Chemokine expression in human 3-dimensional cultured epidermis exposed to PM2.5 collected by cyclonic separation.

Fine particulate matter (PM2.5) exposure has a risk of inducing several health problems, especially in the respiratory tract. The skin is the largest organ of the human body and is therefore the primary target of PM2.5. In this study, we examined the effects of PM2.5 on the skin using a human 3-dimensional cultured epidermis model. PM2.5 was collected by cyclonic separation in Yokohama, Japan. Global analysis of 34 proteins released from the epidermis revealed that the chemokines, chemokine C-X-C motif ligand 1 (CXCL1) and interleukin 8 (IL-8), were significantly increased in response to PM2.5 exposure. These chemokines stimulated neutrophil chemotaxis in a C-X-C motif chemokine receptor 2-dependent manner. The oxidative stress and signal transducer and activator of transcription 3 pathways may be involved in the increased expression of CXCL1 and IL-8 in the human epidermis model. Interestingly, in the HaCaT human keratinocyte cell line, PM2.5 did not affect chemokine expression but did induce IL-6 expression, suggesting a different effect of PM2.5 between the epidermis model and HaCaT cells. Overall, PM2.5 could induce the epidermis to release chemokines, followed by neutrophil activation, which might cause an unregulated inflammatory reaction in the skin.

Airborne microplastics detected in the lungs of wild birds in Japan.

Microplastics (MPs) have been found in a wide range of animal species including humans. The detection of MPs in human lungs suggests that humans inhale airborne microplastics (AMPs). Although birds respire more efficiently than mammals and are therefore more susceptible to air pollution, little is known about their inhalation exposure to MPs. In this study, we analyzed samples isolated from the lungs of several species of wild birds in Japan by attenuated total reflection (ATR) imaging method of micro-Fourier transform infrared (µFTIR) spectroscopy to clear whether AMPs can be inhaled and accumulate within the lungs of wild birds. To isolate MPs from lung samples of rock doves (Columba livia), black kites (Milvus migrans), and barn swallows (Hirundo rustica) euthanized for pest control, digestion and density separation were performed. After each sample collected on an alumina filter was measured by ATR imaging method using µFTIR spectroscopy, the physical and chemical characteristics of the detected MPs were evaluated. Six MPs were detected in 3 of 22 lung samples. Polypropylene and polyethylene were found in rock doves and ethylene vinyl acetate was found in a barn swallow. Most MPs were fragments of 28.0-70.5 µm. Our results demonstrated that in addition to dietary sources, some wild birds are exposed to MPs by inhalation, and these MPs reach the lungs.

Involvement of polycyclic aromatic hydrocarbons and endotoxin in macrophage expression of interleukin-33 induced by exposure to particulate matter.

Air pollutants are important factors that contribute to the development and/or exacerbation of allergic inflammation accompanied by asthma, but experimental evidence still needs to be collected. Interleukin 33 (IL-33) is closely involved in the onset and progression of asthma. In this study, we examined the effects of particulate matter (PM) on IL-33 expression in macrophages. PM2.5 collected in Yokohama, Japan by the cyclone device significantly induced IL-33 expression in human THP-1 macrophages, and the induction was clearly suppressed by pretreatment with the aryl hydrocarbon receptor (AhR) antagonist CH-223191 or the Toll-like receptor 4 (TLR4) antagonist TAK-242. PM2.5-induced IL-33 expression was significantly attenuated in AhR-knockout or TLR4-mutated macrophages, suggesting an important role of polycyclic aromatic hydrocarbons (PAHs) and endotoxin in IL-33 stimulation. PM samples derived from tunnel dust slightly but significantly induced IL-33 expression, while road dust PM did not affect IL-33 expression. The PAH concentration in tunnel dust was higher than that in road dust. Tunnel dust or road dust PM contained less endotoxin than PM2.5 collected in Yokohama. These data suggest that the potency of IL-33 induction could depend on the concentration of PAHs as well as endotoxin in PMs. Caution regarding PAHs and endotoxin levels in air pollutants should be taken to prevent IL-33-induced allergic inflammation.