Umeå University's logo

umu.sePublications
Change search
Link to record
Permanent link

Direct link
Bosson, Jenny A.
Alternative names
Publications (10 of 52) Show all publications
Uski, O., Rankin, G. D., Wingfors, H., Magnusson, R., Boman, C., Muala, A., . . . Sandström, T. (2024). In vitro toxicity evaluation in A549 cells of diesel particulate matter from two different particle sampling systems and several resuspension media. Journal of Applied Toxicology
Open this publication in new window or tab >>In vitro toxicity evaluation in A549 cells of diesel particulate matter from two different particle sampling systems and several resuspension media
Show others...
2024 (English)In: Journal of Applied Toxicology, ISSN 0260-437X, E-ISSN 1099-1263Article in journal (Refereed) Epub ahead of print
Abstract [en]

In urban areas, inhalation of fine particles from combustion sources such as diesel engines causes adverse health effects. For toxicity testing, a substantial amount of particulate matter (PM) is needed. Conventional sampling involves collection of PM onto substrates by filtration or inertial impaction. A major drawback to those methodologies is that the extraction process can modify the collected particles and alter their chemical composition. Moreover, prior to toxicity testing, PM samples need to be resuspended, which can alter the PM sample even further. Lastly, the choice of the resuspension medium may also impact the detected toxicological responses. In this study, we compared the toxicity profile of PM obtained from two alternative sampling systems, using in vitro toxicity assays. One system makes use of condensational growth before collection in water in an impinger – BioSampler (CG-BioSampler), and the other, a Dekati® Gravimetric Impactor (DGI), is based on inertial impaction. In addition, various methods for resuspension of DGI collected PM were compared. Tested endpoints included cytotoxicity, formation of cellular reactive oxygen species, and genotoxicity. The alternative collection and suspension methods affected different toxicological endpoints. The water/dimethyl sulfoxide mixture and cell culture medium resuspended particles, along with the CG-BioSampler sample, produced the strongest responses. The water resuspended sample from the DGI appeared least toxic. CG-BioSampler collected PM caused a clear increased response in apoptotic cell death. We conclude that the CG-BioSampler PM sampler is a promising alternative to inertial impaction sampling.

Place, publisher, year, edition, pages
John Wiley & Sons, 2024
Keywords
apoptosis, diesel exhaust, extraction, impinger, particulate matter, reactive oxygen species, sampling, soot, toxicity
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:umu:diva-224261 (URN)10.1002/jat.4616 (DOI)001214370400001 ()38705171 (PubMedID)2-s2.0-85192155238 (Scopus ID)
Available from: 2024-05-14 Created: 2024-05-14 Last updated: 2024-05-14
Lyytinen, G., Melnikov, G., Brynedal, A., Anesäter, E., Antoniewicz, L., Blomberg, A., . . . Lundbäck, M. (2024). Use of heated tobacco products (IQOS) causes an acute increase in arterial stiffness and platelet thrombus formation. Atherosclerosis, 390, Article ID 117335.
Open this publication in new window or tab >>Use of heated tobacco products (IQOS) causes an acute increase in arterial stiffness and platelet thrombus formation
Show others...
2024 (English)In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 390, article id 117335Article in journal (Refereed) Published
Abstract [en]

Background and aims: Heated tobacco products (HTPs) are novel alternative tobacco products being promoted as an alternative to cigarettes. To evaluate the impact of HTP use on vascular function, we investigated the effects of a brief HTP usage on arterial stiffness and platelet thrombus formation in healthy volunteers.

Methods: In a randomised crossover study, twenty-four healthy young adults with occasional tobacco use smoked the HTP IQOS 3 Multi (Phillip Morris Int.) and “no-exposure” was used as a control, with a wash-out period of at least one week in-between. Arterial stiffness was assessed through pulse wave velocity and pulse wave analysis. Blood samples, collected at baseline and 5 min following exposure, were analysed with the Total-Thrombus-formation analysis system evaluating platelet and fibrin-rich thrombus formation tendency.

