Ppm Cl2 Research Articles

Effectiveness of different antimicrobial washes combined with freezing against Escherichia coli O157:H7, Salmonella Typhimurium, and Listeria monocytogenes inoculated on blueberries

To ensure the safety of produce, including blueberries, elimination of potential pathogens is critical. This study evaluated the efficacy of antimicrobial washes when coupled with frozen storage against Escherichia coli O157:H7, Salmonella Typhimurium and Listeria monocytogenes on wild blueberries. Inoculated blueberries were sprayed with antimicrobial solutions at different concentrations for various contact times (chlorine dioxide -2.5, 5, 10, and 15 ppm for 10 s, 1, 5, and 10 min; chlorine -100, 150, and 200 ppm for 10s, 1, 5, and 10 min; lactic acid 1 and 2% for 5, 10 and 20 min) and following treatment, stored at −12 °C for 1 week. Compared to antimicrobial washing alone, the additional freezing significantly reduced pathogens (P < 0.05). Concentrations of all three antimicrobials combined with freezing reduced L. monocytogenes to undetectable levels (detection limit < 1 log CFU/g). The greatest reduction of E. coli O157:H7 (4.4 log CFU/g) and Salmonella (5.4 log CFU/g) was achieved by 2% lactic acid or 200 ppm Cl2 followed with frozen storage. These antimicrobials maintained the visual quality of blueberries and did not leave detectable residues. In conclusion, antimicrobial washes, when combined with frozen storage, effectively reduce the risk of pathogen contamination on blueberries.

Ultrahigh sensitivity and selectivity chlorine gas sensing of In2O3 hollow microtubules by bio-template method with degreasing cotton

A simple two-stage procedure of immersion-calcination method has been developed for preparing In2O3 hollow microtubules by using degreasing cotton as soft bio-templates. The morphological feature was characterized as hollow microtubules with the range of 50–70 μm in length, 5–6 μm in width, and about 1 μm in thickness. The Cl2 sensing properties were remarkably enhanced in sensitivity and selectivity for In2O3 hollow microtubules. The gas response (Rgas/Rair) of the In2O3 hollow microtubules sensor was 1051 to 10 ppm Cl2 at 200 °C, which was 25 times higher than In2O3 particles. Such outstanding gas sensing performance was ascribed to the hollow morphology, which revealed high specific surface area, abundant oxygen vacancies and low band gap. The gas sensing mechanism was deduced that Cl2 molecules are directly adsorbed on the metal oxide surface and oxygen vacancies.

Effects of interfering gases in electrochemical sensors NH3 and NO2

Electrochemical sensors used for toxic gas measurement. In this paper construction EC sensor and principle of operation has been described. The results of research on the influence of interfering gases on the readings of detectors containing ammonia and nitric oxide (IV) electrochemical sensors are presented. Span gases were used in the tests: 100 ppm CO, 25 ppm H2S, 25 ppm NH3, 10 ppm NO, 25 ppm NO2, 10 ppm Cl2, 10 ppm HCN, 10 ppm HCl, 2% vol. H2, 2.5% by volume CH4, 0.35% by volume of C5H12. The conducted research indicates that the presence of chlorine, hydrogen chloride, hydrogen cyanide, carbon monoxide and saturated hydrocarbons in the atmosphere does not affect the work of the ammonia electrochemical sensor. In the case of this sensor, there was a significant cross effect in relation to hydrogen sulphide and hydrogen. The administration of these substances indicated the presence of ammonia outside the measuring range (200 ppm). In the measurements using the NO2 sensor, in most cases negative interference was found. The test results indicate that the measurements made with electrochemical sensors may be subject to error in the presence of interfering gases. The results obtained may be both understated and overstated.

