Academic journal article Environmental Health Perspectives

Personal and Ambient Air Pollution Is Associated with Increased Exhaled Nitric Oxide in Children with Asthma

Academic journal article Environmental Health Perspectives

Personal and Ambient Air Pollution Is Associated with Increased Exhaled Nitric Oxide in Children with Asthma

Article excerpt

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 (F[E.sub.NO]), a biomarker of airway inflammation. Personal active sampler exposures included continuous particulate matter < 2.5 [micro]m in aerodynamic diameter (P[M.sub.2.5]), 24-hr P[M.sub.2.5] elemental and organic carbon (EC, OC), and 24-hr nitrogen dioxide. Ambient exposures included P[M.sub.2.5], P[M.sub.2.5] EC and OC, and N[O.sub.2]. Data were analyzed with mixed models controlling for personal temperature, humidity and 10-day period.

RESULTS: The strongest positive associations were between F[E.sub.NO] and 2-day average pollutant concentrations. Per interquartile range pollutant increase, these were: for 24 [micro]g/[m.sup.3] personal P[M.sub.2.5], 1.1 ppb F[E.sub.NO] [95% confidence interval (CI), 0.1-1.9]; for 0.6 [micro]g/[m.sup.3] personal EC, 0.7 ppb F[E.sub.NO] (95% CI, 0.3-1.1); for 17 ppb personal N[O.sub.2], 1.6 ppb F[E.sub.NO] (95% CI, 0.4-2.8). Larger associations were found for ambient EC and smaller associations for ambient N[O.sub.2]. Ambient P[M.sub.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 P[M.sub.2.5] in the preceding 5 hr was associated with F[E.sub.NO]. In two-pollutant models, the most robust associations were for personal and ambient EC and N[O.sub.2], and for personal but not ambient P[M.sub.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 [Online 11 July 2006]


Epidemiologic studies have shown associations between asthma outcomes and criteria air pollutants regulated by the U.S. Environmental Protection Agency (EPA), such as nitrogen dioxide and mass concentrations of particulate matter (PM) < 2.5 [micro]m in aerodynamic diameter (P[M.sub.2.5]). It is unclear whether these associations for pollutant gases and particles are independent of each other or are attributable to toxic air pollutants not routinely monitored, such as combustion-related organic compounds (Delfino 2002). Growing experimental evidence suggests that PM organic components, including polycyclic aromatic hydrocarbons (PAHs), have adjuvant effects on cytokine-mediated airway inflammation, at least partly through exposure to redox active chemicals and resultant oxidative stress (Li et al. 2003). The relevance of these findings to people with asthma can be enhanced with an assessment of the impact of personal air pollutant exposures on acute changes in asthma outcomes. Children with asthma at greatest risk of exacerbations from air pollutants likely include those with persistent asthma symptoms.

Airway inflammation is a hallmark of asthma. The fractional concentration of nitric oxide in exhaled air (F[E.sub.NO]) is a noninvasive biomarker of airway inflammation and is higher in subjects with poorly controlled asthma (Jones et al. 2001). Therefore, F[E.sub.NO] is potentially useful in epidemiologic field research to evaluate the impacts of air pollution on the inflammatory state of airways in children with asthma. NO is produced endogenously in the airways from L-arginine by NO synthetase. There are two constitutive isoforms and an inducible isoform involved in airway inflammation. …

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