Results: HTP exposure caused immediate heightened pulse wave velocity (+0.365 m/s, 95% CI: +0.188 to 0.543; p = 0.004) and enhanced augmentation index corrected to heart rate (+6.22%, 95% CI: +2.33 to 10.11; p = 0.003) compared to the no-exposure occasion. Similarly, blood pressure and heart rate transiently increased immediately following HTP inhalation. Platelet thrombus formation significantly increased following HTP exposure (area under the curve +59.5, 95% CI: +25.6 to 93.4; p < 0.001) compared to no-exposure. No effect was seen on fibrin-rich thrombus formation following HTP-exposure.

Conclusions: Brief HTP use in healthy young adults had immediate adverse effects on vascular function resulting in increased arterial stiffness and platelet thrombus formation, known risk factors for the development of atherosclerosis. Further research is needed to address long term health impacts.

Place, publisher, year, edition, pages
Elsevier, 2024
Keywords
Arterial stiffness, Heated tobacco products, Nicotine, Platelets, Thrombosis, Tobacco
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:umu:diva-215940 (URN)10.1016/j.atherosclerosis.2023.117335 (DOI)001203215800001 ()37872010 (PubMedID)2-s2.0-85174705819 (Scopus ID)
Available from: 2023-11-01 Created: 2023-11-01 Last updated: 2024-05-14Bibliographically approved
Lyytinen, G., Brynedal, A., Anesäter, E., Antoniewicz, L., Blomberg, A., Wallén, H., . . . Lundbäck, M. (2023). Electronic cigarette vaping with nicotine causes increased thrombogenicity and impaired microvascular function in healthy volunteers: a randomised clinical trial. Cardiovascular Toxicology, 23(7-8), 255-264
Open this publication in new window or tab >>Electronic cigarette vaping with nicotine causes increased thrombogenicity and impaired microvascular function in healthy volunteers: a randomised clinical trial
Show others...
2023 (English)In: Cardiovascular Toxicology, ISSN 1530-7905, E-ISSN 1559-0259, Vol. 23, no 7-8, p. 255-264Article in journal (Refereed) Published
Abstract [en]

Electronic cigarette (EC) vaping is increasingly popular, despite growing evidence of adverse health effects. To further evaluate the impact of EC use on vascular health, we investigated the effects of brief EC inhalation on flow-dependent thrombus formation and microcirculation in healthy volunteers. The study was performed with a randomised double-blind crossover design. Twenty-two healthy subjects aged between 18 and 45 years with occasional tobacco use were recruited. Subjects inhaled 30 puffs of EC aerosol with and without nicotine on two occasions separated by a wash-out period of at least 1 week. Blood samples were collected at baseline and at 15 and 60 min following exposure and analysed with the Total-Thrombus-formation analysis system evaluating fibrin-rich thrombus formation and platelet thrombus formation in whole blood under flow. Microvascular function was assessed at baseline and 30 min after exposure by laser speckle contrast imaging and iontophoresis of acetylcholine and sodium nitroprusside (SNP) to evaluate the endothelium-dependent and independent pathways of vasodilation. Compared with nicotine free EC aerosol, exposure to EC aerosol with nicotine significantly increased platelet thrombus formation and fibrin-rich thrombus formation at 15 min (p = 0.017 and p = 0.037, respectively) with normalisation after 60 min. Peak SNP-mediated microvascular perfusion, i.e. endothelium-independent vasodilation, was reduced following EC vaping with nicotine compared with baseline (p = 0.006). Thirty puffs of EC aerosol with nicotine increased platelet and fibrin-dependent thrombus formation and reduced microvascular dilatation capacity. No compelling effects of EC vaping without nicotine were observed, indicating nicotine as the main effector.

