Search PubMed⌕ Search

Biomedical subjects

F W Oehme

Publications and source records attributed to F W Oehme.

At least 37 records · Page 2Linked to original sources

Environmental degradation of polyacrylamides. II. Effects of environmental (outdoor) exposure.

The environmental fate of a polyacrylamide thickening agent (PATA), formulated without and with a glyphosate-surfactant herbicide (GH), was examined under various environmental situations: formulation in surface water and ground water, volatility, and soil mobility. Environmental Fate of PATA in Surface Water and Ground Water: PATA was formulated at four concentrations in distilled-deionized water, three surface water samples, and two ground water samples, without and with a GH. Solutions were placed in glass bottles, covered with plastic wrap, and exposed to environmental (outdoor) conditions for 6 weeks. Acrylamide and ammonium concentration, pH, and bacterial and fungal populations were measured weekly. All solutions in this portion of the study had a homogeneous milky appearance but the conclusions of the study were nearly transparent. The results of this study suggest that polyacrylamide can degrade to acrylamide under environmental conditions. Statistically, there was no linear correlation between the various parameters measured. Volatility: PATA was formulated without and with GH. Each solution plus an acrylamide standard (positive control) was placed in a glass beaker and exposed to environmental (outdoor) conditions for 6 days. Acrylamide concentration, ammonium concentration, pH, and solution volume were measured daily. Acrylamide and ammonium concentrations increased during the study in all formulations, except when solutions evaporated to dryness. pH did not change greatly over the course of the study for these samples. Those solutions containing PATA had a homogeneous milky appearance but by the conclusions of the study were nearly transparent. This suggests a physical structural change in the polymer. Soil Mobility: PATA formulated with GH was also applied to soil columns and soil boxes containing sand, Eudora sandy loam, Eudora sandy clay, and Kohola silt loam. Acrylamide could be detected by Day 2 in all soil columns. Acrylamide could not be detected in the runoff of any of the soil boxes.

Acrylamides↗

Fumonisin exposure to Kansans through consumption of corn-based market foods.

Fumonisins are secondary metabolites of the fungus Fusarium moniliforme Sheldon, a common corn contaminant world wide. Presently 6 different fumonisins (FB1, FB2, FB3, FB4, FA1 and FA2) have been identified and characterized. In veterinary medicine fumonisins cause equine leucoencephalomalacia and swine pulmonary edema. In addition, fumonisins have been shown to be carcinogenic in laboratory animals and have been linked to human esophageal cancer in South Africa and China. In this study we examined the prevalence of FB1, FB2 and FB3 in corn-based human foods in Kansas using HPLC equipped with a fluorescent detector. All 3 fumonisins were detected in at least 1 food item. However, only 24/121 samples analyzed (20%), contained detectable (> 40 ppb) fumonisins. Corn flour was the most frequently contaminated as 13/25 items (52%) were positive for fumonisins. For all analyzed human foods, the range of fumonisins was 42-350 ppb in comparison to 765-9953 ppb found in corn meant for animal consumption. This data shows that corn flour is the item most likely to be contaminated with low concentrations of fumonisins. Corn-based foods do not appear a significant source of fumonisins for Kansans although the implications to human health of these low levels are unknown.

Animal Feed↗

Environmental degradation of polyacrylamides. 1. Effects of artificial environmental conditions: temperature, light, and pH.

A polyacrylamide thickening agent (PATA) was formulated at four concentrations in distilled-deionized water, without and with a glyphosate-surfactant herbicide (GH). Over a 6-week period, these mixtures were exposed to various controlled temperature and light conditions. Acrylamide concentration, ammonium concentration, and pH were measured at weekly intervals to assess the degradation of polyacrylamide and acrylamide. Satellite studies were conducted to examine the effect of altered pH on solutions of PATA (i.e., does pH promote polyacrylamide depolymerization?) and GH binding to amine groups (i.e., protection from degradation). The results of these studies suggest that polyacrylamide can degrade to acrylamide by thermal and photolytic effects, that changes in pH do not promote the depolymerization of polyacrylamide, and that GH does protect polyacrylamide and acrylamide from environmental degradation. Statistically there was no linear correlation between the various parameters measured.

Acrylamide↗

Increased neurotoxicity following concurrent exposure to pyridostigmine bromide, DEET, and chlorpyrifos.

