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Background: Potassium nitrate poisoning is a rare but potentially serious condition that can result in methemoglobinemia and subsequent cyanosis. This case report presents a unique instance of rapid-onset methemoglobinemia resulting from the ingestion of a traditional medicine preparation containing potassium nitrate, known as "kalmi shora.", Case Presentation: A 14-year-old Pakistani boy reported to the emergency department with a history of sudden-onset headache, drowsiness agitation, irritability, and generalized cyanosis. Pulse oximetry showed a concerning oxygen saturation level of 58%, whereas arterial blood gas analysis revealed a normal partial pressure of oxygen (90 mmHg). The profile of abrupt onset of symptoms, generalized cyanosis, and the discrepancy between the partial pressure of oxygen and oxygen saturation readings necessitated a comprehensive assessment including inquiries into potential toxins. The peculiar appearance of the blood, resembling chocolate in color, further indicated the possibility of methemoglobinemia. The patient was successfully treated with methylene blue, leading to a prompt resolution of symptoms., Conclusion: This case highlights the significance of considering toxin exposures, such as traditional-medicine-induced poisoning, in emergency settings. The report contributes to the medical literature by highlighting the potential risks associated with traditional remedies and emphasizes the critical role of prompt diagnosis and intervention in optimizing patient outcomes. Recognition of the specific etiology of methemoglobinemia, in this case, traditional medicine ingestion, is essential for effective management in emergency medicine., (© 2024. The Author(s).)

Unintentional exposure to nitrite- or nitrate-containing toxic salts is a recognized cause of acquired methemoglobinemia (MetHb). This systemic alteration of the blood can be fatal if not recognized and treated promptly. The intentional ingestion of sodium nitrite (NaNO 2 ) or sodium nitrate (NaNO 3 ), causing MetHb, is an uncommon and recently identified method of suicide, with the first reported case in the literature occurring in New Zealand in 2010. In this case series we present 28 cases of sudden death of individuals with evidence of MetHb and/or toxic salt ingestion, occurring in the Province of Ontario, Canada, between the years 1980 and 2020, inclusive. Of the 28 deaths in our case series, 25 showed evidence of intentional ingestion of sodium nitrite or sodium nitrate salts. Our year-over-year data demonstrated this is an increasingly used method of suicide in our provincial population, with the majority of cases occurring in the final two years of our study. Postmortem detection of MetHb is typically established via screening techniques such as scene evidence suggesting fatal consumption of a toxic salt in addition to the characteristic grey-purple lividity observed upon the body. The diagnosis can be established via postmortem blood testing demonstrating elevated methemoglobin saturation. Additionally, we have confirmed that postmortem MRI in cases of MetHb demonstrates a T1-bright (hyperintense) signal of the blood; both within intracardiac blood on chest MRIs and postmortem blood samples in tubes., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2021 Elsevier B.V. All rights reserved.)

The National Council of Radiation Protection and Measurements' (NCRP) wound model was applied to the bioassay data from a United States Transuranium and Uranium Registries' whole-body tissue donor, Case 0212. This individual was exposed to plutonium nitrate as a result of an occupational wound injury and he underwent extensive chelation treatment with Ca-DTPA. All major soft tissues and bones were collected post-mortem and radiochemically analyzed for 238Pu, 239,240Pu and 241Am. The 239,240Pu activity in the total body was estimated to be 232.0 Bq, with 80.3 Bq retained in the liver, 115.1 Bq in the skeleton and 14.3 Bq in the wound. The maximum likelihood method was used to simultaneously fit the 'post-treatment' urinary excretion and post-mortem liver and skeleton retention data. It was demonstrated that the deposited material was predominantly a strongly retained soluble compound (nitrate) with a 22% fraction of plutonium particles. The residual intake, the amount of plutonium deposited in the wound that was not removed from the system by Ca-DTPA, was estimated to be 288 Bq. The resulting committed effective dose was 134 mSv. Accounting for plutonium eliminated in the urine during chelation therapy, the actual 'untreated' intake was 1204 Bq, and the projected committed effective dose was 567 mSv. Hence, DTPA treatment reduced the dose by a factor of 4., (© The Author 2017. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Agricultural compounds have been detected in drinking water, some of which are teratogens in animal models. The most commonly detected agricultural compounds in drinking water include nitrate, atrazine, and desethylatrazine. Arsenic can also be an agricultural contaminant, although arsenic often originates from geologic sources. Nitrate has been the most studied agricultural compound in relation to prenatal exposure and birth defects. In several case-control studies published since 2000, women giving birth to babies with neural tube defects, oral clefts, and limb deficiencies were more likely than control mothers to be exposed to higher concentrations of drinking water nitrate during pregnancy. Higher concentrations of atrazine in drinking water have been associated with abdominal defects, gastroschisis, and other defects. Elevated arsenic in drinking water has also been associated with birth defects. Since these compounds often occur as mixtures, it is suggested that future research focus on the impact of mixtures, such as nitrate and atrazine, on birth defects.

