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[Display omitted] • A Fe(III)/NaClO oxidation system was developed for enhanced PAHs degradation. • Fe(III) dosage, NaClO concentration and pH value affected PAHs removal process. • PAHs degradation was ascribed to the synergetic effect of HClO and generated •OH. • Degradation pathways of phenanthrene by Fe(III)/NaClO oxidation was proposed. • The inhibitory effect on plants growth weakened for the remediated soil. Great attention has been paid to the removal of polycyclic aromatic hydrocarbons (PAHs) from polluted soil worldwide, because the refractory PAHs have severe carcinogenic, teratogenic, and mutagenic effects that put substantial threats to ecosystem safety and human health. In this study, a Fe(III)/NaClO catalytic oxidation system was employed to achieve an enhanced remediation of PAHs-contaminated industrial site soil. With an optimal mass ratio of Fe(III)/NaClO at 1/6, the removal efficiency of PAHs was improved by 19.6% and 14.8% after 2 and 48 h of reaction compared with using NaClO alone when the concentration of NaClO was set as 2000 mg/L. The degradation behavior of PAHs by Fe(III)/NaClO catalytic oxidation system was investigated in detail. The influence of Fe(III) dosage, NaClO concentration and pH value on PAHs removal was evaluated in-depth. The degradation products were confirmed and degradation pathways were proposed. Generated hydroxyl radicals (•OH) were identified by quenching experiments and electron paramagnetic resonance (EPR) technology, which played synergetic effects in the degradation of PAHs with HClO molecule. Finally, results of phytotoxicity tests demonstrated that the inhibition effects on plants growth decreased obviously of remediated soil. This work provided a catalytic oxidation method with cost-effectiveness, high efficiency and wide applicability for PAHs degradation in industrial site soil. [ABSTRACT FROM AUTHOR]

• In an exposure and rest model, PM2.5 paradoxically alleviated the disease severity and airway inflammatory responses in COPD-like mice. • PM2.5 and polycyclic aromatic hydrocarbons (PAHs) in PM2.5 induced inhibitory memory alveolar macrophages (AMs). • The induction of inhibitory trained AMs by PM2.5 was dependent on the IL-33 production from epithelial cells through the AhR/ARNT pathway. Fine particulate matter (PM2.5) concentrations have decreased in the past decade. The adverse effects of acute PM2.5 exposure on respiratory diseases have been well recognized. To explore the long-term effects of PM2.5 exposure on chronic obstructive pulmonary disease (COPD), mice were exposed to PM2.5 for 7 days and rest for 21 days, followed by challenges with lipopolysaccharide (LPS) and porcine pancreatic elastase (PPE). Unexpectedly, PM2.5 exposure and rest alleviated the disease severity and airway inflammatory responses in COPD-like mice. Although acute PM2.5 exposure increased airway inflammation, rest for 21 days reversed the airway inflammatory responses, which was associated with the induction of inhibitory memory alveolar macrophages (AMs). Similarly, polycyclic aromatic hydrocarbons (PAHs) in PM2.5 exposure and rest decreased pulmonary inflammation, accompanied by inhibitory memory AMs. Once AMs were depleted, pulmonary inflammation was aggravated. PAHs in PM2.5 promoted the secretion of IL-33 from airway epithelial cells via the aryl hydrocarbon receptor (AhR)/ARNT pathway. High-throughput mRNA sequencing revealed that PM2.5 exposure and rest drastically changed the mRNA profiles in AMs, which was largely rescued in IL-33−/− mice. Collectively, our results indicate that PM2.5 may mitigate pulmonary inflammation, which is mediated by inhibitory trained AMs via IL-33 production from epithelial cells through the AhR/ARNT pathway. We provide the rationale that PM2.5 plays complicated roles in respiratory disease. [ABSTRACT FROM AUTHOR]

[Display omitted] • Mn(Ⅱ) was effective at activating ClO 2 oxidation to promote PAHs degradation in real contaminated industrial soil. • With the increasing of Mn(Ⅱ) concentration, PAHs degradation efficiency first increased and then decreased. • The mechanism of PAHs degradation by Mn(Ⅱ) activated ClO 2 oxidation was ascribed to the HOCl and •OH. Chlorine dioxide (ClO 2) takes effect as a promising chemical oxidant to remove polycyclic aromatic hydrocarbons (PAHs) from contaminated soil in situ. However, the conventional ClO 2 degradation procedure is limited by its reaction selectivity to organic pollutants, as well as its low economic efficiency with huge dosage. Systematical study of activated ClO 2 oxidation which is more efficient to remove PAHs in soil is still scarce. Herein, the impact of divalent manganese ion [Mn(Ⅱ)] on activating ClO 2 to oxidize PAHs in real contaminated soil was currently studied, including the kinetics, degradation products, mechanisms, and biological toxicity. The results revealed that the PAHs removal rate constants (k 1) had a quadratic relationship with Mn(II) concentrations (k 1 = -0.005 × [Mn(Ⅱ)]2 + 0.0033 × [Mn(Ⅱ)] + 0.0222, R2 = 0.9084, [Mn(Ⅱ)] = 0 ∼ 5 mM), the best degradation performance was obtained when the molar ratio of Mn(II)/ClO 2 was 1/20. Furthermore, the optimal initial ClO 2 concentration of 2500 mg/L could satisfy the comprehensive considerations of efficiency and economy. At the pH range of 3 ∼ 11, the removal efficiency decreased with increasing pH. Four representative PAH congeners (anthracene, phenanthrene, pyrene, and fluoranthene) had been chlorine substituted and oxygenated, but benzene ring rupture was observed only in fluoranthene simultaneously. XPS spectra, EPR analysis, and quenching experiments indicated the mechanisms that HOCl and •OH were the principal active species in the oxidation reaction. The toxicity evaluation by earthworms Eisenia fetida resulted out that high toxic effect to organism still remained in remediated soil which should be paid attention to. [ABSTRACT FROM AUTHOR]