title: Effects of Laser Printer-Emitted Engineered Nanoparticles on Cytotoxicity, Chemokine Expression, Reactive Oxygen Species, DNA Methylation, and DNA Damage: A Comprehensive in Vitro Analysis in Human Small Airway Epithelial Cells, Macrophages, and Lymphoblasts.
abstract: BACKGROUND
  Engineered nanomaterials (ENMs) incorporated into toner formulations of printing equipment become airborne during consumer use. Although information on the complex physicochemical and toxicological properties of both toner powders and printer-emitted particles (PEPs) continues to grow, most toxicological studies have not used the actual PEPs but rather have primarily used raw toner powders, which are not representative of current exposures experienced at the consumer level during printing.
  
  
  OBJECTIVE
  We assessed the biological responses of a panel of human cell lines to PEPs.
  
  
  METHODS
  Three physiologically relevant cell lines--small airway epithelial cells (SAECs), macrophages (THP-1 cells), and lymphoblasts (TK6 cells)--were exposed to PEPs at a wide range of doses (0.5-100 μg/mL) corresponding to human inhalation exposure durations at the consumer level of 8 hr or more. Following treatment, toxicological parameters reflecting distinct mechanisms were evaluated.
  
  
  RESULTS
  PEPs caused significant membrane integrity damage, an increase in reactive oxygen species (ROS) production, and an increase in pro-inflammatory cytokine release in different cell lines at doses equivalent to exposure durations from 7.8 to 1,500 hr. Furthermore, there were differences in methylation patterns that, although not statistically significant, demonstrate the potential effects of PEPs on the overall epigenome following exposure.
  
  
  CONCLUSIONS
  The in vitro findings obtained in this study suggest that laser printer-emitted engineered nanoparticles may be deleterious to lung cells and provide preliminary evidence of epigenetic modifications that might translate to pulmonary disorders.
authors.affiliation: Department of Environmental Health, Center for Nanotechnology and Nanotoxicology, Harvard T.H. Chan School of Public Health, Harvard University, Boston, Massachusetts, USA.
authors.forename: Sandra V
authors.initials: SV
authors.lastname: Pirela
authors.forename: Isabelle R
authors.initials: IR
authors.lastname: Miousse
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Lu
authors.forename: Vincent
authors.initials: V
authors.lastname: Castranova
authors.forename: Treye
authors.initials: T
authors.lastname: Thomas
authors.forename: Yong
authors.initials: Y
authors.lastname: Qian
authors.forename: Dhimiter
authors.initials: D
authors.lastname: Bello
authors.forename: Lester
authors.initials: L
authors.lastname: Kobzik
authors.forename: Igor
authors.initials: I
authors.lastname: Koturbash
authors.forename: Philip
authors.initials: P
authors.lastname: Demokritou
mesh_terms: D002460:Cell Line; D018925:Chemokines / Q000235:genetics* / Q000378:metabolism; D003603:Cytotoxins / Q000633:toxicity*; D004249:DNA Damage; D019175:DNA Methylation / Q000187:drug effects*; D004847:Epithelial Cells / Q000187:drug effects; D006801:Humans; D008168:Lung / Q000187:drug effects; D008214:Lymphocytes / Q000187:drug effects; D008264:Macrophages / Q000187:drug effects; D053758:Nanoparticles / Q000633:toxicity*; D011327:Printing; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D018925:Chemokines; D003603:Cytotoxins; D017382:Reactive Oxygen Species