A plutonium-DTPA (Pu-DTPA) biokinetic model was introduced that had originated from the study of a plutonium-contaminated wound. This work evaluated the extension of the Pu-DTPA model to United States Transuranium and Uranium Registry (USTUR) Case 0269 involving an acute inhalation of a plutonium nitrate aerosol. Chelation was administered intermittently for the first 7 mo as Ca-EDTA, mostly through intravenous injection, with Ca-DTPA treatments administered approximately 2.5 y post intake. Urine and fecal bioassays were collected following intake for several years. Tissues were collected and analyzed for plutonium content approximately 38 y post intake. This work employed the Pu-DTPA model for predicting the urine and fecal bioassay and final tissue quantity at autopsy. The Pu-DTPA model was integrated with two separate plutonium systemic models (i.e., ICRP Publication 67 and its proposed modification). This work illustrated that the Pu-DTPA model was useful for predicting urine and fecal bioassay, including final tissue quantity, 38 y post intake.

Methaemoglobinaemia due to nitrite poisoning is rare. Awareness of this condition in the cyanosed patient not responding to oxygenation and timely administration of methylene blue may be life saving. We report a case of methaemoglobinaemia as a result of sodium nitrite poisoning.

A 67-year-old man accidentally ingested 75 g of sodium nitrate. He had instant gastrointestinal symptoms. On physical examination, he was respiratorily and haemodynamically stable and there were no signs of central or peripheral cyanosis. Repeated methaemoglobin levels were normal and he made an uneventful recovery. Sodium nitrate intoxication is rare. Serious effects can occur, mainly through formation of nitrite and nitric oxide, which can cause methaemoglobinaemia and vasodilation. Even if the presenting symptoms are mild, it is important to remain cautious since more serious symptoms can occur later. Monitoring of respiratory and haemodynamic status and repeated blood gas analysis in order to detect methaemoglobinaemia are recommended., (2014 BMJ Publishing Group Ltd.)

Nitrate and nitrite are toxicants that have become increasingly significant environmental chemicals. Increase in environmental distribution of nitrogenous compounds, especially in surface and ground water, has been attributed to the intensive use of nitrate as agricultural fertilizers and to increasing amounts of nitrogenous wastes produced by municipalities, industries, and feedlots. The purpose of this study is to illustrate a fatal nitrate toxicosis in cattle associated with the consumption of fennels (Foeniculum vulgare). Fifteen cows from the same farm suddenly developed weakness, muscular tremors, respiratory distress, and finally convulsions. The affected animals died within 24 to 48 h from the onset of the clinical signs. Five cows underwent a complete post-mortem examination. In all examined animals, gross lesions included presence of dark unclotted blood around the nostrils and the anal region, moderate inflammation of the gastrointestinal mucosa, and brown discoloration of the skeletal muscles and kidneys. The histological examination showed tubular degeneration and congestion of glomerular vessels in the kidney. Toxicological analysis detected nitrates at 4 672.2 ppm in the fennels used to feed the animals. The source of exposure to nitrates was identified in the fennels. The fennels were grown in a polluted area of the Campania region in southern Italy and distributed in a public market for human consumption. The waste from the sale of the fennels was fed to the cows. The accumulation of nitrates in some vegetables poses a risk not only for animal health but also for human and environmental safety.

We wish to report two cases of methaemoglobinaemia secondary to amyl nitrate use. A 55-year-old male presented with saturations in the mid 80s despite FiO2 of 1.0 and GCS 10 and a 22-year-old female who presented with fluctuating GCS and a slate grey colour. Both were found to have high levels of metheamoglobinaemia on ABG, were treated with methylene blue and made excellent recoveries. These cases illustrate the risk of methaemoglobinaemia secondary to amyl nitrate. Appropriate and prompt management can lead to very good outcomes.

