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Association between air pollution exposure and exhaled nitric oxide in an elderly population

¹ Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115, USA
² Exposure, Epidemiology and Risk Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA
³ Department of Chemistry, Franciscan University of Steubenville, Steubenville, OH, USA

Correspondence to:
Correspondence to:
Dr G Adamkiewicz
Exposure, Epidemiology and Risk Program, Harvard School of Public Health, 401 Park Drive, Boston, MA 02115, USA; gadamkie{at}hsph.harvard.edu

ABSTRACT
Background: Animal models suggest that the cardiovascular effects of air pollution result in part from inflammation caused by proinflammatory mediators originating in the lung. In a human study of the cardiovascular effects of air pollution, we aimed to evaluate the potential association between air pollution levels and the fraction of exhaled nitric oxide (FE_NO), a non-invasive measure of airway inflammation.

Methods: Breath samples were collected weekly between September and December 2000 in a community based group of elderly subjects (median age 70.7 years) in Steubenville, Ohio. The samples were analysed for NO. Air pollution levels were measured concurrently at a central site monitor.

Results: An increase in the 24 hour average PM_2.5 concentration of 17.7 µg/m³ was associated with an increase in FE_NO of 1.45 ppb (95% CI 0.33 to 2.57) in models adjusted for subject, week of study, day of the week, hour of the day, ambient barometric pressure, temperature, and relative humidity. This represents a change of approximately 15% compared with the mean FE_NO in the cohort (9.9 ppb). A significant association was also observed for a 24 hour moving average of ambient NO (0.83 ppb increase, 95% CI 0.26 to 1.40). In two-pollutant models, the magnitude and precision of the PM_2.5 effect was not reduced and the ambient NO effect was no longer significant. The associations between FE_NO and PM_2.5 were significantly higher in subjects with a doctor’s diagnosis of COPD (p value for interaction = 0.03).

Conclusions: Ambient pollution may lead to airway inflammation as measured by FE_NO. These subclinical inflammatory changes may be an important step in the pathogenesis of the cardiopulmonary effects induced by exposure to air pollution.

Keywords: exhaled nitric oxide; air pollution; particulate matter; inflammation; geriatrics

Abbreviations: COPD, chronic obstructive pulmonary disease; ECG, electrocardiogram; FE_NO, fraction of exhaled nitric oxide; GLM, generalised linear model; IL-6, interleukin 6; IQR, interquartile range; NO, nitric oxide; NO₂, nitrogen dioxide; NOS, nitric oxide synthase; NOx, oxides of nitrogen; O₃, ozone; PM_2.5, particulate matter less than 2.5 µm in aerodynamic diameter; PM₁₀, particulate matter less than 10 µm in aerodynamic diameter; SO₂, sulphur dioxide; TNF-, tumour necrosis factor

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