Prenatal and early exposure to fine particulate matter <2.5 micrometers (μm) (PM2.5), aeroallergens, and tobacco smoke, together with polymorphisms in glutathione S-transferase P1 (GSTP1) and CAT, overwhelm these defenses, driving epithelial damage, airway remodeling, and corticosteroid resistance—the core of childhood asthma pathogenesis. Here, GSTP1 is linked to childhood onset asthma.