Acute exposure to wood smoke from incomplete combustion - indications of cytotoxicity

Abstract

BackgroundSmoke from combustion of biomass fuels is a major risk factor for respiratory disease, but the underlying mechanisms are poorly understood. The aim of this study was to determine whether exposure to wood smoke from incomplete combustion would elicit airway inflammation in humans.MethodsFourteen healthy subjects underwent controlled exposures on two separate occasions to filtered air and wood smoke from incomplete combustion with PM1 concentration at 314 μg/m3 for 3 h in a chamber. Bronchoscopy with bronchial wash (BW), bronchoalveolar lavage (BAL) and endobronchial mucosal biopsies was performed after 24 h. Differential cell counts and soluble components were analyzed, with biopsies stained for inflammatory markers using immunohistochemistry. In parallel experiments, the toxicity of the particulate matter (PM) generated during the chamber exposures was investigated in vitro using the RAW264.7 macrophage cell line.ResultsSignificant reductions in macrophage, neutrophil and lymphocyte numbers were observed in BW (p < 0.01, <0.05, <0.05, respectively) following the wood smoke exposure, with a reduction in lymphocytes numbers in BAL fluid (<0.01. This unexpected cellular response was accompanied by decreased levels of sICAM-1, MPO and MMP-9 (p < 0.05, <0.05 and <0.01). In contrast, significant increases in submucosal and epithelial CD3+ cells, epithelial CD8+ cells and submucosal mast cells (p < 0.01, <0.05, <0.05 and <0.05, respectively), were observed after wood smoke exposure. The in vitro data demonstrated that wood smoke particles generated under these incomplete combustion conditions induced cell death and DNA damage, with only minor inflammatory responses.ConclusionsShort-term exposure to sooty PAH rich wood smoke did not induce an acute neutrophilic inflammation, a classic hallmark of air pollution exposure in humans. While minor proinflammatory lymphocytic and mast cells effects were observed in the bronchial biopsies, significant reductions in BW and BAL cells and soluble components were noted. This unexpected observation, combined with the in vitro data, suggests that wood smoke particles from incomplete combustion could be potentially cytotoxic. Additional research is required to establish the mechanism of this dramatic reduction in airway leukocytes and to clarify how this acute response contributes to the adverse health effects attributed to wood smoke exposure.Trial registrationNCT01488500Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-015-0111-7) contains supplementary material, which is available to authorized users.

Mass spectrometry profiling of oxylipins, endocannabinoids, and N-acylethanolamines in human lung lavage fluids reveals responsiveness of prostaglandin E2 and associated lipid metabolites to biodiesel exhaust exposure

“…The intricate function of PGE 2 is only one example of the complexity of an adequate inflammatory response that, besides PGE 2 , also involves other studied eicosanoids and associated bioactive lipid mediators that altogether exhibit coordinated and often opposing actions [22]. Our results suggest that PGE 2 portrays a protective response in the more distal parts of the lung, where fewer signs of an inflammatory response have been detected than in BW [17, 18, 50]. But further research is needed to test this hypothesis.…”

“…We have previously demonstrated marked neutrophilic inflammation in the proximal airways sampled by endobronchial biopsies and BW following exposure to petrodiesel, however, with no corresponding inflammatory response in BAL fluids, representing the more peripheral and alveolar lung compartments [17, 18, 47–49]. Moreover, clear differences between the responses of the airway and alveolar regions have been identified following controlled exposure to wood smoke [50]. The approach using BW and BAL fluids has also been advocated in previous studies addressing oxylipin profiles in the airways of healthy and asthmatics subjects [42, 44].…”

“…15-HETE has antioxidant and pro-resolving properties [62] and was significantly downregulated in BAL fluid in a murine cystic fibrosis model after nanoparticle exposure [63]. Hence, the trend towards decreased levels of 15-HETE in BW may indicate a lack of protection against the harmful effects of biodiesel exhaust exposure in more proximal parts of the lung, where, based on previous petrodiesel studies, more signs of an inflammatory response have been detected in traditional inflammatory markers, compared to BAL [17, 18, 50]. 9-HODE previously demonstrated opposite shifts in response to exposure to subway air, with increased concentrations from healthy subjects and decreased concentrations from asthmatics [44].…”

Cytotoxic and genotoxic responses of human lung cells to combustion smoke particles of Miscanthus straw, softwood and beech wood chips

“…Both in-vivo (Forchhammer et al, 2012; Muala et al, 2015) and in-vitro (Kasurinen et al, 2015a; Tapanainen et al, 2011) experiments exploring potential relationships between biomass combustion and health effects have confirmed that PAHs can be adsorbed onto the surface of particles, presenting a potential hazard to biota.…”

Particulate emissions from the combustion of birch, beech, and spruce logs cause different cytotoxic responses in A549 cells

“…Wood smoke PM exerts its negative health effects mainly through the induction of inflammation in the lung as well as low‐grade systemic inflammation (Hejl et al, , Lee et al, , Soukup et al, ), but it has been shown that exposure to wood smoke PM also causes immediate cytotoxicity and oxidative stress in healthy individuals (Muala et al, ), as well as DNA damage in in vitro studies (Danielsen et al, ). The extent of toxicity induced by wood smoke PM depends on several factors: the physicochemical properties of the PM (Kocbach Bølling et al, ), the solubility and lung deposition of the PM (Jalava et al, ) and the dose and duration of the exposure to the PM.…”