Synthetic Respiratory Tract Lining Fluid Research Articles

Assessment of the Oxidative Potential and Oxidative Burden from Occupational Exposures to Particulate Matter.

Oxidative potential (OP) is a toxicologically relevant metric that integrates features like mass concentration and chemical composition of particulate matter (PM). Although it has been extensively explored as a metric for the characterization of environmental particles, this is still an underexplored application in the occupational field. This study aimed to estimate the OP of particles in two occupational settings from a construction trades school. This characterization also includes the comparison between activities, sampling strategies, and size fractions. Particulate mass concentrations (PM4-Personal, PM4-Area, and PM2.5-Area) and number concentrations were measured during three weeks of welding and construction/bricklaying activities. The OP was assessed by the ascorbate assay (OPAA) using a synthetic respiratory tract lining fluid (RTLF), while the oxidative burden (OBAA) was determined by multiplying the OPAA values with PM concentrations. Median (25th-75th percentiles) of PM mass and number concentrations were 900 (672-1730) µg m-3 and 128 000 (78 000-169 000) particles cm-3 for welding, and 432 (345-530) µg m-3 and 2800 (1700-4400) particles cm-3 for construction. Welding particles, especially from the first week of activities, were also associated with higher redox activity (OPAA: 3.3 (2.3-4.6) ρmol min-1 µg-1; OBAA: 1750 (893-4560) ρmol min-1 m-3) compared to the construction site (OPAA: 1.4 (1.0-1.8) ρmol min-1 µg-1; OBAA: 486 (341-695) ρmol min-1 m-3). The OPAA was independent of the sampling strategy or size fraction. However, driven by the higher PM concentrations, the OBAA from personal samples was higher compared to area samples in the welding shop, suggesting an influence of the sampling strategy on PM concentrations and OBAA. These results demonstrate that important levels of OPAA can be found in occupational settings, especially during welding activities. Furthermore, the OBAA found in both workplaces largely exceeded the levels found in environmental studies. Therefore, measures of OP and OB could be further explored as metrics for exposure assessment to occupational PM, as well as for associations with cardiorespiratory outcomes in future occupational epidemiological studies.

Spatial variations in PM2.5 oxidative potential in Toronto and Montreal, Canada

BACKGROUND AND AIM: Particulate matter air pollution is a recognized threat to human health. Recently, measures of particulate air pollution have been developed that incorporate information on the effects that particles may have inside the human respiratory tract. Among these is particle oxidative potential (OP), which is a measure of the ability of PM to cause oxidative reactions. OP can be quantified using assays that measure the ability of PM to deplete antioxidants in a synthetic respiratory tract lining fluid model. An alternative approach considers the ability of particles to generate reactive oxygen species (ROS) in the respiratory tract, as estimated using a mathematical model and concentrations of transition metals. The aim of our study was to develop land-use regression models to characterize the spatial distribution of ROS-generating capacity of PM2.5 and two measures of OP. METHODS: We conducted large-scale spatial monitoring campaigns across Montreal and Toronto, Canada and developed land use regression models to predict the spatial distribution of ROS-generating capacity of PM2.5 and the ability of PM2.5 extracts to deplete the antioxidants ascorbate (OPAA) and glutathione (OPGSH). RESULTS:In Montreal, the best models explained 54% of variation in ROS, 45% in OPAA and 31% in OPGSH. In Toronto, models explained 63% of variation in ROS, 77% in OPAA, and 44% in OPGSH. Variables that were identified as predictors across multiple models included distance to PM2.5 and NOX emitting facilities, total traffic counts, and distance to highways. CONCLUSIONS:These results contribute to existing knowledge of within-city spatial variations in particle oxidative potential using an unprecedented number of sensors. Exposure surfaces generated by these models can be applied in future studies of the health impact of PM2.5. Future work could clarify the sources of the most harmful components of PM2.5 to human health to aid in targeted reductions of emissions. KEYWORDS: particulate matter, oxidative potential, land use regression

Physico-chemical properties and reactive oxygen species generation by respirable coal dust: Implication for human health risk assessment