Trial registration: ClinicalTrials.gov Identifier: NCT04175457 URL: https://clinicaltrials.gov/ct2/show/NCT04175457.

Place, publisher, year, edition, pages
Springer Nature, 2023
Keywords
Coagulation, E-cigarette, Electronic cigarette, Microcirculation, Nicotine, Platelets, Thrombosis
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:umu:diva-212844 (URN)10.1007/s12012-023-09802-9 (DOI)37548804 (PubMedID)2-s2.0-85166954236 (Scopus ID)
Funder
Swedish Heart Lung FoundationThe Swedish Heart and Lung AssociationSwedish Society of MedicineRegion StockholmRegion VästerbottenKarolinska Institute
Available from: 2023-08-15 Created: 2023-08-15 Last updated: 2023-10-13Bibliographically approved
Antoniewicz, L., Kabele, M., Nilsson, U., Pourazar, J., Rankin, G., Bosson, J. A. & Lundbäck, M. (2022). Chronic snus use in healthy males alters endothelial function and increases arterial stiffness. PLOS ONE, 17(6), Article ID e0268746.
Open this publication in new window or tab >>Chronic snus use in healthy males alters endothelial function and increases arterial stiffness
Show others...
2022 (English)In: PLOS ONE, E-ISSN 1932-6203, Vol. 17, no 6, article id e0268746Article in journal (Refereed) Published
Abstract [en]

Background: Snus usage is commonly touted as a safer alternative to cigarette smoking. However, recent studies have demonstrated possible adverse cardiovascular effects in chronic snus users. The present study evaluates the effects of chronic snus use on vascular function by assessing central arterial stiffness and endothelial vasodilatory function in healthy chronic snus users as compared to matched non-users.

Methods and results: Fifty healthy males (24 snus users, 26 age-matched controls) with a mean age of 44 years were included in the study. Arterial stiffness was assessed employing both pulse wave velocity and pulse wave analysis. Endothelial vasodilatory function was measured by venous occlusion plethysmography, utilizing intra-arterial administration of acetylcholine, glyceryl trinitrate and bradykinin to further gauge endothelium-dependent and -independent vasodilatory function. Arterial stiffness was significantly higher in chronic snus users as compared to controls: pulse wave velocity [m/s]: 6.6±0.8 vs 7.1±0.9 resp. (p = 0.026), augmentation index corrected for heart rate [%]: 0.1±13.2 vs 7.3±7.8 resp. (p = 0.023). Endothelial independent vasodilation, i.e. the reaction to glyceryl trinitrate, was significantly lower in snus users as measured by venous occlusion plethysmography.

Conclusions: The results of this study show an increased arterial stiffness and an underlying endothelial dysfunction in daily snus users as compared to matched non-tobacco controls. These findings indicate that long-term use of snus may alter the function of the endothelium and therefore reinforces the assertion that chronic snus use is correlated to an increased risk of development of cardiovascular disease.

Place, publisher, year, edition, pages
Public Library of Science (PLoS), 2022
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:umu:diva-203175 (URN)10.1371/journal.pone.0268746 (DOI)000832307900135 ()35657943 (PubMedID)2-s2.0-85131702456 (Scopus ID)
Funder
The Swedish Heart and Lung AssociationVästerbotten County CouncilSwedish Heart Lung FoundationKarolinska InstituteStockholm County CouncilUmeå UniversityMagnus Bergvall FoundationSwedish Society of Medicine
Available from: 2023-01-16 Created: 2023-01-16 Last updated: 2024-04-08Bibliographically approved
Unosson, J., Kabele, M., Boman, C., Nyström, R., Sadiktsis, I., Westerholm, R., . . . Bosson, J. A. (2021). Acute cardiovascular effects of controlled exposure to dilute Petrodiesel and biodiesel exhaust in healthy volunteers: a crossover study. Particle and Fibre Toxicology, 18(1), Article ID 22.
Open this publication in new window or tab >>Acute cardiovascular effects of controlled exposure to dilute Petrodiesel and biodiesel exhaust in healthy volunteers: a crossover study
Show others...
2021 (English)In: Particle and Fibre Toxicology, E-ISSN 1743-8977, Vol. 18, no 1, article id 22Article in journal (Refereed) Published
Abstract [en]

Background: Air pollution derived from combustion is associated with considerable cardiorespiratory morbidity and mortality in addition to environmental effects. Replacing petrodiesel with biodiesel may have ecological benefits, but impacts on human health remain unquantified.

