Abstract
BackgroundExposure to wood smoke is associated with respiratory symptoms, whereas knowledge on systemic effects is limited. We investigated effects on systemic inflammation, oxidative stress and microvascular function (MVF) after controlled wood smoke exposure.MethodsIn a randomised, double-blinded, cross-over study 20 non-smoking atopic subjects were exposed at rest to 14, 220, or 354 μg/m3 of particles from a well-burning modern wood stove for 3 h in a climate controlled chamber with 2 week intervals. We investigated the level of oxidatively damaged DNA, inflammatory markers and adhesion molecules before and 0, 6 and 20 h after exposure. Six h after exposure we measured MVF non-invasively by digital peripheral artery tonometry following arm ischemia.ResultsThe MVF score was unaltered after inhalation of clean air (1.58 ± 0.07; mean ± SEM), low (1.51 ± 0.07) or high (1.61 ± 0.09) concentrations of wood smoke particles in atopic subjects, whereas unexposed non-atopic subjects had higher score (1.91 ± 0.09). The level of oxidatively damaged DNA, mRNA of ITGAL, CCL2, TNF, IL6, IL8, HMOX1, and OGG1 and surface marker molecules ICAM1, ITGAL and L-selectin in peripheral blood mononuclear cells were not affected by inhalation of wood smoke particles.ConclusionsExposure to wood smoke had no effect on markers of oxidative stress, DNA damage, cell adhesion, cytokines or MVF in atopic subjects.
Highlights
Exposure to wood smoke is associated with respiratory symptoms, whereas knowledge on systemic effects is limited
The present study investigated the impact of different doses of wood smoke-derived PM2.5; a clean air exposure 14 ± 8 μg/m3, a relatively low concentration 220 ± 49 μg/m3 and a relatively high concentration 354 ± 148 μg/m3 (Table 1)
We found no significant associations between the exposure and microvascular function (MVF) score (p = 0.78)
Summary
Exposure to wood smoke is associated with respiratory symptoms, whereas knowledge on systemic effects is limited. Several in vitro studies of cultured cells have previously shown that wood smoke PM increased the expression new study indicated virtually no effect on inflammation and oxidative stress in the airways after inhalation of relative large concentrations (224 ± 22 μg/m3 for 3 h) of PM from a wood pellet burner [16]. It appears that wood smoke PM shows relatively limited effects measured by biomarkers in healthy subjects, but vulnerable subjects such as asthmatics or atopics, who are predisposed to allergy and constitute more than 20% of the Danish population [17], might be sensitive to inhalation exposure of wood smoke PM [18]. The activation of these cells was assessed by expression of inflammatory genes including chemokine (C-C-motif) ligand 2 (CCL2), interleukin 6 (IL6), interleukin 8 (IL8), tumor necrosis factor (TNF) and surface markers including inter cellular adhesion molecule 1 (ICAM1), ITGAL integrin aL (antigen CD11A, lymphocyte function-associated antigen 1; a-polypeptide) and L-selectin
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