Estimation of incidence and social cost of colon cancer due to nitrate in drinking water in the EU: a tentative cost-benefit assessment.

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.

Epidemilogical trends strongly suggest exposures as etiologic agents in the pathogenesis of sporadic Alzheimer's disease, diabetes mellitus, and non-alcoholic steatohepatitis.

Nitrosamines mediate their mutagenic effects by causing DNA damage, oxidative stress, lipid peroxidation, and pro-inflammatory cytokine activation, which lead to increased cellular degeneration and death. However, the very same pathophysiological processes comprise the "unbuilding" blocks of aging and insulin-resistance diseases including, neurodegeneration, diabetes mellitus (DM), and non-alcoholic steatohepatitis (NASH). Previous studies demonstrated that experimental exposure to streptozotocin, a nitrosamine-related compound, causes NASH, and diabetes mellitus Types 1, 2 and 3 (Alzheimer (AD)-type neurodegeneration). Herein, we review evidence that the upwardly spiraling trends in mortality rates due to DM, AD, and Parkinson's disease typify exposure rather than genetic-based disease models, and parallel the progressive increases in human exposure to nitrates, nitrites, and nitrosamines via processed/preserved foods. We propose that such chronic exposures have critical roles in the pathogenesis of our insulin resistance disease pandemic. Potential solutions include: 1) eliminating the use of nitrites in food; 2) reducing nitrate levels in fertilizer and water used to irrigate crops; and 3) employing safe and effective measures to detoxify food and water prior to human consumption. Future research efforts should focus on refining our ability to detect and monitor human exposures to nitrosamines and assess early evidence of nitrosamine-mediated tissue injury and insulin resistance.

Acute poisoning of silver gulls (Larus novaehollandiae) following urea fertilizer spillage.

Two episodes of accidental urea toxicosis are described in wild silver gulls (Larus novaehollandiae) following spillage of fertilizer grade urea at a commercial shipping facility near Perth, Western Australia. In both cases, urea spillage had been seen to contaminate freshwater wash-down pools on the wharves where ships were being unloaded and gulls were seen to be drinking and washing in the pools nearby the spillages. Affected birds were found moribund or dead. Necropsy and histopathological findings were non-specific and consisted of mild to moderate congestion of visceral organs and brain. Analysis of a water sample collected during Case 1 revealed a very high urea concentration of 4.124 mol/l (pH 5.5), and fluid from the proventriculus of two birds had urea concentrations of 382 and 308 mmol/l, respectively. Nine birds were examined during the second episode (Case 2) and, from heparinized heart blood samples collected (n = 5), the mean plasma urea (288 +/- 92.0 mmol/l), ammonia (43.9 +/- 34.2 mmol/l) and uric acid (7.45 +/- 1.99 mmol/l) concentrations were markedly elevated above the reference ranges for all bird species. Proventricular contents (n = 7) similarly contained high concentrations of urea (394 +/- 203 mmol/l) and ammonia (9.3 +/- 15 mmol/l). The probable mechanisms of urea and ammonia toxicity in these birds are discussed.

Acute renal failure following ingestion of manganese-containing fertilizer.

Fertilizers are used to promote the survival and growth of plants and crops and have a good safety record when used properly. The basic elements in fertilizer include phosphorus, nitrite, and potassium. In addition, there are additive agents that vary for different crops and which may include some metals. Acute intoxication by ingesting fertilizer includes damage to various organ systems as well as severe cardiovascular or respiratory distress. We report the case of a 64-year-old man who ingested about 700 mL of fertilizer and suffered acute renal failure, hyperkalemia, and mild methemoglobinemia. After supportive care and emergent hemodialysis for hemodynamic instability due to hyperkalemia, the renal function of the patient recovered in four days.

Acute poisoning of cattle by fertilizer-contaminated water.

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.

Hazardous substances emergency events in the agriculture industry and related services in four mid-western states.

Analysis of Hazardous Substances Emergency Events Surveillance data reported from 14 participating states between 1993 and 1998 found that acute releases are seasonal. This seasonality was more prevalent in four Midwestern states during April-June and coincided with their planting season, suggesting an association of these releases with the agricultural industry. A more detailed analysis of events related to this industry in these states found that ammonia was the chemical most frequently released, and ammonia related events resulted in a significantly higher number of evacuations than all other events (OR = 10.7, [5.25-22.28]). A logistic regression model to identify risk factors for an event with victims found an increased risk for: (1) events with ammonia during April-June (adjusted OR = 3.57, [2.09-6.09]); (2) events in fixed-facilities during April-June (aOR = 3.74, [2.01-6.95]); and (3) events with multiple substances (aOR = 2.33, [1.05-5.17]). The most common causes for the events were equipment failure and operator error. Resulting injuries were mainly respiratory, ocular and traumatic, and included six deaths. Employing more stringent safety measures and educating employees and the public about the health hazards involved with agricultural chemicals may reduce injuries and help contain costs associated with the releases.

Ricinus communis cake poisoning in a dog.

A fatal case of canine poisoning by castor bean (Ricinus communis L) cake used as fertilizer is described, heat treatment The process of R communis cake production should include heat treatment to reduce the risk if the product is accidentally ingested by pets or humans.

Occupation and prostate cancer risk in Sweden.

