Publications
182 results found
, 2004, Inter- and intra-individual vitamin E uptake in healthy subjects is highly repeatable across a wide supplementation dose range, Vol: 1031, Pages: 22-39, ISSN: 0077-8923
Blomberg A, Mudway I, Svensson M, et al., 2003, Clara cell protein as a biomarker for ozone-induced lung injury in humans, EUROPEAN RESPIRATORY JOURNAL, Vol: 22, Pages: 883-888, ISSN: 0903-1936
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- Citations: 69
, 2003, Protein oxidation at the air-lung interface, Vol: 25, Pages: 375-396, ISSN: 0939-4451
, 2003, Air pollution and the elderly: oxidant/antioxidant issues worth consideration, Vol: 40, Pages: 70s-75s, ISSN: 0904-1850
, 2002, Effect of ozone on bronchial mucosal inflammation in asthmatic and healthy subjects, Vol: 96, Pages: 352-358, ISSN: 0954-6111
Mudway IS, Behndig A, Blomberg A, et al., 2002, Supplementation with vitamin C (<i>vitC</i>) and E (<i>vitE</i>) does not protect against the acute effects of low-dose ozone challenges, Publisher: PERGAMON-ELSEVIER SCIENCE LTD, Pages: S163-S163, ISSN: 0891-5849
Duggan S, Mudway IS, Monero ST, et al., 2002, Coarse and fine particle matter (PM) collected from a London curb-side site is highly oxidising, Publisher: PERGAMON-ELSEVIER SCIENCE LTD, Pages: S171-S172, ISSN: 0891-5849
Kelly FJ, Mudway IS, 2002, Oxidant-antioxiant interactions at the surface of the lung, Publisher: PERGAMON-ELSEVIER SCIENCE LTD, Pages: S162-S162, ISSN: 0891-5849
Mudway IS, Duggan S, Kelly FJ, 2001, Influence of sample preparation on diesel exhaust particle (DEP) activity in in-vitro model systems, Publisher: BRITISH MED JOURNAL PUBL GROUP, Pages: 12-12, ISSN: 0040-6376
, 2001, Differences in basal airway antioxidant concentrations are not predictive of individual responsiveness to ozone: a comparison of healthy and mild asthmatic subjects, Vol: 31, Pages: 962-974, ISSN: 0891-5849
, 2000, Ozone and the lung: a sensitive issue, Vol: 21, Pages: 1-48, ISSN: 0098-2997
Mudway IS, Blomberg A, Helleday R, et al., 1999, Even though mild asthmatic subjects have compromised antioxidant status and basal inflammation they do not exhibit heightened responsiveness to ozone, Publisher: BRITISH MED JOURNAL PUBL GROUP, Pages: A70-A70, ISSN: 0040-6376
Blomberg A, Mudway IS, Nordenhäll C, et al., 1999, Ozone-induced lung function decrements do not correlate with early airway inflammatory or antioxidant responses, EUROPEAN RESPIRATORY JOURNAL, Vol: 13, Pages: 1418-1428, ISSN: 0903-1936
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- Citations: 79
Mudway IS, Blomberg A, Helleday R, et al., 1999, Low baseline nasal respiratory tract lining fluid urate concentrations in mild asthmatic subjects restricts their capacity to scrub ozone., Publisher: AMER LUNG ASSOC, Pages: A491-A491, ISSN: 1073-449X
Mudway IS, Zielinski H, BéruBé KA, et al., 1999, Particle-antioxidant interactions in epithelial lining fluid, Publisher: AMER LUNG ASSOC, Pages: A26-A26, ISSN: 1073-449X
, 1999, Modeling the interactions of particulates with epithelial lining fluid antioxidants, Vol: 277, Pages: L719-L726, ISSN: 0002-9513
, 1999, Compromised concentrations of ascorbate in fluid lining the respiratory tract in human subjects after exposure to ozone, Vol: 56, Pages: 473-481, ISSN: 1351-0711
, 1999, Antioxidant consumption and repletion kinetics in nasal lavage fluid following exposure of healthy human volunteers to ozone, Vol: 13, Pages: 1429-1438, ISSN: 0903-1936
, 1999, Altered lung antioxidant status in patients with mild asthma, Vol: 354, Pages: 482-483, ISSN: 0140-6736
Zieliński H, Mudway IS, Kelly FJ, 1998, PM10 and the respiratory tract: What do we know?, Polish Journal of Environmental Studies, Vol: 7, Pages: 273-277, ISSN: 1230-1485
The present review deals mainly with recent developments in research on the impact of PM10 (particulate matter below 10 μm) air pollution on the respiratory system and the possibly oxidant reactions that occur as a result of breathing these particles.