The operating environment of the service personnel during the Persian Gulf War involved psychological, biological, and chemical elements including exposure to pesticides such as the insect repellent DEET (N,N-diethyl-m-toluamide) and the insecticide chlorpyrifos (O,O-diethyl O-3,5,6-trichloropyridinyl phosphorothioate) and to pyridostigmine bromide (PB,3-dimethylaminocarbonyloxy-N-methylpyridinium bromide) that was administered as a prophylactic agent against possible nerve gas attack. The present study was designed to determine the toxicity produced by individual or coexposure of hens 5 days/week for 2 months to 5 mg PB/kg/day in water, by gavage; 500 mg DEET/kg/day, neat, sc; and 10 mg chlorpyrifos kg/day in corn oil, sc. Coexposure to various binary treatments produced greater neurotoxicity than that caused by individual exposures and was characterized by severe neurologic deficit and neuropathological alterations. Also, neurotoxicity was further enhanced following concurrent administration of the three chemicals. Severe inhibition of plasma butyrylcholinesterase (BuChE) activity was produced in hens treated with PB (activity 17% of control) compared to those treated with chlorpyrifos (activity 51% of control) or DEET (activity 83% of control). BuChE inhibition was further increased in binary and tertiary treatment groups compared to individual treatment groups. In contrast, a significant inhibition of brain acetylcholinesterase (AChE) was produced in hens administered chlorpyrifos alone (activity 67% of control), while those given chlorpyrifos in combination with other compounds exhibited a significant inhibition of brain AChE activity ranging from 43 to 76%. Brain neurotoxicity target esterase (NTE) was not inhibited in any of the individual treatment groups or PB/DEET, but was significantly inhibited and had activity expressed as a percentage of control in groups administered combined chlorpyrifos with PB of 73% or DEET of 74% and in the tertiary treatment group of 71%. We hypothesize that test compounds may compete for xenobiotic metabolizing enzymes in the liver and blood and may also compromise the integrity of the blood-brain barrier, leading to an increase in their "effective concentrations" in the nervous system to levels equivalent to the toxic doses of individual compounds. This is consistent with the present observation of increases in (1) the inhibition of brain AChE and NTE, (2) the extent of neurologic dysfunction, and (3) the severity and frequency of neuropathologic lesions in the combined treatment groups compared to those administered individual compounds.

Animals↗

Neurotoxicity resulting from coexposure to pyridostigmine bromide, deet, and permethrin: implications of Gulf War chemical exposures.

Of the three-quarters of a million service personnel involved in the Persian Gulf War, approximately 30,000 have complained of neurological symptoms of unknown etiology. One contributing factor to the emergence of such symptoms may be the simultaneous exposure to multiple agents used to protect the health of service personnel, in particular, the anti-nerve agent pyridostigmine bromide (PB; 3-dimethylaminocarbonyloxy-N-methylpyridinium bromide), the insect repellent DEET (N,N-diethyl-m-toluamide), and the insecticide permethrin (3-(2,2-dichloro-ethenyl)-2,2-dimethylcyclopropanecarboxylic acid (3-phenoxyphenyl)methyl ester). This study investigated neurotoxicity produced in hens by individual or simultaneous exposure to these agents (5 d/wk for 2 months to 5 mg/kg/d PB in water, po; 500 mg/kg/d DEET, neat, sc; and 500 mg/kg/d permethrin in corn oil, sc). At these dosages, exposure to single compounds resulted in minimal toxicity. Combinations of two agents produced greater neurotoxicity than that caused by individual agents. Neurotoxicity was further enhanced following concurrent administration of all three agents. We hypothesize that competition for liver and plasma esterases by these compounds leads to their decreased breakdown and increased transport of the parent compound to nervous tissues. Thus, carbamylation of peripheral esterases by PB reduces the hydrolysis of DEET and permethrin and increases their availability to the nervous system. In effect, PB "pumps" more DEET and permethrin into the central nervous system. Consistent with this hypothesis, hens exposed to the combination of the three agents exhibited neuropathological lesions with several characteristics similar to those previously reported in studies of near-lethal doses of DEET and permethrin. If this hypothesis is correct, then blood and liver esterases play an important "buffering" role in protecting against neurotoxicity in the population at large. It also suggests that individuals with low plasma esterase activity may be predisposed to neurologic deficits produced by exposure to certain chemical mixtures.

Administration, Oral↗

Iron complexation with oral deferoxamine in a swine model.

A controversial therapy in the management of acute iron poisoning is the oral administration of deferoxamine which purportedly complexes unabsorbed iron, exerts protection at the cellular level, and/or enhances the renal elimination of ingested iron. To study the effects of oral deferoxamine on iron absorption, fasted male pigs weighing an average of 10 kg simulated potentially toxic iron overdoses in 12 to 24-mo-old children. A control group of 13 pigs received 60 mg elemental iron/kg via oral gavage followed by 50 ml of distilled water. Serum iron (SI) levels were obtained at 0, 1 2, 4, 6 and 8 h post-iron dosing. The study group of 10 pigs received 60 mg elemental iron/kg po followed by 10 g deferoxamine (1 g/kg). SI levels were obtained at the same intervals. There was no mortality in either group. Statistical differences in SI were noted at 6 and 8 h. Characteristic urine discoloration secondary to deferoxamine was noted at 4 h in the study group. Deferoxamine reduced some peak 51 levels but did not diminish the total absorption of iron.