Purpose: Plutonium-nitrate has a moderately rapid translocation rate from the lung to blood stream. Previous studies have shown an unexpected retention of soluble plutonium in the beagles and human case studied here. The inflammatory responses that may be associated with long-term exposure to ionizing radiation were characterized. These pathways include tissue injury, apoptosis, and gene expression modifications. Other protein modifications related to carcinogenesis and inflammation and the various factors that may play a role in orchestrating complex interactions which influence tissue integrity following irradiation were investigated., Materials and Methods: We have examined numerous lung samples from a plutonium-exposed worker, a human control, and a variety of plutonium-exposed beagle dogs using immunohistochemistry and quantitative Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR)., Results: The exposed human showed interstitial fibrosis in peripheral regions of the lung, but no pulmonary tumors. Beagles with similar doses were diagnosed with tumors in bronchiolo-alveolar, peripheral and sub-pleural alveolar regions of the lung. The terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay showed an elevation of apoptosis in tracheal mucosa, tumor cells, and nuclear debris in the alveoli and lymph nodes of the beagles but not in the human case. In both the beagles and human there were statistically significant modifications in the expression of Fas ligand (FASLG), B-cell lymphoma 2 (BCL2), and Caspase 3 (CASP3)., Conclusions: The data suggests that FASLG, BCL2, CASP3 and apoptosis play a role in the inflammatory responses following prolonged plutonium exposure. Utilizing these unique tissues revealed which pathways are triggered following the internal deposition and long-term retention of plutonium-nitrate in a human and a large animal model.

Background: In April 2013, a hospital in Suzhou City notified authorities of a patient with nitrite poisoning with two other family members who had similar toxic symptoms five days prior. We investigated the event to identify the cause, source and possible route of contamination., Methods: A case was defined as any person living in the Yang Shan Hua Yuan community who had been diagnosed with cyanoderma and food poisoning symptoms from 15 to 25 April 2013. Active case finding was conducted by interviewing community residents and reviewing medical records from local clinics; information was then retrospectively collected on the patient's food history, cooking procedures and food sources., Results: We identified three nitrite poisoning cases, one male and two females, from the same family. The time between dinner and onset of illness was less than an a hour. A retrospective survey showed that a substance presumed to be sugar mixed with asparagus on 17 April and with stir-fried asparagus on 21 April was the suspected contaminant. The presumed sugar came from a clean-up of a neighbouring rental house. Nitrite was detected in a vomitus sample, the sugar substance and two leftover food samples., Conclusion: This family cluster of nitrite poisoning resulted from the mistaken use of nitrite as sugar to cook dishes. We recommend that sodium nitrite be dyed a bright colour to prevent such a mistake and that health departments strengthen food hygiene education to alert people about the danger of eating unidentified food from an unknown source.

Suicide by ingestion of barium is exceptionally rare. Adverse health effects depend on the solubility of the barium compound. Severe hypokalemia, which generally occurs within 2 hours after ingestion, is the predominating feature of acute barium toxicity, subsequently leading to adverse effects on muscular activity and cardiac automaticity. We report one case of acute poisoning with barium nitrate, a soluble barium compound. A 75-year-old woman was hospitalized after suicidal ingestion of a burrow mole fumigant containing 12.375 g of barium nitrate. About 1 hour post-ingestion, she was only complaining of abdominal pain. The ECG recording demonstrated polymorphic ventricular premature complexes (VPCs). Laboratory data revealed profound hypokalemia (2.1 mmol/L). She made a complete and uneventful recovery after early and massive potassium supplementation combined with oral magnesium sulphate to prevent barium nitrate absorption.

