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Exposure and harm to combustion-derived wood particles

Berube, Kelly Ann ORCID:, Wlodarczyk, Anna Julia, Prytherch, Zoe Cariad ORCID:, Jones, Timothy Peter ORCID:, Karg, Ernst, Sippula, Ollie, Harndorf, Hann, Rabe, R., Streibel, T. and Zimmermann, Ralf 2015. Exposure and harm to combustion-derived wood particles. Presented at: 2015 European Aerosol Conference (EAC 2015), Milan, Italy, 6-11 September 2015. European Aerosol Conference 2015 Digital Abstracts. Milan: European Aerosol Conference, p. 1.

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The human respiratory system is the gateway of entry for inhaled detritus from anthropogenic (e.g. combustion-derived (CD) particulate matter (PM; e.g. diesel exhaust and wood-burning PM). Adult humans inhale 20m3 of air and suspended debris (gases and particles) into the airways daily. Inhalation exposure to CDPM (Figure 1) is known to increase the risk of morbidity and mortality of lung and heart diseases in all exposed individuals. The physicochemical properties of size, surface area and presence of transition metals have been implicated as drivers of the oxidative capacity of CDPM. However, the precise role of reactive organic compounds (ROC) in ambient aerosols, present either in the gas or particle phase has not been fully-investigated for their relevance in the induction of the observed adverse health effects. When addressing the toxicity of inhalation hazards such as wood smoke CDPM, a model that resembles the human lung responding to toxic challenges is required. In our in vitro exposure studies, we utilised normal human bronchial epithelial (NHBE) cells grown at the air-liquid interface (ALI) using filter-well technology (Prytherch et al 2011), to create an in vivo-like 3-dimensional lung model. This model is a fully-differentiated, pseudo-stratified, muco-ciliary epithelium containing basal, serous, Clara, goblet and ciliated cells. NHBE cells were exposed to wood smoke derived from Spruce, Beech and Birch at a dose of 152µg/cm2: carbon black (CB; negative control; Monarch 120, Cabot UK; DQ12 quartz (positive control). Following exposure (24 hours), tissue integrity (i.e. transepithelial electrical resistance (TEER) was measured to reveal minor disruption to bronchial tissue integrity (Figure 2). However, changes in cellular energy levels (i.e. ATP) between the types of wood smokes (Figure 3), could infer the smoke acted as an irritant to the lung environment. Wood smoke exposure can depress the immune system and damage the layer of cells in the lungs that protect and cleanse the airways. Further work on the biological and histological impacts of wood smoke will allow us to reveal mechanisms behind the changes observed, as well identifying biomarkers of cell damage by specific CDPM ROCs. For vulnerable populations, such as people with asthma, chronic respiratory disease and those with cardiovascular disease, wood smoke is particularly harmful, even at short exposures it can prove dangerous. Wood smoke interferes with normal lung development in infants and children. It also increases children’s risk of lower respiratory infections such as bronchitis and pneumonia. Prytherch, Z., Job, C., Marshall, H., Oreffo, V., Foster, M. and BéruBé, K.A. (2011) Macro. Bios. 11, 1467–77. This work was supported by HICE (

Item Type: Conference or Workshop Item (Lecture)
Date Type: Publication
Status: Published
Schools: Earth and Environmental Sciences
Subjects: Q Science > Q Science (General)
Publisher: European Aerosol Conference
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Date of First Compliant Deposit: 30 March 2016
Last Modified: 17 Nov 2022 05:05

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