The effect of platinum precursor concentrations on chlorine sensing characteristics of platinum nanoparticles−loaded single walled carbon nanotubes

The correlation between platinum (Pt) functionalization and chlorine (Cl2) sensing capability in single-walled carbon nanotubes (SWCNTs) was investigated. Utilizing a photoreduction technique via ultraviolet (UV) irradiation, the Pt nanoparticles (NPs) with various diameters of 7–80 nm, which were controlled by Pt precursor concentrations, were successfully functionalized on the sidewalls of SWCNTs. The discrete Pt NP−loaded SWCNTs exhibited significantly enhanced response value (−(ΔR/R0) × 100 = 33.8%) for 1 ppm Cl2 at room temperature (25 °C) compared with that (no response) of pure SWCNTs. On the other hand, in case of continuous Pt NP–loaded SWCNTs, Cl2 sensing capabilities were significantly degraded. The Cl2 sensing capabilities of fabricated sensors tended to correlate with geometric configurations of the catalytic Pt NPs on the sidewalls of SWCNTs, due to differences in the electron pathway.

CysLT1 Receptor Is Protective against Oxidative Stress in a Model of Irritant-Induced Asthma.

The bronchoconstrictive and proinflammatory properties of cysteinyl leukotrienes (cysLTs) in allergic asthma mediate their effects predominantly through the cysLT1 receptor (cysLT1R). However, the role of cysLTs and cysLT1R in innate immune-triggered asthma is largely unexplored. We explored the synthesis of cysLTs and cysLT1R as determinants of airway responses in an oxidative stress-induced model of irritant asthma. Wild-type (WT) mice exposed to 100 ppm Cl2 for 5 min had airway neutrophilia, increased cysLT production, and pulmonary expression of cysLT-related biosynthetic genes. CysLT1R-deficient (CysLTr1(-/-)) mice that were exposed to Cl2 demonstrated airway hyperresponsiveness to inhaled methacholine significantly greater than in WT BALB/c mice. Compared to WT mice, airway neutrophilia and keratinocyte chemoattractant production levels were higher in CysLTr1(-/-) mice and airway hyperresponsiveness was ameliorated using a granulocyte depletion Ab. CysLTr1(-/-) mice also demonstrated prolonged bronchial epithelial cell apoptosis following Cl2 WT mice showed increased antioxidant and NF erythroid 2-related factor 2 (Nrf2) gene expression, Nrf2 nuclear translocation in bronchial epithelial cells, and increased reduced glutathione/oxidized glutathione following Cl2 exposure whereas CysLTr1(-/-) mice did not. Furthermore, CysLTr1(-/-) mice demonstrated increased pulmonary E-cadherin expression and soluble E-cadherin shedding compared with WT mice. Loss of a functional cysLT1R results in aberrant antioxidant response and increased susceptibility to oxidative injury, apparently via a cysLT1R-dependent impairment of Nrf2 function.

Chlorine inhalation-induced myocardial depression and failure.

Victims of chlorine (Cl2) inhalation that die demonstrate significant cardiac pathology. However, a gap exists in the understanding of Cl2-induced cardiac dysfunction. This study was performed to characterize cardiac dysfunction occurring after Cl2 exposure in rats at concentrations mimicking accidental human exposures (in the range of 500 or 600 ppm for 30 min). Inhalation of 500 ppm Cl2 for 30 min resulted in increased lactate in the coronary sinus of the rats suggesting an increase in anaerobic metabolism by the heart. There was also an attenuation of myocardial contractile force in an ex vivo (Langendorff technique) retrograde perfused heart preparation. After 20 h of return to room air, Cl2 exposure at 500 ppm was associated with a reduction in systolic and diastolic blood pressure as well echocardiographic/Doppler evidence of significant left ventricular systolic and diastolic dysfunction. Cl2 exposure at 600 ppm (30 min) was associated with biventricular failure (observed at 2 h after exposure) and death. Cardiac mechanical dysfunction persisted despite increasing the inspired oxygen fraction concentration in Cl2-exposed rats (500 ppm) to ameliorate hypoxia that occurs after Cl2 inhalation. Similarly ex vivo cardiac mechanical dysfunction was reproduced by sole exposure to chloramine (a potential circulating Cl2 reactant product). These results suggest an independent and distinctive role of Cl2 (and its reactants) in inducing cardiac toxicity and potentially contributing to mortality.

Neutrophils mediate airway hyperresponsiveness after chlorine-induced airway injury in the mouse.

