| 171. |
- Langrish, Jeremy P, et al.
(författare)
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Altered nitric oxide bioavailability contributes to diesel exhaust inhalation-induced cardiovascular dysfunction in man
- 2013
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Ingår i: Journal of the American Heart Association. - : American stroke association. - 2047-9980 .- 2047-9980. ; 2:1, s. e004309-
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Tidskriftsartikel (refereegranskat)abstract
- Background Diesel exhaust inhalation causes cardiovascular dysfunction including impaired vascular reactivity, increased blood pressure, and arterial stiffness. We investigated the role of nitric oxide (NO) bioavailability in mediating these effects.Methods and Results In 2 randomized double-blind crossover studies, healthy nonsmokers were exposed to diesel exhaust or filtered air. Study 1: Bilateral forearm blood flow was measured during intrabrachial infusions of acetylcholine (ACh; 5 to 20 mu g/min) and sodium nitroprusside (SNP; 2 to 8 mu g/min) in the presence of the NO clamp (NO synthase inhibitor N-G-monomethyl-L-arginine (L-NMMA) 8 mu g/min coinfused with the NO donor SNP at 90 to 540 ng/min to restore basal blood flow). Study 2: Blood pressure, arterial stiffness, and cardiac output were measured during systemic NO synthase inhibition with intravenous L-NMMA (3 mg/kg). Following diesel exhaust inhalation, plasma nitrite concentrations were increased (68 +/- 48 versus 41 +/- 32 nmol/L; P=0.006) despite similar L-NMMA-induced reductions in basal blood flow (-20.6 +/- 14.7% versus -21.1 +/- 14.6%; P=0.559) compared to air. In the presence of the NO clamp, ACh and SNP caused dose-dependent vasodilatation that was not affected by diesel exhaust inhalation (P>0.05 for both). Following exposure to diesel exhaust, L-NMMA caused a greater increase in blood pressure (P=0.048) and central arterial stiffness (P=0.007), but reductions in cardiac output and increases in systemic vascular resistance (P>0.05 for both) were similar to those seen with filtered air.Conclusions Diesel exhaust inhalation disturbs normal vascular homeostasis with enhanced NO generation unable to compensate for excess consumption. We suggest the adverse cardiovascular effects of air pollution are, in part, mediated through reduced NO bioavailability.
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| 172. |
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| 173. |
- Langrish, J. P., et al.
(författare)
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Cardiovascular effects of particulate air pollution exposure : time course and underlying mechanisms
- 2012
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Ingår i: Journal of Internal Medicine. - Hoboken, NJ : Wiley-Blackwell. - 0954-6820 .- 1365-2796. ; 272:3, s. 224-239
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Forskningsöversikt (refereegranskat)abstract
- Objective Air pollution is now recognized as an important independent risk factor for cardiovascular morbidity and mortality and may be responsible for up to 3 similar to million premature deaths each year worldwide. The mechanisms underlying the observed effects are poorly understood but are likely to be multifactorial. Here, we review the acute and chronic effects of air pollution exposure on the cardiovascular system and discuss how these effects may explain the observed increases in cardiovascular morbidity and mortality.
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| 174. |
- Langrish, Jeremy P., et al.
(författare)
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Controlled exposures to air pollutants and risk of cardiac arrhythmia
- 2014
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Ingår i: Journal of Environmental Health Perspectives. - : Environmental Health Perspectives. - 0091-6765 .- 1552-9924. ; 122:7, s. 747-753
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Epidemiological studies have reported associations between air pollution exposure and increases in cardiovascular morbidity and mortality. Exposure to air pollutants can influence cardiac autonomic tone and reduce heart rate variability, and may increase the risk of cardiac arrhythmias, particularly in susceptible patient groups. OBJECTIVES: We investigated the incidence of cardiac arrhythmias during and after controlled exposure to air pollutants in healthy volunteers and patients with coronary heart disease. METHODS: We analyzed data from 13 double-blind randomized crossover studies including 282 participants (140 healthy volunteers and 142 patients with stable coronary heart disease) from whom continuous electrocardiograms were available. The incidence of cardiac arrhythmias was recorded for each exposure and study population. RESULTS: There were no increases in any cardiac arrhythmia during or after exposure to dilute diesel exhaust, wood smoke, ozone, concentrated ambient particles, engineered carbon nanoparticles, or high ambient levels of air pollution in either healthy volunteers or patients with coronary heart disease. CONCLUSIONS: Acute controlled exposure to air pollutants did not increase the short-term risk of arrhythmia in participants. Research employing these techniques remains crucial in identifying the important pathophysiological pathways involved in the adverse effects of air pollution, and is vital to inform environmental and public health policy decisions.
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| 175. |
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| 176. |
- Lanz, Thomas, et al.