This study investigates the mineralogy, micro-morphology, chemical characteristics and oxidation toxicity of respirable dusts generated in underground coal mines. The active sampling was applied to collect airborne particulates with aerodynamic diameter <4 µm (PM4) at depth greater than 500 m from earth surface. The average mass concentration of PM4 was extremely higher than recommended values. QXRD and FESEM-EDS analyses were applied to study the micro-mineralogy and micro-morphology of respirable dusts. The chemical analysis by ICP-MS revealed an enrichment of V, Cr, Cu, Zn, As, Ag, Cd and Sb in respirable dust compared with the background environment and world coals. The EPA’s health risk model showed that the health risk posed by Cr and Co in all workplaces exceeded the acceptable risk value for human health. The synthetic respiratory tract lining fluid (RTLF) model was utilized to achieve a novel insight into the toxicity of respirable coal dust. The result showed an overall depletion of lung surface antioxidants with the decreasing trend of ascorbic acid > reduced glutathione >> urate, implying low- to medium level of oxidative stress. The result of this study can be applied globally by decision-makers to decrease hazardous exposure of mine workers to respirable dust.

Characterization and comparison of PM&amp;lt;sub&amp;gt;2.5&amp;lt;/sub&amp;gt; oxidative potential assessed by two acellular assays

Abstract. The capability of ambient particles to generate in vivo reactive oxygen species (ROS), called oxidative potential (OP), is a potential metric for evaluating the health effects of particulate matter (PM) and is supported by several recent epidemiological investigations. Studies using various types of OP assays differ in their sensitivities to varying PM chemical components. In this study, we systematically compared two health-relevant acellular OP assays that track the depletion of antioxidants or reductant surrogates: (i) the synthetic respiratory-tract lining fluid (RTLF) assay that tracks the depletion of ascorbic acid (AA) and glutathione (GSH) and (ii) the dithiothreitol (DTT) assay that tracks the depletion of DTT. Yearlong daily samples were collected at an urban site in Atlanta, GA (Jefferson Street), during 2017, and both DTT and RTLF assays were performed to measure the OP of water-soluble PM2.5 components. PM2.5 mass and major chemical components, including metals, ions, and organic and elemental carbon were also analyzed. Correlation analysis found that OP as measured by the DTT and AA depletion (OPDTT and OPAA, respectively) were correlated with both organics and some water-soluble metal species, whereas that from the GSH depletion (OPGSH) was exclusively sensitive to water-soluble Cu. These OP assays were moderately correlated with each other due to the common contribution from metal ions. OPDTT and OPAA were moderately correlated with PM2.5 mass with Pearson's r=0.55 and 0.56, respectively, whereas OPGSH exhibited a lower correlation (r=0.24). There was little seasonal variation in the OP levels for all assays due to the weak seasonality of OP-associated species. Multivariate linear regression models were developed to predict OP measures from the particle composition data. Variability in OPDTT and OPAA were not only attributed to the concentrations of metal ions (mainly Fe and Cu) and organic compounds but also to antagonistic metal–organic and metal–metal interactions. OPGSH was sensitive to the change in water-soluble Cu and brown carbon (BrC), a proxy for ambient humic-like substances.

Assessment of Particle Oxidative Potential as an Air Pollution Exposure Metric: A Systematic Review

Ambient particulate air pollution is linked to numerous acute and chronic health outcomes. The standard approach to measuring particulate exposure has been to estimate particle mass concentration. New measures account for oxidative potential, the ability of particles to cause oxidative stress in the body. There has been no systematic comparison of particulate air pollution exposure assessment methods between those that incorporate oxidative potential and those that do not. The aim of this review is to determine if associations between particulate air pollution exposure and health outcomes are stronger when oxidative potential is used as the exposure metric, in comparison to particle mass concentration. The databases Medline and Embase were searched from inception to 28 March 2018 for studies that reported an association between particulate air pollution exposure and a health outcome in a human population, and in which exposure was measured by both particle mass concentration and oxidative potential. Study quality was assessed using a US National Toxicology Program instrument. We identified 18 publications meeting the selection criteria. The most common oxidative potential assay was antioxidant depletion in synthetic respiratory tract lining fluid, used in 12 articles. The rate of consumption of dithiothreitol was also frequently used as an oxidative potential assay and appeared in 5 studies. The dithiothreitol assay most consistently produced stronger effect estimates, as 10/14 endpoints showed higher point estimates of associations compared to particle mass concentration estimates. Other assays showed mixed results. To date there is no consistent evidence that oxidative potential is more strongly associated with health outcomes than particle mass concentrations; however, these assays do have the advantage of not treating all particles as equally harmful and further work should explore which specific assays are most relevant to evaluating air pollution health risks.