Background: Private water systems are more likely to have nitrate levels above the maximum contaminant level (MCL). Pregnant women are considered vulnerable to the effects of exposure to high levels of nitrates in drinking water due to their altered physiological states. The level of methemoglobin in the blood is the biomarker often used in research for assessing exposure to nitrates. The objective of this study was to assess methemoglobin levels and examine how various factors affected methemoglobin levels during pregnancy. We also examined whether differences in water use practices existed among pregnant women based on household drinking water source of private vs. public supply., Methods: A longitudinal study of 357 pregnant women was conducted. Longitudinal regression models were used to examine changes and predictors of the change in methemoglobin levels over the period of gestation., Results: Pregnant women showed a decrease in methemoglobin levels with increasing gestation although <1% had levels above the physiologic normal of 2% methemoglobin, regardless of the source of their drinking water. The multivariable analyses did not show a statistically significant association between methemoglobin levels and the estimated nitrate intake from tap water among pregnant women around 36 weeks gestation (β = 0.046, p = 0.986). Four women had tap water nitrate levels above the MCL of 10 mg/L. At enrollment, a greater proportion of women who reported using water treatment devices were private wells users (66%) compared to public system users (46%) (p < 0.0001). Also, a greater proportion of private well users (27%) compared to public system users (13%) were using devices capable of removing nitrate from water (p < 0.0001)., Conclusion: Pregnant women potentially exposed to nitrate levels primarily below the MCL for drinking water were unlikely to show methemoglobin levels above the physiologic normal. Water use practices such as the use of treatment devices to remove nitrates varied according to water source and should be considered in the assessment of exposure to nitrates in future studies.

Background: Presently, health costs associated with nitrate in drinking water are uncertain and not quantified. This limits proper evaluation of current policies and measures for solving or preventing nitrate pollution of drinking water resources. The cost for society associated with nitrate is also relevant for integrated assessment of EU nitrogen policies taking a perspective of welfare optimization. The overarching question is at which nitrogen mitigation level the social cost of measures, including their consequence for availability of food and energy, matches the social benefit of these measures for human health and biodiversity., Methods: Epidemiological studies suggest colon cancer to be possibly associated with nitrate in drinking water. In this study risk increase for colon cancer is based on a case-control study for Iowa, which is extrapolated to assess the social cost for 11 EU member states by using data on cancer incidence, nitrogen leaching and drinking water supply in the EU. Health costs are provisionally compared with nitrate mitigation costs and social benefits of fertilizer use., Results: For above median meat consumption the risk of colon cancer doubles when exposed to drinking water exceeding 25 mg/L of nitrate (NO3) for more than ten years. We estimate the associated increase of incidence of colon cancer from nitrate contamination of groundwater based drinking water in EU11 at 3%. This corresponds to a population-averaged health loss of 2.9 euro per capita or 0.7 euro per kg of nitrate-N leaching from fertilizer., Conclusions: Our cost estimates indicate that current measures to prevent exceedance of 50 mg/L NO3 are probably beneficial for society and that a stricter nitrate limit and additional measures may be justified. The present assessment of social cost is uncertain because it considers only one type of cancer, it is based on one epidemiological study in Iowa, and involves various assumptions regarding exposure. Our results highlight the need for improved epidemiological studies.

Inadvertent ingestion of sodium nitrite is known to precipitate metheamoglobinaemia. No cases exist, however, of intentional suicide by methaemoglobinaemia following self-poisoning with sodium nitrite. A 76-year-old man collapsed and rapidly developed brady-asystolic cardiac arrest 25 min following self-poisoning with an unknown quantity of crystalline sodium nitrite. On arrival in the ED the patient was asystolic with cardiopulmonary resuscitation in progress. Haemoglobin concentration was 110 g/L, arterial methaemoglobin measured 82.6% and serum lactate 9.6 mmol/L. Antioxidative treatment was undertaken with total 5 mg/kg intravenous methylene blue administered in divided aliquots. Despite prolonged resuscitative efforts the patient died. Resuscitation from methaemoglobinaemia-induced asystole following self-poisoning presents a unique therapeutic challenge. Treatment of methaemoglobinaemia-induced cardiovascular instability and overt cardiopulmonary arrest are discussed., (© 2010 The Authors. Emergency Medicine Australasia © 2010 Australasian College for Emergency Medicine and Australasian Society for Emergency Medicine.)

Multiple stable isotope analysis can be a powerful technique in forensic sciences. Oxygen and nitrogen isotopes were used to determine the source of nitrate that was responsible for the poisoning deaths of 71 wild horses in the Nevada desert. The nitrate was present in a water-filled hole known as 'the Main Lake depression.' Nitrate from the Main Lake depression had delta(18)O and delta(15)N values that were very positive (+32 per thousand, +37 per thousand), and Delta(17)O values of approximately +2 per thousand. The isotopic data suggested that the most probable source of the nitrate was nitrification of nitrogen from horse manure and urine that had leached into the pond. The delta(18)O signal suggested that extreme evaporative concentration had occurred, resulting in toxic levels of nitrate accumulating in the Main Lake depression. The study demonstrates the utility of the multiple stable isotope analysis approach for characterizing sources of nitrate.

