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The experimental study carried out with white rats Wistar trend, which were introduced of sodium nitrate at a rate of 9.6 g/kg of their mass. It follows to the development of considerable activation of lipid peroxidation and depression of antioxidant system in liver. The obtained results permit supposing the significant role of nitric oxide (NO) in liver as a factor resulting in accumulation of peroxidation products. The research has stated that the use hyperbaric oxygenation (HBO) prevents considerable activation of lipid peroxidation and the decrease of antioxidant enzyme (catalase and superoxide dismutase) activity. The results permit supposing that the effect HBO is connected with the decrease of the rate of reduction of nitrate-ions to NO.

The experimental study carried out on white rats, which was introduced of sodium nitrate at a dose of 9,6 g/kg of their mass. It is followed by the development of considerable disturbances of energy metabolism in liver. It has been shown the depression and the uncoupling of oxidation and phosphorylation, decrease of energy quotient in hepatic tissues. The results obtained permit supposing the significant role of nitric oxide (NO) in liver as a factor resulting in decrease of energy potential. The research has stated that the use of hyperbaric oxygenation (HBO) prevents difficult disturbances of energy metabolism in liver of white rats. The results permit supposing that the effect HBO is connected with the decrease of the speed of reduction of nitrate-ions to more toxic products of their biotransformation.

Four cases of rarely reported nitrate toxicosis due to contamination of drinking water or whey were recorded in 2 beef and 2 dairy cattle herds. In the cases associated with water contamination, water containing ammonium nitrate as a fertilizer for irrigating orchards accidentally entered drinking water troughs for cattle through malfunctioning 1-way valves. The whey contamination in 1 instance was caused by transportation in containers which contained traces of concentrated ammonium nitrate; the 2nd case was induced by whey derived from the production of a specialty cheese produced by the incorporation of nitrate. Mortality occurred in 2 herds and abortions in the 2 other herds. Affected cows responded well to treatment, but some animals remained in a deteriorated physical condition for several months.

Three teenagers from a butcher's household were admitted to hospital as emergency case after eating sausages. The local consultant in communicable disease control was immediately asked to help investigate the cause of their food poisoning. The cases were treated for methaemoglobinaemia. Investigations revealed that the sausage meat had been prepared using sodium nitrate (saltpetre) as a preservative at levels well in excess of those legally permitted in meat products. Prompt recognition of the cause of the food poisoning prevented the outbreak from becoming much bigger. A large quantity of the sausage meat had been prepared for commercial sale, but the butcher's children had eaten part of the batch on the evening before it was due to go on sale to the public.

The article deals with changes in color sensation under exposure to nitroesther vapors. Lower sensitivity to blue color is an early sign of exposure to the chemical hazards.

Experimental study of white rats has shown that the intragastric introduction of sodium nitrate at a rate of 9.6 g/kg of their mass is followed by the development of considerable disturbances of energy metabolism in kidneys. It was shown that the depression and separation of oxidation and phosphorylation, decrease energetic potential in the kidney tissues. The results obtained permit supposing the significant role of nitric oxide in kidneys as a factor resulting in bioenergetic disturbances. Maximum maintenance of Fe-NO complexes was marked 24 hours after the introduction of sodium nitrate and it corresponded to maximum disturbances of energy metabolism.

Nitrate-nitrite toxicosis causes numerous cattle deaths every year in western Nebraska. Its role in fetal abortions is complex and still speculative. This paper reports composite fetal nitrate diagnostic levels, fetal abattoir nitrate levels and observations of bovine perinates from cow-calf livestock units.

Methaemoglobinaemia is rare but should be considered in cases of cyanosis unresponsive to oxygen therapy. An example of this is given involving the accidental ingestion of Amyl Nitrite.

Ground water serves as the primary source of drinking water for nearly all of rural Nebraska. However, ground-water contamination by nitrates, largely due to the use of fertilizers, is an increasing problem. In an ecologic study, the author found that counties characterized by high fertilizer usage and significant ground-water contamination by nitrates also had a high incidence of non-Hodgkin's lymphoma. Other potential health effects of nitrates in drinking water are also discussed.

