title: Increased ultrafine particles and carbon monoxide concentrations are associated with asthma exacerbation among urban children.
abstract: OBJECTIVE
  Increased air pollutant concentrations have been linked to several asthma-related outcomes in children, including respiratory symptoms, medication use, and hospital visits. However, few studies have examined effects of ultrafine particles in a pediatric population. Our primary objective was to examine the effects of ambient concentrations of ultrafine particles on asthma exacerbation among urban children and determine whether consistent treatment with inhaled corticosteroids could attenuate these effects. We also explored the relationship between asthma exacerbation and ambient concentrations of accumulation mode particles, fine particles (≤2.5 micrograms [μm]; PM2.5), carbon monoxide, sulfur dioxide, and ozone. We hypothesized that increased 1-7 day concentrations of ultrafine particles and other pollutants would be associated with increases in the relative odds of an asthma exacerbation, but that this increase in risk would be attenuated among children receiving school-based corticosteroid therapy.
  
  
  METHODS
  We conducted a pilot study using data from 3 to 10 year-old children participating in the School-Based Asthma Therapy trial. Using a time-stratified case-crossover design and conditional logistic regression, we estimated the relative odds of a pediatric asthma visit treated with prednisone (n=96 visits among 74 children) associated with increased pollutant concentrations in the previous 7 days. We re-ran these analyses separately for children receiving medications through the school-based intervention and children in a usual care control group.
  
  
  RESULTS
  Interquartile range increases in ultrafine particles and carbon monoxide concentrations in the previous 7 days were associated with increases in the relative odds of a pediatric asthma visit, with the largest increases observed for 4-day mean ultrafine particles (interquartile range=2088p/cm(3); OR=1.27; 95% CI=0.90-1.79) and 7-day mean carbon monoxide (interquartile range=0.17ppm; OR=1.63; 95% CI=1.03-2.59). Relative odds estimates were larger among children receiving school-based inhaled corticosteroid treatment. We observed no such associations with accumulation mode particles, black carbon, fine particles (≤2.5μm), or sulfur dioxide. Ozone concentrations were inversely associated with the relative odds of a pediatric asthma visit.
  
  
  CONCLUSIONS
  These findings suggest a response to markers of traffic pollution among urban asthmatic children. Effects were strongest among children receiving preventive medications through school, suggesting that this group of children was particularly sensitive to environmental triggers. Medication adherence alone may be insufficient to protect the most vulnerable from environmental asthma triggers. However, further research is necessary to confirm this finding.
authors: Department of Public Health Sciences, University of Rochester School of Medicine & Dentistry, 265 Crittenden Boulevard, CU 420644, Rochester, NY 14642, USA. Electronic address: kristin_evans@urmc.rochester.edu.
authors: Kristin A
authors: KA
authors: Evans
authors: Department of Pediatrics, University of Rochester School of Medicine & Dentistry, 601 Elmwood Avenue, Box 777, Rochester, NY 14642, USA. Electronic address: jill_halterman@urmc.rochester.edu.
authors: Jill S
authors: JS
authors: Halterman
authors: Department of Chemical & Biomolecular Engineering, CA206 CAMP/Rowley Annex, Clarkson University, PO Box 5708, Potsdam, NY 13699, USA. Electronic address: hopkepk@clarkson.edu.
authors: Philip K
authors: PK
authors: Hopke
authors: Department of Pediatrics, University of Rochester School of Medicine & Dentistry, 601 Elmwood Avenue, Box 777, Rochester, NY 14642, USA. Electronic address: maria_fagnano@urmc.rochester.edu.
authors: Maria
authors: M
authors: Fagnano
authors: Department of Public Health Sciences, University of Rochester School of Medicine & Dentistry, 265 Crittenden Boulevard, CU 420644, Rochester, NY 14642, USA. Electronic address: david_rich@urmc.rochester.edu.
authors: David Q
authors: DQ
authors: Rich
mesh_terms: D000305:Adrenal Cortex Hormones / Q000008:administration & dosage / Q000627:therapeutic use; D000393:Air Pollutants / Q000009:adverse effects / Q000032:analysis*; D001249:Asthma / Q000139:chemically induced* / Q000453:epidemiology / Q000503:physiopathology / Q000628:therapy; D002248:Carbon Monoxide / Q000009:adverse effects / Q000032:analysis*; D002648:Child; D002675:Child, Preschool; D018450:Disease Progression; D004784:Environmental Monitoring / Q000379:methods / Q000706:statistics & numerical data; D006760:Hospitalization / Q000706:statistics & numerical data; D006801:Humans; D019570:Inhalation Exposure / Q000009:adverse effects / Q000032:analysis* / Q000706:statistics & numerical data; D009518:New York; D010316:Particle Size; D052638:Particulate Matter / Q000009:adverse effects / Q000032:analysis*; D012119:Respiration / Q000187:drug effects; D014505:Urban Population / Q000706:statistics & numerical data
chemical_list: D000305:Adrenal Cortex Hormones; D000393:Air Pollutants; D052638:Particulate Matter; D002248:Carbon Monoxide
keywords: Asthma; Children; Corticosteroids; Intervention; Ultrafine particles