Small airway epithelial cells exposure to printer-emitted engineered nanoparticles induces cellular effects on human microvascular endothelial cells in an alveolar-capillary coculture model

Details

• Personal Author:
  Castranova, Vincent ; Demokritou P ; Farcas M ; Friend S ; Pirela SV ; Qian Y ; Schwegler-Berry D ; Shvedova AA ; Sisler J
• Description:
  The printer is one of the most common office equipment. Recently, it was reported that toner formulations for printing equipment constitute nanoenabled products (NEPs) and contain engineered nanomaterials (ENMs) that become airborne during printing. To date, insufficient research has been performed to understand the potential toxicological properties of printer-emitted particles (PEPs) with several studies using bulk toner particles as test particles. These studies demonstrated the ability of toner particles to cause chronic inflammation and fibrosis in animal models. However, the toxicological implications of inhalation exposures to ENMs emitted from laser printing equipment remain largely unknown. The present study investigates the toxicological effects of PEPs using an in vitro alveolar-capillary co-culture model with Human Small Airway Epithelial Cells (SAEC) and Human Microvascular Endothelial Cells (HMVEC). Our data demonstrate that direct exposure of SAEC to low concentrations of PEPs (0.5 and 1.0 microg/mL) caused morphological changes of actin remodeling and gap formations within the endothelial monolayer. Furthermore, increased production of reactive oxygen species (ROS) and angiogenesis were observed in the HMVEC. Analysis of cytokine and chemokine levels demonstrates that interleukin (IL)-6 and MCP-1 may play a role in the cellular communication observed between SAEC and HMVEC and the resultant responses in HMVEC. These data indicate PEPs at low, non-cytotoxic exposure levels are bioactive and affect cellular responses in an alveolar-capillary co-culture model, which raises concerns for potential adverse health effects. [Description provided by NIOSH]
• Subjects:
  Air Pollutants, Occupational Chemistry Chronic Disease Fibrosis Hazardous Substances Lung Occupational Health Particulate Matter Printing Respiratory System Safety

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• Keywords:
  Airborne-particles Alveolar-cells Analytical-models Bioactivation Cellular-function Cellular-reactions Chemical-composition Chronic-inflammation In-vitro-study Inhalation-studies Lung-cells Morphology Nanotechnology Office-equipment Printers Toxic-effects Toxic-materials

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• ISSN:
  1096-6080
• Document Type:
  Text
• Genre:
  Abstract or Summary
• Place as Subject:
  California ; Massachusetts ; OSHA Region 1 ; OSHA Region 3 ; OSHA Region 9 ; West Virginia
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Division:
  HELD - Health Effects Laboratory Division
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Volume:
  144
• Issue:
  1
• NIOSHTIC Number:
  nn:20045987
• Citation:
  Toxicologist 2015 Mar; 144(1):415
• Federal Fiscal Year:
  2015
• NORA Priority Area:
  Manufacturing
• Peer Reviewed:
  False
• Source Full Name:
  The Toxicologist. Society of Toxicology 54th Annual Meeting and ToxExpo, March 22-26, 2015, San Diego, California
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:c63a71cdfd5ad2dde597486c483de23f70eb9fd193b955b2d5ba2ed1ee04b7e422040afdbfa51b2dee07df0ba8e8688bbb5d62a4b2a87469afbe7a463e4c0aaf
• Download URL:
  https://stacks.cdc.gov/view/cdc/201186/cdc_201186_DS1.pdf
• File Type:
  [PDF - 228.50 KB ]