Chlorine gas (Cl2) inhalation causes oxidative stress, airway epithelial damage, airway hyperresponsiveness (AHR), and neutrophilia. We evaluated the effect of neutrophil depletion on Cl2-induced AHR and its effect on the endogenous antioxidant response, and if eosinophils or macrophages influence Cl2-induced AHR. We exposed male Balb/C mice to 100 ppm Cl2 for 5 minutes. We quantified inflammatory cell populations in bronchoalveolar lavage (BAL), the antioxidant response in lung tissue by quantitative PCR, and nuclear factor (erythroid-derived 2)-like 2 (NRF2) nuclear translocation by immunofluorescence. In vitro, NRF2 nuclear translocation in response to exogenous hypochlorite was assessed using a luciferase assay. Anti-granulocyte receptor-1 antibody or anti-Ly6G was used to deplete neutrophils. The effects of neutrophil depletion on IL-13 and IL-17 were measured by ELISA. Eosinophils and macrophages were depleted using TRFK5 or clodronate-loaded liposomes, respectively. AHR was evaluated with the constant-phase model in response to inhaled aerosolized methacholine. Our results show that Cl2 exposure induced neutrophilia and increased expression of NRF2 mRNA, superoxide dismutase-1, and heme-oxygenase 1. Neutrophil depletion abolished Cl2-induced AHR in large conducting airways and prevented increases in antioxidant gene expression and NRF2 nuclear translocation. Exogenous hypochlorite administration resulted in increased NRF2 nuclear translocation in vitro. After Cl2 exposure, neutrophils occupied 22 ± 7% of the luminal space in large airways. IL-17 in BAL was increased after Cl2, although this effect was not prevented by neutrophil depletion. Neither depletion of eosinophils nor macrophages prevented Cl2-induced AHR. Our data suggest the ability of neutrophils to promote Cl2-induced AHR is dependent on increases in oxidative stress and occupation of luminal space in large airways.

N-acetyl cysteine improves the effects of corticosteroids in a mouse model of chlorine-induced acute lung injury.

Chlorine (Cl2) causes tissue damage and a neutrophilic inflammatory response in the airways manifested by pronounced airway hyperreactivity (AHR). The importance of early anti-inflammatory treatment has previously been addressed. In the previous study, both high-dose and low-dose of dexamethasone (DEX) decreased the risk of developing delayed effects, such as persistent lung injuries, while only high-dose treatment could significantly counteract acute-phase effects. One aim of this study was to evaluate whether a low-dose of DEX in combination with the antioxidant N-acetyl cysteine (NAC) and if different treatments (Triptolide, Reparixin and Rolipram) administered 1h after Cl2-exposure could improve protection against acute lung injury in Cl2-exposed mice. BALB/c mice were exposed to 300 ppm Cl2 during 15 min. Assessment of AHR and inflammatory cells in bronchoalveolar lavage was analyzed 24h post exposure. Neither of DEX nor NAC reduced the AHR and displayed only minor effects on inflammatory cell influx when given as separate treatments. When given in combination, a protective effect on AHR and a significant reduction in inflammatory cells (neutrophils) was observed. Neither of triptolide, Reparixin nor Rolipram had an effect on AHR but Triptolide had major effect on the inflammatory cell influx. Treatments did not reduce the concentration of either fibrinogen or plasminogen activator inhibitor-1 in serum, thereby supporting the theory that the inflammatory response is not solely limited to the lung. These results provide a foundation for future studies aimed at identifying new concepts for treatment of chemical-induced lung injury. Studies addressing combination of anti-inflammatory and antioxidant treatment are highly motivated.

Potential anti‐inflammatory effects of nebulized local anesthetics on inhaled chlorine lung injury (834.8)

