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In the frame of the OFFICAIR project, office buildings were investigated across Europe to assess how the office workers are exposed to different particulate matter (PM) characteristics (i.e. PM2.5 mass concentration, particulate oxidative potential (OP) based on ascorbate and reduced glutathione depletion, trace element concentration and total particle number concentration (PNC)) within the buildings. Two offices per building were investigated during the working hours (5 consecutive days; 8 h per day) in two campaigns. Differences were observed for all parameters across the office buildings. Our results indicate that the monitoring of the PM2.5 mass concentration in different offices within a building might not reflect the spatial variation of the health relevant PM characteristics such as particulate OP or the concentration of certain trace elements (e.g., Cu, Fe), since larger differences were apparent within a building for these parameters compared to that obtained for the PM2.5 mass concentration in many cases. The temporal variation was larger for almost all PM characteristics (except for the concentration of Mn) than the spatial differences within the office buildings. These findings indicate that repeated or long-term monitoring campaigns are necessary to have information about the temporal variation of the PM characteristics. However, spatial variation in exposure levels within an office building may cause substantial differences in total exposure in the long term. We did not find strong associations between the investigated indoor activities such as printing or windows opening and the PNC values. This might be caused by the large number of factors affecting PNC indoors and outdoors. © 2017 Elsevier B.V.

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/m 3, 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. © 2016 Macmillan Publishers Limited.

Background: Particulate matter (PM) from traffic and other sources has been associated with adverse health effects. One unifying theory is that PM, whatever its source, acts on the human body via its capacity to cause damaging oxidation reactions related to its content of pro-oxidants components. Few epidemiological studies have investigated particle oxidative potential (OP) and health. We conducted a time series analysis to assess associations between daily particle OP measures and numbers of deaths and hospital admissions for cardiovascular and respiratory diseases. Methods: During 2011 and 2012 particles with an aerodynamic diameter less than 2.5 and 10 μm (PM2.5 and PM10 respectively) were collected daily on Partisol filters located at an urban background monitoring station in Central London. Particulate OP was assessed based on the capacity of the particles to oxidize ascorbate (OPAA) and glutathione (OPGSH) from a simple chemical model reflecting the antioxidant composition of human respiratory tract lining fluid. Particulate OP, expressed as % loss of antioxidant per μg of PM, was then multiplied by the daily concentrations of PM to derive the daily OP of PM mass concentrations (% loss per m3). Daily numbers of deaths and age- and cause-specific hospital admissions in London were obtained from national registries. Poisson regression accounting for seasonality and meteorology was used to estimate the percentage change in risk of death or admission associated with an interquartile increment in particle OP. Results: We found little evidence for adverse associations between OPAA and OPGSH and mortality. Associations with cardiovascular admissions were generally positive in younger adults and negative in older adults with confidence intervals including 0%. For respiratory admissions there was a trend, from positive to negative associations, with increasing age although confidence intervals generally included 0%. Conclusions: Our study, the first to analyse daily particle OP measures and mortality and admissions in a large population over two years, found little evidence to support the hypothesis that short-term exposure to particle OP is associated with adverse health effects. Further studies with improved exposure assessment and longer time series are required to confirm or reject the role of particle OP in triggering exacerbations of disease. © 2016 The Authors

The adverse effect of short-term exposure to traffic-related pollution on cardiovascular and respiratory health was investigated. For each day for 2011-2012 in London, UK, > 100 air pollutant metrics were assembled using monitors, modeling, and chemical analyses. A priori metrics indicative of traffic sources, e.g., general traffic, petrol exhaust, diesel exhaust, and non-exhaust was considered. For single day exposure, onsistent associations between adult (15-64 yr) cardiovascular and pediatric (0-14 yr) respiratory admissions with elemental and black carbon (EC/BC), ranging from 0.56% to 1.65% increase per IQR change, and to a lesser degree with CO and Al was observed. The average of past 7 days EC/BC exposure was associated with elderly (65+ yr) cardiovascular admissions. Indicated associations were higher during the warm period of the year. These results suggest that exhaust related pollutants are linked with increased numbers of adult cardiovascular and pediatric respiratory hospitalizations.

