Air pollution and subclinical airway inflammation in the SALIA cohort study

Abstract

BackgroundThe association between long-term exposure to air pollution and local inflammation in the lung has rarely been investigated in the general population of elderly subjects before. We investigated this association in a population-based cohort of elderly women from Germany.MethodsIn a follow-up examination of the SALIA cohort study in 2008/2009, 402 women aged 68 to 79 years from the Ruhr Area and Borken (Germany) were clinically examined. Inflammatory markers were determined in exhaled breath condensate (EBC) and in induced sputum (IS). We used traffic indicators and measured air pollutants at single monitoring stations in the study area to assess individual traffic exposure and long-term air pollution background exposure. Additionally long-term residential exposure to air pollution was estimated using land-use regression (LUR) models. We applied multiple logistic and linear regression analyses adjusted for age, indoor mould, smoking, passive smoking and socio-economic status and additionally conducted sensitivity analyses.ResultsInflammatory markers showed a high variability between the individuals and were higher with higher exposure to air pollution. NO derivatives, leukotriene (LT) B4 and tumour necrosis factor-α (TNF-α) showed the strongest associations. An increase of 9.42 μg/m3 (interquartile range) in LUR modelled NO2 was associated with measureable LTB4 level (level with values above the detection limit) in EBC (odds ratio: 1.38, 95% CI: 1.02 -1.86) as well as with LTB4 in IS (%-change: 19%, 95% CI: 7% - 32%). The results remained consistent after exclusion of subpopulations with risk factors for inflammation (smoking, respiratory diseases, mould infestation) and after extension of models with additional adjustment for season of examination, mass of IS and urban/rural living as sensitivity analyses.ConclusionsIn this analysis of the SALIA study we found that long-term exposure to air pollutants from traffic and industrial sources was associated with an increase of several inflammatory markers in EBC and in IS. We conclude that long-term exposure to air pollution might lead to changes in the inflammatory marker profile in the lower airways in an elderly female population.

Ambient Air Pollution and Adult Asthma Incidence in Six European Cohorts (ESCAPE)

“…Increased frailty of the epithelial barrier, inflammation, oxidative stress, and interaction with genetic and epigenetic determinants have been proposed. Research in adults, including subjects from the cohorts included in our analysis, has suggested a role of air pollution in local inflammation measured in exhaled breath condensate and induced sputum (using ESCAPE exposure estimates) ( Vossoughi et al 2014 ), interaction with oxidative stress genes ( Castro-Giner et al 2009 ), or novel DNA methylation markers ( Sofer et al 2013 ). Ambitious programs with comprehensive environmental exposure assessment and biological markers are starting in childhood populations ( Vrijheid et al 2014 ).…”

Particulate Air Pollution and Fasting Blood Glucose in Nondiabetic Individuals: Associations and Epigenetic Mediation in the Normative Aging Study, 2000–2011

“…We chose to focus our analysis on the four inflammatory genes included in these genes, including two inflammatory cytokines ( IFN- γ and IL-6 ), intercellular adhesion molecule 1 ( ICAM-1 ), and Toll-like receptor 2 ( TLR-2 ). The choice of these four inflammatory genes was aligned with previous literature on PM and inflammation, as well as subclinical inflammation and the risk of T2DM (Bind et al 2012; Blüher et al 2002; Herder et al 2013; Madrigano et al 2010; van Eeden et al 2001; Vossoughi et al 2014). Specifically, IFN- γ and IL-6 encode for inflammatory cytokines that facilitate cell-to-cell communications in the inflammatory cascade, ICAM-1 encodes for a glycoprotein that is often expressed on the cell surface of endothelial cells and leukocytes, ICAM-1 glycoproteins are important for cell surface adhesion, transmigration and homing of leukocytes from the circulation to the target tissue.…”

Phenotypes, Risk Factors, and Mechanisms of Adult‐Onset Asthma

“…Most studies on air pollution and asthma have concentrated on children, but whether different mechanisms are involved in patients with adult-onset asthma who often are less atopic remains unclear. In elderly women, long-term exposure to traffic- and industrial-related air pollution was associated with increased inflammatory markers (leukotriene B 4 and TNF- α ) in exhaled breath condensate and induced sputum [ 236 ]. Oxidative stress has been hypothesized as the mechanism of how air pollution might cause asthma.…”