Fine Particulate Matter and Emergency Room Visits for Respiratory Illness. Effect Modification by Oxidative Potential.

Fine particulate air pollution (PM2.5; particulate matter 2.5 μm or less in diameter) is thought to contribute to acute respiratory morbidity in part through oxidative stress. To examine the association between PM2.5 oxidative burden and emergency room visits for respiratory illnesses. We conducted a case-crossover study in Ontario, Canada between 2004 and 2011, including 127,836 cases of asthma, 298,751 cases of chronic obstructive pulmonary disease, and more than 1.1 million cases of all respiratory illnesses. Daily air pollution data were collected from ground monitors, and city-level PM2.5 oxidative potential was measured on the basis of a synthetic respiratory tract lining fluid containing the antioxidants glutathione and ascorbate. Conditional logistic regression was used to estimate associations between air pollution concentrations and emergency room visits, adjusting for time-varying covariates. Three-day mean PM2.5 concentrations were consistently associated with emergency room visits for all respiratory illnesses. Among children (<9 yr), each interquartile change (5.92 μg/m(3)) in 3-day mean PM2.5 was associated with a 7.2% (95% confidence interval, 4.2-10) increased risk of emergency room visits for asthma. Glutathione-related oxidative potential modified the impact of PM2.5 on emergency room visits for respiratory illnesses (P = 0.001) but only at low concentrations (≤10 μg/m(3)). Between-city differences in ascorbate-related oxidative potential did not modify the impact of PM2.5 on respiratory outcomes. Between-city differences in glutathione-related oxidative potential may modify the impact of PM2.5 on acute respiratory illnesses at low PM2.5 concentrations. This may explain in part how small changes in ambient PM2.5 mass concentrations can contribute to acute respiratory morbidity in low-pollution environments.

Ambient PM2.5 and Risk of Emergency Room Visits for Myocardial Infarction: Impact of Regional PM2.5 Oxidative Potential: A Case-Crossover Study

Regional differences in the oxidative potential of fine particulate air pollution (PM2.5) may modify its impact on the risk of myocardial infarction. A case-crossover study was conducted in 16 cities in Ontario, Canada to evaluate the impact of regional PM2.5 oxidative potential on the relationship between PM2.5 and emergency room visits for myocardial infarction. Daily air pollution and meteorological data were collected between 2004 and 2011 from provincial monitoring sites and regional estimates of glutathione (OPGSH) and ascorbate-related (OPAA) oxidative potential were determined using an acellular assay based on a synthetic respiratory tract lining fluid. Exposure variables for the combined oxidant capacity of NO2 and O3 were also examined using their sum (Ox) and a weighted average (Ox wt) based on their redox potentials. In total, 30,101 cases of myocardial infarction were included in the analysis. For regions above the 90th percentile of OPGSH each 5 μg/m3 increase in same-day PM2.5 was associated with a 7.9 % (95 % CI: 4.1, 12) increased risk of myocardial infarction whereas a 4.1 % (95 % CI: 0.26, 8.0) increase was observed in regions above the 75th percentile and no association was observed below the 50th percentile (p-interaction = 0.026). A significant 3-way interaction was detected with the strongest associations between PM2.5 and myocardial infarction occurring in areas with high regional OPGSH and high Ox wt (p-interaction < 0.001). Regional PM2.5 oxidative potential may modify the impact of PM2.5 on the risk of myocardial infarction. The combined oxidant capacity of NO2 and O3 may magnify this effect.