Chlorine (Cl2) is a chemical used in both industry and society alike, despite it being a highly irritant and reactive gas. Acute exposure can result in symptoms of airway obstruction such as wheezing, shortness of breath, mouth/nose/chest pain, and bronchospasm. Currently, there is no known antidote for chlorine’s poisoning effects. Potential treatments include topical exposure of the airways to nebulized drugs such as local anesthetics which have been shown to improve the mobility of monitored animals after exposure to Cl2 gas. In this research project, we assess the effects of the nebulized local anesthetics lidocaine (1% and 4%), 3% 2‐Chloroprocaine following exposure to 100 or 400 ppm of chlorine gas on biochemical measurements of injury to airway. Wet‐to‐dry lung weight ratios, bronchoalveolar lavage (BAL) cell counts and total protein, and lung homogenate cytokine levels were determined 24 hours after Cl2 gas exposure and anesthetic treatment. In mice exposed to 400 ppm Cl2 gas, 1% lidocaine had the greatest decrease of wet‐to‐dry lung weight ratio in addition to lower live cell infiltration and lower protein concentrations in BAL fluids indicating a potential anti‐inflammatory affect. Cytokine levels from lung homogenates after exposure and treatments had a decreasing trend compared to untreated animals. Levels of IL‐10, IFNγ, MCP‐1 and IL‐13 were significantly lower in the 1% lidocaine animal group. Similar but not identical results were found following treatment with 100ppm Cl2. Treatment with 4% lidocaine and 3% 2‐chloroprocaine had potential toxic effects. This study indicates that nebulized 1% lidocaine is potentially a good treatment option after chlorine induced lung injury based on behavioral and biochemical data.Grant Funding Source: Supported by 1R21ES022876

Effects of Aluminum Solids on the under Deposit Corrosion of Copper in Synthetic Potable Water: The Arguments for and against a Semi-Permeable Membrane

Aluminum solids promote under deposit pitting of UNS C11000 copper. The possible roles that aluminum solids (i.e., Al(OH)3) play to promote copper pitting were examined by various characterization methods followed by diagnostic chemical/electrochemical methods in Edwards synthetic drinking water (ESDW). Cathodic polarization scans indicated that aluminum solids did not affect the intrinsic cathodic half-cell kinetics on an isolated copper electrode. Cyclic potentiodynamic polarization (CPP) experiments showed that the pitting potential (EPit) of copper was decreased by the presence of gelatinous aluminum solids deposited on the surface. Multi-electrode arrays (MEAs) with various surface deposition treatments were tested in ESDW under both driven and natural conditions. Lower pitting potentials were found under driven conditions on copper electrodes containing aluminum deposits. Pitting events also occurred on copper electrodes containing aluminum deposits with the presence of 5 ppm Cl2 under freely corroding conditions. MEAs were also tested with an inert Delrin crevice former. In this case, a lower EPit and greater number of pitting events were found outside the crevice former. The drop in EPit was not as severe as in the case of deposited Al(OH)3, pointing to effects besides geometrically occluded sites, produced by inert crevice formers. Preferential sorption/transport of selected anions (OH−, HCO3−, SO42−, and Cl−) through gelatinous Al(OH)3 was studied. Plausible explanations for the detrimental effects of Al(OH)3 were given.

Porous thin sheet-based α-Fe2O3-doped In2O3 structures: hydrothermal synthesis and enhanced Cl2 sensing performance

A facile hydrothermal route was employed to synthesize porous thin sheet-based α-Fe2O3-doped In2O3 structures including nanosheets and microflowers without any surfactant and template. The morphologies of the porous thin sheet-based α-Fe2O3-doped In2O3 structures consisted of many porous thin sheets with lengths of 80–100 nm and widths of 5–10 nm, while the pores in the sheets were 2–10 nm, and the amount of α-Fe2O3-doping significantly affected the overall morphology. The characterization of the porous thin sheet-based α-Fe2O3-doped In2O3 structures was obtained using nitrogen adsorption–desorption isotherms at 77 K. The results showed that the porous thin sheet-based α-Fe2O3-doped In2O3 structures (S4) adsorbed the largest amount of N2 and had the biggest surface area, which contributed to the improvement of the gas sensing characteristics. Furthermore, the gas sensing characteristics of the obtained products were studied. The results demonstrated that the sensors based on α-Fe2O3-doped In2O3 structures exhibited a much higher response to Cl2 than those without α-Fe2O3 (S1), and the In/Fe = 9 : 1 (molar ratio) showed the highest response. The sensor based on porous thin sheet-based α-Fe2O3-doped In2O3 structures (S4) exhibited a high response, up to 48.2 ± 4.8 to 5 ppm Cl2, quick response–recovery behavior and excellent stability, which implies good potential for practical applications. Finally, the gas sensing mechanism was also studied.

