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Reproductive epidemiological studies have suggested associations between perinatal exposure to fine particulate matter (PM2.5) and adverse birth outcomes. To explore the effects of early prenatal exposure to PM2.5 on subsequent generations, pregnant mice were exposed to PM2.5 or filtered clean air in whole body dynamic exposure chambers for 14 consecutive days from gestation day (GD) 1.5 to GD15.5. Neurobehavioral tests showed that spontaneous locomotion and exploratory behaviors in the offspring were significantly enhanced in the open field test. Meanwhile, metabolomics analysis suggested activation of dopamine pathway while inhibition of glycine pathway in murine brains. Administration of the DRD4 antagonist, clozapine; or supplementation of glycine receptor agonist, taurine, to mice offspring attenuated the locomotor hyperactivities to levels indistinguishable from controls. These data provide strong evidence that maternal exposure to air pollution might increase the risk for neural disorders in the offspring during critical periods of brain development.

In the case of fire, explosive spalling often occurs in cementitious composites due to dense microstructure and high pore-pressure. Polymer fibers were proved to be effective in mitigating such behavior. However, deterioration of these fiber-reinforced cementitious composites inevitably occurs, which is vital for the prediction of structural performance and prevention of catastrophic disaster. This paper concentrates on the behavior and mechanism of the deterioration of polyvinyl alcohol fiber-reinforced engineered cementitious composite (PVA-ECC) after exposure to elevated temperatures. Surface change, cracking, and spalling behavior of the cubic specimens were observed at room temperature, and after exposure to 200 &deg, C, 400 &deg, C, 600 &deg, C, 800 &deg, C, and 1200 &deg, C. Losses in specimen weight and compressive strength were evaluated. Test results indicated that explosive spalling behavior was effectively prevented with 2.0 vol% polyvinyl alcohol fiber although the strength monotonically decreased with heating temperature. X-ray diffraction curves showed that the calcium hydroxide initially decomposed in the range of 400&ndash, 600 &deg, C, and finished beyond 600 &deg, C, while calcium silicate hydrate began at around 400 &deg, C and completely decomposed at approximately 800 &deg, C. Micrographs implied a reduction in fiber diameter at 200 &deg, C, exhibiting apparent needle-like channels beyond 400 &deg, C. When the temperature was increased to 600 &deg, C and above, the dents were gradually filled with newly produced substance due to the synergistic effect of thermal expansion, volume expansion of chemical reactions, and pore structure coarsening

Epidemiological studies have associated ambient fine particulate matter (PM2.5) exposure with lung cancer, in which epithelial-mesenchymal transition (EMT) is an initial process. Thus, it is important to identify the key molecule or pathway involved in the PM2.5 induced EMT. Human bronchial epithelial (HBE) cells were exposed to PM2.5 (100 or 500 μg/ml) for 30 passages and analyzed by metabolomics to identify the alteration of metabolites related to PM2.5 exposure. The expression levels of EMT markers were evaluated by qRT-PCR and Western blot assays in HBE cells and murine lung tissues. Reduced epithelial markers, increased mesenchymal markers expression levels and increased capacity of metastasis were observed in PM2.5-exposed HBE cells. Metabolomics analysis suggested upregulation of citrate acid with fold change (FC) of 2.89 or 4.18 in 100 or 500 μg/ml PM2.5 treated HBE cells. For both of the in vitro and in vivo study, the up-regulation of ATP citrate lyase (ACLY) was confirmed following PM2.5 exposure. Importantly, ACLY knockdown in HBE cells reversed EMT, migration and invasion capacities in HBE cells induced by PM2.5. Taken together, our data suggest that inhibition of ACLY demonstrates a protection against PM2.5-induced EMT, providing a concern on the molecular mechanisms of PM2.5-associated pulmonary disorders.

Background Inhaled nanoparticles can deposit in the deep lung where they interact with pulmonary cells. Despite numerous studies on pulmonary nanotoxicity, detailed molecular mechanisms of specific nanomaterial-induced lung injury have yet to be identified. Results Using whole-body dynamic inhalation model, we studied the interactions between aluminum oxide nanoparticles (Al2O3 NPs) and the pulmonary system in vivo. We found that seven-day-exposure to Al2O3 NPs resulted in emphysema and small airway remodeling in murine lungs, accompanied by enhanced inflammation and apoptosis. Al2O3 NPs exposure led to suppression of PTPN6 and phosphorylation of STAT3, culminating in increased expression of the apoptotic marker PDCD4. Rescue of PTPN6 expression or application of a STAT3 inhibitor, effectively protected murine lungs from inflammation and apoptosis, as well as, in part, from the induction of chronic obstructive pulmonary disease (COPD)-like effects. Conclusion In summary, our studies show that inhibition of PTPN6 plays a critical role in Al2O3 NPs-induced COPD-like lesions. Electronic supplementary material The online version of this article (10.1186/s12989-017-0234-0) contains supplementary material, which is available to authorized users.

Particulate matter (PM) exposure has been associated with intestinal disorders. Therefore, there is an urgent need to understand the precise molecular mechanism involved and explore potential prevention strategies. In this study, inhaled PM is shown to activate inflammatory pathways in murine colon. In a panel study, it is found that ambient PM levels are significantly associated with elevated number of fecal white blood cells in healthy subjects. Acting as a promoter, PM exposure accelerates chemical carcinogenesis‐induced colonic tumor formation in a murine model. Mechanistically, RNA‐seq assays suggest activation of phosphoinositide 3‐kinase (PI3K)/AKT cascades in chronically PM‐exposed human colon mucosal epithelial cells. Ablation of up‐stream driver fibroblast growth factor receptor 4 (FGFR4) effectively inhibits inflammation and neoplasia in PM‐exposed murine colons. Notably, dietary curcumin supplement is shown to protect against PM‐induced colonic injuries in mice. Collectively, these findings identify that PM exposure accelerates colonic tumorigenesis in a PI3K/AKT‐dependent manner and suggests potential nutrient supplement for prevention.