"Poppers" is the street name for volatile nitrites offered by online shops and sex-shops for their aphrodisiac and euphoric properties. Although nitrites have been abused since the late 1960s, recently they became popular in Poland. Recreational poppers using was associated with homosexual men at first. Currently they are commonly reported among heterosexual men and regular dicso participants. Advertisements of these substances tempt potential buyers with the promise of a legal narcotic high. Easy access and the sense of safety make these products the reason of acute toxicity. Volatile nitrites relaxes smooth muscle, the consequent intense peripheral vasodilatation produces flushing, a fall in blood pressure, and reflex increase in heart rate. These effects are accompanied by feeling of warmth, euphoria and intensifying of sexual pleasure. Serious poisoning results in severe methaemoglobinaemia, coma, respiratory and cardiovascular failure, and even death. Skin and mucous contact with poppers can produce a crusty lesion at the site. This article presents the case of 44-years old male hospitalized three times in Toxicology Department after history of poppers abusing. Methaemoglobinaemia (26.4%) and tracheobronchial irritation were the main symptoms observed. Patient was given specific therapy with methylene blue.

Objectives: To investigate if live births conceived in months when surface water agrichemicals are highest are at greater risk for birth defects., Methods: Monthly concentrations during 1996-2002 of nitrates, atrazine and other pesticides were calculated using United States Geological Survey's National Water Quality Assessment data. Monthly United States birth defect rates were calculated for live births from 1996 to 2002 using United States Centers for Disease Control and Prevention natality data sets. Birth defect rates by month of last menstrual period (LMP) were then compared to pesticide/nitrate means using logistical regression models., Results: Mean concentrations of agrichemicals were highest in April-July. Total birth defects, and eleven of 22 birth defect subcategories, were more likely to occur in live births with LMPs between April and July. A significant association was found between the season of elevated agrichemicals and birth defects., Conclusion: Elevated concentrations of agrichemicals in surface water in April-July coincided with higher risk of birth defects in live births with LMPs April-July. While a causal link between agrichemicals and birth defects cannot be proven from this study an association might provide clues to common factors shared by both variables.

Nitrate-nitrite poisoning killed four adult alpacas and induced the abortion of a full-term fetus after access to oaten hay (Avena sativa) containing 3.2% KNO(3) equivalent in dry matter. Necropsy findings were cyanosis, dark-coloured blood, and pulmonary congestion and oedema. Aqueous humour from two adults contained 25 mg NO(3)/L and that from the fetus contained 10 mg NO(3)/L. Cyanide poisoning possibly killed two adult wether alpacas that ate a garden-cultivated variety of Osteospermum ecklonis (South African daisy, bietou) with a cyanide potential of 6800 mg HCN/kg dry matter.

Severe acute lead intoxications are rare and are associated with accidental or purposeful ingestion. There were only few cases of severe to fatal poisonings reported in literature in children. We report a case of acute lead intoxication in a child with extremely high lead blood level of 20.4 micromol/L (422.7 microg/dL), who was treated with chelation and in whom significant organ dysfunction did not develop. Documented significant high level above 3.37 micromol/L (corresponding to 70 microg/dL) in this patient persisted for approximately 24 h. Adequate, single or combined chelatation therapy in early phase of acute lead poisoning is essential for the further patient's outcome.

Sediment and nutrients yields especially from farmlands were studied in a watershed in Ishigaki island, Okinawa, Japan. The transport processes of these materials in rivers, mangrove, lagoon and coastal zones were studied by using various observation methods including stable isotope analysis. They were simulated by using a WEPP model which was modified to be applicable to such small islands by identifying several factors from the observations. The model predicts that a proper combination of civil engineering countermeasure and change of farming method can reduce the sediment yield from the watershed by 74%. Observations of water quality and coral recruitment test in Nagura bay indicate that the water is eutrophicated and the corals cannot grow for a long time. Based on these observations, a quantitative target of the reduction of sediment and nutrients yield in watershed can be decided rationally.

