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- Stockfelt, Leo, 1981, et al.
(författare)
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A controlled chamber study of effects of exposure to diesel exhaust particles and noise on heart rate variability and endothelial function
- 2022
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Ingår i: Inhalation Toxicology. - : Taylor and Francis Ltd.. - 0895-8378 .- 1091-7691. ; 34:5-6, s. 159-170
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Tidskriftsartikel (refereegranskat)abstract
- Background: Adverse cardiovascular effects are associated with both diesel exhaust and road traffic noise, but these exposures are hard to disentangle epidemiologically. We used an experimental setup to evaluate the impact of diesel exhaust particles and traffic noise, alone and combined, on intermediary outcomes related to the autonomic nervous system and increased cardiovascular risk. Methods: In a controlled chamber 18 healthy adults were exposed to four scenarios in a randomized cross-over fashion. Each exposure scenario consisted of either filtered (clean) air or diesel engine exhaust (particle mass concentrations around 300 µg/m3), and either low (46 dB(A)) or high (75 dB(A)) levels of traffic noise for 3 h at rest. ECG was recorded for 10-min periods before and during each exposure type, and frequency-domain heart rate variability (HRV) computed. Endothelial dysfunction and arterial stiffness were assessed after each exposure using EndoPAT 2000. Results: Compared to control exposure, HRV in the high frequency band decreased during exposure to diesel exhaust, both alone and combined with noise, but not during noise exposure only. These differences were more pronounced in women. We observed no synergistic effects of combined exposure, and no significant differences between exposure scenarios for other HRV indices, endothelial function or arterial stiffness. Conclusion: Three-hour exposure to diesel exhaust, but not noise, was associated with decreased HRV in the high frequency band. This indicates activation of irritant receptor-mediated autonomic reflexes, a possible mechanism for the cardiovascular risks of diesel exposure. There was no effect on endothelial dysfunction or arterial stiffness after exposure. © 2022 The Author(s).
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| 2. |
- Svensson, Christian, et al.
(författare)
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Validation of an air–liquid interface toxicological set-up using Cu, Pd, and Ag well-characterized nanostructured aggregates and spheres
- 2016
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Ingår i: Journal of Nanoparticle Research. - : Springer Science and Business Media LLC. - 1388-0764 .- 1572-896X. ; 18:4
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Tidskriftsartikel (refereegranskat)abstract
- Abstract: Systems for studying the toxicity of metal aggregates on the airways are normally not suited for evaluating the effects of individual particle characteristics. This study validates a set-up for toxicological studies of metal aggregates using an air–liquid interface approach. The set-up used a spark discharge generator capable of generating aerosol metal aggregate particles and sintered near spheres. The set-up also contained an exposure chamber, The Nano Aerosol Chamber for In Vitro Toxicity (NACIVT). The system facilitates online characterization capabilities of mass mobility, mass concentration, and number size distribution to determine the exposure. By dilution, the desired exposure level was controlled. Primary and cancerous airway cells were exposed to copper (Cu), palladium (Pd), and silver (Ag) aggregates, 50–150 nm in median diameter. The aggregates were composed of primary particles 2, respectively, were achieved. Viability was measured by WST-1 assay, cytokines (Il-6, Il-8, TNF-a, MCP) by Luminex technology. Statistically significant effects and dose response on cytokine expression were observed for SAEC cells after exposure to Cu, Pd, or Ag particles. Also, a positive dose response was observed for SAEC viability after Cu exposure. For A549 cells, statistically significant effects on viability were observed after exposure to Cu and Pd particles. The set-up produced a stable flow of aerosol particles with an exposure and dose expressed in terms of number, mass, and surface area. Exposure-related effects on the airway cellular models could be asserted. Graphical Abstract: [Figure not available: see fulltext.]
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| 3. |
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| 4. |
- Wierzbicka, Aneta, et al.
(författare)
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Indoor PM2.5 from occupied residences in Sweden caused higher inflammation in mice compared to outdoor PM2.5
- 2022
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Ingår i: Indoor Air. - : Hindawi Limited. - 0905-6947 .- 1600-0668. ; 32:12
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Tidskriftsartikel (refereegranskat)abstract
- We spend most of our time indoors; however, little is known about the effects of exposure to aerosol particles indoors. We aimed to determine differences in relative toxicity and physicochemical properties of PM 2.5 collected simultaneously indoors (PM 2.5 INDOOR ) and outdoors (PM 2.5 OUTDOOR ) in 15 occupied homes in southern Sweden. Collected particles were extracted from filters, pooled (indoor and outdoor separately), and characterized for chemical composition and endotoxins before being tested for toxicity in mice via intratracheal instillation. Various endpoints including lung inflammation, genotoxicity, and acute-phase response in lung and liver were assessed 1, 3, and 28 days post-exposure. Chemical composition of particles used in toxicological assessment was compared to particles analyzed without extraction. Time-resolved particle mass and number concentrations were monitored. PM 2.5 INDOOR showed higher relative concentrations (μg mg -1 ) of metals, PAHs, and endotoxins compared to PM 2.5 OUTDOOR . These differences may be linked to PM 2.5 INDOOR causing significantly higher lung inflammation and lung acute-phase response 1 day post-exposure compared to PM 2.5 OUTDOOR and vehicle controls, respectively. None of the tested materials caused genotoxicity. PM 2.5 INDOOR displayed higher relative toxicity than PM 2.5 OUTDOOR under the studied conditions, that is, wintertime with reduced air exchange rates, high influence of indoor sources, and relatively low outdoor concentrations of PM. Reducing PM 2.5 INDOOR exposure requires reduction of both infiltration from outdoors and indoor-generated particles.
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