{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T19:24:42Z","timestamp":1791228282003,"version":"4.1.0"},"reference-count":49,"publisher":"American Physiological Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2014,11,1]]},"abstract":"<jats:p>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 (PM<jats:sub>2.5<\/jats:sub>) during gestation and nursing. Mice were exposed to PM<jats:sub>2.5<\/jats:sub>at an average concentration of 51.69 \u03bcg\/m<jats:sup>3<\/jats:sup>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 PM<jats:sub>2.5<\/jats:sub>pups compared with FA (1.36 \u00b1 0.12 g FA, n = 42 mice; 1.30 \u00b1 0.15 g PM<jats:sub>2.5<\/jats:sub>, n = 67 P = 0.012). At adulthood, mice exposed to perinatal PM<jats:sub>2.5<\/jats:sub>had reduced left ventricular fractional shortening compared with FA-exposed mice (43.6 \u00b1 2.1% FA, 33.2 \u00b1 1.6% PM<jats:sub>2.5<\/jats:sub>, P = 0.001) with greater left ventricular end systolic diameter. Pressure-volume loops showed reduced ejection fraction (79.1 \u00b1 3.5% FA, 35.5 \u00b1 9.5% PM<jats:sub>2.5<\/jats:sub>, P = 0.005), increased end-systolic volume (10.4 \u00b1 2.5 \u03bcl FA, 39.5 \u00b1 3.8 \u03bcl PM<jats:sub>2.5<\/jats:sub>, P = 0.001), and reduced dP\/d t maximum (11,605 \u00b1 200 \u03bcl\/s FA, 9,569 \u00b1 800 \u03bcl\/s PM<jats:sub>2.5<\/jats:sub>, P = 0.05) and minimum (\u22129,203 \u00b1 235 \u03bcl\/s FA, \u22127,045 \u00b1 189 \u03bcl\/s PM<jats:sub>2.5<\/jats:sub>, P = 0.0005) in PM<jats:sub>2.5<\/jats:sub>-exposed mice. Isolated cardiomyocytes from the hearts of PM<jats:sub>2.5<\/jats:sub>-exposed mice had reduced peak shortening (%PS, 8.53 \u00b1 2.82% FA, 6.82 \u00b1 2.04% PM<jats:sub>2.5<\/jats:sub>, P = 0.003), slower calcium reuptake (\u03c4, 0.22 \u00b1 0.09 s FA, 0.26 \u00b1 0.07 s PM<jats:sub>2.5<\/jats:sub>, P = 0.048), and reduced response to \u03b2-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 PM<jats:sub>2.5<\/jats:sub>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 PM<jats:sub>2.5<\/jats:sub>to induce persistent cardiac dysfunction at adulthood.<\/jats:p>","DOI":"10.1152\/ajpheart.00526.2014","type":"journal-article","created":{"date-parts":[[2014,8,30]],"date-time":"2014-08-30T02:35:25Z","timestamp":1409366125000},"page":"H1353-H1360","source":"Crossref","is-referenced-by-count":80,"title":["Early life exposure to air pollution induces adult cardiac dysfunction"],"prefix":"10.1152","volume":"307","author":[{"given":"Matthew W.","family":"Gorr","sequence":"first","affiliation":[{"name":"College of Medicine and the Dorothy M. 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