A 300-strong Angus-Brahman cattle herd near Springsure, central Queensland, was being fed Acacia shirleyi (lancewood) browse during drought and crossed a 5-hectare, previously burnt area with an almost pure growth of Dysphania glomulifera subspecies glomulifera (red crumbweed) on their way to drinking water. Forty cows died of cyanide poisoning over 2 days before further access to the plant was prevented. A digital image of a plant specimen made on a flat-bed scanner and transmitted by email was used to identify D glomulifera. Specific advice on the plant's poisonous properties and management of the case was then provided by email within 2 hours of an initial telephone call by the field veterinarian to the laboratory some 600 km away. The conventional method using physical transport of a pressed dried plant specimen to confirm the identification took 5 days. D glomulifera was identified in the rumen of one of two cows necropsied. The cyanogenic potential of D glomulifera measured 4 days after collection from the site of cattle deaths was 18,600 mg HCN/kg in dry matter. The lethal dose of D glomulifera for a 420 kg cow was estimated as 150 to 190 g wet weight. The plant also contained 4.8% KNO3 equivalent in dry matter, but nitrate-nitrite poisoning was not involved in the deaths.

Infants for whom formula may be prepared with well water remain a high-risk group for nitrate poisoning. This clinical report reinforces the need for testing of well water for nitrate content. There seems to be little or no risk of nitrate poisoning from commercially prepared infant foods in the United States. However, reports of nitrate poisoning from home-prepared vegetable foods for infants continue to occur. Breastfeeding infants are not at risk of methemoglobinemia even when mothers ingest water with very high concentrations of nitrate nitrogen (100 ppm).

A 22-year-old woman with an initial diagnosis of 'ruptured ectopic pregnancy' and 'hemorrhagic shock' was sent to the operation room for surgical treatment. The mucocutaneous color was deeply cyanosed and the pulse oximeter oxygen saturation (SpO2) was only 86% after tracheal intubation (100% O2). 'Chocolate-brown' blood was observed and methemoglobinemia was considered. Then the arterial blood gas (ABG) sample was obtained, an intravenous infusion of methylene blue and vitamin C followed. The patient recovered quickly, and later two other patients with similar symptoms were treated in the same way. The success was due to a correct diagnosis accompanied with prompt treatment and quick recognition of the etiology.

A 22-year-old male was admitted to hospital with diarrhea and vomiting, cardiac arrhythmias, severe hypokalemia and gradual onset of muscular weakness. A potassium infusion was started, but for several hours serum potassium remained low. Evidence of toxic ingestion was initially lacking. When it became clear -- after a considerable delay -- that the patient had ingested barium nitrate, hemodialysis was started. This resulted in rapid clinical improvement with correction of hypokalemia and restored muscular function. Intoxication with barium causes hypokalemia, arrhythmias, muscular weakness and paralysis, often requiring respiratory support. This patient presented with symptoms typical of severe barium intoxication, non-responsive to potassium supplementation. There are few published reports on the use of hemodialysis in barium poisoning. This case confirms the possible benefit of hemodialysis in severe cases, where potassium supplementation alone is insufficient.

Nitrates and nitrites, accumulating in toxic concentrations in soil, plants, water and foodstuffs, can cause lethal intoxication. The method of isolation, identification and quantitation has been elaborated for their diagnosis. It is based on the isolation of water and subsequent chromogenic test plus photoelectrocolorimetry.

On behalf of the World Health Organization (WHO), I have undertaken a series of literature-based investigations examining the global burden of disease related to a number of environmental risk factors associated with drinking water. In this article I outline the investigation of drinking-water nitrate concentration and methemoglobinemia. The exposure assessment was based on levels of nitrate in drinking water greater than the WHO guideline value of 50 mg/L. No exposure-response relationship, however, could be identified that related drinking-water nitrate level to methemoglobinemia. Indeed, although it has previously been accepted that consumption of drinking water high in nitrates causes methemoglobinemia in infants, it appears now that nitrate may be one of a number of co-factors that play a sometimes complex role in causing the disease. I conclude that, given the apparently low incidence of possible water-related methemoglobinemia, the complex nature of the role of nitrates, and that of individual behavior, it is currently inappropriate to attempt to link illness rates with drinking-water nitrate levels.

