Inhalation of Printer-Emitted Particles Impairs Cardiac Conduction, Hemodynamics, and Autonomic Regulation and Induces Arrhythmia and Electrical Remodeling in Conscious Rats. Carll AP, Salatini R, Pirela SV, Wang Y, Xie Z, Lorkiewicz P, Naeem N, Qian Y, Castranova V, Godleski JJ, Demokritou P (2020).of Environmental Health, Program in Molecular and Integrative Physiological Sciences Post-doctoral Research Fellow, 2013-2015, Harvard School of Public Health, Dept. Environmental Protection Agency, National Health and Environmental Effects Research Laboratory, Cardiopulmonary and Immunotoxicology Branch. 2004, Duke University, Environmental Science & Policy 2008, UNC-Chapel Hill, School of Public Health, Environmental Sciences & Engineering.Ī.B. 2012, University of North Carolina (UNC)-Chapel Hill, Gillings School of Global Public Health, Environmental Health Sciences. Chan School of Public Health, Molecular and Integrative Physiological Sciences. How do VOCs contribute to the cardiac risks of exposure to pollutant aerosols?.How do e-cigarette and office printer aerosols adversely affect cardiac function, intracellular signaling, and neuroregulation?.What are the neural and cellular pathways underlying pollutant-induced myocardial dysfunction and remodeling?.Currently we are investigating in both rodents and humans several emerging questions in environmental health sciences, including: The Carll lab also conducts basic biochemical and molecular toxicologic assays while analyzing physiologic signals, including the electrocardiogram (ECG), arterial and left ventricular pressure waveforms, and echocardiogram. Carll’s team assesses rodent and human hearts for adverse changes in electrical activity, mechanical performance, and neural regulation following exposure to multiple pollutants, including PM from highways, office printers, and ambient urban airsheds, as wells as diesel exhaust, volatile organic compounds (VOCs), mainstream cigarette smoke, and electronic cigarette aerosols. The Carll lab applies healthy, diseased, and genetic rodent models to inhalation exposure studies to investigate the biological plausibility and elucidate the mechanisms of air pollutant-induced cardiac mortality and morbidity.ĭr. Carll’s recent findings suggest that exposure to suspended particulate matter (PM) at near-ambient levels promotes concomitant arrhythmia, autonomic imbalance, blunted baroreflexes, and respiratory dysfunction. The Carll laboratory studies the biological mechanisms by which air pollutants weaken the heart, impair cardiac conduction, and compromise hemodynamics, and whether such effects occur through the autonomic nervous system.
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