Background There is ample evidence of adverse associations between short-term exposure to ambient particle mass concentrations and health but little is known about the relative contribution from various sources. Methods We used air particle composition and number networks in London between 2011 and 2012 to derive six source-related factors for PM10 and four factors for size distributions of ultrafine particles (NSD). We assessed the associations of these factors, at pre-specified lags, with daily total, cardiovascular (CVD) and respiratory mortality and hospitalizations using Poisson regression. Relative risks and 95% confidence intervals (CI) were expressed as percentage change per interquartile range increment in source-factor mass or number concentration. We evaluated the sensitivity of associations to adjustment for multiple other factors and by season. Results We found no evidence of associations between PM10 or NSD source-related factors and daily mortality, as the direction of the estimates were variable with 95% CI spanning 0%. Traffic-related PM10 and NSD displayed consistent associations with CVD admissions aged 15–64 years (1.01% (95%CI: 0.03%, 2.00%) and 1.04% (95%CI: − 0.62%, 2.72%) respectively) as did particles from background urban sources (0.36% for PM10 and 0.81% for NSD). Most sources were positively associated with pediatric (0–14 years) respiratory hospitalizations, with stronger evidence for fuel oil PM10 (3.43%, 95%CI: 1.26%, 5.65%). Our results did not suggest associations with cardiovascular admissions in 65 + or respiratory admissions in 15 + age groups. Effect estimates were generally robust to adjustment for other factors and by season. Conclusions Our findings are broadly consistent with the growing evidence of the toxicity of traffic and combustion particles, particularly in relation to respiratory morbidity in children and cardiovascular morbidity in younger adults. © 2016 The Authors

The six week eruption of Eyjafjallajokull volcano in 2010 produced heavy ash fall in a sparsely populated area of southern and south eastern Iceland and disrupted European commercial flights for at least 6 days. We adopted a protocol for the rapid analysis of volcanic ash particles, for the purpose of informing respiratory health risk assessments. Ash collected from deposits underwent a multi-laboratory physicochemical and toxicological investigation of their mineralogical parameters associated with bio-reactivity, and selected in vitro toxicology assays related to pulmonary inflammatory responses. Ash from the eruption of Grimsvotn, Iceland, in 2011 was also studied. The results were benchmarked against ash from Soufriere Hills volcano, Montserrat, which has been extensively studied since the onset of eruptive activity in 1995. For Eyjafjallajokull, the grain size distributions were variable: 2–13 vol% of the bulk samples were

Background: Proximity to traffic-related pollution has been associated with poor respiratory health in adults and children. Objectives: We wished to test the hypothesis that particulate matter (PM) from high-traffic sites would display an enhanced capacity to elicit inflammation. Methods: We examined the inflammatory potential of coarse [2.5–10 μm in aerodynamic diameter (PM2.5–10)] and fine [0.1–2.5 μm in aerodynamic diameter (PM0.1–2.5)] PM collected from nine sites throughout Europe with contrasting traffic contributions. We incubated murine monocytic-macrophagic RAW264.7 cells with PM samples from these sites (20 or 60 μg/cm2) and quantified their capacity to stimulate the release of arachidonic acid (AA) or the production of interleukin-6 and tumor necrosis factor-α (TNFα) as measures of their inflammatory potential. Responses were then related to PM composition: metals, hydrocarbons, anions/cations, and endotoxin content. Results: Inflammatory responses to ambient PM varied markedly on an equal mass basis, with PM2.5–10 displaying the largest signals and contrasts among sites. Notably, we found no evidence of enhanced inflammatory potential at high-traffic sites and observed some of the largest responses at sites distant from traffic. Correlation analyses indicated that much of the sample-to-sample contrast in the proinflammatory response was related to the content of endotoxin and transition metals (especially iron and copper) in PM2.5–10. Use of the metal chelator diethylene triamine pentaacetic acid inhibited AA release, whereas recombinant endotoxin-neutralizing protein partially inhibited TNFα production, demonstrating that different PM components triggered inflammatory responses through separate pathways. Conclusions: We found no evidence that PM collected from sites in close proximity to traffic sources displayed enhanced proinflammatory activity in RAW264.7 cells. Key words: copper, endotoxin, inflammation, iron, macrophages, metals, particulate matter, polyaromatic hydrocarbons. Environ Health Perspect 118:1728–1734 (2010). doi:10.1289/ehp.1002105 [Online 27 July 2010]

