Cellular senescence has beneficial biological roles during development and tissue repair, however, prolonged senescence triggers chronic inflammation and tissue damage. This study aimed to investigate whether pre- and postnatal long-term fine particulate matter (PM2.5) exposure could impair age-related senescence in the kidney contributing to renal damage progression. We examined the impact of developmental PM2.5 exposure on the senescence trajectories combined with postnatal angiogenesis and chronic inflammation in the rat kidneys. Pregnant Sprague–Dawley rats were randomly exposed to normal saline (NS, controls) or PM2.5 during gestation and lactation (N=3/group, during the kidney development period). Their respective male rat offspring were subsequently exposed to NS or PM2.5 for 5 weeks after weaning (from 3 to 8 weeks after birth) (n=4-5/group). Offspring kidneys were taken for morphometric, immunohistochemical, and Western blot studies at two time points, postnatal day (P)21 and P56. PM2.5-exposed offspring exhibited renal structural disturbances that persisted into adulthood. Glomerular and tubulointerstitial injuries with capillary loss were increased in the rats exposed to PM2.5 at both time points. On P21, maternal PM2.5-exposed pups showed the downregulation of intrarenal protein levels of senescence marker p53, p21, and p16 along with a reduced expression of key regulators of angiogenesis and anti-apoptotic protein Bcl-2. On P56, intrarenal expressions of p53, p21, and p16 were all upregulated combined with the activation of nuclear factor-κB and various pro-inflammatory cytokines in the PM2.5 group. The number of CD68-positive macrophages was also greater in the long-term PM2.5 -exposed adult kidneys, compared to the controls. Prenatal exposure to PM2.5 may impair developmental renal senescence, suppressing renal angiogenesis. Prolonged postnatal PM2.5 exposure can promote premature renal senescence and chronic inflammation later in life.