Ambient fine and coarse particles in Japan affect nasal and bronchial epithelial cells differently and elicit varying immune response

Ambient particulate matter (PM) epidemiologically exacerbates respiratory and immune health, including allergic rhinitis (AR) and bronchial asthma (BA). Although fine and coarse particles can affect respiratory tract, the differences in their effects on the upper and lower respiratory tract and immune system, their underlying mechanism, and the components responsible for the adverse health effects have not been yet completely elucidated. In this study, ambient fine and coarse particles were collected at three different locations in Japan by cyclone technique. Both particles collected at all locations decreased the viability of nasal epithelial cells and antigen presenting cells (APCs), increased the production of IL-6, IL-8, and IL-1β from bronchial epithelial cells and APCs, and induced expression of dendritic and epithelial cell (DEC) 205 on APCs. Differences in inflammatory responses, but not in cytotoxicity, were shown between both particles, and among three locations. Some components such as Ti, Co, Zn, Pb, As, OC (organic carbon) and EC (elemental carbon) showed significant correlations to inflammatory responses or cytotoxicity. These results suggest that ambient fine and coarse particles differently affect nasal and bronchial epithelial cells and immune response, which may depend on particles size diameter, chemical composition and source related particles types

Effects of Ambient PM2.5 Collected Using Cyclonic Separator from Asian Cities on Human Airway Epithelial Cells

Recent studies have shown that air pollution is intense and hazardous in Asia compared to other parts of the world due to the late and poor implementation of updated technology in automobiles and industry as well as to the high population density. Respiratory disease, including asthma, is exacerbated by air pollution. However, the effects of PM₂.₅, especially on respiratory allergies in Asian cities, have not yet been examined in detail. In this study, airway epithelial cells were exposed to crude PM₂.₅ particles collected by cyclonic separation from three different Asian cities, namely, Sakai, Bangkok, and Taipei. We compared the cytotoxicity and inflammatory potential of the PM₂.₅ from these cities by measuring IL-6 and IL-8. The samples from Sakai and Bangkok caused cytotoxic effects at a dose of 75 µg mL⁻¹ and, moreover, induced the release of IL-6 and IL-8 even at low doses. The release of these two interleukins was highly associated with fluoranthene derivatives, microbial factors (endotoxin and β-glucan), metals (e.g., Ti), and organic (OC2 and OC3) and elemental carbon (EC1) in the PM₂.₅. Thus, these components potentially contribute to cellular damage and a pro-inflammatory response in the airway epithelial cells, and the effect depends on PM₂.₅ sources in the locations

Synergistic effect of carbon nuclei and polyaromatic hydrocarbons on respiratory and immune responses

Particulate matter with aerodynamic diameter ≤2.5 μm (PM₂.₅) is generally composed of carbon nuclei associated with various organic carbons, metals, ions and biological materials. Among these components, polyaromatic hydrocarbons (PAHs) such as benzo(a)pyrene (BaP) and quinones have detrimental effects on airway epithelial cells and immunodisrupting effects, which leads to the exacerbation of respiratory allergies. The effects of PAHs and the carbon nuclei, separately as well as in combination, remain to be established. We investigated the effects of BaP, 9, 10‐phenanthroquinone (9, 10‐PQ), and 1, 2‐napthoquinone (1, 2‐NQ) and their combined effects with heated diesel exhaust particle (H‐DEP) as carbon nuclei of typical PM₂.₅. We exposed human airway epithelial cells (BEAS‐2B), murine bone marrow‐derived antigen‐presenting cells (APCs), and murine splenocytes to BaP, 9, 10‐PQ, or 1, 2‐NQ in the presence and absence of H‐DEP. Several important inflammatory cytokines and cell surface molecules were measured. PAHs alone did not have apparent cytotoxic effects on BEAS‐2B, whereas combined exposure with H‐DEP induced noticeable detrimental effects which mainly reflected the action of H‐DEP itself. BaP increased CD86 expression as an APC surface molecule regardless of the presence or absence of H‐DEP. None of the BaP, 9, 10‐PQ, or 1, 2‐NQ exposure alone or their combined exposure with H‐DEP resulted in any significant activation of splenocytes. These results suggest that PAHs and carbon nuclei show additive effects, and that BaP with the carbon nuclei may contribute to exacerbations of allergic respiratory diseases including asthma by PM₂.₅, especially via antigen‐presenting cell activation

Exposure of Lung Epithelial Cells to Photochemically Aged Secondary Organic Aerosol Shows Increased Toxic Effects

Adverse health effects due to exposure to particulate matter (PM) are among the most important global environmental health risks. However, the effects of exposure to secondary organic aerosols (SOA), a major component of the global aerosol, are largely unknown. Here we exposed lung epithelial cells (A549) to fresh and aged SOA particles and investigated the effect of SOA atmospheric aging on cell viability and gene expression. Naphthalene- and α-pinene-derived SOA were formed in an oxidation flow reactor that simulates atmospheric SOA formation and aging dominated by OH radical oxidation under NO_<i>x</i>-free conditions. The SOA mass and chemical composition were characterized on-line using a scanning mobility particle sizer and aerosol mass spectrometer. Fresh and aged SOA were directed to an air–liquid interface cell exposure system. Aged naphthalene- and α-pinene-derived SOA were somewhat more toxic than fresh SOA. Aged naphthalene SOA contained peroxide levels that were higher than those of fresh SOA. The level of induction of Nrf2 signaling increased following exposure to aged naphthalene SOA. Given the global prevalence of SOA and its observed toxicity, this study calls for more studies aimed at understanding the underlying mechanics