Online monitoring of volatile organic compounds emitted from human bronchial epithelial cells as markers for oxidative stress

Cassagnes, L E; Leni, Z; Håland, A; Bell, D M; Zhu, L; Bertrand, A; Baltensperger, U; El Haddad, I; Wisthaler, A; Geiser, M; Dommen, J (2020). Online monitoring of volatile organic compounds emitted from human bronchial epithelial cells as markers for oxidative stress. Journal of breath research, 15(1) IOP Science 10.1088/1752-7163/abc055

[img]
Preview
Text
Cassagnes_2021_J._Breath_Res._15_016015.pdf - Published Version
Available under License Creative Commons: Attribution (CC-BY).

Download (919kB) | Preview

Particulate air pollution is associated with adverse respiratory effects and is a major factor for premature deaths. In-vitro assays are commonly used for investigating the direct cytotoxicity and inflammatory impacts due to particulate matter (PM) exposure. However, biological tests are often labor-intensive, destructive and limited to endpoints measured offline at single time points, making it impossible to observe the progression of cell response upon exposure. Here we explored the potential of a high-resolution proton transfer reaction mass spectrometer (PTR-MS) to detect the volatile organic compounds (VOCs) emitted by human bronchial epithelial cells (BEAS-2B) upon exposure to PM. Cells were exposed to single components (1,4-naphthoquinone and Cu(II)) known to induce oxidative stress. We also tested filter extracts of aerosols generated in a smog chamber, including fresh and aged wood burning emissions, as well as α-pinene secondary organic aerosol (SOA). We found that 1,4-naphthoquinone was rapidly internalized by the cells. Exposing cells to each of these samples induced the emission of VOCs, which we tentatively assigned to acetonitrile, benzaldehyde and dimethylbenzaldehyde, respectively. Emission rates upon exposure to fresh and aged OA from α-pinene oxidation and from biomass burning significantly exceeded those observed after exposure to similar doses of Cu(II), a proxy for transition metals with high oxidative potential. Emission rates of biomarkers from cell exposure to α-pinene SOA exhibited a statistically significant, but weak dose dependence. The emission rates of benzaldehyde scaled with cell death, estimated by measuring the apical release of cytosolic lactate dehydrogenase. Particle mass doses delivered to the BEAS-2B cells match those deposited in the human tracheobronchial tract after several hours of inhalation at elevated ambient air pollution. The results presented here show that our method has the potential to determine biomarkers of PM induced pulmonary damage in toxicological and epidemiological research on air pollution.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Anatomy

UniBE Contributor:

Leni, Zaira and Geiser, Marianne

Subjects:

600 Technology > 610 Medicine & health
500 Science
500 Science > 540 Chemistry
500 Science > 570 Life sciences; biology
600 Technology

ISSN:

1752-7163

Publisher:

IOP Science

Funders:

[42] Schweizerischer Nationalfonds ; [UNSPECIFIED] Horizon 2020 (EUROCHAMP-2020)

Language:

English

Submitter:

Marianne Geiser Kamber

Date Deposited:

27 Jan 2021 15:08

Last Modified:

27 Jan 2021 15:17

Publisher DOI:

10.1088/1752-7163/abc055

PubMed ID:

33045691

Uncontrolled Keywords:

particulate air pollution, human bronchial epithelial cells, pulmonary oxidative stress, proton transfer reaction mass spectrometry, volatile organic compounds

BORIS DOI:

10.48350/150244

URI:

https://boris.unibe.ch/id/eprint/150244

Actions (login required)

Edit item Edit item
Provide Feedback