eCite Digital Repository

The Dose-Response Association between Nitrogen Dioxide Exposure and Serum Interleukin-6 Concentrations

Citation

Perret, JL and Bowatte, G and Lodge, CJ and Knibbs, LD and Gurrin, LC and Kandane-Rathnayake, R and Johns, DP and Lowe, AJ and Burgess, JA and Thompson, BR and Thomas, PS and Wood-Baker, R and Morrison, S and Giles, GG and Marks, G and Markos, J and Tang, MLK and Abramson, MJ and Walters, EH and Matheson, MC and Dharmage, SC, The Dose-Response Association between Nitrogen Dioxide Exposure and Serum Interleukin-6 Concentrations, International Journal of Molecular Sciences, 18, (5) pp. 1-14. ISSN 1661-6596 (2017) [Refereed Article]


Preview
PDF
802Kb
  

Copyright Statement

2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

DOI: doi:10.3390/ijms18051015

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.

Item Details

Item Type:Refereed Article
Keywords:Pollution, nitogen dioxide, lung function
Research Division:Medical and Health Sciences
Research Group:Cardiorespiratory Medicine and Haematology
Research Field:Respiratory Diseases
Objective Division:Health
Objective Group:Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:Respiratory System and Diseases (incl. Asthma)
UTAS Author:Johns, DP (Associate Professor David Johns)
UTAS Author:Wood-Baker, R (Professor Richard Wood-Baker)
UTAS Author:Walters, EH (Professor Haydn Walters)
ID Code:118084
Year Published:2017
Web of Science® Times Cited:5
Deposited By:Medicine
Deposited On:2017-07-04
Last Modified:2018-09-11
Downloads:39 View Download Statistics

Repository Staff Only: item control page