Inflammation-Related Effects of Diesel Engine Exhaust Particles: Studies on Lung CellsIn Vitro

Abstract

Diesel exhaust and its particles (DEP) have been under scrutiny for health effects in humans. In the development of these effects inflammation is regarded as a key process. Overall, in vitro studies report similar DEP-induced changes in markers of inflammation, including cytokines and chemokines, as studies in vivo. In vitro studies suggest that soluble extracts of DEP have the greatest impact on the expression and release of proinflammatory markers. Main DEP mediators of effects have still not been identified and are difficult to find, as fuel and engine technology developments lead to continuously altered characteristics of emissions. Involved mechanisms remain somewhat unclear. DEP extracts appear to comprise components that are able to activate various membrane and cytosolic receptors. Through interactions with receptors, ion channels, and phosphorylation enzymes, molecules in the particle extract will trigger various cell signaling pathways that may lead to the release of inflammatory markers directly or indirectly by causing cell death. In vitro studies represent a fast and convenient system which may have implications for technology development. Furthermore, knowledge regarding how particles elicit their effects may contribute to understanding of DEP-induced health effects in vivo, with possible implications for identifying susceptible groups of people and effect biomarkers.

Combined exposure of diesel exhaust particles and respirable Soufrière Hills volcanic ash causes a (pro-)inflammatory response in an in vitro multicellular epithelial tissue barrier model

“…Nonetheless, in the current study, DEP did cause an increased release of measured (pro-)inflammatory markers (TNF-α, IL-8 and IL-1β) compared to the negative control (supplemented cell culture medium). These findings concur with previous observations of monoculture in vitro studies, which reported DEP to be highly (pro)-inflammatory [38, 39], as well as with studies using the same triple cell co-culture system [20]. …”

“…The observations indicate that combined exposure to VA and DEP induces a (pro-)inflammatory response in cells at the respiratory epithelial tissue barrier, but it is not yet clear whether this effect is directly driven by the individual particle-cell interactions, secondary toxicology mechanisms incited via the particles’ physicochemical characteristics, or through particle-particle interactions leading to the combined effect noted. It is known that increased release of (pro-)inflammatory mediators may augment, as well as prolong, inflammatory reactions and, if the exposure persists, can result in chronic inflammation [38]. Airway inflammation not only promotes the development of lung diseases, but it may increase the susceptibility to acute cardiovascular disease [55].…”

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

“…In developing countries, emissions from combustion of biomass for domestic heat production are the main source of indoor and outdoor air pollution in rural areas, and, increasingly, in urban areas, too (Chen et al, 2016; Sigsgaard et al, 2015). The amount of particulate matter (PM) generated and its toxicological properties depends on the biomass fuel type and source, the combustion technology used and the combustion conditions (Fachinger et al, 2017; Jalava et al, 2012; Schwarze et al, 2013) Combustion of biomass can create emissions that include solid particles made of crystalline materials, amorphous substances, heavy metals, soot and organic substances like PAHs (Jokiniemi et al, 2008). Three competitive mechanisms have been identified for particle formation during biomass combustion: coarse ash particle entrainment, inorganic vapor (e.g., KOH, KCl, K 2 SO 4 , Zn) condensation, and pyrolysis product condensation (Kocbach Bølling et al, 2009).…”

Serum cytokine levels related to exposure to volatile organic compounds and PM_2.5 in dwellings and workplaces in French farmers – a mechanism to explain nonsmoking COPD

“…The researchers concluded that subjects who are repeatedly exposed to organic matter might develop a certain adaptation 15. Furthermore, toxicological studies have shown inhibition of IL6 and IL8 after exposure to PM 30–34. Recently, Rodriguez-Cotto et al20 showed that PM in the city of Rio de Janeiro can either increase or decrease the secretion of cytokines in vitro while being site specific and time dependent.…”