Evaluating the metallic pollution of riverine water and sediments: a case study of Aras River.

Metallic pollution caused by elements Zn, Cu, Fe, Pb, Ni, Cd, and Hg in water and sediments of Aras River within a specific area in Ardabil province of Iran is considered. Water and sediment samples were collected seasonally and once respectively from the five selected stations. Regarding WHO published permissible values, only Ni concentration in spring and summer water samples has exceeded the acceptable limit up to four times greater than the limit. The concentration of metals Ni, Pb, and Fe in river water shows a direct relationship with river water discharge and the amount of precipitation. Enhanced soil erosion, bed load dissolution, and runoffs may play a key role in remarkable augmentation of metallic ions concentration. Furthermore, excessive use of pesticides which contain a variety of metallic ions (mainly Cu) in spring and summer may also result in an increase in the metals' concentration. The potential risk of Ni exposure to the water environment of the study area is assigned to juice, dairy products, edible oil, and sugar cane factories as well as soybean crop lands which are located within the sub-basin of Aras River in the study area. Regarding the sediment samples, the bioavailable metal concentrations indicate an ascending order from the first station towards the last one. In comparison with earth crust, sedimental and igneous rocks the reported metallic concentration values, except for Cd, lie within the low-risk status. Regarding Cd, the reported values in some stations (S2, S4, and S5) are up to ten times greater than that of shale which may be considered as a remarkable risk potential. The industrial and municipal wastewater generated by Parsabad moqan industrial complex and residential areas, in addition to the discharges of animal husbandry centers, may be addressed as the key factors in the sharp increase of metallic pollution potential in stations 4 and 5.

Findings on the phytoextraction and phytostabilization of soils contaminated with heavy metals.

As a result of human activities such as mining, metal pollution has become one of the most serious environmental problems today. Phytoremediation, an emerging cost-effective, non-intrusive, and aesthetically pleasing technology that uses the remarkable ability of plants to concentrate elements can be potentially used to remediate metal-contaminated sites. The aim of this work was to assess the extent of metal accumulation by plants found in a mining area in Hamedan province with the ultimate goal of finding suitable plants for phytoextraction and phytostabilization (two processes of phytoremediation). To this purpose, shoots and roots of the 12 plant species and the associated soil samples were collected and analyzed by measurement of total concentrations of some elements (Fe, Mn, Zn, and Cu) using atomic absorption spectrophotometer and then biological absorption coefficient, bioconcentration factor, and translocation factor parameters calculated for each element. Our results showed that none of the plants were suitable for phytoextraction and phytostabilization of Fe, Zn, and Cu, while Chenopodium botrys, Stipa barbata, Cousinia bijarensis, Scariola orientalis, Chondrila juncea, and Verbascum speciosum, with a high biological absorption coefficient for Mn, were suitable for phytoextraction of Mn, and C. bijarensis, C. juncea, V. speciosum, S. orientalis, C. botrys, and S. barbata, with a high bioconcentration factor and low translocation factor for Mn, had the potential for the phytostabilization of this element.

Effect of p38 MAPK inhibition on corticosteroid suppression of cytokine release in severe asthma.

Patients with severe asthma respond less well to corticosteroids than those with non-severe asthma. Increased p38 mitogen-activated protein kinase (MAPK) activation in alveolar macrophages (AMs) from severe asthma patients has been associated with a reduced inhibition of cytokine release by dexamethasone. We determined whether p38 MAPK inhibitors would modulate corticosteroid suppression of cytokine release from AMs and peripheral blood mononuclear cells (PBMCs). PBMCs were isolated from venous blood and AMs by bronchoalveolar lavage in severe and non-severe asthma patients. PBMCs and AMs were exposed to lipopolysaccharide (LPS) with and without the p38 MAPK inhibitor, SD282, or dexamethasone. We determined the concentration-dependent effects of another p38 MAPK inhibitor, GW-A, on dexamethasone-induced inhibition of interleukin (IL)-8 release from PBMCs. Cytokines were assayed using an ELISA-based method. SD282 (10(-7) M), with dexamethasone (10( -6) M), caused a greater inhibition of release of IL-1beta, IL-6, macrophage inflammatory protein-1alpha and IL-10, than with dexamethasone alone in AMs from severe and non-severe asthma. At 10(-9) and 10(-10) M, GW-A, that had no direct effects, increased the inhibitory activity of dexamethasone (10(-8) and 10( -6) M) on LPS-induced IL-8 release in PBMCs from severe asthma. Corticosteroid insensitivity in severe asthma patients may be improved by inhibitors of p38 MAPK.

