Processing of carbon-reinforced construction materials releases PM2.5 inducing inflammation and (secondary) genotoxicity in human lung epithelial cells and fibroblasts

Research output: Contribution to journalResearch articleContributedpeer-review

Contributors

  • Jana Pantzke - , University of Rostock (Author)
  • Arne Koch - , University of Rostock (Author)
  • Elias J. Zimmermann - , University of Rostock (Author)
  • Rastak Narges - , Helmholtz Zentrum München - German Research Center for Environmental Health (Author)
  • Svenja Offer - , University of Rostock (Author)
  • Christoph Bisig - , Helmholtz Zentrum München - German Research Center for Environmental Health (Author)
  • Stefanie Bauer - , Helmholtz Zentrum München - German Research Center for Environmental Health (Author)
  • Sebastian Oeder - , Helmholtz Zentrum München - German Research Center for Environmental Health (Author)
  • Jürgen Orasche - , Helmholtz Zentrum München - German Research Center for Environmental Health (Author)
  • Petra Fiala - , Institute of Process Engineering and Environmental Technology, Mechanical Process Engineering Group (Author)
  • Michael Stintz - (Author)
  • Christoph Paul Rüger - , University of Rostock (Author)
  • Thorsten Streibel - , Helmholtz Zentrum München - German Research Center for Environmental Health (Author)
  • Sebastiano di Bucchianico - , Helmholtz Zentrum München - German Research Center for Environmental Health (Author)
  • Ralf Zimmermann - , University of Rostock (Author)

Abstract

Building demolition following domestic fires or abrasive processing after thermal recycling can release particles harmful for the environment and human health. To mimic such situations, particles release during dry-cutting of construction materials was investigated. A reinforcement material consisting of carbon rods (CR), carbon concrete composite (C³) and thermally treated C³ (ttC³) were physicochemically and toxicologically analyzed in monocultured lung epithelial cells, and co-cultured lung epithelial cells and fibroblasts at the air-liquid interface. C³ particles reduced their diameter to WHO fibre dimensions during thermal treatment. Caused by physical properties or by polycyclic aromatic hydrocarbons and bisphenol A found in the materials, especially the released particles of CR and ttC³ induced an acute inflammatory response and (secondary) DNA damage. Transcriptome analysis indicated that CR and ttC³ particles carried out their toxicity via different mechanisms. While ttC³ affected pro-fibrotic pathways, CR was mostly involved in DNA damage response and in pro-oncogenic signaling.

Details

Original languageEnglish
Article number104079
Number of pages12
JournalEnvironmental Toxicology and Pharmacology
Volume98
Publication statusPublished - Mar 2023
Peer-reviewedYes

External IDs

Scopus 85148366165

Keywords

Sustainable Development Goals