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Updated: Jul 18, 2026

Measuring Carbon Content in Airway Macrophages Exposed to Carbon-Containing Particulate Matters
Published on: July 12, 2024
Personal and ambient air pollution is associated with increased exhaled nitric oxide in children with asthma
Ralph J Delfino1, Norbert Staimer, Dan Gillen
1Epidemiology Division, Department of Medicine, School of Medicine, University of California, Irvine, Irvine, California 92617-7555, USA. rdelfino@uci.edu
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 (FeNO), a biomarker of airway inflammation. Personal active sampler exposures included continuous particulate matter < 2.5 microm in aerodynamic diameter (PM2.5), 24-hr PM2.5 elemental and organic carbon (EC, OC), and 24-hr nitrogen dioxide. Ambient exposures included PM2.5, PM2.5 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 FeNO and 2-day average pollutant concentrations. Per interquartile range pollutant increase, these were: for 24 microg/m3 personal PM2.5, 1.1 ppb FeNO [95% confidence interval (CI), 0.1-1.9]; for 0.6 microg/m3 personal EC, 0.7 ppb FeNO (95% CI, 0.3-1.1); for 17 ppb personal NO2, 1.6 ppb FeNO (95% CI, 0.4-2.8). Larger associations were found for ambient EC and smaller associations for ambient NO2. Ambient PM2.5 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 PM2.5 in the preceding 5 hr was associated with FeNO. In two-pollutant models, the most robust associations were for personal and ambient EC and NO2, and for personal but not ambient PM2.5.
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.
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