| 1. |
- Beko, Gabriel, et al.
(författare)
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Contribution of various microenvironments to the daily personal exposure to ultrafine particles: Personal monitoring coupled with GPS tracking
- 2015
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Ingår i: Atmospheric Environment. - : Elsevier BV. - 1352-2310. ; 110, s. 122-129
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Tidskriftsartikel (refereegranskat)abstract
- Exposure to ultrafine particles (UFP) may have adverse health effects. Central monitoring stations do not represent the personal exposure to UFP accurately. Few studies have previously focused on personal exposure to UFP. Sixty non-smoking residents living in Copenhagen, Denmark were asked to carry a backpack equipped with a portable monitor, continuously recording particle number concentrations (PN), in order to measure the real-time individual exposure over a period of similar to 48 h. A GPS logger was carried along with the particle monitor and allowed us to estimate the contribution of UFP exposure occurring in various microenvironments (residence, during active and passive transport, other indoor and outdoor environments) to the total daily exposure. On average, the fractional contribution of each microenvironment to the daily integrated personal exposure roughly corresponded to the fractions of the day the subjects spent in each microenvironment. The home environment accounted for 50% of the daily personal exposure. Indoor environments other than home or vehicles contributed with similar to 40%. The highest median UFP concentration was obtained during passive transport (vehicles). However, being in transit or outdoors contributed 5% or less to the daily exposure. Additionally, the subjects recorded in a diary the periods when they were at home. With this approach, 66% of the total daily exposure was attributable to the home environment. The subjects spent 28% more time at home according to the diary, compared to the GPS. These results may indicate limitations of using diaries, but also possible inaccuracy and miss-classification in the GPS data. (C) 2015 Elsevier Ltd. All rights reserved.
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| 2. |
- Bekö, Gabriel, et al.
(författare)
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Ultrafine Particles: Exposure and Source Apportionment in 56 Danish Homes
- 2013
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Ingår i: Environmental Science & Technology. - : American Chemical Society (ACS). - 1520-5851 .- 0013-936X. ; 47:18, s. 10240-10248
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Tidskriftsartikel (refereegranskat)abstract
- ABSTRACT: Particle number (PN) concentrations (10−300 nm in size) were continuously measured over a period of ∼45 h in 56 residences of nonsmokers in Copenhagen, Denmark. The highest concentrations were measured when occupants were present and awake (geometric mean, GM: 22.3 × 103 cm−3), the lowest when the homes were vacant (GM: 6.1 × 103 cm−3) or the occupants were asleep (GM: 5.1 × 103 cm−3). Diary entries regarding occupancy and particle related activities were used to identify source events and apportion the daily integrated exposure among sources. Source events clearly resulted in increased PN concentrations and decreased average particle diameter. For a given event, elevated particle concentrations persisted for several hours after the emission of fresh particles ceased. The residential daily integrated PN exposure in the 56 homes ranged between 37 × 103 and 6.0 × 106 particles per cm3·h/day (GM: 3.3 × 105 cm−3·h/day). On average, ∼90% of this exposure occurred outside of the period from midnight to 6 a.m. Source events, especially candle burning, cooking, toasting, and unknown activities, were responsible on average for ∼65% of the residential integrated exposure (51% without the unknown activities). Candle burning occurred in half of the homes where, on average, it was responsible for almost 60% of the integrated exposure.
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| 3. |
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| 4. |
- Bräuner, Elvira Vaclavik, et al.
(författare)
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Exposure to ambient concentrations of particulate air pollution does not influence vascular function or inflammatory pathways in young healthy individuals.
- 2008
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Ingår i: Particle and fibre toxicology. - : Springer Science and Business Media LLC. - 1743-8977. ; 5
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Tidskriftsartikel (refereegranskat)abstract
- ABSTRACT: BACKGROUND: Particulate air pollution is associated with increased risk of cardiovascular events although the involved mechanisms are poorly understood. The objective of the present study was to investigate the effects of controlled exposure to ambient air fine and ultrafine particles on microvascular function and biomarkers related to inflammation, haemostasis and lipid and protein oxidation. METHODS: Twenty-nine subjects participated in a randomized, two-factor crossover study with or without biking exercise for 180 minutes and with 24 hour exposure to particle rich (number concentrations, NC: 11600 +/- 5600 per cm3, mass concentrations: 13.8 +/- 7.4 mug/m3 and 10.5 +/- 4.8 mug/m3 for PM10-2.5 and PM2.5, respectively) or particle filtered (NC: 555 +/- 1053 per cm3) air collected above a busy street. Microvascular function was assessed non-invasively by measuring digital peripheral artery tone following arm ischemia. Biomarkers included haemoglobin, red blood cells, platelet count, coagulation factors, C-reactive protein, fibrinogen, interleukin-6, tumour necrosis factor alpha, lag time to copper-induced oxidation of plasma lipids and protein oxidation measured as 2-aminoadipic semialdehyde in plasma. RESULTS: No statistically significant differences were observed on microvascular function or the biomarkers after exposure to particle rich or particle filtered air. CONCLUSION: This study indicates that exposure to air pollution particles at outdoor concentrations is not associated with detectable systemic inflammation, lipid or protein oxidation, altered haemostasis or microvascular function in young healthy participants.