Enhanced Cl2 sensing performance by decorating discrete Au nanoparticles on octahedral CdIn2O4 crystals

High response to low-concentration Cl2 gas was achieved by a sensor based on octahedral crystals of CdIn2O4 decorated by Au nanoparticles (Au NPs). CdIn2O4 crystals were synthesized in a one-step hydrothermal reaction and Au NPs were functionalized onto CdIn2O4 also in a hydrothermal reaction. Systematic investigations revealed that the Au NPs-decorated CdIn2O4 samples possessed a superior sensing capability, compared with bare CdIn2O4 crystals. The optimal Au NPs loading (2 wt%) resulted in 8.3-fold enhancement in gas response to 1 ppm Cl2 at the working temperature, 190 °C, compared to bare CdIn2O4. The Au NPs on the surface enhanced the sensor response due to the catalytic activity of Au NPs and the strong electronic interaction between Au NPs and CdIn2O4 support. This work provides a promising approach for fabricating such a hybrid structure with excellent gas sensing capabilities.

Antioxidant consumption in squalane and polyethylene exposed to chlorinated aqueous media

Squalane stabilized with 0.2 wt.% of Irganox 1010 and a medium-density polyethylene containing 0.1 wt.% of the same antioxidant were exposed to two different aqueous media (water solutions containing either 10 ppm Cl2 or 10 ppm ClO2, both buffered to pH = 6.8) at different temperatures between 30 and 70 °C. The squalane phase was characterized by differential scanning calorimetry (oxidation induction time, OIT) and infrared spectroscopy, and the aqueous media were analysed after concentrating the analytes using liquid–liquid extraction by liquid chromatography, mass spectrometry and infrared spectroscopy. OIT measurements were carried out on the polyethylene samples after exposure to the chlorinated aqueous media. Exposure of the squalane systems to water containing ClO2 resulted in discolouration by the formation of quinoid structures and a faster depletion of the antioxidant than exposure to water containing Cl2. The activation energy for the loss of antioxidant activity on exposure to ClO2-water was very low (<10 kJ mol−1) in the squalane test (no diffusion control) and 21 ± 2 kJ mol−1 at a depth of 1–2 mm from the surface of polyethylene plaques (diffusion control). Calculation from earlier published OIT data from a HDPE exposed to Cl2-water yielded an activation energy for the loss antioxidant activity of 68 kJ mol−1. The antioxidant degradation products obtained from the exposure to the ClO2 aqueous medium were found at a higher concentration, were more polar and exhibited a higher proportion of low molar mass species than those obtained after exposure to the Cl2 aqueous medium. The important chemical difference between ClO2 and Cl2 is that the former is a one-electron oxidant whereas the latter preferentially reacts by hydrogen substitution. Possible further reactions, in agreement with the observations made, are proposed.

Chlorine contaminants poisoning of solid oxide fuel cells

Investigation has been conducted on the poisoning effect of various contaminants containing chlorine at ppm level (<10 ppm) on the performance of Ni-YSZ anode-supported solid oxide fuel cells. The results indicate that cell performance drops by exposure to 1 ppm Cl2(g) at 750 °C, whereas the introduction of Cl2(g) with concentration higher than 5 ppm causes only a slight degradation at 850 °C. The presence of 2–6 ppm CH3Cl(g) and C2H3Cl(g) can also induce measurable cell performance decline at 750 and 850 °C and this deterioration cannot be completely removed after switching to pure fuel at 850 °C. No performance loss is found when the cell is operated in fuel containing 1–8 ppm HCl(g) at 750 and 850 °C. It is thus concluded that chlorine in the form of Cl2(g) yields the largest poisoning effect at 750 °C, while the degradation rate caused by addition of C2H3Cl(g) increases with the increase of operation temperature. Agglomerations at anodic region are observed in the samples after poisoning test by Cl2(g), CH3Cl(g), and C2H3Cl(g), but the anode microstructure is uniform for the sample exposed to HCl(g) for poisoning test.