Nitrite incubation in mitochondria and nitrate intoxication of rats have been studied for their effect on aerobic energetic processes in the liver. Sodium nitrite in concentration of 2 mg/l causes an inhibition of ADP-stimulated respiration and provides uncoupling processes of oxidative phosphorylation and respiration in mitochondria, when adding succinate as a substrate. Low doses of nitrate in vivo promote oxygen economization in mitochondria. Intoxication of rats with nitrate in a dose of 50 mg/l for 30 days induces a decrease of the respiration rate after ADP-phosphorylation and an increase of the coefficient of oxidative phosphorylation efficiency (ADP/O). Intraperitoneal administration of adrenalin in a dose of 25 micrograms/100 g to rats after 30-day nitrate intoxication in a concentration of 10 mg/l induces no typical increase of ADP-stimulated respiration and rate of oxidative phosphorylation and succinate oxidation.

Nitrates are frequently found in vegetables and ground water. Nitrate levels in ground water have increased over the past two decades because of the heightened use of nitrogenous fertilizers. Following ingestion, nitrates are converted to nitrites by fecal organisms. Nitrites are absorbed and form methemoglobin, which interferes with the oxygen-carrying capacity of hemoglobin. Infants are particularly susceptible to nitrate poisoning because fetal hemoglobin is more readily oxidized to methemoglobin. In infants, the most common source of nitrate exposure is well water, which is mixed with infant formula. Affected infants may present with asymptomatic cyanosis, which can progress to dyspnea and lethargy or coma. Blood methemoglobin concentrations are elevated. Treatment consists of the administration of oxygen and intravenous and oral methylene blue.

Three children of nitrate oral intoxication with symptoms of meta-hemoglobinemia and respiratory insufficiency have been described. All cases have been recovered.

A retrospective study was done on corrosive oesophageal burns to ascertain the preventive effect of corticosteroids on stricture development. Within the last 12 years 351 children were admitted to our medical centre with a history of corrosive agent ingestion. In 235 of these the diagnosis of oesophageal burn was confirmed by means of oesophagoscopy. Children admitted within the first 48 hours received steroid, antibiotic and fluid therapy while fluid and antibiotics were given, if needed, in the rest. Forty-six of the children were lost to follow-up. The type of corrosive agent, the admission period, the degree of the burn and the stricture development were used as parameters. Stricture development was found statistically significant in late admitted patients vs. early admissions. This retrospective study suggests the effectiveness of corticosteroid treatment in preventing the stricture development.

A 37-year-old man presented to the emergency department after an attempt to self-treat his priapism with saltpeter (K+NO3). Initially he had a potassium of 7.6 with electrocardiographic changes and a markedly elevated CO2. The potassium and carbon dioxide normalized in less than 24 hours with standard treatment for hyperkalemia. Hyperkalemia is expected with large oral potassium ingestion; and the elevated CO2 was spurious, caused by the misreading of serum nitrates by the Ektachrom 700 system. Ingestion of K+NO3 should be added to the differential of hyperkalemia with a markedly elevated CO2.

Two clinically different episodes of nitrate toxicosis in heifers at the same dairy were evaluated to determine whether dietary supplements could have contributed to the confounding signs of illness. The first episode followed a 24-hour period of feeding mismanagement and resultant overconsumption of both a protein/nonprotein nitrogen supplement and a monensin supplement. This episode was characterized by ataxia, bloating, and death, without the classic clinical signs of dyspnea, salivation, cyanosis, and dark-colored blood, or the cardinal histologic changes of cyanosis, tissue staining, petechiations, or congestion. Approximately 5 weeks later, another episode developed, without the feeding mismanagement or the presence of supplements, and was characterized by classic signs of nitrate toxicosis along with response to methylene blue treatment. In both episodes, the feed source was the same, with high concentrations of nitrate. Heifers of both episodes had high ocular nitrate values, confirming the toxicoses. The difference was the availability of supplements. Calculation of exposure makes it unlikely that either the nonprotein moiety or the monensin moiety could have reached toxic values. However, the cell-level effects of monensin may have caused the animals to not display classic signs of nitrate toxicosis, confusing the diagnosis and treatment. This report demonstrates how field toxicosis can differ from reports of toxicoses caused by single etiologic agents. Practitioners must be aware of the potential for interactions between (and confounding by) commercially used feed components.