The objective was to compare acute cardiovascular effects of blended and pure biodiesel exhaust exposure against known adverse effects of petrodiesel exhaust (PDE) exposure in human subjects.

In two randomized controlled double-blind crossover studies, healthy volunteers were exposed to PDE or biodiesel exhaust for one hour. In study one, 16 subjects were exposed, on separate occasions, to PDE and 30% rapeseed methyl ester biodiesel blend (RME30) exhaust, aiming at PM10 300 μg/m3. In study two, 19 male subjects were separately exposed to PDE and exhaust from a 100% RME fuel (RME100) using similar engine load and exhaust dilution. Generated exhaust was analyzed for physicochemical composition and oxidative potential. Following exposure, vascular endothelial function was assessed using forearm venous occlusion plethysmography and ex vivo thrombus formation was assessed using a Badimon chamber model of acute arterial injury. Biomarkers of inflammation, platelet activation and fibrinolysis were measured in the blood.

Results: In study 1, PDE and RME30 exposures were at comparable PM levels (314 ± 27 μg/m3; (PM10 ± SD) and 309 ± 30 μg/m3 respectively), whereas in study 2, the PDE exposure concentrations remained similar (310 ± 34 μg/m3), but RME100 levels were lower in PM (165 ± 16 μg/m3) and PAHs, but higher in particle number concentration. Compared to PDE, PM from RME had less oxidative potential. Forearm infusion of the vasodilators acetylcholine, bradykinin, sodium nitroprusside and verapamil resulted in dose-dependent increases in blood flow after all exposures. Vasodilatation and ex vivo thrombus formation were similar following exposure to exhaust from petrodiesel and the two biodiesel formulations (RME30 and RME100). There were no significant differences in blood biomarkers or exhaled nitric oxide levels between exposures.

Conclusions: Despite differences in PM composition and particle reactivity, controlled exposure to biodiesel exhaust was associated with similar cardiovascular effects to PDE. We suggest that the potential adverse health effects of biodiesel fuel emissions should be taken into account when evaluating future fuel policies.

Trial registration: ClinicalTrials.gov, NCT01337882/NCT01883466. Date of first enrollment March 11, 2011, registered April 19, 2011, i.e. retrospectively registered.

Place, publisher, year, edition, pages
BioMed Central (BMC), 2021
Keywords
Air pollution, Biodiesel, Cardiovascular system, Diesel, Endothelial function, Particulate matter, Thrombosis, Vascular function, Vasomotor dysfunction
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:umu:diva-186143 (URN)10.1186/s12989-021-00412-3 (DOI)000661490800001 ()34127003 (PubMedID)2-s2.0-85107933281 (Scopus ID)
Funder
AFA InsuranceSwedish Heart Lung FoundationWellcome trust, WT103782AIARegion Västerbotten
Available from: 2021-07-14 Created: 2021-07-14 Last updated: 2023-07-07Bibliographically approved
Rankin, G. D., Kabéle, M., Brown, R., Macefield, V. G., Sandström, T. & Bosson, J. A. (2021). Acute Exposure to Diesel Exhaust Increases Muscle Sympathetic Nerve Activity in Humans. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 10(10), Article ID e018448.
Open this publication in new window or tab >>Acute Exposure to Diesel Exhaust Increases Muscle Sympathetic Nerve Activity in Humans
Show others...
2021 (English)In: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, ISSN 2047-9980, E-ISSN 2047-9980, Vol. 10, no 10, article id e018448Article in journal (Refereed) Published
Abstract [en]

Background: Diesel exhaust (DE) emissions are a major contributor to ambient air pollution and are strongly associated with cardiovascular morbidity and mortality. Exposure to traffic-related particulate matter is linked with acute adverse cardiovascular events; however, the mechanisms are not fully understood. We examined the role of the autonomic nervous system during exposure to DE that has previously only been indirectly investigated.