Relative corticosteroid insensitivity of alveolar macrophages in severe asthma compared with non-severe asthma.

BACKGROUND: About 5-10% of patients with asthma suffer from poorly controlled disease despite corticosteroid (CS) treatment, which may indicate the presence of CS insensitivity. A study was undertaken to determine whether relative CS insensitivity is present in alveolar macrophages from patients with severe asthma and its association with p38 mitogen-activated protein kinase (MAPK) activation and MAPK phosphatase-1 (MKP-1). METHODS: Fibreoptic bronchoscopy and bronchoalveolar lavage (BAL) were performed in 20 patients with severe asthma and 19 with non-severe asthma and, for comparison, in 14 normal volunteers. Alveolar macrophages were exposed to lipopolysaccharide (LPS, 10 mug/ml) and dexamethasone (10(-8) and 10(-6) M). Supernatants were assayed for cytokines using an ELISA-based method. p38 MAPK activity and MKP-1 messenger RNA expression were assayed in cell extracts. RESULTS: The inhibition of LPS-induced interleukin (IL)1beta, IL6, IL8, monocyte chemotactic protein (MCP)-1 and macrophage inflammatory protein (MIP)-1alpha release by dexamethasone (10(-6) M) was significantly less in macrophages from patients with severe asthma than in macrophages from patients with non-severe asthma. There was increased p38 MAPK activation in macrophages from patients with severe asthma. MKP-1 expression induced by dexamethasone and LPS, expressed as a ratio of LPS-induced expression, was reduced in severe asthma. CONCLUSION: Alveolar macrophages from patients with severe asthma demonstrate CS insensitivity associated with increased p38 MAPK activation that may result from impaired inducibility of MKP-1.

Modulation of ozone-induced airway hyperresponsiveness and inflammation by interleukin-13.

The present study aimed to determine whether the T-helper cell type 2-derived cytokines, interleukin (IL)-4 and -13, can modulate the lung response to ozone exposure. IL-13(-/-), IL-4/13(-/-) and IL-13-overexpressing transgenic (Tg) mice were exposed to ozone (3 ppm; 3 h) or air. Wild-type (Wt) Balb/c mice and transgenic-negative littermates (IL-13Wt) were used as controls for gene-deficient and IL-13Tg mice, respectively. IL-4/13(-/-) and IL-13(-/-) mice developed a lesser degree of ozone-induced airway hyperresponsiveness (AHR) while IL-13Tg mice developed a greater degree of AHR compared with ozone-exposed wild-type or IL-13Wt mice, respectively. Ozone caused a time-dependent increase of bronchoalveolar lavage (BAL) neutrophils and macrophages in wild-type mice, maximal at 20-24 h, which was attenuated in the IL-13(-/-) and IL-4/13(-/-) mice. In IL-13Tg mice, there was a greater increase in BAL neutrophils after ozone exposure compared with IL-13Wt mice. Using quantitative real-time PCR, ozone-induced mRNA expression for IL-6 and keratinocyte chemokine was further enhanced in IL-13(-/-) and IL-4/13(-/-) mice, and was inhibited in IL-13Tg mice. Macrophage inflammatory protein (MIP)-3alpha/CCL20 expression was enhanced after ozone exposure in wild-type mice, inhibited in IL-13(-/-) and IL-4/13(-/-) mice, while in IL-13Tg mice it was enhanced. A similar pattern of expression was observed with lipopolysaccharide-induced cytokine (LIX/CXCL5/ENA-78) expression. In conclusion, interleukin-13 augments ozone-induced airway hyperresponsiveness and neutrophilic inflammation, possibly through modulation of certain cytokines induced by ozone exposure.