Publications
588 results found
Menni C, Metrustry SJ, Mohney RP, et al., 2015, Circulating Levels of Antioxidant Vitamins Correlate with Better Lung Function and Reduced Exposure to Ambient Pollution, American Journal of Respiratory and Critical Care Medicine, Vol: 191, Pages: 1203-1207, ISSN: 1073-449X
Patelarou E, Tzanakis N, Kelly F, 2015, Exposure to Indoor Pollutants and Wheeze and Asthma Development during Early Childhood, International Journal of Environmental Research and Public Health, Vol: 12, Pages: 3993-4017
Mihucz VG, Szigeti T, Dunster C, et al., 2015, An integrated approach for the chemical characterization and oxidative potential assessment of indoor PM<sub>2.5</sub>, MICROCHEMICAL JOURNAL, Vol: 119, Pages: 22-29, ISSN: 0026-265X
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- Citations: 16
Kelly FJ, Fussell JC, 2015, Linking ambient particulate matter pollution effects with oxidative biology and immune responses, Annals of the New York Academy of Sciences, Vol: 1340, Pages: 84-94, ISSN: 0077-8923
<jats:p>Exposure to combustion‐related particulate matter (PM), at concentrations experienced by populations throughout the world, contributes to pulmonary and cardiac disease through multiple mechanistic pathways that are complex and interdependent. Current evidence supports an interactive chain of events linking pollution‐induced pulmonary and systemic oxidative stress, inflammatory events, and translocation of particle constituents with an associated risk of vascular dysfunction, atherosclerosis, altered cardiac autonomic function, and ischemic cardiovascular and obstructive pulmonary diseases. Because oxidative stress is believed to play such an instrumental role in these pathways, the capacity of particulate pollution to cause damaging oxidative reactions (the oxidative potential) has been used as an effective exposure metric, identifying toxic components and sources within diverse ambient PM mixes that vast populations are subjected to—from traffic emissions on busy roads in urban areas to biomass smoke that fills homes in rural areas of the developing world.</jats:p>
Janssen NAH, Strak M, Yang A, et al., 2015, Associations between three specific a-cellular measures of the oxidative potential of particulate matter and markers of acute airway and nasal inflammation in healthy volunteers, Occupational and Environmental Medicine, Vol: 72, Pages: 49-56, ISSN: 1351-0711
Bohnenstengel SI, Belcher SE, Aiken A, et al., 2015, Meteorology, air quality, and health in London, The ClearfLo project, Vol: 96, Pages: 779-804, ISSN: 0003-0007
The Clean Air for London (ClearfLo) project provides integrated measurements of the meteorology, composition, and particulate loading of the urban atmosphere in London, United Kingdom, to improve predictive capability for air quality.
Atkinson R, Analytis A, Samoli E, et al., 2015, Short-term exposure to traffic-related air pollution and daily mortality in London, UK, Journal of Exposure Science and Environmental Epidemiology, Vol: 26, Pages: 125-132, ISSN: 1559-0631
Epidemiological studies have linked daily concentrations of urban air pollution to mortality, but few have investigated specific traffic sources that can inform abatement policies. We assembled a database of >100 daily, measured and modelled pollutant concentrations characterizing air pollution in London between 2011 and 2012. Based on the analyses of temporal patterns and correlations between the metrics, knowledge of local emission sources and reference to the existing literature, we selected, a priori, markers of traffic pollution: oxides of nitrogen (general traffic); elemental and black carbon (EC/BC) (diesel exhaust); carbon monoxide (petrol exhaust); copper (tyre), zinc (brake) and aluminium (mineral dust). Poisson regression accounting for seasonality and meteorology was used to estimate the percentage change in risk of death associated with an interquartile increment of each pollutant. Associations were generally small with confidence intervals that spanned 0% and tended to be negative for cardiovascular mortality and positive for respiratory mortality. The strongest positive associations were for EC and BC adjusted for particle mass and respiratory mortality, 2.66% (95% confidence interval: 0.11, 5.28) and 2.72% (0.09, 5.42) per 0.8 and 1.0 μg/m3, respectively. These associations were robust to adjustment for other traffic metrics and regional pollutants, suggesting a degree of specificity with respiratory mortality and diesel exhaust containing EC/BC.
