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Sodium nitrate was administered through rumen cannulae to produce NO-3 intoxication in four cows (382 to 445 kg body wt) fed prairie grass hay and a protein-mineral supplement. The cows were fed 0, 1.6 or 3.2 kg of dry rolled corn daily for 10 d prior to sodium nitrate administration. Sodium nitrate administration was followed by a marked increase in intraruminal NO-2 and NH3 and blood NO-2 and methemoglobin. Six of eight cows fed 0 and 1.6 kg of corn were given methylene blue to treat severe methemoglobinemia, while none of the cows fed 3.2 kg corn required such therapy. Feeding of 3.2 kg of corn protected against nitrate poisoning by reducing intraruminal nitrite and blood methemoglobin (P less than .05).

Trace element analyses were performed on 144 livers from perinatal calves submitted to the Veterinary Science Laboratory, North Platte, NE. All calves originated from herds in west-central Nebraska and ranged in age from 8 months of gestation up to 6-week-old neonates. Calves were divided into 5 categories based on objectives gross examination and ocular fluid evaluation: abomasal ulcers, abomasal tympany, diarrhea, stillborn and excessive nitrate exposure. Excessive zinc concentrations were found in 4 of the 5 categories. Only in the abomasal ulcer category could a correlation be found; this category routinely was found to have deficient to low normal liver copper concentrations and highest liver molybdenum concentrations. Both excesses and deficiencies of selenium and iron occurred in all categories.

Six cases of nitrate poisoning in cattle are reported. The fact that the symptoms were highly acute and appeared as rapidly as within a few hours after feeding, was a striking feature in dairy cows. Deaths occurred among yearlings without the stock owners having previously noticed any changes. In those cases in which post-mortem studies were done, characteristic changes were not observed, with the exception of engorgement of the lungs with blood or paleness of the mucosae. Nitrate levels were found to vary markedly within a single lot of roughage. Early administration of methylene blue to reduce methaemoglobin and treatment with hypertensive agents may be life-saving.

We report on two children who experienced delayed complete obstruction of the gastric antrum following concentrated acid ingestion. Both patients required initial tube gastrostomy and subsequent antrectomy with intestinal reconstruction. Unlike the more common alkaline corrosives, ingested acids tend to spare the esophagus and gastric fundus. While gastric perforation and vascular collapse may occur immediately following overwhelming acid ingestion, the more common course is chronic gastric antral inflammation with subsequent fibrosis and, in some cases, complete stricture. Delayed surgical reconstruction is recommended to permit the acute inflammation and edema to subside.

Corrosive damage to the small bowel is not common; stasis of acid in the stomach usually prevents extensive jejunal damage. The case presented herein is unusual because the patient had a gastroenterostomy and sustained extensive injury of the jejunum after ingesting acid. The patient survived but developed a jejunal stricture that eventually required resection.

The typical occupational cohort study includes all causes of mortality. However, emphasis is usually placed on the presence or absence of excess cancer mortality. A systematic review of completed occupational cohort studies to assess the findings and patterns of cardiovascular mortality would be useful. Although many of these studies will illustrate the "healthy worker effect" with deficits in mortality, particularly from cardiovascular causes, a thorough review should indicate certain exposures needing further research. A recently published study of heart disease mortality in the rubber industry illustrates the potential use of such a literature review with subsequent follow up. Production workers in the rubber industry have shown small excesses in CAHD mortality. A follow-up study at one plant confirmed the known association between carbon disulfide and atherosclerosis, as well as suggested two new causal associations between CAHD and the use of phenol and ethanol as solvents. What additional techniques can be used to generate hypotheses on heart disease and occupation? Some possibilities include: A recent article describes the use of the results of occupational disease surveillance systems for occupational cancer research. A review of such systems for heart disease would be equally useful. It would be useful to review the quality and quantity of occupational data that has been collected in prospective cohort studies, such as those in Framingham and Evans County. The importance of examining the association between occupational exposures and heart disease include: Assessing whether adequate protection is afforded by current limits on exposure to substances known to cause heart disease (carbon disulfide, nitrates, and carbon monoxide).(ABSTRACT TRUNCATED AT 250 WORDS)

Studies were carried out on some paraclinical indices of the blood with sheep in the case of experimental nitrate intoxication. The animals were divided into five groups and were offered nitrates at the rates of 0.4, 0.5, 1.5, and 2.0 per cent of the dry matter in the ration. The feed given to group V was obtained in a natural way (through the overrate dressing of maize with nitrogen fertilizers), while that given to the remaining groups was prepared by adding nitrates in the corn mash. The blood of the test animals was sampled on the 15th, 30th, 45th, 60th, and 75th day to assess the erythrocyte and leukocyte counts and the level of hemoglobin, methemoglobin, blood sugar, carotene, vitamin A, nitrates and nitrites. The leukocyte count was found to drop, and the erythrocyte one -- to rise. Rose also the level of hemoglobin in the sheep of group V. The level of methemoglobin rose proportionally to the increased amount of nitrates swallowed, and the blood sugar was increased with the increase of methemoglobin. Carotene and vitamin A levels dropped, and nitrates rose. No changes were found in the level of nitrites.

Nitrites and nitrates are often responsible for methemoglobinemy. Infants, on account of their greater sensibility to oxidizing agents, are particularly liable to poison by nitrates and nitrites. Sodium nitrite can be responsible for poisoning after accidental ingestion or owing to an overdose when preparing salt provisions, or because it has been mistaken for another product. Then it is often a case of collective poisoning. Nitrates generally produce methenoglobinemy when they are changed into nitrites under the influence of a bacterial proliferation or of a reductase held in plants. It happens with spinach and carrot soup. Nitrates can pollute municipal water supply and chiefly well water. As regards therapy, cases of methemoglobinemy have been noted after an overdose of potassium nitrate and especially of bismuth subnitrate. The treatment of methemoglobinemy caused by nitrates and nitrites is not specific: suppression of the oxidizing agents, oxygenation, prescription of reducing agents.

