Bioaccumulation of microplastics in the edible tissues of fish collected from urban lakes of Bangladesh: a potential exposure to public health.

Microplastic (MP) pollution is an emerging environmental problem, due to its universal dispersion. In the present study, we determined the MP pollution in water, sediment, and fish samples of three different urban lakes of Bangladesh to assess the bioaccumulation of MPs from the lake environment to fish's edible (flesh) and inedible tissue (gut), ecological risk and consequent human exposure to MPs by fish consumption. A total of forty-three fishes were collected from Jahangirnagar Co-Operative Housing Society (JCHS), Dhanmondi Lake (DL), and Saturia Thana Lake (MST). The average MP concentration in sediment and water of the lakes is 7588 ± 4353 MPs/kg dry weights; 142 ± 22 MPs/L, respectively. MPs were identified in the edible (2.8-20.2 MPs/g) and inedible (2.27-20.93 MPs/g) tissue of all fish species. The highest number of MPs was observed in the flesh of Labeo bata of the JCHS Lake and in the gut of Catla catla of DL. The most dominant shape of MPs was fiber and fragment, 0.1-0.4 mm was the dominant size range, and blue, purple, and transparent were the dominant colors. The presence of six polymer types was revealed by FT-IR analysis, which were polystyrene, polypropylene, nitrile, ethylene vinyl acetate, high-density polyethylene, and nylon. The concentration of MPs in fish is found to increase with the increment in body weight. The bioconcentration factor (BCF) analysis reveals that among all the fish species, Labeo bata and Oreochromis mossambicus accumulate the highest number of MPs from the lake environment. The pollution load index of MPs indicates that the sampling sites were within hazard levels III-IV. Estimated annual intake reveals that humans will be exposed to the highest number of MPs if they consume the flesh of Labeo bata of DL and JCHS Lake.

Oral itraconazole for the treatment of severe seborrhoeic dermatitis.

BACKGROUND: Seborrheic dermatitis (SD) is an inflammatory skin disorder in which colonies of Malassezia furfur have been found in affected areas. AIM: The aim of this study was to evaluate the efficacy of itraconazole in the treatment of severe SD. MATERIALS AND METHODS: Itraconazole was given to 30 patients of SD in a dose of 100 mg twice daily for 1 week followed by 200 mg/day for first 2 days of the following 2 months. The response was noted on day 15, 30, 60, and 90. The clinical response was graded as markedly effective, effective, or ineffective. RESULTS: Clinical improvement (evaluated as markedly effective or effective) was observed in 83.3% cases. CONCLUSION: The anti-inflammatory activity of oral itraconazole suggests that it should be the first-line therapy in severe SD.

Packed blood cells stored in AS-5 become proinflammatory during storage.

BACKGROUND: Studies have shown that packed blood cells (PBCs) stored in AS-1 (Adsol, Baxter) and AS-3 (Nutricel, Medsep Corp.) accumulate proinflammatory substances, which may contribute to increased complications from allogeneic blood transfusion. This study assessed whether supernates from PBCs stored in AS-5 (Optisol, Terumo Corp.) prime neutrophils (PMNs), activate platelets (PLTs), and accumulate proinflammatory cytokines and PMN granule constituents. STUDY DESIGN AND METHODS: PBC units were prepared in AS-5 from nonleukoreduced (NLR) and leukoreduced (LR) whole-blood units and stored at 4 degrees C. Supernates from samples of PBCs collected at various storage times were analyzed by multiplex enzyme-linked immunosorbent assay for proinflammatory cytokines and myeloperoxidase (MPO) and were incubated with type-matched blood, which was assessed by flow cytometry for expression of CD11b on PMNs, CD62P on PLTs, and formation of PMN-PLT aggregates. RESULTS: Supernates from NLR PBCs stored for at least 14 days elevated CD11b expression on PMNs and the number of PMN-PLT aggregates compared to supernates from collection day PBCs. The magnitude of these effects correlated with storage age. Supernates from LR PBCs did not elicit these responses. Expression of CD62P on PLTs was not affected by supernates from either NLR or LR PBCs. Levels of interleukin (IL)-1beta, IL-6, IL-8, IL-18, NAP-2, MCP-1, RANTES, and MPO were elevated in supernates from 28- and 42-day NLR units. Tumor necrosis factor alpha and MIP-1alpha did not increase, and cytokine levels in LR PBC units did not increase. CONCLUSION: Units of NLR PBCs stored in AS-5 become increasingly proinflammatory as a function of storage time. Leukoreduction prevents this change.

Effects of nitrogen dioxide on the expression of intercellular adhesion molecule-1, neutrophil adhesion, and cytotoxicity: studies in human bronchial epithelial cells.

