|Title:||Synergistic effect of carbon nuclei and polyaromatic hydrocarbons on respiratory and immune responses|
|Authors:||Chowdhury, Pratiti H.|
Honda, Akiko https://orcid.org/0000-0002-7358-4372 (unconfirmed)
Ueda, Kayo https://orcid.org/0000-0002-2104-1384 (unconfirmed)
|Author's alias:||本田, 晶子|
|Journal title:||Environmental Toxicology|
|Abstract:||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.|
|Rights:||This is the peer reviewed version of the following article: 'Environmental Toxicology' 32(9) 2172-2181, which has been published in final form at https://doi.org/10.1002/tox.22430. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.|
The full-text file will be made open to the public on 16 August 2018 in accordance with publisher's 'Terms and Conditions for Self-Archiving'.
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|Appears in Collections:||Journal Articles|
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