Tests have been carried out on 50 ex-workers of a hat-factory who had been exposed to mercury nitrate in order to investigate whether a symptomatological pattern attributable to professional exposure would be still present as a consequence of long term exposure and after a long latency period. Because of the small number of examined workers, the collected data have been compared with those of a control group in order to assess the significance of the results. The incidence of subjective and objective signs has been detected to be higher in female group. The symptoms and objective signs may only partially be included in the chronic hydrargiric pattern described by many Authors. These signs are not so marked as to be expected from heavy hydrargiric chronic poisoning and they include: changes in the oral cavity, psychic erethism and neurologycal signs of sensibility impairment.

The present paper is a report on a case of nitrate poisoning in young calves. Supplying feed high in nitrates to these very young calves would appear to be more hazardous than it would to the older calves.

On the societal level, risks are the result of collective processes of definition. Accepted risks are mainly the output and secondarily the (scientific) input of these processes. As a consequence, in this paper the question of risk management of the nitrate burden to ground and drinking water is analysed within the framework of comparative policy analysis. Various actors pursue their respective interests in different policy arenas within the given rules of the policy game. The impacts of the policy outputs on the policy addressees, namely farmers and water companies, (substantially) determine the level of actual risk. Different national regulatory styles and traditions towards nitrate regulation shape the policy outputs. Consequently, the assumption or normative postulate of a 'rational' (scientific) risk assessment and risk management appears to be utterly heroic and, in the end, misleading.

Twelve eighteen-month-old calves contracted nitrate poisoning as a result of overfeeding with turnips. Four animals died before treatment was instituted. Intravenous injection of methylene blue resulted in prompt and complete recovery of the other animals.

Cardiovascular effects of potential occupational hazards have received relatively little attention. The major inhalant occupational exposures of concern are carbon disulfide, nitrates, halogenated hydrocarbons and carbon dioxide. Occupational exposure to certain trace metals may also be associated with adverse cardiovascular effects. Of concern is potential toxicity from cobalt, antimony, lead, cadmium and arsenic. Potential physical hazards exist in association with noise, heat and radiofrequency radiation. In most instances, the data are suggestive rather than conclusive. Further epidemiologic studies with careful control for potentially complicating factors, such as baseline differences in blood pressure, cigarette smoking habits and age, are needed. In some areas where epidemiologic studies have provided clues, the mechanisms of action of potential occupational hazards require further basic scientific investigation.

The effect was studied of nitrates and nitrites in drinking water on the methemoglobin level in blood and pathomorphological changes in fourteen-day-old pheasant chickens. The concentrations of 500 ppm of NO3- and 15 ppm NO2- in the drinking water were not lethal, they caused only the increase in the methemoglobin in blood to 7.1% (NO3-) and 16.5% (NO2-). The pheasants exposed to NO3- suffered from hyperaemia of liver, kidneys and mucosa of the small intestine and from the multiplication of the eosinophilic granulocytes in the villus stroma. The exposition to NO2- resulted in the non-specific dystrophic changes in liver and kidneys and in the villus edema of the small intestine. Lethal levels of nitrates and nitrites in drinking water were estimated in relation to the age of pheasants.

The controversial situation of chronic low level nitrate intoxication may involve oxidation of important iron-containing enzymes, much like oxidation of hemoglobin (Fe++) iron to methomoglobin (Fe+++). This oxication causes enzyme inhibition and unlike hemoglobin, which has the methemoglobin reduction system, these enzymes remain in the oxidized state, resulting in the clinical signs and conditions described. This condition may be diagnosed more accurately by measuring erythrocyte catalase activity in addition to blood or dietary levels of nitrate.

Hypertension can be considered work-related and, therefore, compensable when it[occurs] causes cardiac disease in occupational groups for whom cardiac ailments are legislated as being work-incurred and in workers exposed to certain nitrate explosives. In legal circles job related stresses are often invoked as a cause of hypertension and judicial precedent has accepted the medically unproven theory that hypertension develops after an exposure for long hours over a period of several years to the exasperations, frustrations, pressures, strains, and stresses of work. Apportionment of liability between industrial and non-industrial factors is a legal concept with negotiations often open to forensic debate. This could be minimized if epidemiologic information permitting the calculation of attributable risk were available. Also desirable is a better understanding of the possible contributions of common physical hazards e.g., noise and vibration, to sustained hypertension.

The occurrence of a suspected mixed ammonia and nitrate fertiliser poisoning that led to acute illness and fatalities in cattle is described. The circumstances leading to the incident included the method of application of the fertiliser, low rainfall and the absence of subsequent irrigation of the fertilised pastures. The clinical and gross post mortem findings, principally dehydration and fluid distension of the rumen, were not pathognomonic. The complex of nitrate, nitrite and ammonia toxicity is discussed.

Nitrate poisoning was induced in a cow by giving it 200 g potassium nitrate through a rumen fistula for three to four days in succession. The effect of treatment with methylene blue, ascorbic acid and menadione, administered intravenously in different dosages was assessed by measuring methaemoglobin as a percentage of total haemoglobin and comparing the results with those from the untreated cow. The results obtained indicate that ascorbic acid and menadione are unsuitable for treatment of methaemoglobinaemia in nitrate poisoned cattle, but treatment with methylene blue at 1 mg/kg body weight appears to be adequate.