Hungry cattle and sheep introduced to stockyards containing a dominant or pure growth of Dactyloctenium radulans (button grass) suffered acute nitrate-nitrite toxicity in four incidents in inland Queensland between 1993 and 2001. Deaths ranged from 16 to 44%. Methaemoglobinaemia was noted at necropsies in all incidents. An aqueous humour sample from one dead steer contained 75 mg nitrate/L and from one dead sheep contained 100 mg nitrate and 50 mg nitrite/L (normal = ca 5 mg nitrate/L). Both lush and dry button grass were toxic. The nitrate content of button grass from within the stockyards ranged from 4.0 to 12.9% as potassium nitrate equivalent in dry matter and from outside the stockyards ranged from <0.2 to 0.4%. These data suggest that urine and faeces in stockyard soil may boost the nitrate content of button grass to a concentration hazardous to hungry ruminants.

Background: Nitrate is a widespread contaminant of drinking water, but its potential health effects are unclear. In the body, nitrate is reduced to nitrite, which can react with amines and amides by nitrosation to form N-nitroso compounds, known animal carcinogens. N-nitroso compound formation is inhibited by certain nutrients, such as vitamin C, and increased by meat intake., Methods: We investigated the association of nitrate in public water supplies with incident colon and rectum cancers in a case-control study conducted in Iowa from 1986 to 1989. Nitrate levels in Iowa towns were linked to the participants' water source histories. We focused our analyses on the period from 1960 onward, during which nitrate measurements were more frequent, and we restricted analyses to those persons with public water supplies that had nitrate data (actual or imputed) for greater than 70% of this time period (376 colon cancer cases, 338 rectum cancer cases, and 1244 controls)., Results: There were negligible overall associations of colon or rectum cancers with measures of nitrate in public water supplies, including average nitrate and the number of years with elevated average nitrate levels. For more than 10 years with average nitrate greater than 5 mg/L, the odds ratio (OR) for colon cancer was 1.2 (95% confidence interval [CI] = 0.9-1.6) and for rectum the OR was 1.1 (CI = 0.7-1.5). However, nitrate exposure (>10 years with average nitrate >5 mg/L) was associated with increased colon cancer risk among subgroups with low vitamin C intake (OR = 2.0; CI = 1.2-3.3) and high meat intake (OR = 2.2; CI = 1.4-3.6). These patterns were not observed for rectum cancer., Conclusions: Our analyses suggest that any increased risk of colon cancer associated with nitrate in public water supplies might occur only among susceptible subpopulations.

An autoerotic fatality due to mechanical compression of the neck by a sophisticated construction used for breath control games is reported. The presence of signs of methemoglobinemia as well as an empty "poppers" flask found beside the passed indicated the use of volatile nitrites to enhance sexual pleasure. It was assumed that vasodilatation had caused a sudden unconsciousness with consecutive hanging.

Three cases of accidental acute fertilizer poisoning in cattle resulted in substantial death loss. Water hauled in tanks previously contaminated with a nitrogen-based fertilizer was the source in all cases. In 2 cases, analysis of the water measured urea at 1,640 and 2,300 ppm and ammonia-nitrogen at 640 and 750 ppm, respectively. Confirmation of urea toxicosis was made by measurement of toxic levels of ammonia-nitrogen in the rumen contents (>800 ppm) and blood (>8.0 ppm). In Case 3, no urea was detected in the water but ammonia-nitrogen was measured at 1,670 ppm and nitrate at 1.1%. Toxic levels of nitrate were measured in ocular fluid from 2 animals (60 ppm). Rumen contents contained toxic levels of ammonia-nitrogen (300 ppm) and a pH of 8.7. Interpretation of ammonia levels in rumen contents should take into account the source of ammonia as well as the pH since urea is more toxic than some ammonium salts. When the source is unknown, analysis of blood and/or serum ammonia-nitrogen instead of rumen content is recommended. The rapid progression of signs to death with ammonium nitrate poisoning may explain the lower levels of nitrate attained in ocular fluid than observed with pure nitrate intoxications.

Three cows fed Chenopodium album hay died 30 min after showing ataxia, bluish-brown mucous membranes, rapid and difficult breathing, increased heart rates, tremors and coma. Brown-colored and badly coagulated blood was the prominent necropsy finding. Slight pulmonary edema was prominent and all visceral organs were hyperemic. The hay contained 2,500 ppm nitrate-nitrogen and 11 ppm nitrite nitrogen.

