posure to ambient air pollution contributes to the progression of cardiovascular disease, particularly in susceptible populations. The objective of the present study was to determine whether early life exposure to air pollution causes persistent cardiovascular conse-quences measured at adulthood. Pregnant FVB mice were exposed to filtered (FA) or concentrated ambient particulate matter (PM2.5) dur-ing gestation and nursing. Mice were exposed to PM2.5 at an average concentration of 51.69 g/m3 from the Columbus, OH region for 6 h/day, 7 days/wk in utero until weaning at 3 wk of age. Birth weight was reduced in PM2.5 pups compared with FA (1.36 0.12 g FA, n 42 mice; 1.30 0.15 g PM2.5, n 67 P 0.012). At adulthood, mice exposed to perinatal PM2.5 had reduced left ventricular fractional shortening compared with FA-exposed mice (43.6 2.1 % FA, 33.2 1.6 % PM2.5, P 0.001) with greater left ventricular end systolic diameter. Pressure-volume loops showed reduced ejectio
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