Perret, Jennifer L; Bowatte, Gayan; Lodge, Caroline J; Knibbs, Luke D; Gurrin, Lyle C; Kandane-Rathnayake, Rangi; Johns, David P; Lowe, Adrian J; Burgess, John A; Thompson, Bruce R; Thomas, Paul S; Wood-Baker, Richard; Morrison, Stephen; Giles, Graham G; Marks, Guy; Markos, James; Tang, Mimi L K; Abramson, Michael J; Walters, E Haydn; Matheson, Melanie C; Dharmage, Shyamali C

doi:10.3390/ijms18051015

Author(s)

Perret, Jennifer L

Bowatte, Gayan

Lodge, Caroline J

Knibbs, Luke D

Gurrin, Lyle C

Kandane-Rathnayake, Rangi

Johns, David P

Lowe, Adrian J

Burgess, John A

Thompson, Bruce R

Thomas, Paul S

Wood-Baker, Richard

Morrison, Stephen

Giles, Graham G

Marks, Guy

Markos, James

Tang, Mimi L K

Abramson, Michael J

Walters, E Haydn

Matheson, Melanie C

Dharmage, Shyamali C

Publication Date

2017-05-08

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.

Citation

International journal of molecular sciences 2017; 18(5): 1015.

Jornal Title

International journal of molecular sciences

OrcId

0000-0001-7034-0615

Link

https://ahro.austin.org.au/austinjspui/handle/1/28162

Subject

airflow obstruction

interleukin

nitrogen dioxide

systemic inflammation

traffic-related air pollution

tumor necrosis factor-α

Title

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

Type of document

Journal Article

Austin Health

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

Files:

Author(s)	Perret, Jennifer L Bowatte, Gayan Lodge, Caroline J Knibbs, Luke D Gurrin, Lyle C Kandane-Rathnayake, Rangi Johns, David P Lowe, Adrian J Burgess, John A Thompson, Bruce R Thomas, Paul S Wood-Baker, Richard Morrison, Stephen Giles, Graham G Marks, Guy Markos, James Tang, Mimi L K Abramson, Michael J Walters, E Haydn Matheson, Melanie C Dharmage, Shyamali C
Publication Date	2017-05-08
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.
Citation	International journal of molecular sciences 2017; 18(5): 1015.
Jornal Title	International journal of molecular sciences
OrcId	0000-0001-7034-0615
Link	https://ahro.austin.org.au/austinjspui/handle/1/28162
Subject	airflow obstruction interleukin nitrogen dioxide systemic inflammation traffic-related air pollution tumor necrosis factor-α
Title	The Dose-Response Association between Nitrogen Dioxide Exposure and Serum Interleukin-6 Concentrations.
Type of document	Journal Article