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Original article
Chronic electronic cigarette exposure in mice induces features of COPD in a nicotine-dependent manner
  1. Itsaso Garcia-Arcos1,2,
  2. Patrick Geraghty1,2,
  3. Nathalie Baumlin3,
  4. Michael Campos3,
  5. Abdoulaye Jules Dabo1,2,
  6. Bakr Jundi4,
  7. Neville Cummins5,
  8. Edward Eden5,
  9. Astrid Grosche3,
  10. Matthias Salathe3,
  11. Robert Foronjy1,2
  1. 1Division of Pulmonary and Critical Care Medicine, SUNY Downstate Medical Center, Brooklyn, New York, USA
  2. 2Department of Cell Biology, State University of New York Downstate Medical Center, Brooklyn, New York, USA
  3. 3Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, University of Miami Miller School of Medicine, Miami, Florida, USA
  4. 4Department of Medicine, Royal College of Surgeons in Ireland, Dublin, Ireland
  5. 5Division of Pulmonary, Critical Care and Sleep Medicine, Mount Sinai St. Luke's Roosevelt Health Sciences Center, New York, New York, USA
  1. Correspondence to Dr Robert Foronjy, Division of Pulmonary and Critical Care Medicine, SUNY Downstate Medical Center, Brooklyn, NY 11203, USA; Robert.Foronjy{at}downstate.edu

Abstract

Background The use of electronic (e)-cigarettes is increasing rapidly, but their lung health effects are not established. Clinical studies examining the potential long-term impact of e-cigarette use on lung health will take decades. To address this gap in knowledge, this study investigated the effects of exposure to aerosolised nicotine-free and nicotine-containing e-cigarette fluid on mouse lungs and normal human airway epithelial cells.

Methods Mice were exposed to aerosolised phosphate-buffered saline, nicotine-free or nicotine-containing e-cigarette solution, 1-hour daily for 4 months. Normal human bronchial epithelial (NHBE) cells cultured at an air-liquid interface were exposed to e-cigarette vapours or nicotine solutions using a Vitrocell smoke exposure robot.

Results Inhalation of nicotine-containing e-cigarettes increased airway hyper-reactivity, distal airspace enlargement, mucin production, cytokine and protease expression. Exposure to nicotine-free e-cigarettes did not affect these lung parameters. NHBE cells exposed to nicotine-containing e-cigarette vapour showed impaired ciliary beat frequency, airway surface liquid volume, cystic fibrosis transmembrane regulator and ATP-stimulated K+ ion conductance and decreased expression of FOXJ1 and KCNMA1. Exposure of NHBE cells to nicotine for 5 days increased interleukin (IL)-6 and IL-8 secretion.

Conclusions Exposure to inhaled nicotine-containing e-cigarette fluids triggered effects normally associated with the development of COPD including cytokine expression, airway hyper-reactivity and lung tissue destruction. These effects were nicotine-dependent both in the mouse lung and in human airway cells, suggesting that inhaled nicotine contributes to airway and lung disease in addition to its addictive properties. Thus, these findings highlight the potential dangers of nicotine inhalation during e-cigarette use.

  • COPD ÀÜ Mechanisms
  • Emphysema
  • COPD Pathology

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

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Footnotes

  • IG-A and PG contributed equally. MS and RF shared senior authorship.

  • Contributors IG-A and PG: responsible for study design and execution, data collection and manuscript preparation. NB, MC, AJD, BJ, NC, AG and EE: responsible for study execution. MS: responsible for study design and execution and manuscript preparation. RF: responsible for study design, execution, data collection and overall manuscript preparation. He is the guarantor.

  • Funding This work was supported by grants made available to RF (Flight Attendant Medical Research Institute YCSA 24039, CIA 074047 and the US National Institutes of Health 1R01HL098528-05), MS (Flight Attendant Medical Research Institute, CIA 130033 and the James and Esther King Florida Biomedical Research Program grant#5JK02), PG (Flight Attendant Medical Research Institute YCSA 113380) and IG-A (Flight Attendant Medical Research Institute YCSA 13005).

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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