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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.

Epidemiologic studies have revealed that Asian sand dust particles (ASDs) can affect respiratory and immune health represented by asthma. Factors responsible for the exacerbation of asthma remain unclear. The fungus Bjerkandera adusta (B.ad) and polycyclic aromatic hydrocarbons such as benzo[a]pyrene (BaP) have been identified in ASDs collected from the atmosphere when an ASD event occurred. We investigated the effects of B.ad and BaP related to ASDs on respiratory and immune systems. Bone marrow-derived antigen-presenting cells (APCs) and splenocytes from atopic prone NC/Nga mice and human airway epithelial cells were exposed to the B.ad or to BaP in the presence and absence of heated-ASDs (H-ASDs). B.ad and BaP in both the presence and absence of H-ASDs increased the expression of cell surface molecules on APCs. H-ASDs alone slightly activated APCs. The expressions induced by B.ad were higher than those induced by BaP in the presence and absence of H-ASDs. There were no remarkable effects on the activation of splenocytes or the proinflammatory responses in airway epithelial cells. These results suggest that B.ad rather than BaP contributes to the exacerbation of asthma regardless of the presence or absence of sand particles, particularly by the activation of the immune system via APCs. Copyright © 2016 John Wiley & Sons, Ltd.

Epidemiologic studies have reported that Asian sand dust (ASD) particles can affect respiratory health; however, the mechanisms remain unclear. We investigated the effects of ASD on airway epithelial cells and immune cells, and their contributing factors to the effects. Human airway epithelial cells were exposed to ASD collected on 1-3 May (ASD1) and on 12-14 May (ASD2) 2011 in Japan and heat-treated ASD1 for excluding heat-sensitive substances (H-ASD) at a concentration of 0, 3, 30 or 90 µg ml(-1) for 4 or 24 h. Furthermore, bone marrow-derived dendritic cells (BMDC) from atopic prone mice were differentiated by culture with granulocyte-macrophage colony-stimulating factor (GM-CSF) then these BMDC were exposed to the ASD for 24 h. Also splenocytes as mixture of immune cells were exposed to the ASD for 72 h. All ASD dose dependently reduced viability of airway epithelial cells. Non-heated ASD showed a dose-dependent increase in the protein release of interleukin (IL)-6 and IL-8. The raises induced by ASD1 were higher than those by ASD2. ASD1 and ASD2 also elevated ICAM-1 at the levels of mRNA, cell surface protein and soluble protein in culture medium. In contrast, H-ASD did not change most of these biomarkers. Non-heated ASD showed enhancement in the protein expression of DEC205 on BMDC and in the proliferation of splenocytes, whereas H-ASD did not. These results suggest that ASD affect airway epithelial cells and immune cells such as BMDC and splenocytes. Moreover, the difference in ASD events and components adhered to ASD can contribute to the health effects.

This study was designed to investigate the effect of high-impact and low-repetition jump training on bones in ovariectomized (OVX) rats. Forty female Wistar rats were sham-operated (sham) or OVX at the age of 11 weeks. The rats were divided randomly into the following four groups: sham-sedentary (SS; n = 10), sham-exercised (SE; n = 10), OVX-sedentary (OS; n = 10), and OVX-exercised (OE; n = 10). The rats started the jump training at the age of 12 weeks. The jump-training protocol was 10 times/day, 5 days/week and the jumping-height was 40 cm. After 8 weeks of training, the mass and breaking force in the tibia and ulna, cross-sectional areas of diaphysis in the tibia, and serum bone turnover markers were measured. The jump training significantly increased the fat-free dry weight, ash weight, and ultimate breaking force in the tibia. The rate of increase in these parameters was similar in both the sham and the OVX groups. On the other hand, in the ulna, there were no significant changes in the ultimate breaking force. The jump training significantly increased the periosteal perimeter and cortical area, although the increase in these parameters in OE compared with OS was lower than that in SE compared with SS. The jump training significantly increased serum osteocalcin in the OVX groups, as well as in the sham groups. These results suggest that high-impact and low-repetition training had beneficial effects on bone formation and bone biomechanical properties in OVX rats, as well as in sham rats.

The hypothesis of the present study was that low-repetition and high-impact training of 10 maximum vertical jumps/day, 3 times/wk would be effective for improving bone mineral density (BMD) in ordinary young women. Thirty-six female college students, with mean age, height, and weight of 20.7 ± 0.7 yr, 158.9 ± 4.6 cm, and 50.4 ± 5.5 kg, respectively, were randomly divided into two groups: jump training and a control group. After the 6 mo of maximum vertical jumping exercise intervention, BMD in the femoral neck region significantly increased in the jump group from the baseline (0.984 ± 0.081 vs. 1.010 ± 0.080 mg/cm2; P < 0.01), although there was no significant change in the control group (0.985 ± 0.0143 vs. 0.974 ± 0.134 mg/cm2). And also lumbar spine (L2–4) BMD significantly increased in the jump training group from the baseline (0.991 ± 0.115 vs. 1.015 ± 0.113 mg/cm2; P < 0.01), whereas no significant change was observed in the control group (1.007 ± 0.113 vs. 1.013 ± 0.110 mg/cm2). No significant interactions were observed at other measurement sites, Ward's triangle, greater trochanter, and total hip BMD. Calcium intakes and accelometry-determined physical daily activity showed no significant difference between the two groups. From the results of the present study, low-repetition and high-impact jumps enhanced BMD at the specific bone sites in young women who had almost reached the age of peak bone mass.