Methods and Results: Using microneurography, we measured muscle sympathetic nerve activity (MSNA) directly in the peroneal nerve of 16 healthy individuals. MSNA, heart rate, and respiration were recorded while subjects rested breathing filtered air, filtered air with an exposure mask, and standardized diluted DE (300 µg/m3) through the exposure mask. Heart rate variability was assessed from an ECG. DE inhalation rapidly causes an increase in number of MSNA bursts as well as the size of bursts within 10 minutes, peaking by 30 minutes (P<0.001), compared with baseline filtered air with an exposure mask. No significant changes occurred in heart rate variability indices during DE exposure; however, MSNA frequency correlated negatively with total power (r2=0.294, P=0.03) and low frequency (r2=0.258, P=0.045). Heart rate correlated positively with MSNA frequency (r2=0.268, P=0.04) and the change in percentage of larger bursts (burst amplitude, height >50% of the maximum burst) from filtered air with an exposure mask (r2=0.368, P=0.013).

Conclusions: Our study provides direct evidence for the rapid modulation of the autonomic nervous system after exposure to DE, with an increase in MSNA. The quick increase in sympathetic outflow may explain the strong epidemiological data associating traffic-related particulate matter to acute adverse cardiovascular events such as myocardial infarction.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02892279.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2021
Keywords
air pollution, autonomic nervous system, diesel, heart rate variability, muscle sympathetic nerve activity, sympatho‐excitation
National Category
Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:umu:diva-183918 (URN)10.1161/JAHA.120.018448 (DOI)000651436300025 ()33942621 (PubMedID)2-s2.0-85106552074 (Scopus ID)
Funder
Swedish Heart Lung FoundationForte, Swedish Research Council for Health, Working Life and WelfareVästerbotten County Council
Available from: 2021-06-04 Created: 2021-06-04 Last updated: 2023-03-24Bibliographically approved
Mobarrez, F., Antoniewicz, L., Hedman, L., Bosson, J. A. & Lundbäck, M. (2020). Electronic cigarettes containing nicotine increase endothelial and platelet derived extracellular vesicles in healthy volunteers. Atherosclerosis, 301, 93-100
Open this publication in new window or tab >>Electronic cigarettes containing nicotine increase endothelial and platelet derived extracellular vesicles in healthy volunteers
Show others...
2020 (English)In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 301, p. 93-100Article in journal (Refereed) Published
Abstract [en]

BACKGROUND AND AIMS: E-cigarette use is increasingly common. Whether e-cigarettes are harmful to human health is an intensely debated subject. In order to investigate whether e-cigarettes with and without nicotine cause different vascular responses, we obtained blood samples from healthy young volunteers who performed brief active e-cigarette inhalations. Extracellular vesicles (EVs) of endothelial and platelet origin were measured to determine vascular changes.

METHODS: Using a randomized, double-blind, crossover design, 17 healthy occasional smokers inhaled 30 puffs of e-cigarette vapor during 30 min. Blood samples were collected at baseline, as well as at 0, 2, 4 and 6 h post-exposure. EVs from platelets and endothelial cells were measured by flow cytometry.

RESULTS: Platelet and endothelial derived EVs were significantly increased with peak levels seen at 4 h following exposure to active inhalation of e-cigarette vapor with nicotine. Moreover, platelet derived EVs, expressing platelet activation marker P-selectin and the inflammation marker, CD40 ligand, were also significantly increased following inhalation of e-cigarette vapor with nicotine. In addition, platelet derived EVs expressing CD40 ligand was increased after inhalation of e-cigarette vapor without nicotine.