Fine particulate air pollution and adverse birth outcomes: Effect modification by oxidative potential

Introduction: Oxidative stress has been identified as one of the toxic effects of fine particulate air pollution (PM2.5) that is most relevant for adverse birth outcomes. The aim of this study was to evaluate the association between PM2.5 oxidative burden and adverse birth outcomes. Methods: Data on 191,539 singleton births that occurred in the province of Ontario, Canada from 2003 to 2011 were obtained from a birth registry. Daily air pollution data were collected from ground monitors and regional PM2.5 oxidative potential was measured using a synthetic respiratory tract lining fluid containing the anti-oxidants glutathione and ascorbate. We used logistic regression models to examine the associations between air pollution concentrations and preterm birth (gestational age &lt; 37 weeks) birth weight, term low birth weight (&lt;2500 g) and small for gestational age (SGA, &lt;10th percentile of birth weight for gestational age) adjusting for individual covariates and neighbourhood socioeconomic status (SES). Results: We observed that a 10 μg/m3 increase in PM2.5 over the entire pregnancy was associated with term low birth weight (OR = 1.22, 95% CI 1.02, 1.47) and SGA (OR = 1.04, 95% CI 1.01, 1.07). Regional differences in ascorbate-related oxidative potential modified the impact of PM2.5 on term low birth weight (p for interaction = 0.02). Glutathione-related oxidative potential did not modify the impact of PM2.5 on birth outcomes. Conclusions: Ascorbate-related oxidative potential may modify the impact of PM2.5 on term low birth weight. These findings may have implications in assessing regional differences in PM2.5 related health impacts.

Oxidative potential and chemical composition of PM2.5 in office buildings across Europe – The OFFICAIR study

In the frame of the OFFICAIR project, indoor and outdoor PM2.5 samples were collected in office buildings across Europe in two sampling campaigns (summer and winter). The ability of the particles to deplete physiologically relevant antioxidants (ascorbic acid (AA), reduced glutathione (GSH)) in a synthetic respiratory tract lining fluid, i.e., oxidative potential (OP), was assessed. Furthermore, the link between particulate OP and the concentration of the PM constituents was investigated.The mean indoor PM2.5 mass concentration values were substantially lower than the related outdoor values with a mean indoor/outdoor PM2.5 mass concentration ratio of 0.62 and 0.61 for the summer and winter campaigns respectively. The OP of PM2.5 varied markedly across Europe with the highest outdoor OPAA m−3 and OPGSH m−3 (% antioxidant depletion/m3 air) values obtained for Hungary, while PM2.5 collected in Finland exhibited the lowest values. Seasonal variation could be observed for both indoor and outdoor OPAA m−3 and OPGSH m−3 with higher mean values during winter. The indoor/outdoor OPAA m−3 and OPGSH m−3 ratios were less than one with 4 and 17 exceptions out of the 40 cases respectively. These results indicate that indoor air is generally less oxidatively challenging than outdoors. Correlation analysis revealed that trace elements play an important role in determining OP, in particular, the Cu content. Indoor air chemistry might affect OP since weaker correlations were obtained for indoor PM2.5. Our findings also suggest that office workers may be exposed to health relevant PM constituents to a different extent within the same building.

Ambient PM2.5 and risk of emergency room visits for myocardial infarction: impact of regional PM2.5 oxidative potential: a case-crossover study.