Basic laboratory evaluation of water quality for livestock should include measurement of TDS, sulfate, nitrate-nitrite, and coliform bacteria. Supplementary water tests may include pH, sodium, iron, magnesium, chloride, calcium, potassium, manganese, and contaminants specific to the situation. Using the best-quality drinking water available contributes to the optimal production of livestock. Restricted quantity of drinking water or drinking water containing excessive levels of nitrate, TDS, sulfate, and other constituents can affect growth and production of all classes of animals. Drinking-water quality and availability should be evaluated as a cause of poor performance or nonspecific disease conditions in livestock. It is important that attempts to evaluate water quality include obtaining a thorough history, making astute observations, and asking intelligent questions. A thorough laboratory examination of animal specimens and water samples should be evaluated in view of existing standards for livestock drinking-water quality.

Subacute intoxication was induced by the oral administration of sodium nitrate 200 mg/kg during 150 days to Wistar rats. After the time had been up severe damaging were found in liver, kidney, heart and thymic tissues. In the liver cells the DNA fragmentation in "scale" manner was found, but not in kidney and heart cells. Simultaneously, the Ca2+, Mg(2+)-depended endonucleases activity were increased in the liver nuclei extracts under intoxication. It was suggested that increasing of apoptosis in liver is the universal reaction to toxins.

Background: An epidemiological investigation was undertaken in all age groups to assess the prevalence of methaemoglobinaemia in areas with high nitrate concentration in drinking water., Methods: Five areas were selected with an average nitrate concentration (as nitrate) of 26, 45, 95, 222 and 459 mg nitrate ions/litre in drinking water. These areas were visited and the house schedule (containing name, age, sex and weight of the family members) prepared in accordance with the statistically designed protocol. In all, 178 persons, matched for age and weight, were selected and arranged in five age groups. They constituted 10% of the total population of each of these areas. A detailed history of the selected population was taken, medical examination conducted and blood samples taken to ascertain the level of methaemoglobin. The collected data were subjected to statistical analysis to ascertain a relationship between nitrate concentration and methaemoglobinaemia., Results: High nitrate concentrations cause severe methaemoglobinaemia (7%-27% of Hb) in all age groups, especially in the age group of less than 1 year and above 18 years. The lower levels of methaemoglobin in the age group of 1-18 years is probably due to better reserve of cytochrome b5 reductase activity and its adaptation to increasing nitrate concentration in water to compensate for methaemoglobinaemia in this age group., Conclusion: We conclude that high nitrate ingestion causes methaemoglobinaemia in all age groups. Cytochrome b5 reductase activity and its adaptation with increasing water nitrate ingestion plays a role in compensating for the methaemoglobinaemia.

A case of fatal methemoglobinemia (MetHb-emia) which was presumably due to ingestion of nitrate is presented. An unidentified man was taken to a local emergency hospital suffering from deep cyanosis and 7 h later he was found dead in the hospital bed. The post-mortem examination of the blood revealed a methemoglobin (MetHb) concentration of 78% and the concentrations of nitrate and nitrite were 1.50 and 0.76 microg/mL, respectively. Capillary gas chromatography coupled to mass spectrometry (GC-MS) and capillary gas chromatography with a nitrogen-phosphorus detector (NPD) were used to detect nitrates and nitrites in the blood.

Sulphite is widely used as a preservative and antioxidant in foods, beverages, and pharmaceuticals. Endogenous sulphite is generated during the normal metabolism of sulphur-containing amino acids, and alterations in sulphur amino acid metabolism occur in some neurodegenerative diseases. In particular, sulphite oxidase deficiency produces severe mental retardation, seizures, spastic quadriparesis, dislocated lenses, and early death. Exposure of a neuronal cell line (rat mesencephalic cells) to high levels of sulphite induced a time-dependent decrease in viability. Peroxynitrite was also toxic to this cell line, and sulphite affected the toxicity of ONOO-. Sulphite concentrations of < or = 0.5 mM markedly potentiated cell damage induced by 200 microM ONOO-. We propose that sulphite can act as a neurotoxic agent, especially in combination with peroxynitrite. Sulphite radicals may be involved in the neurotoxic effect.