Behndig AF, Shanmuganathan K, Whitmarsh L, et al., 2015, Effects of controlled diesel exhaust exposure on apoptosis and proliferation markers in bronchial epithelium - an in vivo bronchoscopy study on asthmatics, rhinitics and healthy subjects, BMC Pulm Med, Vol: 15, ISSN: 1471-2466
BACKGROUND: Epidemiological evidence demonstrates that exposure to traffic-derived pollution worsens respiratory symptoms in asthmatics, but controlled human exposure studies have failed to provide a mechanism for this effect. Here we investigated whether diesel exhaust (DE) would induce apoptosis or proliferation in the bronchial epithelium in vivo and thus contribute to respiratory symptoms. METHODS: Moderate (n = 16) and mild (n = 16) asthmatics, atopic non-asthmatic controls (rhinitics) (n = 13) and healthy controls (n = 21) were exposed to filtered air or DE (100 mug/m(3)) for 2 h, on two separate occasions. Bronchial biopsies were taken 18 h post-exposure and immunohistochemically analysed for pro-apoptotic and anti-apoptotic proteins (Bad, Bak, p85 PARP, Fas, Bcl-2) and a marker of proliferation (Ki67). Positive staining was assessed within the epithelium using computerized image analysis. RESULTS: No evidence of epithelial apoptosis or proliferation was observed in healthy, allergic or asthmatic airways following DE challenge. CONCLUSION: In the present study, we investigated whether DE exposure would affect markers of proliferation and apoptosis in the bronchial epithelium of asthmatics, rhinitics and healthy controls, providing a mechanistic basis for the reported increased airway sensitivity in asthmatics to air pollutants. In this first in vivo exposure investigation, we found no evidence of diesel exhaust-induced effects on these processes in the subject groups investigated.
Ho TR, Pfeffer PE, Mann E, et al., 2014, AIR POLLUTION PARTICULATE MATTER PROMOTES DC MATURATION AND ENHANCES THEIR STIMULATION OF CD8 LYMPHOCYTE RESPONSES, Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A27-A28, ISSN: 0040-6376
Pfeffer PE, Kelly FJ, Hawrylowicz CM, 2014, VITAMIN D ENHANCES BRONCHIAL EPITHELIAL CELL ANTIOXIDANT RESPONSES AND REDUCES THEIR PRO-INFLAMMATORY CYTOKINE RESPONSE TO STIMULATION BY URBAN PARTICULATE MATTER, Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A1-A1, ISSN: 0040-6376
Sinharay R, Barratt B, Gong J, et al., 2014, THE EFFECTS OF REAL-WORLD EXPOSURES TO DIESEL TRAFFIC EMISSIONS ON CARDIO-RESPIRATORY OUTCOMES IN COPD : 'OXFORD STREET 2', Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A56-A56, ISSN: 0040-6376
O'Farrell G, McDonald M, Kelly F, 2014, 'Tea trolley' difficult airway training: a novel approach, Annual Congress of the Association-of-Anaesthetists-of-Great-Britain-and-Ireland (AAGBI), Publisher: WILEY-BLACKWELL, Pages: 85-85, ISSN: 0003-2409
Kelly F, 2014, London air quality: A real world experiment in progress, 50th Congress of the European-Societies-of-Toxicology, Publisher: ELSEVIER IRELAND LTD, Pages: S23-S23, ISSN: 0378-4274