BackgroundRegional differences in the oxidative potential of fine particulate air pollution (PM2.5) may modify its impact on the risk of myocardial infarction.MethodsA case-crossover study was conducted in 16 cities in Ontario, Canada to evaluate the impact of regional PM2.5 oxidative potential on the relationship between PM2.5 and emergency room visits for myocardial infarction. Daily air pollution and meteorological data were collected between 2004 and 2011 from provincial monitoring sites and regional estimates of glutathione (OPGSH) and ascorbate-related (OPAA) oxidative potential were determined using an acellular assay based on a synthetic respiratory tract lining fluid. Exposure variables for the combined oxidant capacity of NO2 and O3 were also examined using their sum (Ox) and a weighted average (Oxwt) based on their redox potentials.ResultsIn total, 30,101 cases of myocardial infarction were included in the analysis. For regions above the 90th percentile of OPGSH each 5 μg/m3 increase in same-day PM2.5 was associated with a 7.9 % (95 % CI: 4.1, 12) increased risk of myocardial infarction whereas a 4.1 % (95 % CI: 0.26, 8.0) increase was observed in regions above the 75th percentile and no association was observed below the 50th percentile (p-interaction = 0.026). A significant 3-way interaction was detected with the strongest associations between PM2.5 and myocardial infarction occurring in areas with high regional OPGSH and high Oxwt (p-interaction < 0.001).ConclusionsRegional PM2.5 oxidative potential may modify the impact of PM2.5 on the risk of myocardial infarction. The combined oxidant capacity of NO2 and O3 may magnify this effect.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-016-0129-9) contains supplementary material, which is available to authorized users.

Oxidative burden of fine particulate air pollution and risk of cause-specific mortality in the Canadian Census Health and Environment Cohort (CanCHEC)

BackroundFine particulate air pollution (PM2.5) is known to contribute to cardiorespiratory mortality but it is not clear how PM2.5 oxidative burden (i.e. the ability of PM2.5 to cause oxidative stress) may influence long-term mortality risk. MethodsWe examined the relationship between PM2.5 oxidative burden and cause-specific mortality in Ontario, Canada. Integrated PM2.5 samples were collected from 30 provincial monitoring sites between 2012 and 2013. The oxidative potential (% depletion/µg) of regional PM2.5 was measured as the ability of filter extracts to deplete antioxidants (glutathione and ascorbate) in a synthetic respiratory tract lining fluid. PM2.5oxidative burden was calculated as the product of PM2.5 mass concentrations and regional estimates of oxidative potential. In total, this study included 193,300 people who completed the Canadian long-form census in 1991 and who lived within 5km of a site where oxidative potential was measured. Deaths occurring between 1991 and 2009 were identified through record linkages and Cox proportional hazard models were used to estimate hazard ratios (and 95% confidence intervals) for interquartile changes in exposure adjusting for individual-level covariates and indirect-adjustment for smoking and obesity. ResultsGlutathione-related oxidative burden was associated with cause-specific mortality. For lung cancer specifically, this metric was associated with a 12% (95% CI: 5.0–19) increased risk of mortality whereas a 5.0% (95% CI: 0.1, 10) increase was observed for PM2.5. Indirect adjustment for smoking and obesity decreased the lung cancer hazard ratio for glutathione-related oxidative burden but it remained significantly elevated (HR=1.07, 95% CI: 1.005, 1.146). Ascorbate-related oxidative burden was not associated with mortality. ConclusionsOur findings suggest that glutathione-related oxidative burden may be more strongly associated with lung cancer mortality than PM2.5 mass concentrations.

Changes in chemical composition and oxidative potential of urban PM2.5 between 2010 and 2013 in Hungary

A comprehensive chemical characterization and oxidative potential (OP) assessment of PM2.5 was carried out at an urban site of Budapest between June 2010 and May 2013 to investigate the seasonal variability of particulate phase air pollutants and their oxidative activity. Chemical analyses included the determination of the concentration of trace elements, major water-soluble inorganic ions and carbonaceous fractions (total carbon, water-soluble organic carbon, organic carbon, elemental carbon). The OP of PM2.5 was assessed by antioxidant depletion using a synthetic respiratory tract lining fluid containing ascorbate, reduced glutathione and urate.The mean PM2.5 mass concentration (21.0μgm−3) was just below the 25μgm−3 annual mean PM2.5 limit value set by the European Commission and showed a seasonal pattern with higher levels during winter. On average, 84% of the gravimetric mass could be reconstructed by the chemical measurements. Organic matter and secondary inorganic ions were the most dominant PM2.5 constituents contributing 40 and 29% of its mass, respectively. Changes in the yearly concentrations were not identified for the investigated compounds between 2010 and 2013. Temporal differences in both ascorbate and glutathione oxidation could be observed during the 3-year long sampling period; however, no clear seasonal trend was apparent. OP metrics were associated mainly with traffic-related trace elements; however, other PM sources (i.e., long-range transport, secondary aerosol formation) could also contribute to particulate OP in Budapest. The weak correlation between OP metrics and PM2.5 mass concentration suggests the possibility of using OP as an additional metric in epidemiology.

