The human long noncoding RNAs CoroMarker, MALAT1, CDR1as, and LINC00460 in whole blood of individuals after controlled short-term exposure with ultrafine metal fume particles at workplace conditions, and in human macrophages in vitro

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Abstract

Background

Short-term inhalation of occupationally relevant ultrafine zinc/copper (Zn/Cu) containing welding fumes has been shown to induce subclinical systemic inflammation, associated with an elevated risk for cardiovascular diseases. The involvement of noncoding RNAs (lncRNAs) in this setting is currently unknown. However, lncRNAs have been reported to fulfill essential roles in, e.g., cardiovascular diseases, inflammation, infectious diseases, and pollution-related lung disorders.

Methods

In this study, the specific lncRNAs levels of the 4 lncRNAs CoroMarker, MALAT1, CDR1as and LINC00460 were determined by RT-qPCR in THP-1 macrophages exposed to Zn/Cu metal fume suspensions for 1, 2, and 4 hours in vitro. Furthermore, 14 subjects were exposed to Zn/Cu containing welding fumes (at 2.5 mg/m ³) for 6 hours. Before, 6, 10, and 29 hours after exposure start, whole blood cell lncRNAs levels were determined by RT-qPCR.

Results

In THP-1 macrophages, we observed a 2.3-fold increase of CDR1as at 1 h (Wilcoxon p = 0.03), a non-significant increase of CoroMarker at 1 h, and an increase of LINC00460 at 2 h ( p = 0.03) and at 4 h ( p = 0.06). In whole blood cells, we determined a non-significant upregulation of CDR1as at 6 h ( p = 0.2), a significant downregulation of CoroMarker at 6 h ( p = 0.04), and a significant upregulation of LINC00460 levels at 10 h ( p = 0.04) and 29 h ( p = 0.04). MALAT-1 remained unchanged in both settings.

Conclusion

The orientation of regulation of the lncRNAs is (except for CoroMarker) similar in the in vitro and in vivo experiments and in line with their described functions. Therefore, these results, e.g. the upregulation of the potential risk marker for cardiovascular diseases, CDR1as, contribute to understanding the underlying mechanisms of Zn/Cu-induced subclinical inflammation in metal workers.

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Comparative toxicity of 24 manufactured nanoparticles in human alveolar epithelial and macrophage cell lines

Sophie Lanone, Françoise Rogerieux, Jorina Geys … (2009)

Background A critical issue with nanomaterials is the clear understanding of their potential toxicity. We evaluated the toxic effect of 24 nanoparticles of similar equivalent spherical diameter and various elemental compositions on 2 human pulmonary cell lines: A549 and THP-1. A secondary aim was to elaborate a generic experimental set-up that would allow the rapid screening of cytotoxic effect of nanoparticles. We therefore compared 2 cytotoxicity assays (MTT and Neutral Red) and analyzed 2 time points (3 and 24 hours) for each cell type and nanoparticle. When possible, TC50 (Toxic Concentration 50 i.e. nanoparticle concentration inducing 50% cell mortality) was calculated. Results The use of MTT assay on THP-1 cells exposed for 24 hours appears to be the most sensitive experimental design to assess the cytotoxic effect of one nanoparticle. With this experimental set-up, Copper- and Zinc-based nanoparticles appear to be the most toxic. Titania, Alumina, Ceria and Zirconia-based nanoparticles show moderate toxicity, and no toxicity was observed for Tungsten Carbide. No correlation between cytotoxicity and equivalent spherical diameter or specific surface area was found. Conclusion Our study clearly highlights the difference of sensitivity between cell types and cytotoxicity assays that has to be carefully taken into account when assessing nanoparticles toxicity.

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Progressive severe lung injury by zinc oxide nanoparticles; the role of Zn2+ dissolution inside lysosomes

Wan-Seob Cho, Rodger Duffin, Sarah EM Howie … (2011)

Background Large production volumes of zinc oxide nanoparticles (ZnONP) might be anticipated to pose risks, of accidental inhalation in occupational and even in consumer settings. Herein, we further investigated the pathological changes induced by ZnONP and their possible mechanism of action. Methods Two doses of ZnONP (50 and 150 cm2/rat) were intratracheally instilled into the lungs of rats with assessments made at 24 h, 1 wk, and 4 wks after instillation to evaluate dose- and time-course responses. Assessments included bronchoalveolar lavage (BAL) fluid analysis, histological analysis, transmission electron microscopy, and IgE and IgA measurement in the serum and BAL fluid. To evaluate the mechanism, alternative ZnONP, ZnONP-free bronchoalveolar lavage exudate, and dissolved Zn2+ (92.5 μg/rat) were also instilled to rats. Acridine orange staining was utilized in macrophages in culture to evaluate the lysosomal membrane destabilization by NP. Results ZnONP induced eosinophilia, proliferation of airway epithelial cells, goblet cell hyperplasia, and pulmonary fibrosis. Bronchocentric interstitial pulmonary fibrosis at the chronic phase was associated with increased myofibroblast accumulation and transforming growth factor-β positivity. Serum IgE levels were up-regulated by ZnONP along with the eosinophilia whilst serum IgA levels were down-regulated by ZnONP. ZnONP are rapidly dissolved under acidic conditions (pH 4.5) whilst they remained intact around neutrality (pH 7.4). The instillation of dissolved Zn2+ into rat lungs showed similar pathologies (eg., eosinophilia, bronchocentric interstitial fibrosis) as were elicited by ZnONP. Lysosomal stability was decreased and cell death resulted following treatment of macrophages with ZnONP in vitro. Conclusions We hypothesise that rapid, pH-dependent dissolution of ZnONP inside of phagosomes is the main cause of ZnONP-induced diverse progressive severe lung injuries.

