Frederick W. Oehme

Acrylamide and Polyacrylamide: A Review of Production, Use, Environmental Fate and Neurotoxicity

Acrylamide is a highly water soluble vinyl monomer formed from the hydration of acrylonitrile. The major commercial use of acrylamide is the formation of polymers. In the environment acrylamide has a high mobility in soil, may travel great distances in ground-water, is biodegradable, and is not absorbed by sediments or affected by water treatment. It is absorbed by all routes of animal exposure. The main metabolite is N-acetyl-S-(3-amino-3-oxypropyl)-cysteine and is excreted predominantly in the urine. Acrylamide produces an ascending central/peripheral axonopathy in man and animals. The major histological findings are swelling of axons and/or decrease in number of large diameter axons. Acrylamide axonopathy is reversible with time, but full recovery depends upon the severity of the intoxication. All reported cases of acrylamide toxicity have been attributed to handling the monomer. Polyacrylamide is non-toxic. Specific clinical features of acrylamide intoxication are more conclusive than electrophysiological, histological or biochemical laboratory tests for diagnosis. Acrylamide can be detected by titration, colorimetry, high performance chromatography, gas chromatography and polarography in air, water, biological fluids, tissues and polyacrylamides. Present research on the effects of acrylamide focuses on developmental and reproductive effects, genotoxicity and carcinogenicity.

Cyanides and their toxicity: a literature review

Summary Cyanide is a potent and rapidly-acting asphyxiant which prevents tissue utilization of oxygen by inhibition of the cellular respiratory enzyme, cytochrome oxidase. Inhalation or ingestion of cyanide produces reactions within a few seconds and death within minutes. Cyanide toxicity of dietary origin has been implicated in acute animal deaths and as major etiologic factors in toxic ataxic neuropathy in man and as a cause of vision failure in humans suffering from tobacco amblyopia and lebers hereditary optic atrophy. Diagnosis of cyanide toxicity may be confirmed by a variety of laboratory procedures, but accurate assay is essential for proper conclusions from analysis of animal tissues several hours after death or from human samples in instances of chronic dietary exposure. Biological detoxification of cyanide is available through several routes, and the application of sodium nitrite with sodium thiosulfate or administration of methylene blue are effective treatment procedure. The environmental availability of cyanide in its various forms necessitates an understanding of its pathophysiology and responsible management of hazardous situations.

The toxicity and biotransformation of single doses of acetaminophen in dogs and cats

The biotransformation of single oral doses of acetaminophen (APAP) was studied in dogs an cats. Each animal received APAP at a no-effect (low), mildly toxic (medium), and severely toxic (high) dosage; dosages for each species were selected to produce similar clinical effects at each respective dosage. For dogs, these dosages were 100, 200, and 500 mg APAP/kg, while for cats, the similar effective dosages were 20, 60, and 120 mg APAP/kg. Plasma half-lives in dogs remained constant at the lower two dosages, but nearly tripled at the high dosage. The plasma half-lives in cats rose with increased dosage. Although the cats were given lower APAP dosages than the dogs, the plasma half-lives of cats were greater than those of the dogs at the medium and high dosages. Both species excreted about 85% of the administered single dose within the first 24 hr. APAP-glucuronide was the principal metabolite excreted in the urine of dogs; its fraction of the total metabolites excreted in urine remained constant at the three dose levels. In cats, APAP-sulfate was the major metabolite in urine at all three dosage levels, but the fraction of the total urinary metabolites represented by APAP-sulfate decreased as the dosage increased. Hepatic centrilobular pathology was seen in dogs, while cats had more diffuse liver pathologic changes. The results indicate that the cat is at increased risk from APAP exposure because of impaired glucuronidation and saturation of its sulfate conjugation pathway.

Mechanisms of Heavy Metal Toxicities

(1972). Mechanisms of Heavy Metal Toxicities. Clinical Toxicology: Vol. 5, No. 2, pp. 151-167.

Carbaryl: A Literature Review

Carbaryl (1-naphthyl-N-methylcarbamate; Sevin),1 a reversible inhibitor of cholinesterase, is an agricultural pesticide used in the control of over 150 major pests (BACK 1965). It belongs to the major class of insecticidal compounds, the carbamates.

Lead, cadmium, and mercury tissue residues in healthy swine, cattle, dogs, and horses from the midwestern United States