Administration, Oral↗

A review of the toxicology of air pollutants: toxicology of chemical mixtures.

On a temporal basis, air has immense capacity for moving a large mass of pollutants. Mammals and birds are exposed to pollutants in air by the inhalation (nose and mouth), cutaneous or ocular routes. Most laboratory studies on air pollutants have been limited to single air pollutants and very little research has been done on the complex mixture of compounds that exist in ambient air. Complex mixtures are further complicated by dynamic chemical reactions that occur after the emissions leave point sources. Exposure parameters are also important in the toxicity of air pollutants. Intermittent exposure of monkeys to ozone increased the adverse pulmonary effects. Superimposing spikes of 0.8 ppm nitrogen dioxide on a baseline of 0.2 ppm, as occurs on a calm winter day, increased the susceptibility of mice to bacteria-induced pneumonia. Sulfur dioxide at concentrations of 5 ppm increased pulmonary resistance by 39%. Sulfuric acid is the predominate acid particle in the atmosphere. Exposure for 1 h to > 200 micrograms sulfuric acid/m3 depressed bronchomucociliary clearance. Concentrations of 100 micrograms/m3 of photochemical products caused headaches and 510 micrograms/m3 produced cough and chest pain. For chemical interactions in dose response, nitrogen dioxide is synergistic with ozone and ammonium sulfate. When all 3 chemicals are used in mixture, the response was 340%. Atmospheric conditions, such as fog, can alter the toxicity of air pollutants. The dose response to a single chemical can be altered by chemical mixtures and pre-existing disease conditions. Understanding these relationships is important for establishing no observable adverse effect levels. Mechanisms for multiple chemical interactions are multifaceted. One chemical may interfere with the metabolism or detoxification of another. Others may interact at cell receptors. To understand the effects of multiple chemical interactions of air pollutants, there is a need for a blend of epidemiological, laboratory and field studies. Studies are expensive. In the rural agricultural settings, the economic and environmental health risks are high. Should field observations and chemical problems be used as "red flags" for action?

Air Pollutants↗

Comparison of N-acetylcysteine and methylene blue, alone or in combination, for treatment of acetaminophen toxicosis in cats.

Acetaminophen is widely used in human beings for analgesic purposes, but is one of the most frequent causes of poisoning in cats. Acetaminophen-poisoned cats develop methemoglobinemia and sometimes hepatic failure. To determine the benefit of using methylene blue, a treatment for methemoglobinemia, along with N-acetylcysteine (NAC), the recommended treatment for acetaminophen-poisoned cats, groups of 3 male and 3 female cats each were given methylene blue NAC, or both after administration of acetaminophen (120 mg/kg of body weight, PO). Male cats seemed more susceptible than female cats to acetaminophen toxicosis, because 3 males died of hepatic failure (2 cats given acetaminophen/methylene blue and 1 given acetaminophen/NAC/methylene blue). Although NAC alone seemed to elicit the best overall response, methylene blue, alone or in combination with NAC, may be useful in female cats.

Acetaminophen↗

Total and respirable dust in swine confinement buildings: the benefit of respiratory protective masks and effect of recirculated air.

Caretakers and pigs in dusty environments inhale particles and toxic gases which can cause subclinical illness. We determined the reduction in sampled dust elicited by respiratory masks mounted on glass funnels. Open-faced filters or British cyclones were sampled to measure quantities of dust which the masks had trapped. Respiratory masks reduced the sampled total suspended particulates (open-faced filters) by > or = 75% with NIOSH/MSHA certified protectant (2-tie) masks and > or = 50% with NIOSH/MSHA non-certified comfort (1-tie) masks. Respirable particulates (British cyclones) were reduced by > or = 45% with NIOSH/MSHA certified protectant (2-tie) masks. These data suggest properly worn respiratory protective masks afford significant protection against both total suspended and respirable particulates in swine confinement facilities. Penetration of 3-25% of total aerosol mass through masks allowing only 1% penetration of a silica aerosol with an aerodynamic diameter of 0.6-1.0 microns suggested that measurable portions of the aerosol mass in these confinement houses behaved as if they were less than 1 micron in diameter. Because of the small size of the aerosol, NIOSH/MSHA certified respiratory protective masks should be worn when working in those facilities. We also studied concentrations of ammonia, endotoxin and total and respirable dust particles to determine effects of a recirculation fan which increased the nominal air flow capacity of the building by 10%. Recirculated air had minimal effects on ammonia, total airborne endotoxin or total particulate mass.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Conditioning↗

Perinatal hypocuprosis affects synthesis and composition of neonatal lung collagen, elastin, and surfactant.