PM10 Oxidative Properties and Asthma and COPD

To the Editor: Oxidative stress is a possible mechanism to explain the toxic effects of particulate matter (PM). Conceptually, PM oxidative burden is an appealing exposure metric because it captures a biological process thought to be responsible for PM-induced airway inflammation. However, few epidemiologic studies have examined this exposure metric, and results have been inconsistent.1 Direct measurement of PM oxidative properties could improve the ability to estimate PM effects and enhance the understanding of its mechanism of action, potentially leading to targeted public health strategies aimed at removing the most toxic PM components. We previously reported adverse effects of PM10 (mean aerodynamic diameter <10 μm) mass on asthma and chronic obstructive pulmonary disease (COPD) exacerbations, increased by low antioxidant status (vitamin C) and variation in antioxidant genes.2 Here, we investigate the effects of PM10 oxidative properties on respiratory exacerbations. We conducted a bi-directional case-crossover study in patients admitted to the hospital for asthma/COPD exacerbation, comparing PM10 oxidative potential (OP) on the admission day with that on 14 days before/after (controls). PM10 was collected using a high-volume sampler located near the hospital, and oxidative potential was measured as depletion of three antioxidants (ascorbic acid, AA; glutathione, GSH; uric acid, UA) in a synthetic respiratory tract lining fluid model. The oxidative potential effects were estimated using conditional logistic regressions for paired data, adjusting for PM10 mass, temperature, and humidity. Effect modification by vitamin C serum levels was also assessed. Details on study methods are provided in the eAppendix (https://links.lww.com/EDE/A776). The analyses included 160 exacerbations in 151 patients with data available from at least one case and one control filter. Patients’ characteristics are presented in eTable 1; https://links.lww.com/EDE/A776. With the exception of a high positive correlation between OPAA and OPGSH (r = 0.69), there was no substantial correlation between the three oxidative potential readings and PM10 mass. PM10 oxidative potentials showed no association with asthma/COPD admissions, with similarly negative results after adjustment for PM10 mass (Table) and when stratifying by vitamin C serum levels (eTable 2; https://links.lww.com/EDE/A776).TABLE: Associationa of Asthma/COPD Exacerbations with a Unit Increase in OP m−3 for Each Antioxidant (n = 160 Exacerbations; n = 156 Filters)Our findings suggest that intrinsic oxidative properties are not driving the adverse effect of PM10 effects on respiratory exacerbations.2 PM10 effects could be due instead to indirect oxidative effects mediated by host reactions through cellular activation,1,3 such as that resulting in an influx of activated inflammatory cells to the lung, which cannot be captured by our particles’ oxidative potential measurement method based on oxidation reactions in an acellular respiratory tract lining fluid model. The association between particles’ oxidative potential and respiratory outcomes was evaluated in three recent epidemiologic panel studies.4–6 Only one of these studies found a positive association of outdoor PM2.5 oxidative potential, but not mass, with airway inflammation in 45 asthmatic children.6 The other two, using a semi-experimental design in 31 volunteers exposed to various levels of ambient PM, found no association of either PM mass or oxidative potential with lung function and exhaled nitric oxide4 or acute nasal airway inflammation.5 Although 85% of the patients in our study lived around the Chelsea and Westminster Hospital where PM10 was sampled,2 the use of monitoring sites to derive individual exposure is problematic due to temporal and spatial variation in PM oxidative properties, with higher oxidative potential in proximity to traffic.7,8 PM personal-sampling methods are more accurate but are not an option in a case-crossover design. Also, we measured the oxidative potential of PM10, and smaller particles may have different oxidative properties. However, previous measurements in London showed greater oxidative potential for PM10, suggesting an enrichment of redox-active components in the coarse fraction.7 Further studies with larger sample sizes, more accurate measurements of exposure (such as personal sampling), sampling several PM fractions, and comparing assays to measure oxidative potential are needed to establish the exact mechanism of PM oxidative potential on respiratory exacerbations. Cristina Canova Department of Molecular Medicine University of Padova Padova, Italy Imperial College London, United Kingdom [email protected]; [email protected] Cosetta Minelli Imperial College London, United Kingdom Christina Dunster Frank Kelly King’s College London, United Kingdom Pallav L. Shah NHLI, Imperial College London, United Kingdom Chelsea and Westminster Hospital London, United Kingdom Cielito Caneja Chelsea and Westminster Hospital London, United Kingdom Michael K. Tumilty Peter Burney Imperial College London, United Kingdom

