Chronically inhaled ambient particles cause cardiac inflammation in normal, diseased, and elderly rat hearts

Exposure to ambient particulate matter (PM) is linked to increases in cardiovascular morbidity and mortality. The exact mechanism by which PM induces cardiovascular toxicity is not completely understood. We sought to study histopathological changes in the heart muscle in young healthy (Wistar–Kyoto, WKY) and spontaneously hypertensive (SHR) rats and old (22-month-old) Sprague–Dawley rats (SD) chronically exposed to PM. WKY rats and SHR were exposed for 3 months to ultrafine particles (UFP) or filtered air (FA). SD rats were exposed for 9 months to coarse (CP), fine (FP), and ultrafine particles or FA. In addition, we studied effects of PM on mean arterial blood pressure (MABP) and echocardiograms in WKY rats and SHR. Chronic exposure to PM caused histopathological changes in the hearts of all studied strains. The effects ranged from cardiac inflammation caused by 3 months of exposure to UFP in WKY rats and SHR to more severe changes in SD rats exposed to PM for 9 months. Changes in SD rats were inflammation, intracellular edema, and vacuolization in hearts exposed to FP and UFP and vacuolization and collagen accumulation in CP-exposed hearts. In addition, evidence of only mild inflammation was seen in the respiratory tract. We did not observe any statistically significant changes in the MABP (constantly recorded over the entire period of exposure by implanted telemetric devices) and in the echocardiograms in WKY rats and SHR exposed to UFP or FA. MABP at the end of 3 months exposure comprised 153.3 ± 13.9 and 160.3 ± 14.7 mmHg in the SHR-FA and SHR-UFP, respectively, and 124.4 ± 11.2 and 107.9 ± 9.2 mmHg in the WKY-FA and WKY-UFP, respectively (mean ± SD). Our data indicate that chronic exposure to particulate air pollutants causes histopathological changes in healthy (WKY), diseased (SHR), and old SD rat hearts.