PubMedID: 16036329 The hypothesis was tested that Werner syndrome (WS) phenotype might be associated with an in vivo prooxidant state. A set of redox-related endpoints were measured in three WS patients, two of their parents, and 99 controls within a study of some cancer-prone and/or ageing-related genetic disorders. The following analytes were measured: (a) leukocyte 8-hydroxy-2'-deoxyguanosine; (b) glutathione from whole blood, and (c) plasma levels of glyoxal, methylglyoxal, 8-isoprostane, and some plasma antioxidants (uric acid, ascorbic acid, ?- and ?-tocopherol). Leukocyte 8-hydroxy-2'-deoxyguanosine levels showed a significant increase in the 3 WS patients vs. 85 controls (p < 10-7). The disulfide glutathione:glutahione ratio was significantly altered in WS patients (p = 0.005). Glyoxal and methylglyoxal levels were significantly increased (p = 0.018 and p = 0.007, respectively). The plasma levels of uric acid (p = 0.002) and ascorbic acid (p = 0.003) were also increased significantly in WS patients and in their parents. No significant alterations were found in the plasma levels of ?- and ?-tocopherol, nor of 8-isoprostane. This is the first report of in vivo alterations of oxidative stress parameters in WS patients. Further investigations on more extensive study populations are warranted to verify the relevance of an in vivo prooxidant state in WS patients. © 2005 Taylor & Francis Group Ltd. Universitat de València National Cancer Institute 1Italian National Cancer Institute, I-80131 Naples, Italy, 2Department of Genetics, “Elena d’Aosta” Hospital, I-80136 Naples, Italy, 3Italian National Cancer Institute, IST I-16132 Genoa, Italy, 4Department of Organic Chemistry and Biochemistry, “Federico II” Naples University, I-80126 Naples, Italy, 5Division of Life Sciences, King’s College, London SE1 9NN, UK, 6Department of Physiology, University of Valencia, E-46010 Valencia, Spain, 7Department of Pediatrics, C¸ ukurova University, TK-01330 Adana, Turkey, 8Department of Metabolism and Pathologic Biochemistry, Istituto Superiore di Sanità, I-00161 Rome, Italy, and 9International Atomic Energy Agency-MEL, MC-98000 Principality of Monaco

Item does not contain fulltext In recent years, there has been increasing interest in noninvasive monitoring of airway inflammation and oxidative stress. Several volatile and nonvolatile substances can be measured in exhaled breath and have been suggested as potential biomarkers of these events. Exhaled gases, including carbon monoxide (CO), alkanes (ethane, pentane), and substances measured in breath condensate, such as hydrogen peroxide (H2O2) and isoprostanes were all suggested as potential markers of oxidative stress in the lung. A European Respiratory Society (ERS) International Research Seminar entitled "Haemoxygenase-1 induction and exhaled markers of oxidative stress in lung diseases" was organized by the Airway Regulation and Provocation Group of the Clinical Allergy and Immunology Assembly in Budapest, Hungary in September, 1999 to integrate the latest knowledge on these issues and accelerate further improvement in this area. During this 2-day event several issues were raised about: the use and standardization of measurements in exhaled breath; problems of measuring expired H2O2 and other mediators in breath condensate; role and regulation of haemoxygenase (HO)-1 in the lung; and conditions and factors influencing exhaled CO. This report is a summary of the main presentations at the seminar, together with the current areas of research in this rapidly expanding field.