Szigeti T, Kertesz Z, Dunster C, et al., 2014, Exposure to PM<sub>2.5</sub> in modern office buildings through elemental characterization and oxidative potential, ATMOSPHERIC ENVIRONMENT, Vol: 94, Pages: 44-52, ISSN: 1352-2310
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- Citations: 41
Knox K, Kelly F, Mey A, et al., 2014, Mental Health Consumers' and Carers' Experiences of Community Pharmacy Services in Australia, Publisher: INT CTR MENTAL HEALTH POLICY & ECONOMICS-ICMPE, Pages: S11-S11, ISSN: 1091-4358
Sinharay R, Barratt B, Goward C, et al., 2014, Cardio-respiratory outcomes in COPD folio ng ambient exposures to diesel traffic emissions:"Oxford Street 2", Publisher: EUROPEAN RESPIRATORY SOC JOURNALS LTD, ISSN: 0903-1936
Kelly F, Moloney B, Jadaan M, et al., 2014, An Unusual Presentation of Psoas Abscess in a Patient Following a Road Traffic Accident, Publisher: SPRINGER LONDON LTD, Pages: S185-S186, ISSN: 0021-1265
Amato F, Cassee FR, Denier van der Gon HAC, et al., 2014, Urban air quality: The challenge of traffic non-exhaust emissions, Journal of Hazardous Materials, Vol: 275, Pages: 31-36, ISSN: 0304-3894
Canova C, Minelli C, Dunster C, et al., 2014, PM<sub>10</sub> Oxidative Properties and Asthma and COPD, EPIDEMIOLOGY, Vol: 25, Pages: 467-468, ISSN: 1044-3983
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- Citations: 17
Brugha RE, Mustaq N, Round T, et al., 2014, Carbon in airway macrophages from children with asthma, Thorax, Vol: 69, Pages: 654-659, ISSN: 0040-6376
Background Airway macrophage (AM) phagocytosis is impaired in severe asthma. Prostaglandin (PG) E2 and D2 are increased in severe asthma and suppress AM phagocytic function in vitro. In this study, we sought evidence for PG-mediated impairment of phagocytosis of inhalable carbonaceous particulate matter (PM) by AM in children with severe asthma compared with mild asthmatics and healthy controls.Methods AM were obtained from children with asthma and healthy controls using induced sputum. AM carbon area (μm2) was assessed by image analysis. In a subgroup of asthmatics, urinary PGE2 and PGD2 metabolites were measured by high-performance liquid chromatography, and PM exposure at the home address was modelled. Phagocytosis of PM by human monocyte-derived macrophages and rat AM was assessed in vitro by image analysis.Results AM carbon was 51% lower in children with moderate-to-severe asthma (n=36) compared with mild asthmatics (n=12, p<0.01) and healthy controls (n=47, p<0.01). There was no association between modelled PM exposure and AM carbon in 33 asthmatics who had a urine sample, but there was an inverse association between AM carbon and urinary metabolites of PGE2 and D2 (n=33, rs=−0.40, p<0.05, and rs=−0.44, p<0.01). PGE2 10−6 M, but not PGD2 10−6 M, suppressed phagocytosis of PM10 by human macrophages in vitro (p<0.05 vs control). PGE2 10−6 M also suppressed phagocytosis of PM10 by rat AM in vitro (p<0.01 vs control).Conclusions Phagocytosis of inhaled carbonaceous PM by AMs is impaired in severe asthma. PGE2 may contribute to impaired AM phagocytic function in severe asthma.
