tolerance (7–13). The gene discussed is IL1B; the disease is tuberculosis.