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Health effects of welding.

James Antonini (2003)

Many of the epidemiology studies performed are difficult to compare because of differences in worker populations, industrial settings, welding techniques, duration of exposure, and other occupational exposures besides welding fumes. Some studies were conducted in carefully controlled work environments, others during actual workplace conditions, and some in laboratories. Epidemiology studies have shown that a large number of welders experience some type of respiratory illness. Respiratory effects seen in full-time welders have included bronchitis, airway irritation, lung function changes, and a possible increase in the incidence of lung cancer. Pulmonary infections are increased in terms of severity, duration, and frequency among welders. Although epidemiological studies have demonstrated an increase in pulmonary illness after exposure to welding fumes, little information of the causality, dose-response, and possible underlying mechanisms regarding the inhalation of welding fumes exists. Even less information is available about the neurological, reproductive, and dermal effects after welding fume exposure. Moreover, carcinogenicity and short-term and long-term toxicology studies of welding fumes in animals are lacing or incomplete. Therefore, an understanding of possible adverse health effects of exposure to welding fumes is essential to risk assessment and the development of prevention strategies and will impact a large population of workers.

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Author and article information

Contributors

Theresa Scheurer: theresa@scheurermail.de

Jan Steffens:

ORCID: http://orcid.org/0000-0002-9672-5713

jan.steffens@rwth-aachen.de , jan.steffens@medicalschool-hamburg.de , jasteffens@ukaachen.de

Agnieszka Markert: amarkert@ukaachen.de

Miriam Du Marchie Sarvaas: msarvaas@ukaachen.de

Christoph Roderburg: christoph.roderburg@charite.de , Christoph.Roderburg@med.uni-duesseldorf.de

Lothar Rink: lrink@ukaachen.de

Frank Tacke:

ORCID: http://orcid.org/0000-0001-6206-0226

frank.tacke@charite.de

Tom Luedde: tom.luedde@med.uni-duesseldorf.de

Thomas Kraus: tkraus@ukaachen.de

Ralf Baumann: rbaumann@ukaachen.de , ralf.baumann@medicalschool-hamburg.de

Journal

Journal ID (nlm-ta): J Occup Med Toxicol

Journal ID (iso-abbrev): J Occup Med Toxicol

Title: Journal of Occupational Medicine and Toxicology (London, England)

Publisher: BioMed Central (London )

ISSN (Electronic): 1745-6673

Publication date (Electronic): 1 August 2022

Publication date PMC-release: 1 August 2022

Publication date Collection: 2022

Volume: 17

Electronic Location Identifier: 15

Affiliations

[1 ]GRID grid.1957.a, ISNI 0000 0001 0728 696X, Institute for Occupational, Social and Environmental Medicine, Medical Faculty, University Hospital RWTH Aachen University, ; Pauwelsstr. 30, 52074 Aachen, Germany

[2 ]GRID grid.461732.5, Institute for Translational Medicine (ITM), Medical School Hamburg (MSH) – Am Kaiserkai 1, ; 20457 Hamburg, Germany

[3 ]GRID grid.1957.a, ISNI 0000 0001 0728 696X, Department of Medicine III, , Medical Faculty, University Hospital RWTH Aachen University, ; Pauwelsstr. 30, 52074 Aachen, Germany

[4 ]GRID grid.6363.0, ISNI 0000 0001 2218 4662, Department of Hepatology and Gastroenterology, , Charité - Universitätsmedizin Berlin, ; Augustenburger Platz 1, 13353 Berlin, Germany

[5 ]GRID grid.14778.3d, ISNI 0000 0000 8922 7789, Clinic for Gastroenterology, Hepatology and Infectious Diseases, , University Hospital Düsseldorf, ; Moorenstr. 5, 40225 Duesseldorf, Germany

[6 ]GRID grid.1957.a, ISNI 0000 0001 0728 696X, Institute of Immunology, Medical Faculty, University Hospital RWTH Aachen University, ; Pauwelsstr. 30, 52074 Aachen, Germany

Author information

Jan Steffens http://orcid.org/0000-0002-9672-5713

Frank Tacke http://orcid.org/0000-0001-6206-0226

Article

Publisher ID: 356

DOI: 10.1186/s12995-022-00356-0

PMC ID: 9344619

PubMed ID: 35915466

SO-VID: 2b6d9f53-1688-4548-945a-6c368736f57b

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 3 February 2022

Date accepted : 12 July 2022

Funding

Funded by: RWTH Aachen University (3131)

Open Access :

Open Access funding enabled and organized by Projekt DEAL.

Custom metadata

ScienceOpen disciplines: Occupational & Environmental medicine

Keywords: lncrna,occupational health,zinc/copper (zn/cu) metal fume exposure,nanotoxicology,macrophages

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ScienceOpen disciplines: Occupational & Environmental medicine

Keywords: lncrna, occupational health, zinc/copper (zn/cu) metal fume exposure, nanotoxicology, macrophages

The human long noncoding RNAs CoroMarker, MALAT1, CDR1as, and LINC00460 in whole blood of individuals after controlled short-term exposure with ultrafine metal fume particles at workplace conditions, and in human macrophages in vitro

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Abstract

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Conclusion

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China Occupational Medicine

Most cited references 43

Comparative toxicity of 24 manufactured nanoparticles in human alveolar epithelial and macrophage cell lines

Progressive severe lung injury by zinc oxide nanoparticles; the role of Zn2+ dissolution inside lysosomes

Health effects of welding.

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