Janssen NAH, Yang A, Strak M, et al., 2014, Oxidative potential of particulate matter collected at sites with different source characteristics, SCIENCE OF THE TOTAL ENVIRONMENT, Vol: 472, Pages: 572-581, ISSN: 0048-9697
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- Citations: 201
Matthews NC, Faith A, Pfeffer P, et al., 2014, Urban Particulate Matter Suppresses Priming of T Helper Type 1 Cells by Granulocyte/Macrophage Colony–Stimulating Factor–Activated Human Dendritic Cells, American Journal of Respiratory Cell and Molecular Biology, Vol: 50, Pages: 281-291, ISSN: 1044-1549
Pfeffer PE, Lu H, Kelly FJ, et al., 2014, Vitamin D Enhances Expression Of Antioxidant G6pd By Bronchial Epithelial Cells And Reduces Their Production Of Pro-Inflammatory Il-6 Upon Stimulation By Ambient Particulate Matter, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
Patelarou E, Kelly FJ, 2014, Indoor exposure and adverse birth outcomes related to fetal growth, miscarriage and prematurity-a systematic review, Int J Environ Res Public Health, Vol: 11, Pages: 5904-5933, ISSN: 1660-4601
The purpose of this review was to summarize existing epidemiological evidence of the association between quantitative estimates of indoor air pollution and all-day personal exposure with adverse birth outcomes including fetal growth, prematurity and miscarriage. We carried out a systematic literature search of MEDLINE and EMBASE databases with the aim of summarizing and evaluating the results of peer-reviewed epidemiological studies undertaken in ""westernized"" countries that have assessed indoor air pollution and all-day personal exposure with specific quantitative methods. This comprehensive literature search identified 16 independent studies which were deemed relevant for further review and two additional studies were added through searching the reference lists of all included studies. Two reviewers independently and critically appraised all eligible articles using the Critical Appraisal Skills Programme (CASP) tool. Of the 18 selected studies, 14 adopted a prospective cohort design, three were case-controls and one was a retrospective cohort study. In terms of pollutants of interest, seven studies assessed exposure to electro-magnetic fields, four studies assessed exposure to polycyclic aromatic hydrocarbons, four studies assessed PM2.5 exposure and three studies assessed benzene, phthalates and noise exposure respectively. Furthermore, 12 studies examined infant growth as the main birth outcome of interest, six examined spontaneous abortion and three studies assessed gestational age at birth and preterm delivery. This survey demonstrates that there is insufficient research on the possible association of indoor exposure and early life effects and that further research is needed.
Steenhof M, Janssen NA, Strak M, et al., 2014, Air pollution exposure affects circulating white blood cell counts in healthy subjects: the role of particle composition, oxidative potential and gaseous pollutants - the RAPTES project, Inhal Toxicol, Vol: 26, Pages: 141-165, ISSN: 1091-7691
Studies have linked air pollution exposure to cardiovascular health effects, but it is not clear which components drive these effects. We examined the associations between air pollution exposure and circulating white blood cell (WBC) counts in humans. To investigate independent contributions of particulate matter (PM) characteristics, we exposed 31 healthy volunteers at five locations with high contrast and reduced correlations amongst pollutant components: two traffic sites, an underground train station, a farm and an urban background site. Each volunteer visited at least three sites and was exposed for 5 h with intermittent exercise. Exposure measurements on-site included PM mass and number concentration, oxidative potential (OP), elemental- and organic carbon, metals, O3 and NO2. Total and differential WBC counts were performed on blood collected before and 2 and 18 h post-exposure (PE). Changes in total WBC counts (2 and 18 h PE), number of neutrophils (2 h PE) and monocytes (18 h PE) were positively associated with PM characteristics that were high at the underground site. These time-dependent changes reflect an inflammatory response, but the characteristic driving this effect could not be isolated. Negative associations were observed for NO2 with lymphocytes and eosinophils. These associations were robust and did not change after adjustment for a large suite of PM characteristics, suggesting an independent effect of NO2. We conclude that short-term air pollution exposure at real-world locations can induce changes in WBC counts in healthy subjects. Future studies should indicate if air pollution exposure-induced changes in blood cell counts results in adverse cardiovascular effects in susceptible individuals.
