Direct Electrochemical Sensing of Hydrogen Sulfide without Sulfur Poisoning.

An electrochemical method capable of direct, real-time detection of hydrogen sulfide was developed using triple pulse amperometry (TPA) to mitigate sulfur poisoning and its related passivation of the working electrode surface. Through repeated cycles of discrete potential pulses, the electrooxidation of surface-adsorbed elemental sulfur to water-soluble sulfate ions was exploited to regenerate the glassy carbon electrode surface and maintain consistent sensor performance. Amperometric measurements and X-ray photoelectron spectroscopy surface analysis demonstrated that the TPA sensors provided enhanced analytical performance via decreased sulfur accumulation relative to low-potential (≤+0.7 V) constant potential amperometry. Sensors operated under optimized TPA parameters retained high sensitivity (57.4 ± 13.0 nA/µM), a wide linear dynamic range (150 nM-15 µM), fast response times (<10 s), and a submicromolar detection limit (<100 nM) upon consecutive calibration cycles. The sensitivity and response time achieved were comparable to or better than current electrochemical sensors. Moreover, the simplicity of the method eliminates the need for external redox mediators or semipermeable membranes.

Temporal changes in nitrogen pollution in northeastern Estonia.

During the last 5 decades the northeastern part of Estonia (the region where oil shale and the chemical industry are located) has been subjected to pollution with acidic compounds. In 1981-1988 the yearly mean nitrogen (N) deposition load was up to 11.1 kg ha(-1). This N pollution level combined with the deposition of sulphur (S) could have seriously endangered the environment, but the simultaneous emission of strongly alkaline fly ash restrained acidification processes. After 1989-1991 the situation changed, and in 1994-1996 the N deposition load in northeastern Estonia remained within the range of 2.6 to 6.6 kg ha(-1) year(-1) and that of S within 2 to 50 kg ha(-1) year(-1). Because the fly ash deposition is permanently decreasing, more sensitive lichens and mosses can be subjected to critical N+S loads in the future. The proportion of oil shale industry in total emission of NOx in Estonia from stationary sources equals approximately 65 to 75%. During 1996-2000 the yearly mean concentration of NO2 in the air of towns increased from 9 to 12 to 16 to 29 g m(-3). The emission of N compounds was mainly caused by N oxides in flue gases from power plants, as well as ammonia and carbamide discharges from chemical plants. In 1988-1990 the estimated yearly total emission of NOx (as NO2 equivalent) was about 18 to 18.6 thousand t and in 1994-2000, 9.9 to 11.8 thousand t.

Update on sulfur-related polioencephalomalacia.

Sulfur-related polioencephalomalacia is frequently associated with a high total sulfur intake by ruminants. The onset of clinical signs coincides with excessive ruminal sulfide production. Measurement of ruminal gas cap hydrogen sulfide makes it possible to identify cattle with potentially hazardous total sulfur intake. Evaluation of all potential sulfur sources is necessary to estimate total dietary sulfur concentration, which can lead to prevention strategies.

Elemental sulfur toxicosis in a flock of sheep.

Two thousand Panama X Rambouillet ewes from a flock of 2,200 developed signs of acute toxicosis after being moved to a field that had been sprayed 16 hours earlier with elemental sulfur. Acute signs were lethargy, abdominal discomfort, and prostration. Two hundred six (10%) of the affected ewes died within 24 hours. Polioencephalomalacia that was unresponsive to thiamine treatment developed in another 40 (2%) of the ewes; 28 (70%) of the ewes with polioencephalomalacia recovered. Sulfur is converted to hydrogen sulfide in the rumen. Signs of sulfur toxicosis are a result of absorption of hydrogen sulfide and interaction with the cytochrome system and hemoglobin. Sulfide is detoxified in the RBC and by the liver.

Toxicopathology of oilfield poisoning in cattle: a review.