Nitrogen Dioxide (NO2) is a product of high-temperature combustion and an environmental oxidant of concern. We have recently reported that early changes in NO2-exposed human bronchial epithelial cells are causally linked to increased generation of proinflammatory mediators, such as nitric oxide/nitrite and cytokines like interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and IL-8. The objective of the present in vitro study was to further delineate the cellular mechanisms of NO2-mediated toxicity, and to define the nature of cell death that ensues upon exposure of normal human bronchial epithelial (NHBE) cells to a brief high dose of NO2. Our results demonstrate that the NHBE cells undergo apoptotic cell death during the early post-NO2 period, but this is independent of any significant increase in caspase-3 activity. However, necrotic cell death was more prevalent at later time intervals. Interestingly, an increased expression of HO-1, a redox-sensitive stress protein, was observed in NO2-exposed NHBE cells at 24 h. Since neutrophils (PMNs) play an active role in acute lung inflammation and resultant oxidative injury, we also investigated changes in human PMN-NHBE cell interactions. As compared to normal cells, increased adhesion of PMNs to NO2-exposed cells was observed, which resulted in an increased NHBE cell death. The latter was also increased in the presence of IL-8 and TNF-alpha + interferon (IFN)-gamma, which correlated with upregulation of intercellular adhesion molecule-1 (ICAM-1). Our results confirmed an involvement of nitric oxide (NO) in NO2-induced cytotoxicity. By using NO synthase inhibitors such as L-NAME and 3-aminoguanidine (AG), a significant decrease in cell death, PMN adhesion, and ICAM-1 expression was observed. These findings indicate a role for the L-arginine/NO synthase pathway in the observed NO2-mediated toxicity in NHBE cells. Therapeutic strategies aimed at controlling excess generation of NO and/or inflammatory cytokines may be useful in alleviating NO2-mediated adverse effects on the bronchial epithelium.

Assessment of inflammatory response and sequestration of blood iron transferrin complexes in a rat model of lung injury resulting from exposure to low-frequency shock waves.

OBJECTIVE: Impact of air blast overpressure waves (OPW), or shock wave, with the body wall or body armor produces two types of energy waves: high-frequency low-amplitude stress waves and long-duration low-frequency share waves. These types of energy waves are characterized by different mechanisms of primary tissue injury that mostly affect lung. Systemic inflammation and resultant acute respiratory distress syndrome are known major secondary causative agents of delayed multiple organ failure and subsequent death after OPW exposure. However, association of each pattern of the blast OPW-produced energy waves with postexposure inflammatory events has not yet been delineated. The objectives of the present research were a) establishment of a rat model for assessment of the inflammatory response following lung injury produced by exposure to medium-amplitude (approximately 120 kPa) low-frequency (260+/-5 Hz) OPWs; and b) assessment of the dynamics of alteration in polymorphonuclear leukocyte counts and expression of CD11b adhesion molecules on the surface of polymorphonuclear leukocytes and status of iron-transferrin complexes in peripheral blood after OPW exposure. DESIGN: This study focused on the OPW effects at different time periods, using a sequential approach to postexposure events. Lung injury in rat was induced by OPW generated in a laboratory shock tube. Animals were exposed to OPW (at peak overpressure of 118+/-7 kPa) that produced "moderate" lung injury. SETTING: Military research institute. SUBJECTS: Twenty-seven CVF Sprague-Dawley rats were subjected to OPW exposures, and 17 sham-treated animals were used as control. INTERVENTIONS: Lung tissue and blood samples were collected at 1, 3, 6, 12, and 24 hrs following OPW exposures and compared with samples collected from nonexposed animals. MEASUREMENTS AND MAIN RESULTS: OPW-induced lung injury caused a 2.7-fold increase in the number of circulatory polymorphonuclear leukocytes as early as 1 hr postexposure, which is indicative of mobilization of the pool of marginated polymorphonuclear leukocytes into the free circulation. Polymorphonuclear leukocyte counts increased through the following 3- and 6-hr periods, when they were, respectively, 5-fold and 3.5-fold higher than in controls. These effects were accompanied by a pronounced expression of CD11b in polymorphonuclear leukocytes and tissue sequestration of blood iron-transferrin complexes during the entire 24-hr period of observations. The increase in circulatory polymorphonuclear leukocytes was accompanied by a decrease in iron-transferrin complex concentrations that apparently reflected implication of blood plasma iron in the inflammatory cell response to OPW-induced injury. CONCLUSIONS: The observed dynamics in polymorphonuclear leukocyte alterations in peripheral blood after OPW exposure were similar to those found recently in clinical observations of nonpenetrating injury and in animal models of infectious insults. Therefore, our data suggest that the main pattern of proinflammatory alterations in the rat model of lung injury induced by exposure to long-duration shock wave is similar to patterns that are characteristic of major trauma. The data further suggest that the expression of polymorphonuclear leukocyte CD11b and the response of iron-transferrin complex can be considered as potential surrogate markers in blood for systemic alterations following OPW-induced injury and, therefore, warrant further investigation in a human pilot study.

