Human chromosomal anomalies, notably trisomies, disrupt gene expression, leading to diverse cellular and organ phenotypes. Increased cellular senescence (SEN) and oxidative stress in trisomies have gained recent attention. We assessed SEN, senescence-associated secretory phenotype (SASP) and oxidative stress on trisomy 13, 18, and 21 (T13, T18, T21) human fetal lung tissues and isolated primary human fetal lung fibroblasts. Telomerase associated foci (TAF) staining showed DNA damage primarily within T21 and T18 lungs. These results were confirmed by RT-qPCR showing an increase of the SEN marker