The toxicologic pathology of petroleum and oilfield-related chemicals is reviewed, and a field guide for toxicopathologic evaluation of cattle is given. Cattle will voluntarily ingest petroleum and chemicals used in the exploration, production and transportation of crude petroleum. Variability in chemical composition of petroleum from different fields will alter the type and severity of lesions observed. When airborne pollutants are present, cattle are continually exposed and make excellent sentinel animals. The lung, kidney, liver, gastrointestinal tract, heart and brain are target organs for petroleum hydrocarbons. Exposure to elemental sulfur can produce pulmonary pathology. Sulfur-containing gases are irritating to the mucosa of the eye and respiratory tract. Arsenic and lead cause lesions in the gastrointestinal tract, brain, liver and kidney. Glycols are hepato-, nephro- and neurotoxic, and oral exposure to diethylene glycol produces corneal lesions. Invert drilling fluids are fetotoxic. Nonpesticide organophosphate esters target the peripheral and central nervous systems. Toxicopathy is a strategic tool in the diagnosis of intoxications occurring in cattle after exposure to oilfield chemicals. Cattle are sensitive to oilfield pollutants and are a useful biomonitoring species.

[Several aspects of clinical signs and pathogenesis of pneumopathies in acute poisoning caused by sulfur-containing natural gas]. / Nekotorye aspekty kliniki i patogeneza pnevmopatii pri ostrykh otravleniiakh serovodorodsoderzhashchim prirodnym gazom.

The article summarizes and analyzes data on 32 cases of acute intoxication varying in severity and caused by inhalation of sulfur-containing natural gas of Astrakhan gas deposit (SCNGAGD). The data were obtained in experimental poisoning of 120 Wistar rats with the gas. Pneumopathies (toxic pulmonary edema, pneumonitis, asthmatic bronchitis, alveolitis) appeared to play the central role among other syndromes of the intoxication by SCNGAGD. Mechanisms of the pneumopathies were traced to morphologic disorders of blood-lung barrier, compromised functions of lung surfactant, disturbances in lipid peroxidation and anaerobic glycolysis.

Mortality studies of machining fluid exposure in the automobile industry. III: A case-control study of larynx cancer.

A case-control study of larynx cancer was conducted within a cohort of automobile workers exposed to metal working fluids, commonly referred to as machining fluids (MF). Results are based on 108 cases of larynx cancer and 5:1 matched controls. Risks associated with specific types of MF, as well as specific components of the fluids were evaluated. Based on a retrospective exposure assessment, lifetime exposures to straight and soluble fluids, grinding particulate, biocides, selected metals, sulfur, and chlorine were examined. Exposure to asbestos and acid mists at two of the three study sites was also characterized. Results suggest that straight mineral oils are associated with almost a two-fold excess in larynx cancer risk. There was also evidence of an association with elemental sulfur, commonly added to straight MF to improve the integrity of the materials under extreme pressure and heat. It is not clear whether sulfur is causally related to an excess relative risk of larynx cancer or whether the observed association is the result of unmeasured confounding by another contaminant or process feature. For example, the high stress operations that require MF enriched with sulfur are also more likely to produce polycyclic aromatic hydrocarbons (PAHs) during the process. Thus, the observed association with sulfur may be due to an association with PAH. The finding of excess risk of laryngeal cancer associated with MF is consistent with several previous reports in the literature. This is the first study, however, to distinguish straight mineral oils from other types of MF. Based on these findings, a general reduction in concentrations of straight mineral oil particulate in occupational environments would be prudent.

[Rapeseed poisoning of wild herbivores]. / Rapsvergiftung wildlebender Pflanzenfresser.

Beginning with the simultaneous occurrence of the first extensive sowing of 00-rape and local increased losses among hares and roe deer in Western Germany and Austria at the end of 1986, the clinical and morphological symptoms of rape poisoning are discussed. They consist of damage to endo- and epithelium, cell membranes, blood, liver and in the so called "rape-blindness". Subsequently, the most important toxic agents of rape including their metabolites are presented. They consist in alkenyl- and indolyl-glucosinolates, leading to isothiocyanates (mustard oils), thiocyanates or thiocyanate ions resp., nitriles and antithyroid agents (e.g. goitrin) as well as S-methylcysteine sulphoxide and its metabolites, particularly dimethyl disulphide. Finally, the activity spectrum of the toxic agents or the metabolites and the clinical picture of the affected wildlife in 1986 are compared with the result that the losses of that period are most likely to be traced back to rape poisoning and that the rape-blindness mentioned is to be interpreted as a thiocyanate-psychosis.

[Subchronic toxic effect of the grain fungicide PF-70 on the electrolyte barrier of the gastric mucosa in rats]. / Wplyw podprzewleklego zatrucia fungicydem do zbóz PF-70 na bariere elektrolitowa blony sluzowej zoladka szczurów.

