- Full (HTML) - Full (PDF) - Supplemental Material - Related EHP Articles - PubMed:Related Articles - PubMed:Citation - Cited in PMC - Purchase This Issue

Ralph J. Delfino,¹ Norbert Staimer,¹ Dan Gillen,² Thomas Tjoa,¹ Constantinos Sioutas,³ Kochy Fung,⁴ Steven C. George,⁵ and Michael T. Kleinman⁶

¹Epidemiology Division, Department of Medicine, School of Medicine, University of California, Irvine, Irvine, California, USA; ²Department of Statistics, University of California, Irvine, Irvine, California, USA; ³Department of Civil and Environmental Engineering, School of Engineering, University of Southern California, Los Angeles, California, USA; ⁴AtmAA, Inc., Calabasas, California, USA; ⁵Department of Biomedical Engineering, University of California, Irvine, Irvine, California, USA; ⁶Department of Community and Environmental Medicine, School of Medicine, University of California, Irvine, Irvine, California, USA

Abstract
Background: Research has shown associations between pediatric asthma outcomes and airborne particulate matter (PM) . The importance of particle components remains to be determined.

Methods: We followed a panel of 45 schoolchildren with persistent asthma living in Southern California. Subjects were monitored over 10 days with offline fractional exhaled nitric oxide (FE_NO) , a biomarker of airway inflammation. Personal active sampler exposures included continuous particulate matter < 2.5 µm in aerodynamic diameter (PM_2.5) , 24-hr PM_2.5 elemental and organic carbon (EC, OC) , and 24-hr nitrogen dioxide. Ambient exposures included PM_2.5, PM_2.5 EC and OC, and NO₂. Data were analyzed with mixed models controlling for personal temperature, humidity and 10-day period.

Results: The strongest positive associations were between FE_NO and 2-day average pollutant concentrations. Per interquartile range pollutant increase, these were: for 24 µg/m³ personal PM_2.5, 1.1 ppb FE_NO [95% confidence interval (CI) , 0.1–1.9] ; for 0.6 µg/m³ personal EC, 0.7 ppb FE_NO (95% CI, 0.3–1.1) ; for 17 ppb personal NO₂, 1.6 ppb FE_NO (95% CI, 0.4–2.8) . Larger associations were found for ambient EC and smaller associations for ambient NO₂. Ambient PM_2.5 and personal and ambient OC were significant only in subjects taking inhaled corticosteroids (ICS) alone. Subjects taking both ICS and antileukotrienes showed no significant associations. Distributed lag models showed personal PM_2.5 in the preceding 5 hr was associated with FE_NO. In two-pollutant models, the most robust associations were for personal and ambient EC and NO₂, and for personal but not ambient PM_2.5.

Conclusion: PM associations with airway inflammation in asthmatics may be missed using ambient particle mass, which may not sufficiently represent causal pollutant components from fossil fuel combustion.

Key words: asthma, epidemiology, exhaled nitric oxide, longitudinal data analysis, nitrogen dioxide, ozone, panel study, particulate air pollution. Environ Health Perspect 114:1736–1743 (2006) . doi:10.1289/ehp.9141 available via http://dx.doi.org/ [Online 11 July 2006]

Address correspondence to R.J. Delfino, Epidemiology Division, Department of Medicine, School of Medicine, University of California, Irvine, 100 Theory, Suite 100, Irvine, CA 92617-7555 USA. Telephone: (949) 824-1767. Fax: (949) 824-1343. E-mail: rdelfino@uci.edu

Supplemental Material is available online at http://www.ehponline.org/docs/2006/9141/suppl.pdf

We thank the staff at the General Clinical Research Center, University of California, Irvine, and the South Coast Air Quality Management District (SCAQMD) .

The project described was supported by grant ES11615 from the National Institute of Environmental Health Sciences (NIEHS) , National Institutes of Health (NIH) , and its contents are solely the responsibility of the author and do not necessarily represent the official views of the NIEHS. Support for exhaled nitric oxide measurements was provided by SCAQMD, through the University of California, Los Angeles, Asthma and Outdoor Air Quality Consortium (Contract UCLA-35692) . The contents of this paper and the findings of its authors do not necessarily reflect the views of the SCAQMD that has not approved or disapproved this report.

The authors declare they have no competing financial interests.

Received 3 March 2006 ; accepted 11 July 2006.