Mitigation of chlorine-induced lung injury by low-molecular-weight antioxidants

Chlorine (Cl(2)) is a highly reactive oxidant gas used extensively in a number of industrial processes. Exposure to high concentrations of Cl(2) results in acute lung injury that may either resolve spontaneously or progress to acute respiratory failure. Presently, the pathophysiological sequelae associated with Cl(2)-induced acute lung injury in conscious animals, as well as the cellular and biochemical mechanisms involved, have not been elucidated. We exposed conscious Sprague-Dawley rats to Cl(2) gas (184 or 400 ppm) for 30 min in environmental chambers and then returned them to room air. At 1 h after exposure, rats showed evidence of arterial hypoxemia, respiratory acidosis, increased levels of albumin, IgG, and IgM in bronchoalveolar lavage fluid (BALF), increased BALF surfactant surface tension, and significant histological injury to airway and alveolar epithelia. These changes were more pronounced in the 400-ppm-exposed rats. Concomitant decreases of ascorbate (AA) and reduced glutathione (GSH) were also detected in both BALF and lung tissues. In contrast, heart tissue AA and GSH content remained unchanged. These abnormalities persisted 24 h after exposure in rats exposed to 400 ppm Cl(2). Rats injected systemically with a mixture of AA, deferoxamine, and N-acetyl-L-cysteine before exposure to 184 ppm Cl(2) had normal levels of AA, lower levels of BALF albumin and normal arterial Po(2) and Pco(2) values. These findings suggest that Cl(2) inhalation damages both airway and alveolar epithelial tissues and that resulting effects were ameliorated by prophylactic administration of low-molecular-weight antioxidants.

Time course of airway remodelling after an acute chlorine gas exposure in mice

Accidental chlorine (Cl2) gas inhalation is a common cause of acute airway injury. However, little is known about the kinetics of airway injury and repair after Cl2 exposure. We investigated the time course of airway epithelial damage and repair in mice after a single exposure to a high concentration of Cl2 gas. Mice were exposed to 800 ppm Cl2 gas for 5 minutes and studied from 12 hrs to 10 days post-exposure. The acute injury phase after Cl2 exposure (≤ 24 hrs post-exposure) was characterized by airway epithelial cell apoptosis (increased TUNEL staining) and sloughing, elevated protein in bronchoalveolar lavage fluid, and a modest increase in airway responses to methacholine. The repair phase after Cl2 exposure was characterized by increased airway epithelial cell proliferation, measured by immunoreactive proliferating cell nuclear antigen (PCNA), with maximal proliferation occurring 5 days after Cl2 exposure. At 10 days after Cl2 exposure the airway smooth muscle mass was increased relative to controls, suggestive of airway smooth muscle hyperplasia and there was evidence of airway fibrosis. No increase in goblet cells occurred at any time point. We conclude that a single exposure of mice to Cl2 gas causes acute changes in lung function, including pulmonary responsiveness to methacholine challenge, associated with airway damage, followed by subsequent repair and airway remodelling.

Effect of Calcination Temperature on Interface Properties Between In2O3 and Au Electrode in Micro Gap Semiconductor Gas Sensors

AbstractThe In2O3 thin film nanosensors were fabricated by dropping In(OH)3 sol on nano gap electrode with 0.1-2.5 micron of gap size, dried, and calcined at various temperatures. The grain size of In2O3 and thus the number of In2O3 grains were changed by calcining at 600-850 °C. The size of grain was increased from 15 nm at 600 °C to 55 nm at 850 °C, and thus the number of grains in 0.3 micron gap was decreased from 19 to 5.3. Contrary to the expectation, the small resistance changes to both 1 ppm Cl2 (resistance increase) and 0.5 ppm Cl2 (resistance decrease) were obtained for In2O3 nanosensors calcined at 700-850 °C. These were contributed to the changes in the surface and interface chemical state to suppress the adsorption of or substitution with Cl2 molecule.

Effect of micro-gap electrode on sensing properties to dilute chlorine gas of indium oxide thin film microsensors