A survey was conducted in 1975–1976 to determine the background levels of lead, cadmium, and mercury in tissues of healthy swine, cattle, dogs, and horses from the midwestern United States. Blood, muscle, liver, and kidney were assayed from cattle and swine slaughtered at federal meat inspection plants and in dogs and horses obtained from local pounds and sales barns. A total of 959 samples for lead, 972 samples for cadmium, and 827 samples for mercury were analyzed. The maximum muscle lead concentration was less than 0.10 ppm in dogs and horses. Fourteen percent of the cattle muscle samples contained between 0.16 and 0.34 ppm lead. The blood lead concentration was generally lower than 0.10 ppm in cattle, swine and horses; however, in dogs 44% of the blood lead values were between 0.11 and 0.37 ppm. The liver and kidney lead content was generally less than 0.50 ppm in all species, and the maximum lead content detected in either tissue was less than 2.0 ppm. Elevated tissue levels of cadmium were observed in horses as compared to other species. While the maximum muscle cadmium content in cattle, swine, and dogs rarely exceeded 0.05 ppm, levels in excess of 0.06 ppm were found in all the 19 horse muscle samples. Blood cadmium levels in all species were near or below the detection limit of 0.005 ppm. The median cadmium concentration in liver and kidney was below 0.2 and 0.6 ppm, respectively, in cattle, swine, and dogs. However, in horses the median concentration was 20 times greater in liver and 4 times higher in kidney. The mercury concentrations in muscle and blood of all species were near or below the detection limit of 0.02 ppm. The median concentrations of mercury in liver and kidney, respectively, were: 0.02 ppm each in swine and cattle; 0.02 ppm and 0.05 ppm in dogs; and 0.12 ppm and 0.72 ppm in horses. The results suggest that exposure of animals to dietary or environmental lead, cadmium, and mercury in the midwestern United States is not significant. The specific cumulation of cadmium and mercury in tissues of horses suggests the need to explore the role these metals play in selective biological processes.

The effect of various dietary zinc concentrations on the biological interactions of zinc, copper, and iron in rats

Three groups (14 rats each) were fed one of the following diets for 8 wks: a control purified basal diet containing 12 ppm zinc, 5 ppm copper, and 35 ppm iron; the basal diet with <2 ppm zinc; or the basal diet supplemented with 1000 ppm zinc. Rats fed the zinc-deficient diet had decreased weight gain, moderate polydipsia, and intermittent mild diarrhea. The zinc-supplemented rats had a cyclical pattern of food intake and weight loss from weeks 5 to 8. Tissue concentrations suggest that zinc and copper were not mutually antagonistic with chronic dietary imbalances. If tissue element concentrations reflected intestinal uptake, then competition and/or inhibition of intestinal uptake occurred between zinc and iron. The fluctuations in tissue element concentrations that occurred with increased duration of the study were at variance with previous studies of shorter time periods. The dietary proportions of zinc, copper, and iron appear to influence zinc, copper, and iron metabolism at the intestinal and cellular transport levels over a given period of time.

Nitrates as an Environmental, Animal, and Human Hazard*

The publics awareness of foreign chemicals polluting our environment during the previous decade has promoted the governments current high interest in the pollution problem. As a result, the applied fields of health (medicine, dentistry, veterinary medicine, nursing, public health, and others including social and psychological health) have been stimulated to increase their concern, We, as practicing scientists, must keep up-to-date in this area of applied health, When considering our environment in regards to environmental pollution, we must consider three basic surroundings-air, water, and soil. Each of these constitutes a dynamic system incorporating sensitive and balanced ecologic systems. In many instances, the biotic and abiotic entities of one biologic system are interconnected, and the entities within the ecologic systems of each biologic system are cyclic and interrelated. The most studied relationship is that involved in the phases of the food chain cycle within an ecologic system.

Carbaryl residues in tissues and cholinesterase activities in brain and blood of rats receiving carbaryl

Abstract The diagnostic value of measuring insecticide levels and cholinesterase activity in carbaryl-poisoned rats was studied. Mature, male rats received 450, 800, or 1200 mg carbaryl/kg orally, and carbaryl residues in liver, heart, and brain and/or cholinesterase (ChE) activity in brain, red blood cells, and plasma of sacrificed, moribund, and dead rats were compared. Significant tissue residues were still present 24–48 hr after dosing. The lowest liver, heart, and brain carbaryl levels were 11.7, 3.6, and 5 ppm, respectively, in fatally poisoned rats. The brain ChE activity of fatally poisoned rats was less than 35% of normal, while surviving rats had greater than 55% of normal ChE activity 48 hr after dosing. Following dosing, red blood cells and plasma ChE activity was near 30% of normal. Cholinesterase activity in brain, red blood cells, and plasma was back to 70% of normal 96 hr after dosing. Blood studies on gastrointestinal tract absorption of carbaryl indicated that prolonged absorption may account for extended clinical signs observed. Whole blood was superior to plasma for carbaryl determination.

Blood and liver cyanide concentrations in rats poisoned with oral doses of potassium cyanide

Abstract Male rats were employed to study the blood and liver cyanide (CN) concentrations after oral doses of 6, 10 and 14 mg potassium cyanide (KCN)/kg body weight. Animals killed 10 min after administration had higher blood CN concentrations than those killed near death or at survival. The minimum lethal blood CN concentration in rats was found to be in the range 2.60–2.92 μg/ml. Liver CN concentrations were generally lower than the corresponding blood CN concentration for all dosage groups studied. This was probably due to the CN detoxification capability of the liver. Lethal liver CN concentrations were in the range 0.54–6.05 μg/g.