(författare)
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A light–emission textile device : conformal spray-sintering of a woven fabric electrode
- 2016
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Ingår i: Flexible and Printed Electronics. - : Institute of Physics (IOP). - 2058-8585. ; 1:2
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Tidskriftsartikel (refereegranskat)abstract
- We report on the realization of an ultra-flexible, light-weight and large-area emissive textile device. The anode and active material of a light-emitting electrochemical cell (LEC) were deposited by conformal spray-coating of a transparent fabric-based electrode, comprising a weave of fine Ag-coated Cu wires and poly(ethylene naphthalene) monofilament fibers embedded in a polyurethane matrix. The yellow-emitting textile featured low turn-on voltage (5 V), high maximum brightness (>4000 cd m−2), good efficiency (3.4 cd A−1), and reasonable lifetime (180 h at >100 cd m−2). Uniform emission to the eye was attained from thin and highly flexible textiles featuring a large emission area of 42 cm2, without resorting to planarization of the partially wavy-shaped (valley-to-peak height = 2.7 μm) fabric electrode. The key enabling factors for the functional emissive textile are the characteristic in situ electrochemical doping of LEC devices, the 'dry' spray-sintering deposition of the active material, and the attractive mechanical, electronic and optical properties of the fabric-based electrode.
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| 177. |
- Larsson, Britt-Marie, et al.
(författare)
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Limited airway effects in mild asthmatics after exposure to air pollution in a road tunnel
- 2010
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Ingår i: Respiratory Medicine. - : Elsevier BV. - 0954-6111 .- 1532-3064. ; 104:12, s. 1912-1918
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Tidskriftsartikel (refereegranskat)abstract
- Ambient air pollution is a contributing factor to respiratory morbidity and mortality and asthmatics are a particularly vulnerable population. The aim of the study was to investigate whether acute exposure to traffic related air pollution in a road tunnel would increase bronchial responsiveness in mild asthmatics, and if this would be accompanied by increased measures of inflammatory markers in the airways assessed by nasal lavage (NAL) and induced sputum. Fourteen mild asthmatics (7 treated with inhaled corticosteroids) were exposed for 2 h in a road tunnel and a control environment, respectively, separated by at least 3 weeks. Symptoms and peak expiratory flow (PEF) were recorded. Seven hours following exposure sessions, subjects underwent measurements of fraction of exhaled nitric oxide (FENO), spirometry, and a bronchial provocation test. NAL, induced sputum and blood samples were collected. The median PM(2.5) and PM(10) levels during the exposure occasions in the road tunnel were 80 (range 41-93) μg/m(3) and 183 (72-213) μg/m(3) respectively. Irritative symptoms from the airways increased and PEF decreased after road tunnel exposure. Increased levels of IL-10, IL-12 and TNF-α were observed in NAL fluid from subjects without ongoing inhaled corticosteroid treatment. Forced expiratory volume in 1 s (FEV(1)) and the degree of bronchial responsiveness in asthmatics did not change significantly after tunnel exposure. We conclude that asthmatics exhibit increased symptoms, decreased PEF and signs of inflammatory response in the upper airways, after a 2 h road tunnel exposure. Our findings may further emphasize asthmatics as a vulnerable group to common air pollutants.
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| 178. |
- Larsson, B-M, et al.
(författare)
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Road tunnel air pollution induces bronchoalveolar inflammation in healthy subjects
- 2007
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Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 29:4, s. 699-705
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Tidskriftsartikel (refereegranskat)abstract
- Traffic-related air pollution is associated with adverse respiratory effects. The aim of the present study was to investigate whether exposure to air pollution in a road tunnel causes airway inflammatory and blood coagulation responses. A total of 16 healthy subjects underwent bronchoscopy with bronchial mucosal biopsies and bronchoalveolar lavage (BAL) on two occasions, in random order: once at 14 h after a 2-h exposure to air pollution in a busy road tunnel, and once after a control day with subjects exposed to urban air during normal activities. Peripheral blood was sampled prior to bronchoscopy. The road tunnel exposures included particulate matter with a 50% cut-off aerodynamic diameter of 2.5 μm, particulate matter with a 50% cut-off aerodynamic diameter of 10 μm and nitrogen dioxide which had median concentrations of 64, 176 and 230 µg·m−3, respectively. Significantly higher numbers of BAL fluid total cell number, lymphocytes and alveolar macrophages were present after road tunnel exposure versus control. Significantly higher nuclear expression of the transcription factor component c-Jun was found in the bronchial epithelium after exposure. No upregulation of adhesion molecules or cellular infiltration was present and blood coagulation factors were unaffected. In conclusion, exposure of healthy subjects to traffic-related air pollution resulted in a lower airway inflammatory response with cell migration, together with signs of an initiated signal transduction in the bronchial epithelium.
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| 179. |
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| 180. |
- Larsson, Kjell, et al.
(författare)
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Så blir KOL-vården bättre
- 2011
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Ingår i: Läkartidningen. - 0023-7205 .- 1652-7518. ; 108:35, s. 1604-1605
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Tidskriftsartikel (refereegranskat)
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