To investigate the role of iron, ascorbate, and fructose on copper depletion and the effect of copper depletion on neonatal lung collagen, elastin, and surfactant, female rabbits were fed a control diet [10 parts per million (ppm) copper], a basal marginal copper diet (1.5 ppm), or a basal diet containing a high concentration of iron (1,750 ppm), ascorbic acid (1%, wt/wt), or fructose (20% of carbohydrates, wt/wt) or a combination of iron, ascorbic acid, and fructose throughout gestation. Whereas 10% of neonates in the control group died in the first 24 h, 27-67% of the offspring of rabbits fed the marginal copper diet died. Birth weight was also lower for the pups of the females fed the marginal copper diets. Lungs of neonates born to females fed iron or ascorbate and marginal copper diets had low levels of copper, high proportions of acid-extractable, high-molecular-weight collagen, and low lysyl-oxidase activities, consistent with incomplete maturation of collagen. The bronchoalveolar lavage fluids of newborns whose mothers were fed marginal copper diets alone or in combination with iron and/or ascorbate had lower levels of total surfactant phospholipids than the fluids from lungs of control newborns. The lower surfactant phospholipid content of these groups could be attributed mainly to lower phosphatidylcholine and, in particular, dipalmitoylphosphatidylcholine levels. These results suggest that high maternal intakes of iron, ascorbate, or their combination in pregnancy deplete biologically available copper, which in turn induces neonatal lung abnormalities.

Animals↗

The effect of a single oral dose of tri-o-cresyl phosphate on neurotoxic esterase and acetylcholinesterase activities in the central nervous system, erythrocytes and plasma.

This study reports the activity of neurotoxic esterase (NTE) and acetylcholinesterase (AChE) in the blood and central nervous system (CNS) of swine 6, 12, 24 and 48 h after a single oral dose of 800 mg tri-o-cresyl phosphate (TOCP)/kg. At all evaluated intervals, inhibition of NTE activity in leukocytes and the CNS was 88% or higher, with only slight differences in NTE inhibition apparent among the various tissues examined. This extreme inhibition of NTE activity precluded correlation between inhibition of NTE in peripheral leukocytes and the CNS. However, the similarity in NTE response in leukocytes and the CNS following TOCP administration indicates the potential for leukocyte NTE as a biochemical marker for organophosphorus ester-induced delayed neurotoxicity (OPIDN) development. As the distribution pattern of NTE in the CNS of swine closely parallels that of man, these results further suggest that swine may prove a useful animal model for the study of OPIDN. The activity of AChE was highly variable based on time of assay and tissue examined. In general, plasma AChE activity was more severely depressed in all animals and responded more rapidly to TOCP administration. However, erythrocyte AChE more accurately reflected the enzyme's activity in the CNS and the clinical response to TOCP. Based on the data provided by this study, a threshold inhibition of erythrocyte AChE between 59 and 74% is required for production of acute cholinergic signs.

Acetylcholinesterase↗

Clinical manifestations and leukocyte neurotoxic esterase and red blood cell and plasma acetylcholinesterase activities in swine following a single oral dose of tri-o-cresyl phosphate.

We report the clinical signs and the effects on leukocyte neurotoxic esterase and red blood cell and plasma acetylcholinesterase (AChE) activities in swine orally administered a single dose of tri-o-cresyl phosphate (TOCP) at 400, 800 or 1000 mg/kg. Swine in all dosage groups exhibited signs consistent with inhibition of nervous tissue cholinesterase 3-48 h after TOCP administration. Onset was dose-related, and 2/3 1000 mg/kg dosed swine died 3 or 35 h postdosing. In surviving swine, significant depressions in plasma AChE activity were apparent at 6 h postdosing, ranging from 16-23% of predosing levels. Similar depressions of red blood cell AChE were not observed until 24 h postdosing. Plasma AChE activities appeared to more accurately reflect the development of acute cholinergic signs observed in the 1000 mg/kg dosed swine at 3 h postdosing while red blood cell AChE activities were more consistent with the delayed cholinergic signs exhibited by the 400 and 800 mg/kg dosed swine at 24 h postdosing. All survivors developed signs of delayed neurotoxicity 10-12 d after TOCP administration, and 70% or greater inhibition of neurotoxic esterase activity in leukocytes was apparent during the first 48 h postdosing.