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| 5. |
- Bräuner, Elvira Vaclavik, et al.
(författare)
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Indoor particles affect vascular function in the aged: an air filtration-based intervention study.
- 2008
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Ingår i: American journal of respiratory and critical care medicine. - 1535-4970. ; 177:4, s. 419-25
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Tidskriftsartikel (refereegranskat)abstract
- RATIONALE: Exposure to particulate matter is associated with risk of cardiovascular events, possibly through endothelial dysfunction, and indoor air may be most important. OBJECTIVES: We investigated effects of controlled exposure to indoor air particles on microvascular function (MVF) as the primary endpoint and biomarkers of inflammation and oxidative stress as secondary endpoints in a healthy elderly population. METHODS: A total of 21 nonsmoking couples participated in a randomized, double-blind, crossover study with two consecutive 48-hour exposures to either particle-filtered or nonfiltered air (2,533-4,058 and 7,718-12,988 particles/cm(3), respectively) in their homes. MEASUREMENTS AND MAIN RESULTS: MVF was assessed noninvasively by measuring digital peripheral artery tone after arm ischemia. Secondary endpoints included hemoglobin, red blood cells, platelet count, coagulation factors, P-selectin, plasma amyloid A, C-reactive protein, fibrinogen, IL-6, tumor necrosis factor-alpha, protein oxidation measured as 2-aminoadipic semialdehyde in plasma, urinary 8-iso-prostaglandin F(2alpha), and blood pressure. Indoor air filtration significantly improved MVF by 8.1% (95% confidence interval, 0.4-16.3%), and the particulate matter (diameter < 2.5 mum) mass of the indoor particles was more important than the total number concentration (10-700 nm) for these effects. MVF was significantly associated with personal exposure to iron, potassium, copper, zinc, arsenic, and lead in the fine fraction. After Bonferroni correction, none of the secondary biomarkers changed significantly. CONCLUSIONS: Reduction of particle exposure by filtration of recirculated indoor air for only 48 hours improved MVF in healthy elderly citizens, suggesting that this may be a feasible way of reducing the risk of cardiovascular disease.
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| 6. |
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| 7. |
- Danielsen, Pernille Hogh, et al.
(författare)
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Oxidatively damaged DNA and its repair after experimental exposure to wood smoke in healthy humans.
- 2008
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Ingår i: Mutation research. - : Elsevier BV. - 0027-5107. ; 642:1-2, s. 37-42
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Tidskriftsartikel (refereegranskat)abstract
- Particulate matter from wood smoke may cause health effects through generation of oxidative stress with resulting damage to DNA. We investigated oxidatively damaged DNA and related repair capacity in peripheral blood mononuclear cells (PBMC) and measured the urinary excretion of repair products after controlled short-term exposure of human volunteers to wood smoke. Thirteen healthy adults were exposed first to clean air and then to wood smoke in a chamber during 4h sessions, 1 week apart. Blood samples were taken 3h after exposure and on the following morning, and urine was collected after exposure, from bedtime until the next morning. We measured the levels of DNA strand breaks (SB), oxidized purines as formamidopyrimidine-DNA-glycosylase (FPG) sites and activity of oxoguanine glycosylase 1 (hOGG1) in PBMC by the comet assay, whereas mRNA levels of hOGG1, nucleoside diphosphate linked moiety X-type motif 1 (hNUDT1) and heme oxygenase 1 (hHO1) were determined by real-time RT-PCR. The excretion of 8-oxo-7,8-dihydro-oxoguanine (8-oxoGua) and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in urine was measured by high performance liquid chromatography purification followed by gas chromatography with mass spectrometry. The morning following exposure to wood smoke the PBMC levels of SB were significantly decreased and the mRNA levels of hOGG1 significantly increased. FPG sites, hOGG1 activity, expression of hNUDT1 and hHO1, urinary excretion of 8-oxodG and 8-oxoGua did not change significantly. Our findings support that exposure to wood smoke causes systemic effects, although we could not demonstrate genotoxic effects, possibly explained by enhanced repair and timing of sampling.
