Early life exposure to air pollution induces adult cardiac dysfunction

Exposure 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 consequences measured at adulthood. Pregnant FVB mice were exposed to filtered (FA) or concentrated ambient particulate matter (PM2.5) during gestation and nursing. Mice were exposed to PM2.5 at an average concentration of 51.69 mu g/m(3) 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 ejection fraction (79.1 +/- 3.5% FA, 35.5 +/- 9.5% PM2.5, P = 0.005), increased end-systolic volume (10.4 +/- 2.5 mu l FA, 39.5 +/- 3.8 mu l PM2.5, P = 0.001), and reduced dP/dt maximum (11,605 +/- 200 mu l/s FA, 9,569 +/- 800 mu l/s PM2.5, P = 0.05) and minimum (-9,203 +/- 235 mu l/s FA, -7,045 +/- 189 mu l/s PM2.5, P = 0.0005) in PM2.5-exposed mice. Isolated cardiomyocytes from the hearts of PM2.5-exposed mice had reduced peak shortening (%PS, 8.53 +/- 2.82% FA, 6.82 +/- 2.04% PM2.5, P = 0.003), slower calcium reuptake (tau, 0.22 +/- 0.09 s FA, 0.26 +/- 0.07 s PM2.5, P = 0.048), and reduced response to beta-adrenergic stimulation compared with cardiomyocytes isolated from mice that were exposed to FA. Histological analyses revealed greater picro-sirius red-positive-stained areas in the PM2.5 vs. FA group, indicative of increased collagen deposition. We concluded that these data demonstrate the detrimental role of early life exposure to ambient particulate air pollution in programming of adult cardiovascular diseases and the potential for PM2.5 to induce persistent cardiac dysfunction at adulthood.