Sinharay R, Barratt B, Meesang W, et al., 2014, Ambient Exposure To Diesel Traffic Particles And Cardio-Respiratory Outcomes In Healthy And In COPD Subjects: 'oxford Street 2', AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 189, ISSN: 1073-449X
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- Citations: 2
Polak N, Read DS, Jurkschat K, et al., 2014, Metalloproteins and phytochelatin synthase may confer protection against zinc oxide nanoparticle induced toxicity in Caenorhabditis elegans, Comp Biochem Physiol C Toxicol Pharmacol, Vol: 160, Pages: 75-85, ISSN: 1532-0456
Zinc oxide nanoparticles (ZnONPs) are used in large quantities by the cosmetic, food and textile industries. Here we exposed Caenorhabditis elegans wild-type and a metal sensitive triple knockout mutant (mtl-1;mtl-2;pcs-1) to ZnONPs (0-50mg/L) to study strain and exposure specific effects on transcription, reactive oxygen species generation, the biomolecular phenotype (measured by Raman microspectroscopy) and key endpoints of the nematode life cycle (growth, reproduction and lifespan). A significant dissolution effect was observed, where dissolved ZnO constituted over 50% of total Zn within a two day exposure to the test medium, suggesting that the nominal exposure to pure ZnONPs represents in vivo, at best, a mixture exposure of ionic zinc and nanoparticles. Nevertheless, the analyses provided evidence that the metallothioneins (mtl-1 and mtl-2), the phytochelatin synthase (pcs-1) and an apoptotic marker (cep-1) were transcriptionally activated. In addition, the DCFH-DA assay provided in vitro evidence of the oxidative potential of ZnONPs in the metal exposure sensitive triple mutant. Raman spectroscopy highlighted that the biomolecular phenotype changes significantly in the mtl-1;mtl-2;pcs-1 triple knockout worm upon ZnONP exposure, suggesting that these metalloproteins are instrumental in the protection against cytotoxic damage. Finally, ZnONP exposure was shown to decrease growth and development, reproductive capacity and lifespan, effects which were amplified in the triple knockout. By combining diverse toxicological strategies, we identified that individuals (genotypes) housing mutations in key metalloproteins and phytochelatin synthase are more susceptible to ZnONP exposure, which underlines their importance to minimize ZnONP induced toxicity.
Kuhlbusch T, Quincey P, Fuller G, et al., 2014, The Future of European Urban Air Quality Monitoring, ATMOSPHERIC ENVIRONMENT, Vol: 87, Pages: 258-260, ISSN: 1352-2310
Williams ML, Atkinson RW, Anderson HR, et al., 2014, Associations between daily mortality in London and combined oxidant capacity, ozone and nitrogen dioxide, Air quality atmosphere and health, Vol: 7, Pages: 407-414, ISSN: 1873-9318
Both nitrogen dioxide (NO2) and ozone (O3) are powerful oxidants in ambient air that are intimately linked through atmospheric chemistry and which continuously interchange over very short timescales. Based upon atmospheric chemistry alone, there is a strong, a priori, reason for considering O3 and NO2 together in epidemiological studies, rather than either of the two pollutants separately in single-pollutant models. This paper compares two approaches to this, using Ox, defined as O3 + NO2, as a single metric and also using O3 and NO2 together in two-pollutant models. We hypothesised that the magnitude of the association between Ox and daily mortality would be greater than for NO2 and O3 individually. Using collocated hourly measurements for O3 and NO2 in London, from 2000 to 2005, we carried out a time series analysis of daily mortality. We investigated O3, NO2 and Ox individually in single-pollutant Poisson regression models and NO2 and O3 jointly in two-pollutant models in both all-year and season-specific analyses. We observed larger associations for mean 24-h concentrations of Ox (1.30 % increase in mortality per 10 ppb) than for O3 (0.87 %) and NO2 (0 %) individually. However, when analysed jointly in two-pollutant models, associations for O3 (1.54 %) and NO2 (1.07 %) were comparable to the Ox association. Season-specific analyses broadly followed this pattern irrespective of whether the Ox concentrations were driven by O3 production (summer) or depletion (winter). This novel approach in air pollution epidemiology captures the simultaneous impact of both oxidants whilst avoiding many of the statistical issues associated with two-pollutant models and potentially simplifies health impact calculations.
Bosson JA, Blomberg A, Stenfors N, et al., 2013, Peripheral Blood Neutrophilia as a Biomarker of Ozone-Induced Pulmonary Inflammation, PLoS ONE, Vol: 8, Pages: e81816-e81816
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