The causes of abortion in cattle in the San Joaquin Valley of California were surveyed from submissions to the California Veterinary Diagnostic Laboratory at Tulare. Four hundred sixty-eight abortion cases were examined. Most submissions (89%) were from large drylot dairies, milking an average of 814 cows. Abortion evaluations included necropsy, histopathology, bacteriology, virology, and other immunologic and serologic tests. A specific cause was identified in 29.5% of the abortions. Bacterial infections, most of which were sporadic, accounted for 16% of all abortions. Viral causes and protozoal infections were diagnosed in 5.6% and 3.2% of the abortions, respectively. Fetuses with protozoal infection had histologic lesions of focal nonsuppurative necrotizing encephalitis, and protozoa were detected. Similar histologic lesions were seen in 80 additional fetuses (17.1%), and although an etiologic agent was not identified for these cases, a protozoal infection was suspected.

Insecticides, nitrates, gossypol, copper, and plants are a few of the common toxicoses observed in livestock in a particular specie due to various factors. Some species may have anatomical or physiological uniquenesses making them more susceptible to certain agents. Another specie may be exposed to some agents more frequently than others, increasing the likelihood of toxicosis in that specie. Once recognized, therapy is often unrewarding due to the advanced stage of the condition when first recognized, the stress involved in administering the treatment, and the unfeasibility of multiple treatments on many animals. Because of the poor response to treatment and the large number of animals potentially at risk, prevention assumes a greater importance in food animals than in companion animals. Prevention consists of making the diagnosis, findings and removing the source of the toxicant, and educating the owner on how future problems can be avoided.

An ion chromatographic method was used to simultaneously determine nitrate and nitrite ions in biological samples. Ultrafiltration was used to produce a protein-free filtrate. Chloride interferences were eliminated by precipitation as the silver salt. Detection limits and average recoveries were 0.5 mg/L and 102% for nitrate and 0.2 mg/L and 78% for nitrite, respectively. Nitrate concentration was 2.1 +/- 1.8 mg/L and 4.9 +/- 0.8 mg/L in serum and ocular fluid of healthy cattle, respectively; nitrite was not detected. A severe case of nitrate poisoning in cattle was described and used to study the concentrations of nitrate and nitrite in samples obtained under natural conditions. Nitrate concentration of acutely poisoned cattle was 35% lower in ocular fluid at 158.1 +/- 51.4 mg/L, than in serum at 256.3 +/- 113.4 mg/L. Nitrite was not detected, because of the long processing time (greater than 3 hours) required for samples obtained in the field. A gradual decrease in ocular fluid nitrate of 29.4% at 24 hours, 25.9% at 36 hours, 51.6% at 48 hours, and 73.2% at 60 hours was observed; however, concentrations remained diagnostically significant (73.2 mg/L) 60 hours after death. Twenty-four hours after poisoning, the serum nitrate concentration of severely ill (52.7 +/- 51.9 mg/L) and moderately affected (12.4 +/- 5.7 mg/L) cattle that survived was indicative of the severity of clinical signs previously observed. Nitrate in serum and ocular fluid was stable in samples stored for 24 hours at 23 C, 1 week at 4 C, and 1 month at -20 C.

Three young men died of rapidly progressive pulmonary edema of delayed onset after inhalation of fumes from an accidental nitric acid explosion. Electron microscopy revealed altered neutrophils and necrotic endothelial cells in alveolar capillaries. Immunohistochemistry showed small and large serum proteins, including immunoglobulin M, in the edema fluid and hyaline membranes. Increased permeability is a consequence of direct microvascular injury by inhaled nitrogen dioxide. However, our findings, implicating neutrophils and serum-derived mediators in the pathogenesis of the pulmonary edema, are consistent with recent proposals on their roles in the maintenance and/or progression of edema initiated by toxic inhalations.