CONCLUSION: As few as 30 puffs of nicotine-containing e-cigarette vapor caused an increase in levels of circulating EVs of endothelial and platelet origin, which may signify underlying vascular changes. Although e-cigarette vapor without nicotine caused an increase in platelet EVs expressing CD40 ligand, nicotine, as a component in the vapor, seems to have a more compelling effect on extracellular vesicle formation and protein composition.

Place, publisher, year, edition, pages
Elsevier, 2020
Keywords
Electronic cigarette, Endothelial microvesicles, Extracellular vesicles, Microparticles, Platelet microvesicles, e-cigarette
National Category
Respiratory Medicine and Allergy
Identifiers
urn:nbn:se:umu:diva-168670 (URN)10.1016/j.atherosclerosis.2020.02.010 (DOI)000537191700007 ()32122618 (PubMedID)2-s2.0-85080115794 (Scopus ID)
Funder
Swedish Heart Lung FoundationSwedish Society of MedicineStockholm County Council
Available from: 2020-03-05 Created: 2020-03-05 Last updated: 2023-03-23Bibliographically approved
Antoniewicz, L., Brynedal, A., Hedman, L., Lundbäck, M. & Bosson, J. A. (2019). Acute Effects of Electronic Cigarette Inhalation on the Vasculature and the Conducting Airways. Cardiovascular Toxicology, 19(5), 441-450
Open this publication in new window or tab >>Acute Effects of Electronic Cigarette Inhalation on the Vasculature and the Conducting Airways
Show others...
2019 (English)In: Cardiovascular Toxicology, ISSN 1530-7905, E-ISSN 1559-0259, Vol. 19, no 5, p. 441-450Article in journal (Refereed) Published
Abstract [en]

The use of electronic cigarettes has increased exponentially since its introduction onto the global market in 2006. However, short- and long-term health effects remain largely unknown due to the novelty of this product. The present study examines the acute effects of e-cigarette aerosol inhalation, with and without nicotine, on vascular and pulmonary function in healthy volunteers. Seventeen healthy subjects inhaled electronic cigarette aerosol with and without nicotine on two separate occasions in a double-blinded crossover fashion. Blood pressure, heart rate, and arterial stiffness measured by pulse wave velocity and pulse wave analysis were assessed at baseline, and then at 0 h, 2 h, and 4 h following exposure. Dynamic spirometry and impulse oscillometry were measured following vascular assessments at these time points, as well as at 6 h following exposure. e-Cigarette aerosol with nicotine caused a significant increase in heart rate and arterial stiffness. Furthermore, e-cigarette aerosol-containing nicotine caused a sudden increase in flow resistance as measured by impulse oscillometry, indicating obstruction of the conducting airways. Both aerosols caused an increase in blood pressure. The present study indicates that inhaled e-cigarette aerosol with nicotine has an acute impact on vascular and pulmonary function. Thus, chronic usage may lead to long-term adverse health effects. Further investigation is warranted.