Pro-inflammatory responses of human bronchial epithelial cells to acute nitrogen dioxide exposure.

Nitrogen dioxide (NO2) is an environmental oxidant, known to be associated with lung epithelial injury. In the present study, cellular pro-inflammatory responses following exposure to a brief high concentration of NO2 (45 ppm) were assessed, using normal human bronchial epithelial (NHBE) cells as an in vitro model of inhalation injury. Generation and release of pro-inflammatory mediators such as nitric oxide (NO), IL-8, TNF-alpha, IFN-gamma and IL-1beta were assessed at different time intervals following NO2 exposure. Effects of a pre-existing inflammatory condition was tested by treating the NHBE cells with different inflammatory cytokines such as IFN-gamma, IL-8, TNF-alpha, IL-1beta, either alone or in combination, before exposing them to NO2. Immunofluorescence studies confirmed oxidant-induced formation of 3-nitrotyrosine in the NO2-exposed cells. A marked increase in the levels of nitrite (as an index of NO) and IL-8 were observed in the NO2-exposed cells, which were further enhanced in the presence of the cytokines. Effects of various NO inhibitors combined, with immunofluorescence and Western blotting data, indicated partial contribution of the nitric oxide synthases (NOSs) toward the observed increase in nitrite levels. Furthermore, a significant increase in IL-1beta and TNF-alpha generation was observed in the NO2-exposed cells. Although NO2 exposure alone did induce slight cytotoxicity (<12%), but presence of inflammatory cytokines such as TNF-alpha and IFN-gamma resulted in an increased cell death (28-36%). These results suggest a synergistic role of inflammatory mediators, particularly of NO and IL-8, in NO2-mediated early cellular changes. Our results also demonstrate an increased sensitivity of the cytokine-treated NHBE cells toward NO2, which may have significant functional implications in vivo.

Electron paramagnetic resonance analysis of transferrin-bound iron in animal models of blunt trauma.

BACKGROUND: Blood iron sequestration is known to be implicated in the systemic acute-phase response to trauma injury. The objective of the present research was to assess the effect of iron sequestration in animal models of blunt trauma by means of electron paramagnetic resonance spectroscopy of iron in complex with transferrin, a main iron-transporting protein in blood, and to correlate this effect with the extent of induced injury. METHODS: Two animal models of blunt trauma were explored in the present study. Blunt trauma in the rat model was produced by exposure of 14 animals to blast overpressure (BOP) (at peak BOP of either 86 +/- 5 kPa or 112 +/- 2 kPa) generated in a shock tube. Blunt trauma in the porcine model was produced by impact of high-speed projectiles made from a rubber-tipped, plastic composite weighing 28.64 +/- 0.12 g (mean +/- SEM, n = 8) with a length of approximately 6 cm and a diameter of approximately 4 cm. The projectiles were propelled by compressed helium onto eight animals at a velocity of 101.8 +/- 3.8 m/s (mean +/- SEM, n = 8) at the point of impact. Each experiment was accompanied by a pathology assessment using an injury scoring system developed for blunt trauma injuries to derive a severity score for whole-body involvement. Amounts of transferrin-bound iron (TRF-[Fe3+]) in whole blood and blood plasma samples were measured using quantitative electron paramagnetic resonance spectroscopy. The observed alterations in the amounts of blood TRF-[Fe3+] were correlated with estimated injury score ratios in each animal. RESULTS: Blunt trauma produced by either BOP exposure of rats or projectile impacts in pigs was accompanied by TRF-[Fe3+] sequestration observed in both blood and blood plasma. The amount of TRF-[Fe3+] in blood was shown to have inverse correlation with the extent of injury (Pearson r = -0.90 in the rat model and r = -0.93 in the porcine model) estimated by injury score ratios and was not dependent on location of the injury (lung, liver, spleen, or jejunum). CONCLUSION: The presented data suggest that assessment of TRF-[Fe3+] in blunt trauma can provide a good deal of information on severity of injury. The response of TRF-[Fe3+] can be considered as a potential surrogate marker of the systemic alterations in blunt trauma and, therefore, warrants further investigation in a human pilot study.