Oxidative Stress, DNA Damage, and Inflammation Induced by Ambient Air and Wood Smoke Particulate Matter in Human A549 and THP-1 Cell Lines

Abstract

Combustion of biomass and wood for residential heating and/or cooking contributes substantially to both ambient air and indoor levels of particulate matter (PM). Toxicological characterization of ambient air PM, especially related to traffic, is well advanced, whereas the toxicology of wood smoke PM (WSPM) is poorly assessed. We assessed a wide spectrum of toxicity end points in human A549 lung epithelial and THP-1 monocytic cell lines comparing WSPM from high or low oxygen combustion and ambient PM collected in a village with many operating wood stoves and from a rural background area. In both cell types, all extensively characterized PM samples (1.25-100 μg/mL) induced dose-dependent formation of reactive oxygen species and DNA damage in terms of strand breaks and formamidopyrimidine DNA glycosylase sites assessed by the comet assay with WSPM being most potent. The WSPM contained more polycyclic aromatic hydrocarbons (PAH), less soluble metals, and expectedly also had a smaller particle size than PM collected from ambient air. All four types of PM combined increased the levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine dose-dependently in A549 cells, whereas there was no change in the levels of etheno-adducts or bulky DNA adducts. Furthermore, mRNA expression of the proinflammatory genes monocyte chemoattractant protein-1, interleukin-8, and tumor necrosis factor-α as well as the oxidative stress gene heme oxygenase-1 was upregulated in the THP-1 cells especially by WSPM and ambient PM sampled from the wood stove area. Expression of oxoguanine glycosylase 1, lymphocyte function-associated antigen-1, and interleukin-6 did not change. We conclude that WSPM has small particle size, high level of PAH, low level of water-soluble metals, and produces high levels of free radicals, DNA damage as well as inflammatory and oxidative stress response gene expression in cultured human cells.

Effects ofPassiflora edulis(Yellow Passion) on Serum Lipids and Oxidative Stress Status of Wistar Rats

“…Mechanisms that contribute to the formation of free radicals may include metabolic stress resulting from changes in energy metabolism, the levels of inflammatory mediators, and the status of antioxidant defense. 35,36 Our results did not show significant alteration in SOD and GSH-Px activities and GSH-t concentration after treatment with P. edulis juice ( Table 2). There is increasing evidence that in certain pathological conditions the increased production and/or ineffective scavenging of such reactive species may play a crucial role in determining tissue injury by lipid peroxidation, especially in atherosclerotic and cardiovascular diseases, even in the presence of hypertension, hyperlipidemias, and smoking.…”

Dithiothreitol activity by particulate oxidizers of SOA produced from photooxidation of hydrocarbons under varied NO<sub><i>x</i></sub> levels

“…Primary combustion particulates (e.g., wood smoke particles, vehicle emissions) are known to be causative agents of these diseases (Danielsen et al, 2011;Nel, 2005); however, increasing attention is also being paid to secondary organic aerosols (SOAs; Fujitani et al, 2012;Jang et al, 2006;Kramer et al, 2016;Lin et al, 2016;McDonald et al, 2010;McWhinney et al, 2013;Tuet et al, 2017aTuet et al, , 2017b, which are produced from the atmospheric transformation of hydrocarbons (HCs) in the presence of atmospheric oxidants (e.g., NO x , OH radicals, O 3 ; Hallquist et al, 2009). Although SOA comprises a large fraction of9966 H. Jiang et al: Dithiothreitol activity by particulate oxidizers 2005), its mechanistic role in causing adverse health effects remains unclear.…”

“…The toxicity of organic aerosols has been ascribed to the generation of reactive oxygen species (ROS) and the modification of biomolecules (e.g., DNA and cellular enzymes; Danielsen et al, 2011;Nel, 2005). ROS can induce oxidative stress in pulmonary systems, followed by a cascade of inflammation responses and ultimately the apoptosis of lung cells (Danielsen et al, 2011;Li et al, 2003Li et al, , 2008.…”

“…ROS can induce oxidative stress in pulmonary systems, followed by a cascade of inflammation responses and ultimately the apoptosis of lung cells (Danielsen et al, 2011;Li et al, 2003Li et al, , 2008. Particulate organic compounds such as quinones and polyaromatic hydrocarbons can react with cellular reducing agents (e.g., NADPH) and form ROS (i.e., H 2 O 2 and O − 2 ; Kumagai et al, 2012).…”

Characterizing residential wood smoke at the neighbourhood scale: An evaluation of five communities in British Columbia.

“…Results indicate that immune response to wood smoke and traffic particles is triggered through different mechanistic pathways (Kocbach et al, 2008;Samuelsen et al, 2009) and that wood smoke may have relatively less inflammatory but greater mutagenic effects (Cavanagh et al, 2011;Kocbach et al, 2008;Danielsen et al, 2009). The organic fraction of wood smoke appears to elicit the strongest responses (Cavanagh et al, 2011;Danielsen et al, 2009;Danielsen et al, 2011;Jalava et al, 2010;Kocbach et al, 2008). The results from these toxicology studies are limited in that they cannot be extrapolated to humans and do not consider mediating processes such as respiratory tract deposition (Londahl et al, 2008;Londahl et al, 2009).…”