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PM10 Oxidative Properties and Asthma and COPD

Canova, Cristina; Minelli, Cosetta; Dunster, Christina; Kelly, Frank; Shah, Pallav L.; Caneja, Cielito; Tumilty, Michael K.; Burney, Peter

doi: 10.1097/EDE.0000000000000084

Department of Molecular Medicine, University of Padova, Padova, Italy, Imperial College, London, United Kingdom,;

Imperial College, London, United Kingdom

King’s College, London, United Kingdom

NHLI, Imperial College, London, United Kingdom, Chelsea and Westminster Hospital, London, United Kingdom

Chelsea and Westminster Hospital, London, United Kingdom

Imperial College, London, United Kingdom

Supported by grants from the UK Department of Health’s Policy Research Programme, and the Medical Research Council and the Health Protection Agency through the MRC-HPA Centre for Health and the Environment.

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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 (

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; 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;

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;

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

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1. Weichenthal SA, Godri-Pollitt K, Villeneuve PJ. PM2.5, oxidant defence and cardiorespiratory health: a review. Environ Health. 2013;12
2. Canova C, Dunster C, Kelly FJ, et al. PM10-induced hospital admissions for asthma and chronic obstructive pulmonary disease: the modifying effect of individual characteristics. Epidemiology. 2012;23:607–615
3. Ayres JG, Borm P, Cassee FR, et al. Evaluating the toxicity of airborne particulate matter and nanoparticles by measuring oxidative stress potential—a workshop report and consensus statement. Inhal Toxicol. 2008;20:75–99
4. Strak M, Janssen NA, Godri KJ, et al. Respiratory health effects of airborne particulate matter: the role of particle size, composition, and oxidative potential-the RAPTES project. Environ Health Perspect. 2012;120:1183–1189
5. Steenhof M, Mudway IS, Gosens I, et al. Acute nasal pro-inflammatory response to air pollution depends on characteristics other than particle mass concentration or oxidative potential: the RAPTES project. Occup Environ Med. 2013;70:341–348
6. Delfino RJ, Staimer N, Tjoa T, Gillen DL, Schauer JJ, Shafer MM. Airway inflammation and oxidative potential of air pollutant particles in a pediatric asthma panel. J Expo Sci Environ Epidemiol. 2013;23:466–473
7. Kelly F, Armstrong B, Atkinson R, et al. The London low emission zone baseline study. Res Rep Health Eff Inst. 2011;163:3–79
8. Boogaard H, Janssen NA, Fischer PH, et al. Contrasts in oxidative potential and other particulate matter characteristics collected near major streets and background locations. Environ Health Perspect. 2012;120:185–191

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