Oxidative potential of smoke from burning wood and mixed biomass fuels

More than half the world's population still rely on burning biomass fuels to heat and light their homes and cook food. Household air pollution, a common component of which is inhalable particulate matter (PM), emitted from biomass burning is associated with increased vulnerability to respiratory infection and an enhanced risk of developing chronic obstructive pulmonary disease. In the light of an emerging hypothesis linking chronic PM exposure during childhood and increased vulnerability to respiratory diseases in adulthood, in a chain of events involving oxidative stress, reduced immunity and subsequent infection, the aim of this study was to characterise the oxidative potential (OP) of PM collected during the burning of wood and mixed biomass, whilst cooking food in the Kathmandu Valley, Nepal. Our assessments were based on the capacity of the particles to deplete the physiologically relevant antioxidants from a validated, synthetic respiratory tract lining fluid (RTLF). Incubation of mixed biomass and wood smoke particles suspensions with the synthetic RTLF for 4 h resulted in a mean loss of ascorbate of 64.76 ± 16.83% and 83.37 ± 14.12% at 50 μg/ml, respectively. Reduced glutathione was depleted by 49.29 ± 15.22% in mixed biomass and 65.33 ± 13.01% in wood smoke particles under the same conditions. Co-incubation with the transition metal chelator diethylenetriaminepentaacetate did not inhibit the rate of ascorbate oxidation, indicating a negligible contribution by redox-active metals in these samples. The capacity of biomass smoke particles to elicit oxidative stress certainly has the potential to contribute towards negative health impacts associated with traditional domestic fuels in the developing world.

Increased oxidative burden associated with traffic component of ambient particulate matter at roadside and urban background schools sites in London.

As the incidence of respiratory and allergic symptoms has been reported to be increased in children attending schools in close proximity to busy roads, it was hypothesised that PM from roadside schools would display enhanced oxidative potential (OP). Two consecutive one-week air quality monitoring campaigns were conducted at seven school sampling sites, reflecting roadside and urban background in London. Chemical characteristics of size fractionated particulate matter (PM) samples were related to the capacity to drive biological oxidation reactions in a synthetic respiratory tract lining fluid. Contrary to hypothesised contrasts in particulate OP between school site types, no robust size-fractionated differences in OP were identified due high temporal variability in concentrations of PM components over the one-week sampling campaigns. For OP assessed both by ascorbate (OPAA m−3) and glutathione (OPGSH m−3) depletion, the highest OP per cubic metre of air was in the largest size fraction, PM1.9–10.2. However, when expressed per unit mass of particles OPAA µg−1 showed no significant dependence upon particle size, while OPGSH µg−1 had a tendency to increase with increasing particle size, paralleling increased concentrations of Fe, Ba and Cu. The two OP metrics were not significantly correlated with one another, suggesting that the glutathione and ascorbate depletion assays respond to different components of the particles. Ascorbate depletion per unit mass did not show the same dependence as for GSH and it is possible that other trace metals (Zn, Ni, V) or organic components which are enriched in the finer particle fractions, or the greater surface area of smaller particles, counter-balance the redox activity of Fe, Ba and Cu in the coarse particles. Further work with longer-term sampling and a larger suite of analytes is advised in order to better elucidate the determinants of oxidative potential, and to fuller explore the contrasts between site types.