To provide new leads regarding occupational prostate cancer risk factors, we linked 36,269 prostate cancer cases reported to the Swedish National Cancer Registry during 1961 to 1979 with employment information from the 1960 National Census. Standardized incidence ratios for prostate cancer, within major (1-digit), general (2-digit), and specific (3-digit) industries and occupations, were calculated. Significant excess risks were seen for agriculture-related industries, soap and perfume manufacture, and leather processing industries. Significantly elevated standardized incidence ratios were also seen for the following occupations: farmers, leather workers, and white-collar occupations. Our results suggest that farmers; certain occupations and industries with exposures to cadmium, herbicides, and fertilizers; and men with low occupational physical activity levels have elevated prostate cancer risks. Further research is needed to confirm these findings and identify specific exposures related to excess risk in these occupations and industries.

[Pesticide poisoning]. / Intoxications par produits agricoles.

Pesticide intoxications are mainly accidental with a benign course, such as ingestions of diluted fertilizers or low concentration antivitamin K rodenticides, ant-killing products or granules of molluscicides containing 5% metaldehyde. Voluntary intoxications by chloralose, strychnine, organophosphorus or organochlorine insecticides, concentrated anti-vitamin K products, herbicides such as paraquat, chlorophenoxy compounds, glyphosate or chlorates may be severe. Toxicity is due to active substances but also to solvents or surfactants included in the composition. Analysis done in a toxicology laboratory help in establishing diagnosis, prognosis and treatment. Poison centres may be called constantly to help for the evaluation of these intoxications.

A case of fatal intoxication with ammonium sulfate and a toxicological study using rabbits.

Agricultural fertilizers such as ammonium sulfate are widely used in house gardens as well as in agriculture, but few case reports or toxicological studies of ingested fertilizers have been reported. This paper investigates a fatal case of ammonium sulfate poisoning and demonstrates its clinical and biochemical findings in rabbits. An 85-year-old woman was found dead lying on the ground outside her house in the middle of March, but the autopsy could not determine the cause of her death. Examination at the police laboratory of the solution in the beer can found next to her showed that it was very likely ammonium sulfate. Our measurement showed a significant increase of ammonium and sulfate ions in serum and gastric contents. The cause of her death was determined as poisoning by ammonium sulfate. The total dose of 1500 mg/kg of ammonium sulfate was administered to three rabbits, all of which showed similar symptoms such as mydriasis, irregular respiratory rhythms, local and general convulsions, until they fell into respiratory failure with cardiac arrest. EEG showed slow, suppressive waves and high-amplitude slowing wave pattern, which is generally observed clinically in hyperammonemia in man and animal. There was a remarkable increase in the concentration of ammonium ion and inorganic sulfate ion in serum, and blood gas analysis showed severe metabolic acidosis. These results, mainly findings by EEG, have shown that a rapid increase in ammonium ions in blood can cause damaging the central nervous system without microscopic change. When the cause of death can not be determined, measurement of ammonium ion, inorganic ion and electrolytes in blood as well as in stomach contents at forensic autopsy is necessary.

Chronic gypsum fertiliser ingestion as a significant contributor to a multifactorial cattle mortality.

OBJECTIVE: To assess the validity of claims that heavy metal contamination from an open-cut mine caused the death of 226 cattle on a nearby farm over a period of 18 months, and to investigate other possible contributing factors. PROCEDURE: A retrospective assessment of previous investigations combined with additional chemical analyses. RESULTS: Extensive chemical analyses produced no evidence of heavy metal contamination associated with the mine. Analysis of bones indicated exposure to fluoride in greater than normal amounts. The main source of fluoride seems to have been gypsum that was included in a feed supplement and also ingested from fertiliser dumps on paddocks. The gypsum itself may have contributed significantly to the ill health. Other factors probably affected some classes of animals, notably the young calves. CONCLUSIONS: What originally seemed to be a disease problem of single aetiology probably was an expression of interacting multifactorial causes. This investigation has highlighted the potential toxicity of gypsum to livestock and the need for further studies to establish its basis.

Accidental superphosphate fertilizer poisoning in pregnant ewes.

Consumption of superphosphate fertilizer by 200 pregnant ewes resulted in signs of toxicosis in 41 ewes, 14 of which died. Predominant clinical signs were marked teeth grinding, voluminous diarrhea, CNS depression, apparent blindness, and a stiff-legged atactic gait. Biochemical abnormalities were hypocalcemia, hypoglycemia, and a high anion gap. The primary toxic principal in superphosphate fertilizers is the fluorine contaminant; however, calcium pyrophosphate and calcium orthophosphate also contribute to toxicosis, which results in acute proximal renal tubular necrosis. Voluntary consumption of superphosphate fertilizer in well-fed livestock is not expected, and was believed to be related to the lack of availability of salt.

Urea poisoning in suckler cows.

Accidental urea intoxication resulted in the death of 17 of 29 suckler cows within six hours after the contamination of their drinking water with urea fertiliser. The other cows showed no lasting ill effects and neither their three-month-old calves nor the stock bull were affected. The urea concentration in the water was 86 mmol/litre, and the concentrations of ammonia nitrogen in the rumen fluid of two of the cows which were examined after death were 1825 and 957 mg/litre. The clinical signs and post mortem findings are described.