The fungicide for corn PF-70 contains 21% of sulphur, 8.4% of mancozeb, and 0.6% of triadimefon . The aim of the study was to determine the effect of the fungicide on the gastric mucosa electrolyte barrier in rats. Mucosa lesion is known to be one of the risk factors of chronic peptic ulcer disease. The experiments were carried out on 80 rats of Wistar strain. The animals were divided into 5 groups--males and females, separately. The fungicide was given for 13 weeks, at the following doses: 100, 400, 1600, and 6400 mg of active substance per 1 kg of fodder. The gastric mucosa electrolyte barrier was examined by determining the transmural electric potential differences (PD) in mucosa before and after treatment with 150 mmlo of hydrochloric acid and 40 mmol of acetylsalicylic acid solutions. No changes in general condition of the animals were observed. An increase in fodder consumption was observed in males receiving the fungicide at doses of 1600 and 6400 mg per 1 kg of fodder. Females exhibited a decrease in body mass after intoxication at concentration of 6400 mg/kg fodder. A decrease in PD was found in all groups intoxicated with the fungicide, irrespective of the animal sex.

Sulfur-induced polioencephalomalacia in sheep: some biochemical changes.

The effect of high dietary sulfur (S) supplementation on blood thiamine (B1) concentration, biochemical indices of liver, muscle and kidney damage and selected plasma electrolytes was studied in six sheep. Three of these sheep received an additional 230 mg thiamine/kg diet (Group 2). After approximately 2.5-3 weeks on this diet, all three sheep in the non-B1-supplemented group (Group 1) showed loss of appetite and developed mild neurological signs: depression, intermittent signs of excitation and head pressing. Increases in blood B1 concentration and plasma creatine kinase (CK) and aspartate aminotransferase (AST) were observed during this time in all affected animals. Clinical signs lasted only for two to five days. Sheep in group 2 were clinically normal throughout the experiment, but all of these animals also had elevated blood B1 concentrations and plasma CK activity at the 3 wk sampling. Plasma magnesium concentrations of group 1 sheep were elevated at the 2.5-3 wk and 6 wk samplings but they declined significantly (p less than 0.05) to low normal levels thereafter. Magnesium concentrations of group 2 sheep were low at the beginning but progressively increased during the course of the experiment. At necropsy, brain lesions suggestive of polioencephalomalacia (PEM) were observed in all sheep but were most marked in group 1. It is speculated that PEM may be caused by a direct toxic effect of S, S metabolites or B1 antimetabolites in the brain rather than by an in vivo B1 deficiency per se.

Early evaluation of potential worker exposure problems associated with the Claus-type sulfur recovery process.

Early evaluation of process plants, such as the Claus-type SRU (sulfur recovery unit), in the design stage not only minimizes worker exposure to toxic chemicals and noise, but also reduces costs for retrofit engineering controls. The Claus-type SRU converts the hydrogen sulfide in refinery acid gas into elemental sulfur. In the process, the SRU handles toxic gases containing high concentrations of H2S, SO2, and other sulfur compounds. These gases can be emitted into the worker's breathing zone during start-ups, shutdowns, routine operations, emergencies, and turnarounds. This paper describes the Claus-type sulfur recovery process, the potential sources of worker exposure to toxic chemicals and noise, and the engineering controls that should be adopted at the plant design stage to minimize the risks of worker exposure. Engineering controls include improved pump seals and a choice of sample configurations based on the physical form and concentration of H2S in the process lines.

[Pathomorphological studies of experimental thiazole-80 poisoning in sheep]. / Patomorfologichni prouchvaniia pri eksperimentalno otraviane na ovtse s tiazol-80.

Investigations on the pathomorphological changes occurring in the organisms of 4 sheep poisoned experimentally by varying Thiazole-80 doses applied orally were made. It was established macroscopically that after opening the rumen a smell of sulfuric hydrogen is felt. The abomasum was with rusty brown haemorrhages and liver distrophy as well as enlarged gall bladder were observed. The histological studies of parenchymal organs revealed vascular disturbances, hyperemia, oedema and intervascular haemolysis. A heavy diffuse nephrosis, hyaline and protein cylinders were found in the kidney cortex, while in the ganglial cells of medula oblongata were evident degenerative changes. Histochemically, in sheep poisoned by thiazole-80, a well expressed reaction to iron in the lungs, leptomeniges and distrophic hepatocytes were established. Glycogen quantity in the liver was considerably reduced.