Evaluation of cytokine expression in BEAS cells exposed to fine particulate matter (PM_2.5) from specialized indoor environments

Abstract

Fine particles were collected in three indoor environments and an outdoor reference site. Samples were acid and aqueous extracted for metal analyses and cytokine expression study using a BEAS-2B line. Results revealed that the average PM2.5 concentration indoors was 5.8 mg/m3 while outside, it was 9.4 mg/m3. The airborne metal concentrations in indoor air ranged from 0.01 ng/m3 (Cd) to 620 ng/m3 (Al). All metals analyzed were higher indoors when compared to outdoor (I/O ratio) indicating a contribution from the workplace. Some metals were more efficiently extracted (e.g., Ni, V, As) in the aqueous phase than others (e.g., Fe and Al). Toxicological assays showed that the aqueous extracts at 20% induced IL-6 and subsequently inhibited it at a higher concentration (50%); both IL-8 and MCP-1 were inhibited at 20 and 50%. As, Ni and V concentrations seem to be the most important metals associated with the cytokine induction/inhibition response probably due to the higher bioavailability.

Particle pollution in Rio de Janeiro, Brazil: Increase and decrease of pro-inflammatory cytokines IL-6 and IL-8 in human lung cells

“…Urban PM has a strong component of fossil fuel due to concentration of engine emissions and burning in the city as compared to the other sites. It has been well established that, PM 10, PM 2.5 and diesel exhaust particles (DEP) can induce the secretion of inflammatory cytokines and chemokines in epithelial cells and macrophages (Alfaro-Moreno et al, 2007; Becker et al, 2005; Fuentes-Mattei et al, 2010; Gioda et al, 2011b; Hiraiwa and van Eeden, 2013;Ortiz-Martínez et al, 2010; Rodriguez-Cotto et al, 2013; Schwarze et al, 2013). In addition, cytokine induction can be mainly attributed to the effects of heavy metals in PM 2.5 (Rodriguez-Cotto et al, 2013) and residual oil fly ash (Carter et al, 1997).…”

“…Few reports exist on IL-6 or IL-8 inhibition due to PM exposure (Alfaro-Moreno et al, 2007; Alfaro-Moreno et al, 2009; Fuentes-Mattei et al, 2010; Gioda et al, 2011b; Schwarze et al, 2013). It has been reported that exposure to PM could induce (Becker et al, 2005) or inhibit (Veranth et al, 2006) IL-8 cellular secretion.…”

Airborne Fine Particulate Matter Induces Oxidative Stress and Inflammation in Human Nasal Epithelial Cells

“…Previous studies have suggested that PM 2.5 has a potential to stimulate cells to produce and release inflammatory cytokines (Ogino et al 2014). In vitro studies have found that diesel exhaust particles (DEP) and PM increase the expression of granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor-α (TNF-α), interleukin 8 (IL-8), IL-6, IL-1β and eotaxin (C-C motif chemokine ligand 11) in airway epithelial cells (Boland et al 1999;Gioda et al 2011;Patel et al 2011;Tang et al 2012). Since nasal epithelial cells function as the first epithelial barrier in the nasal cavity to protect from inhaled particles, PM 2.5 may induce inflammatory responses in nasal epithelial cells.…”

Analytical methods for assessing metal bioaccessibility in airborne particulate matter: A scoping review

“…Although there is some evidence which indicates that insoluble metal forms are also capable of causing ROS-mediated damage in the lungs [7], it is widely accepted that soluble metals are likely contributors to the toxic potential of airborne PM [8,9]. The many epidemiological and toxicity studies which have reported an association between various respective cardiorespiratory and toxicological endpoints and the concentration of water soluble metal fractions in airborne PM, most notably Zn, Ni, Cu, V and Fe, support this [e.g., [10][11][12][13].…”