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| 8. |
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| 9. |
- Haghdoost, Siamak, 1968-
(författare)
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Biomarkers of oxidative stress and their application for assessment of individual radiosensitivity
- 2005
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Radiotherapy is one of the most common therapeutic methods for treatment of many types of cancer. Despite many decades of development and experience there is much to improve, both in efficacy of treatment and to decrease the incidences of adverse healthy tissue reactions. Around 20 % of the radiotherapy patients show a broad range in the severity of normal tissue reactions to radiotherapy, and dose limits are governed by severe reactions in the most radiosensitive patients (< 5 %). Identification of patients with low, moderate or high clinical radiosensitivity before commencing of radiotherapy would allow individual adaptation of the maximum dose with an overall increase in the cure rate. Characterization of factors that may modify the biological effects of ionizing radiation has been a subject of intense research efforts. Still, there is no assay currently available that can reliably predict the clinical radiosensitivity. The aim of this work has been to investigate the role of oxidative stress in individual radiosensitivity and evaluate novel markers of radiation response, which could be adapted for clinical use.8-Oxo-7,8-dihydro-2'-deoxyguanosine (8-oxo-dG), a general marker of oxidative stress, is one of the major products of interaction of ionizing radiation with DNA and the nucleotide pool of the cell. As 8-oxo-dG is highly mutagenic due to incorrect base pairing with deoxyadenosine, various repair mechanisms recognize and remove 8-oxo-dG. The repaired lesions are released from cells to the extracellular milieu (serum, urine and cell culture medium) where they can be detected as markers for free radical reactions with the nucleic acids.Significant variations in background levels as well as in radiation induced levels of 8-oxo-dG in urine have been demonstrated in breast cancer patients (paper 1). Two major patterns were observed: high background and no therapy-related increase vs. low background and significant increase during radiotherapy for the radiosensitive and non radiosensitive patients respectively.Studies in paper 2 indicated major contribution of the nucleotide pool to the extracellular 8-oxo-dG levels. The results also implicated induction of prolonged endogenous oxidative stress in the irradiated cells. RNA “knock-down” experiments on the nucleotide pool sanitization enzyme hMTH1 in paper 3 lend further experimental evidence to this assumption.The applicability of 8-oxo-dG as a diagnostic marker of oxidative stress was demonstrated in paper 4. Studies on dialysis patients revealed a good correlation between inflammatory responses (known to be associated with persistent oxidative stress) and extracellular 8-oxo-dG.In summary, our results confirm that extracellular 8-oxo-dG is a sensitive in vivo biomarker of oxidative stress, primarily formed by oxidative damage of dGTP in the nucleotide pool with a potential to become a clinical tool for prediction of individual responses to radiotherapy.
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| 10. |
- Hemmingsen, Jette Gjerke, et al.
(författare)
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Controlled exposure to diesel exhaust and traffic noise - Effects on oxidative stress and activation in mononuclear blood cells.
- 2015
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Ingår i: Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis. - : Elsevier BV. - 1879-2871 .- 0027-5107. ; 775, s. 66-71
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Tidskriftsartikel (refereegranskat)abstract
- Particulate air pollution increases risk of cancer and cardiopulmonary disease, partly through oxidative stress. Traffic-related noise increases risk of cardiovascular disease and may cause oxidative stress. In this controlled random sequence study, 18 healthy subjects were exposed for 3h to diesel exhaust (DE) at 276μg/m(3) from a passenger car or filtered air, with co-exposure to traffic noise at 48 or 75dB(A). Gene expression markers of inflammation, (interleukin-8 and tumor necrosis factor), oxidative stress (heme oxygenase (decycling-1)) and DNA repair (8-oxoguanine DNA glycosylase (OGG1)) were unaltered in peripheral blood mononuclear cells (PBMCs). No significant differences in DNA damage levels, measured by the comet assay, were observed after DE exposure, whereas exposure to high noise levels was associated with significantly increased levels of hOGG1-sensitive sites in PBMCs. Urinary levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine were unaltered. In auxiliary ex vivo experiments whole blood was incubated with particles from the exposure chamber for 3h without effects on DNA damage in PBMCs or intracellular reactive oxygen species production and expression of CD11b and CD62L adhesion molecules in leukocyte subtypes.
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