Inhalation of Printer-Emitted Particles Impairs Cardiac Conduction, Hemodynamics, and Autonomic Regulation and Induces Arrhythmia and Electrical Remodeling in Rats

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• Personal Author:
  Carll AP ; Castranova, Vincent ; Demokritou P ; Godleski JJ ; Lorkiewicz P ; Naeem N ; Pirela SV ; Qian Y ; Salatini R ; Wang Y ; Xie Z
• Description:
  Background: Using engineered nanomaterial-based toners, laser printers generate aerosols with alarming levels of nanoparticles that bear high bioactivity and potential health risks. Yet, the cardiac impacts of printer-emitted particles (PEPs) are unknown. Inhalation of particulate matter (PM) promotes cardiovascular morbidity and mortality, and ultra-fine particulates (<0.1µm aerodynamic diameter) may bear toxicity unique from larger particles. Toxicological studies suggest that PM impairs left ventricular (LV) performance; however, such investigations have heretofore required animal restraint, anesthesia, or ex vivo preparations that can confound physiologic endpoints and/or prohibit LV mechanical assessments during exposure. To assess the acute and chronic effects of PEPs on cardiac physiology, male Sprague Dawley rats were exposed to PEPs (21days, 5h/day) while monitoring LV pressure (LVP) and electrocardiogram (ECG) via conscious telemetry, analyzing LVP and heart rate variability (HRV) in four-day increments from exposure days 1 to 21, as well as ECG and baroreflex sensitivity. At 2, 35, and 70days after PEPs exposure ceased, rats received stress tests. Results: On day 21 of exposure, PEPs significantly (P <0.05 vs. Air) increased LV end systolic pressure (LVESP, +18 mmHg) and rate-pressure-product (+19%), and decreased HRV indicating sympathetic dominance (root means squared of successive differences [RMSSD], -21%). Overall, PEPs decreased LV ejection time (-9%), relaxation time (-3%), tau (-5%), RMSSD (-21%), and P-wave duration (-9%). PEPs increased QTc interval (+5%) and low:high frequency HRV (+24%; all P <0.05 vs. Air), while tending to decrease baroreflex sensitivity and contractility index (-15% and-3%, P <0.10 vs. Air). Relative to Air, at both 2 and 35days after PEPs, ventricular arrhythmias increased, and at 70days post-exposure LVESP increased. PEPs impaired ventricular repolarization at 2 and 35days postexposure, but only during stress tests. At 72days post-exposure, PEPs increased urinary dopamine 5-fold and protein expression of ventricular repolarizing channels, Kv1.5, Kv4.2, and Kv7.1, by 50%. Conclusions: Our findings suggest exposure to PEPs increases cardiovascular risk by augmenting sympathetic influence, impairing ventricular performance and repolarization, and inducing hypertension and arrhythmia. PEPs may present significant health risks through adverse cardiovascular effects, especially in occupational settings, among susceptible individuals, and with long-term exposure. [Description provided by NIOSH]
• Subjects:
  Aerosols Cardiovascular Diseases Cardiovascular System Electrocardiography Environmental Exposure Laboratories Occupational Health Particulate Matter Printing Respiratory System Risk Assessment Risk Factors Safety Toxicology

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• Keywords:
  Author Keywords: Arrhythmia Autonomic Cardiac Cardiac Function Cardiovascular Function Cardiovascular System Disorders Contractility Electrical Remodeling Electrocardiogram Electrophysiological Effects Exposure Assessment Exposure Levels Heart Disease Heart Rate Hypertension Inhalation Inhalation Studies Laboratory Animals Lasers Left Ventricular Pressure Nanomaterials Nanoparticles Nanotechnology Nanotoxicology Organic Compounds Particulate Matter Particulates Physiological Chemistry Physiology Printers Printing Inks Repolarization Risk Factors Telemetry Toners Ultrafine Particles Ultrafine Particulates Volatiles

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• ISSN:
  1743-8977
• Document Type:
  Text
• Funding:
  Contract
• Genre:
  Journal Article
• Place as Subject:
  Kentucky ; Massachusetts ; OSHA Region 1 ; OSHA Region 3 ; OSHA Region 4 ; West Virginia
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  HELD - Health Effects Laboratory Division
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Pages in Document:
  7
• Volume:
  17
• NIOSHTIC Number:
  nn:20058473
• Citation:
  Part Fibre Toxicol 2020 Jan; 17:7
• Contact Point Address:
  Philip Demokritou, Center for Nanotechnology and Nanotoxicology. Department of Environmental Health, T.H. Chan School of Public Health, Harvard University, 665 Huntington Avenue, Room 1310, Boston, MA 02115, USA
• Email:
  pdemokri@hsph.harvard.edu
• Federal Fiscal Year:
  2020
• Peer Reviewed:
  True
• Source Full Name:
  Particle and Fibre Toxicology
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:a75afb7d5cace92ea5390f63d50cc1fc87ca4ad76a286564e5cee074f9d88c62e07bd3d15da7975188a5edffdc225818ee32448e8d4aaf352cccfd8e28d6acff
• Download URL:
  https://stacks.cdc.gov/view/cdc/221562/cdc_221562_DS1.pdf
• File Type:
  [PDF - 1.91 MB ]