Place, publisher, year, edition, pages
John Wiley & Sons, 2019
Keywords
Arterial stiffness, Augmentation index, ENDS, Electronic cigarettes, IOS, Pulse wave velocity, e-Cig
National Category
Occupational Health and Environmental Health Cardiac and Cardiovascular Systems
Identifiers
urn:nbn:se:umu:diva-158824 (URN)10.1007/s12012-019-09516-x (DOI)000486337400006 ()30963443 (PubMedID)2-s2.0-85064438540 (Scopus ID)
Available from: 2019-05-09 Created: 2019-05-09 Last updated: 2023-03-24Bibliographically approved
Muala, A., Österdahl, R., Sehlstedt, M., Rankin, G., Pourazar, J., Bosson, J. A., . . . Öhberg, F. (2019). Small airways effects of exposure to wood smoke. Paper presented at European-Respiratory-Society (ERS) International Congress, Madrid, SPAIN, SEP 28-OCT 02, 2019.. European Respiratory Journal, 54
Open this publication in new window or tab >>Small airways effects of exposure to wood smoke
Show others...
2019 (English)In: European Respiratory Journal, ISSN 0903-1936, E-ISSN 1399-3003, Vol. 54Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
Sheffield: European Respiratory Society Journals, 2019
Keywords
Asthma, Air pollution
National Category
Respiratory Medicine and Allergy
Identifiers
urn:nbn:se:umu:diva-168166 (URN)10.1183/13993003.congress-2019.PA2829 (DOI)000507372403325 ()
Conference
European-Respiratory-Society (ERS) International Congress, Madrid, SPAIN, SEP 28-OCT 02, 2019.
Projects
Bio4Energy
Funder
Bio4Energy
Available from: 2020-03-17 Created: 2020-03-17 Last updated: 2023-05-09Bibliographically approved
Rankin, G. D., Wingfors, H., Uski, O., Hedman, L., Ekstrand-Hammarström, B., Bosson, J. & Lundbäck, M. (2019). The toxic potential of a fourth-generation E-cigarette on human lung cell lines and tissue explants. Journal of Applied Toxicology, 39(8), 1143-1154
Open this publication in new window or tab >>The toxic potential of a fourth-generation E-cigarette on human lung cell lines and tissue explants
Show others...
2019 (English)In: Journal of Applied Toxicology, ISSN 0260-437X, E-ISSN 1099-1263, Vol. 39, no 8, p. 1143-1154Article in journal (Refereed) Published
Abstract [en]

The use of electronic cigarettes (E‐cigs) is rapidly increasing. The latest generation of E‐cigs is highly customizable, allowing for high heating coil temperatures. The aim of this study was to assess the toxic potential of a fourth‐generation E‐cig. Aerosols generated from E‐liquid with (24 mg/mL) and without nicotine, using a fourth‐generation E‐cig, were chemically analysed and compared with cigarette smoke (K3R4F). Human lung epithelial cell lines and distal lung tissue explants were exposed to E‐cig vapour extract (EVE) and cigarette smoke extract for 24 hours and assessed for viability, inflammation, oxidative stress and genotoxicity. E‐cig aerosols contained measurable levels of volatile organic compounds, aldehydes and polycyclic aromatic hydrocarbons, in general, to a much lesser extent than cigarette smoke. Higher levels of certain carbonyls, e.g. formaldehyde, were detected in the E‐cig aerosols. EVEs decreased cell viability of BEAS‐2B cells, whereas little effect was seen in A549 cells and distal lung tissue. The nicotine‐containing EVE caused a greater decrease in cell viability and significant increase in DNA damage than the nicotine‐free EVE. Increased cytotoxicity, reactive oxygen species production and genotoxicity were seen with cells and tissue exposed to cigarette smoke extract compared with EVEs. Although E‐cig aerosols were less toxic than cigarette smoke, it was not benign. Moreover, the EVE containing nicotine was more toxic than the nicotine‐free EVE. More research is needed on the short‐ and long‐term health effects of vaping and the usage of newly emerging E‐cig devices to evaluate better the potential negative effects of E‐cigs on human health.

Place, publisher, year, edition, pages
John Wiley & Sons, 2019
Keywords
A549, BEAS-2B, DNA damage, aerosol characterization, cell cycle, electronic cigarette extract, human distal lung tissue, inflammatory cytokines, viability
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-158814 (URN)10.1002/jat.3799 (DOI)000475406700006 ()30957912 (PubMedID)2-s2.0-85063979647 (Scopus ID)
Available from: 2019-05-09 Created: 2019-05-09 Last updated: 2019-08-12Bibliographically approved
Organisations

Search in DiVA

Show all publications