Roxborough HE, Mudway IS, Blomberg A, et al., 1998, Nasal Respiratory Tract Lining Fluid (RTLF) antioxidant reposnses to Deisel Exhaust (DE) in healthy human subjects, Thorax, Vol: 53, ISSN: 0040-6376
25 healthy, non-smoking subjects (9 female, 16 male; age 24.5± 4.3 years) were exposed to DE (100 μg/m3 particles + 0.6 ppm NO2) and air (A) to determine the impact of this pollutant complex on RTLF redox status. Exposures were conducted in a randomised, single blinded, crossover control fashion, with successive exposures conducted at least 3 weeks apart. Exposures lasted 2h during which subjects performed alternate 15 min cycles of exercise (VE=20L/min/m3) and rest. Nasal lavage (NL) was performed at set intervals throughout the challenge, pre- (Pre-E), 1h into- (1h-PE), immediately post- (0h-PE), and at 5.5h post-exposure (5.5h-PE) according to the spray method of Harder et al (Am.J.Resp.Crit.Care.Med. 1994;151:A565). Reduced glutathione (GSH), ascorbate (AA), and urate (UA) concentrations were then determined in the recovered NL fluid. Data are summarised in the table below, all concentrations are expressed as μmol/L, n=25. NL Sampling Time Antioxidants Pre-E 1h-E 0h-PE 5.5h-PE GSH A 1.7 (1.2-2.6) 1.0 (0.5-1.7)* 0.8 (0.5-1.1)* 0.8 (0.5-1.6)* DE 1.5 (0.7-2.1) 1.0 (0.5-1.6)* 0.7 (0.4-1.2) * 1.4 (0.6-1.7)* AA A 0.5 (0.2-1.2) 0.3 (0.2-0.5)* 0.3 (0.1-0.5)* 0.5 (0.2-1.9) DE 0.7 (0.3-1.7) 0.4 (0.2-0.5)* 0.3 (0.2-0.4)* 1.0 (0.3-1.6) UA A 18.6 (14.2-30.8) 23.4 (14.9-36.3) 20.3 (14.0-27.9) 20.0 (16.2-35.4) DE 17.8 (13.0-28.6) 19.9 (14.2-28.0) 19.1 (12.6-21.4) 20.3 (12.6-33.5) Values represented as medians (23th-75th percentiles). Analysis performed using the Quade-Two-Way-ANOVA with multiple comparisons using the t-distribution. '*' indicates a significant difference in conc. at 1h-E, 0h-PE, and 5.5h-PE vs. Pre-E values; '+' a significant difference between A and DE exposure concentrations across the same time interval. Following washout by sequential lavage, recovery of GSH over the post exposure period was significantly more rapid after DE, increasing 1.8-fold (p<0.05) over parallel air control values at 5.5h-PE. In contrast, no effects on NL fluid AA or
, 1998, Effects of 0.2 ppm ozone on biomarkers of inflammation in bronchoalveolar lavage fluid and bronchial mucosa of healthy subjects, Vol: 11, Pages: 1294-1300, ISSN: 0903-1936
, 1998, Modeling the interactions of ozone with pulmonary epithelial lining fluid antioxidants
, 1998, Antioxidant defenses in lung lining fluid of broilers: impact of poor ventilation conditions, Vol: 77, Pages: 516-522, ISSN: 0032-5791
Mudway IS, Tetley TD, Charalambous K, et al., 1997, Ozone-exposed respiratory tract lining fluid-mediated toxicity in lung macrophages and epithelial type II cells, ISSN: 0954-6111
, 1997, Sensitivity to ozone: could it be related to an individual's complement of antioxidants in lung epithelium lining fluid?, Vol: 3, Pages: 199-206, ISSN: 1351-0002
Mudway IS, Kelly FJ, 1996, Modelling the interaction between ozone (O<inf>3</inf>) and pulmonary Epithelial Lining Fluid (ELF) antioxidants, Thorax, Vol: 51, ISSN: 0040-6376
Pulmonary ELF antioxidants; ascorbate (AH2), urate (UA) and reduced glutathione (GSH) confer protection against O3 by acting as preferential sacrificial substrates, preventing its reaction with more sensitive components within this compartment. In order to determine their individual importance in this respect, the following models of ELF were employed: Pure biochemical solutions of GSH/GSSG (412/17 μmol/L) AH2 (200 μmol/L.) and UA (200 μmol/L), composite mixtures of the above antioxidants, and composite antioxidant solutions containing 5 mg/mL human albumin. Each model was examined over the range 0-1500 ppb O3 using a continually mixed interfacial exposure system, maintained at 37°C. All solutions were adjusted to pH 7.4 prior to exposure. The rate of consumption for each antioxidant was determined as the loss in concentration per unit time over a 720 min exposure period, under each of the ozone exposure concentrations. Consumption rates are expressed as mol L-1 s-1 ppb O3-1; (c. Table). Consumption rates (mol L-1s-1ppb-1) Antioxidant Pure antioxidant Composite antioxidant Composite antioxidant solutions solutions solutions + protein AH2 8.45±0.31 x 10-12 5.39±1.04 x 10-12 3.12±0.30 x 10-12†* UA 9.87±0.43 x 10-12* 6.73±1.03 x 101†* 6.30±0.20 x 10-12†* GSH 5.82±0.51 x 10-12* 4.17±0.56 x 10-12†* 2.19±1.07 x 10-12‡* Values represent mean ±SD (n=3). '†', significant difference from pure biochemical solution: '‡', significant difference between the composite solutions. For comparison of antioxidant consumption rates within each exposure model; '*' significance difference between UA and GSH vs. AH2, and UA vs. GSH. In all cases significance was assumed when P < 0.05. These data indicate, that in all models, UA represented the most reactive substrate toward O3. Generally, as the model complexity increased, the consumption rate of each antio
Kelly F, Cotgrove M, Mudway IS, 1996, Respiratory tract lining fluid antioxidants: the first line of defence against gaseous pollutants
, 1996, Differential depletion of human respiratory tract antioxidants in response to ozone challenge, Vol: 25, Pages: 499-513, ISSN: 1071-5762
, 1995, The free radical basis of air pollution: focus on ozone, Vol: 89, Pages: 647-656, ISSN: 0954-6111
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