Abstract
Systemic inflammation is an integral part of chronic obstructive pulmonary disease (COPD), and air pollution is associated with cardiorespiratory mortality, yet the interrelationships are not fully defined. We examined associations between nitrogen dioxide (NO2) exposure (as a marker of traffic-related air pollution) and pro-inflammatory cytokines, and investigated effect modification and mediation by post-bronchodilator airflow obstruction (post-BD-AO) and cardiovascular risk. Data from middle-aged participants in the Tasmanian Longitudinal Health Study (TAHS, n = 1389) were analyzed by multivariable logistic regression, using serum interleukin (IL)-6, IL-8 and tumor necrosis factor-α (TNF-α) as the outcome. Mean annual NO2 exposure was estimated at residential addresses using a validated satellite-based land-use regression model. Post-BD-AO was defined by post-BD forced expiratory ratio (FEV1/FVC) < lower limit of normal, and cardiovascular risk by a history of either cerebrovascular or ischaemic heart disease. We found a positive association with increasing serum IL-6 concentration (geometric mean 1.20 (95% CI: 1.1 to 1.3, p = 0.001) per quartile increase in NO2). This was predominantly a direct relationship, with little evidence for either effect modification or mediation via post-BD-AO, or for the small subgroup who reported cardiovascular events. However, there was some evidence consistent with serum IL-6 being on the causal pathway between NO2 and cardiovascular risk. These findings raise the possibility that the interplay between air pollution and systemic inflammation may differ between post-BD airflow obstruction and cardiovascular diseases.
Highlights
In 2012, the World Health Organization (WHO) attributed exposure to outdoor air pollution as the cause for 389,000 premature deaths related to chronic obstructive pulmonary disease (COPD) [1]
We observed a modest direct relationship between NO2 exposure and serum IL-6 concentrations (10.8%), with a correspondingly minor indirect effect through Cardiovascular Disease (CVD) (0.6% (−1 to +2.8))
Our finding of a dose–response main association between NO2 exposure and serum IL-6 levels is consistent with the linear relationship that has been seen for PM2.5 as adverse health effects occur at low levels of exposure [8,9]
Summary
In 2012, the World Health Organization (WHO) attributed exposure to outdoor air pollution as the cause for 389,000 premature deaths related to chronic obstructive pulmonary disease (COPD) [1]. A recent meta-analysis of 13 studies from across North America, Europe and Asia has shown a modest increase in the relative risk (RR) of respiratory mortality with increasing chronic exposure to nitrogen dioxide (NO2) (RR 1.02 (95% confidence interval (CI): 1.02–1.03) per 10 μg/m3 (or equivalent to per 5.32 ppb increase)). This estimate comparable to the major air pollutant, particulate matter less than 2.5 μm in diameter (PM2.5) (RR 1.05 (1.01–1.09) per 10 μg/m3) [3]. The epidemiological data regarding the relationship between NO2 exposure and chronic obstructive pulmonary disease (COPD), an inflammatory lung condition that is characterized by progressive airflow obstruction (AO), are limited [10]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
