The oxidative capacity of indoor source combustion derived particulate matter and resulting respiratory toxicity

Zebrafish irritant responses to wildland fire-related biomass smoke are influenced by fuel type, combustion phase, and byproduct chemistry

“…The concentrations used, however, are comparable with PM exposure concentrations used in published in vitro human lung cell studies (Lyu et al, 2018;Niu et al, 2021:). Moreover, the biologically conserved sensory mechanisms and responsiveness to chemicals among zebrafish skin and mammalian lung epithelium suggest that the interaction of particulates with skin epithelium in this zebrafish model may be comparable and predictive of the irritant responses resulting from the interaction of inhaled particles with mammalian lung epithelium.…”

“…Inhalation of PM2.5 has for decades been demonstrated to produce and/or exaggerate adverse health outcomes such as pulmonary distress and cardiovascular diseases (Lim et al, 2012;Wettstein et al, 2018;Samet et al, 2009;Cochard et al 2020;Shkirkova et al 2020). Further, human and experimental evidence indicates that the severity of adverse health effects is influenced heavily by air pollution source (Hime et al, 2018;Park et al, 2018). This includes studies that have demonstrated enhanced toxicity of combustion emissions from petroleum diesel relative to biodiesel (Shvedova et al 2013; Mutlu et al, 2015;Hazari et al, 2015;Farraj et al, 2015;Gavett et al, 2015), of metalrich residual oil-fly ash relative to carbon black (Wellenius et al, 2002), and of near road PM relative to rural PM (Hargrove et al,.…”

The Adverse Impact of Incense Smoke on Human Health: From Mechanisms to Implications

“… 96 Literature has reported that DNA may be one of critical targets for ROS induced by incense burning, resulting in oxidative DNA lesions and even impediment of the ensuing transcription, replication, and repair processes. 117 In fact, temple workers were found to have a twofold increase in the levels of biomarker of oxidative DNA damage namely 8-oxo-2ʹ-deoxyguanosine (8-OHdG) than those of control workers, and so was DNA strand breaks. 118 Similarly, oxidative DNA damage in human alveolar epithelial A549 cells was also triggered by exposure to PM generated from incense burning, as characterized by the levels of 8-OHdG.…”

“… 118 Similarly, oxidative DNA damage in human alveolar epithelial A549 cells was also triggered by exposure to PM generated from incense burning, as characterized by the levels of 8-OHdG. 117 To cope with the consequences of DNA lesions, living beings are equipped with the tools that serve to remove or tolerate DNA damages called DNA repair mechanisms/pathways. 119 Unfortunately, a significant reduction in DNA repair capacity was observed among temple workers by using cytogenetic challenge assay.…”

The critical roles of histone deacetylase 3 in the pathogenesis of solid organ injury

“…PM2.5 can invade small airways and interfere with pulmonary gas exchange, eventually causing chronic lung injury and lung cancers [ 99 , 100 ]. Mechanistically, PM2.5 causes ultrastructural alterations in mitochondria and membrane lysis in alveolar epithelial cells, in addition to inducing DNA damage and the production of reactive oxygen species (ROS) [ 101 – 103 ]. Furthermore, accumulating evidence suggests that PM2.5 can also activate TLR4, TLR4/NF-κB, and TGF-β/Smads, causing pulmonary inflammation and fibrosis [ 98 , 104 ].…”