Acetylcholinesterase↗

Characterization of particles, ammonia and endotoxin in swine confinement operations.

To define the atmospheres swine confinement operations, we measured concentrations of total and respirable dust particles, ammonia and endotoxin in the nursery and grower areas of 4 swine confinement houses. Increased ventilation in spring-summer relative to that in winter reduced concentrations of large dust particles more rapidly than it did smaller particles or ammonia. The greater decrease in large particles correlating to increased room air velocity may reflect larger particles' momentum causing impaction on surfaces. There was significant spatial variation in the concentration of airborne endotoxin within individual swine rooms and pens reflecting different mixing of large feed and smaller manure particles. Smaller particles had 4-fold higher concentrations of endotoxin than did larger particles, suggesting they had higher fecal material concentrations. Total airborne endotoxin and total suspended particulates correlated to the fraction of functional endotoxin contained in large particles, suggesting that small particles (0.5-2.0 micrometers) collide with large particles (50 micrometers). These data suggest that large non-respirable particles remove smaller respirable particles from indoor atmospheres due to kinematic coagulation.

Air Pollution, Indoor↗

A review of thallium toxicity.

Thallium (Tl) is one of the most toxic of the heavy metals. Its continued use as a rodenticide in many developing countries and its increasing use in an expanding number of new technologies raise concerns about exposure risk to animals and humans. Because Tl and potassium (K) have the same charge and similar ionic radii, Tl follows K distribution pathways and alters and number of K-dependent processes. Possible toxic mechanisms of Tl include ligand formation with protein sulfhydryl groups, inhibition of cellular respiration, interaction with riboflavin and riboflavin-based cofactors, and disruption of calcium homeostasis. The principal clinical features of thallotoxicosis are gastroenteritis, peripheral neuropathy of unknown etiology, and alopecia. The presence of elevated Tl levels in the urine or other biologic materials confirms the diagnosis of Tl poisoning. Treatment with prussian blue (or activated charcoal) will interrupt the enterohepatic cycling of Tl, thus enhancing fecal elimination of the metal. Forced diuresis with potassium loading will increase the renal clearance of Tl, but should be used cautiously because neurologic and cardiovascular symptom may be exacerbated. If recognized and treated early, Tl poisoning carries a favorable prognosis for full recovery.

Animals↗

Ototoxicity in dogs and cats.

Ears are special sense organs whose principal functions are hearing and maintaining equilibrium. Aminoglycoside antibiotics, erythromycin, polymyxin B, and cisplatin can affect either or both of these functions by binding with, injuring, and/or destroying special receptor cells associated with these functions. Severe hearing loss manifests itself as deafness, whereas loss of equilibrium will present as abnormal righting reflexes, nausea, and vomiting. Damage is proportional to levels of these ototoxins in the endolymphatic fluids. Evidence suggests that toxicity may be influenced by endolymphatic calcium concentrations, and levels of cAMP and cGMP are altered in specialized cochlear cells during ototoxicity, suggesting an additional mechanism for ototoxicity. The administration of salicylates and loop diuretics may potentiate the action of ototoxins, especially aminoglycoside antibiotics, probably by increasing the levels of these toxins in the endolymphatic fluid. Although many of these assessments have been made in laboratory animals, applicability may also be expected in small domestic animals, and extreme care should be taken in prescribing potentially ototoxic drugs to small animals. Cochlear damage from ototoxic compounds occurs initially in the cells detecting high-frequency sounds located at the lower basal region. In aging dogs and humans, this sensitivity of receptors in the lower basal region is enhanced. Early auditory damage is detectable by BAER and cochlear microphonic potentials. Vestibular responses can also be detected early as vestibular ocular reflexes and visual-vestibulo-ocular reflexes. Early detection is especially important because early changes can sometimes be reversible. Cavinton (apovincaminic acid) and fosfomycin represent examples of experimental agents being evaluated in laboratory animals for application as potential treatments to limit the ototoxicity associated with various drugs.

Aminoglycosides↗

The biological activity of glyphosate to plants and animals: a literature review.

Glyphosate is a widely-used broad-spectrum herbicide with little to no hazard to man or the environment. Glyphosate is highly effective against 90 kinds of emerged grasses, brush and broad-leaf weeds. There is no residual soil activity, it does not leach into non-target areas, and it is non-volatile. It is practically nontoxic to mammals, birds and fish, showing no bioaccumulation in the food chain; it is biodegraded into natural products. When used correctly, glyphosate poses no threat to the environment and its inhabitants.

Animals↗