The physician is ethically obligated to improve medical knowledge and to transmit those improvements to colleagues. Some occupational physicians are restricted from such professional communication by their employers, and some of these potential communications have major significance in other fields of medicine. For example, the failure to report the cardiovascular toxic manifestations of aliphatic nitrates in explosives and munitions workers involved a number of large U.S. corporations over a period of several decades. Most occupational physicians feel a strong obligation to their corporate employers which poses a dilemma shared by salaried physicians in academic and governmental careers. The solution to the occupational medical communication problem will be materially aided by the recent promulgation of a set of ethical principles for occupational physicians, and would be further advanced by the development of a review process for complaints and by the initiation of a public censure procedure for corporations which do not permit their physicians the opportunity to practice ethically.

In a series of experiments the effect of administering KNO2 was studied, during parturition, on the capability of oxygen transport of maternal blood and on oxygen transfer to foetal blood. The following blood parameters were analysed, MHb percentage, pO2, O2-saturation, pH, pCO2, and (NO2) in maternal arterial blood (carotid art.) and venous blood (jugular vein) and in foetal arterial blood (umbilical art.) and venous blood (umbilical vein). The relative O2-saturation was calculated from the estimated O2-saturation by multiplying with the factor Hb (mmol/l) minus MHb (mmol/l), divided by Hb (mmol/l). In addition, blood pressure in the carotid artery, heart rate, and respiration rate in the dam were continuously recorded for some hours. A dosage of 9 to 12 mg of NO1/kg body weight intravenously or of 30 mg of NO2/kg body weight orally to the dam caused much higher MHb percentages and NO2 contents in the maternal blood than in the foetal blood. In maternal blood the ratio of NO2 content to MHb percentage was proportional to that in foetal blood. In the arterial blood, MHb percentages were almost as high as in the venous blood. After administering of nitrite, relative O2-saturation dropped simultaneously with the increase in methaemoglobin. Nitrite treatment caused a drop in the maternal blood pressure; heart rate and respiration rate increased. O2-saturation in the blood in the umbilical vein was much lower in the animals with nitrite treatment than in those without. These experimental results show clearly that the oxygen capacity of the blood decreases after nitrite treatment. In pregnant cows the oxygen supply to the foetus will be adversely affected after nitrate intake, especially by the lower oxygen transfer via the placenta, though hardly at all by methaemoglobin formation in the foetal blood. When the oxygen transfer to the foetal blood decreases too sharply, intra-uterine death and ultimately abortion may result.

Disposable ammonium nitrate cold packs are widely used in emergency departments instead of ice bags. Five confused or suicidal patients who tore open a pack and ingested from 64 to 234 grams of ammonium nitrate in a single dose, and another patient who attempted to do so, are reported. It is known that chronic ingestion of 6 to 12 grams/day of ammonium nitrate may cause gastritis, acidosis, isosmotic diuresis, and nitrite toxicity manifesting as methemoglobinemia or vasodilatation. None of these patients developed severe toxicity, although three had symptoms of gastritis, three had slight methemoglobinemia, and two had mild hypotension. The product was removed from the stomach promptly in three of the five patients. None had pre-existing renal or intestinal dysfunction, which are known to enhance ammonium nitrate toxicity.

This study was designed to investigate whether exposure to nitrate-containing dust during fertiliser manufacture was associated with an excess of deaths from cancer in general or specifically from cancers of the digestive tract, liver, lung, and bladder. It was based on data extracted from census schedules by the Office of Population Censuses and Surveys, occupational characteristics recorded by fertiliser workers at the 1961 and 1971 censuses of England and Wales being related to subsequent mortality ascertained through the National Health Service Central Register. The 1961 cohort, followed up until 1978, showed a "healthy worker effect" and no evidence of excess mortality from cancer at any site. The 1971 cohort also showed below average mortality during 1971-7 for all causes of death and for circulatory diseases, but there were more deaths from cancer than expected, due mainly to an excess of cancers of the lung and digestive tract. The excess of cancer was more pronounced, but not statistically significant, when compared with other employed men. Though the numbers for comparison were small, there was weak evidence of an association between cancer mortality and frequency of exposure to nitrate-containing dust in this cohort. It is difficult to reconcile the excess cancer mortality in the 1971 cohort with the more favorable level in the earlier cohort, since industrial hygiene has improved and the cohorts showed a similar distribution by region and social class. To examine further these conflicting results the 1971 cohort will be followed for a longer period and re-examined when more deaths have accrued.