Effects of gap size on dilute Cl2 gas sensing properties have been investigated for the In2O3 thin film microsensors equipped with micro-gap electrode. The micro-gap electrodes with various gap sizes (0.1–2μm) were fabricated on SiO2/Si substrate by means of MEMS techniques (photolithography and FIB). Then the In2O3 thin film was deposited on the micro-gap electrode to be micro gas sensor. The resistance of In2O3 microsensor was increased upon exposure to dilute Cl2 gas of ppm-level, while the sensor responded to Cl2 gas less than 0.5ppm with resistance decrease. Interestingly, in both cases the sensitivities were increased with decreasing gap size, although the starting gap size of sensitivity increase were different from each other. The high sensitivity was obtained for In2O3 microsensor with 0.1μm gap. The number of grains was decreased with decreasing gap size, inducing the increasing contribution of interface between electrode and oxide. The sensitivity was increased due to the high sensitivity at interface. The similar effect of number of grains in the micro-gap was examined for the grains with different size packed in the 0.1μm gap electrode. The different grain size was obtained after calcinations at 600–850°C. With decreasing number of grains, the sensitivity to 1ppm Cl2 (resistance increase) was increased, while the sensitivity to 0.5ppm Cl2 (resistance decrease) was decreased. It is assumed that the condition of oxide–electrode interface or In2O3 surface is changed with calcination.

Impact of Three Piscicides on Nitrogen-Mineralizing and Cellulose-Decomposing Bacterial Populations

The effects of three selective piscicides: (1) mahua, Bassia latifolia, oil cake (at a concentration of 200 ppm); (2) dimethyl-dichlorovenyl phosphate (DDVP) (at a concentration of 5 ppm); and (3) a combination of bleaching powder and urea (at a concentration of 5 ppm Cl2 and 5 ppm NH3, respectively), on nitrogen-mineralizing and cellulose-decomposing bacterial populations were tested under simulated fish culture conditions in outdoor cement cisterns (180 L).Water samples were collected aseptically at 10-day intervals. Enumeration of denitrifying and ammonifying bacteria was done by spread-plate technique following the method as described by Alexander (1978); ammonia oxidizing bacteria by Drews (1974); and nitrogen-fixing and cellulose-decomposing bacteria by applying the procedures of APHA (1995). Bacterial populations declined immediately following application of any of the piscicides with a highest decrease in bacterial numbers associated with treatment with DDVP (80-96.5%). The recovery of the bacterial populations to pre-treatment level was faster in the mahua (25-30 days) treatment compared to the other treatments. Application of bleaching powder and urea resulted in a phosphorus-limited environment with high N:P ratio (10-45:1) whereas, DDVP application caused the environment to be nitrogen-limited (2-3:1). Nitrogen-fixing bacterial population decreased exponentially with increasing values of total inorganic nitrogen of water (y = 49.948e∼2.394x). Therefore, mahua oil cake, a natural plant derivative, appears to act as an effective piscicide in a more environmentally-sustainable way than the other two chemical piscicides tested in the present investigation.

Efficacy of Acidic Electrolyzed Water Ice for Pathogen Control on Lettuce

Acidic electrolyzed water (AcEW) was used as frozen AcEW (AcEW-ice) for inactivation of Listeria monocytogenes and Escherichia coli O157:H7 on lettuce. AcEW-ice was prepared from AcEW with 20, 50, 100, and 200 ppm of available chlorine by freezing at −40°C and generated 30, 70, 150, and 240 ppm of chlorine gas (Cl2), respectively. The AcEW-ice was placed into styrene-foam containers with lettuce samples at 20°C for 24 h. Although AcEW-ice generating 30 ppm Cl2 had no effect on L. monocytogenes cell counts, AcEW-ice generating 70 to 240 ppm of Cl2 significantly (P < 0.05) reduced L. monocytogenes by ca. 1.5 log CFU/g. E. coli O157:H7 cell counts were reduced by 1.0 log CFU/g with AcEW-ice generating 30 ppm of Cl2. AcEW-ice generating 70 and 150 ppm of Cl2 reduced E. coli O157:H7 by 2.0 log CFU/g. Further significant reduction of E. coli O157:H7 (2.5 log CFU/g) was demonstrated by treatment with AcEW-ice generating 240 ppm of Cl2. However, treatment with AcEW-ice generating 240 ppm of Cl2 resulted in a physiological disorder resembling leaf burn. AcEW-ice that generated less than 150 ppm of Cl2 had no effect on the surface color of the lettuce. AcEW-ice, regardless of the concentration of the emission of Cl2, had no effect on the ascorbic acid content in the lettuce. The weight ratio of lettuce to AcEW-ice required was determined to be over 1:10. The bactericidal effect of AcEW-ice appeared within the first 2 h. The use of AcEW-ice provides simultaneously for low temperature storage and inactivation of bacteria.