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Results for “FLUORIDE POISONING”

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At least 19 recordsLinked to original sources
PubMed1976

Acute fluoride poisoning.

Fluoride poisoning is a potentially severe environmental hazard for children. A case of fluoride poisong is presented which was manifested by severe hypocalcemia, ventricular arrhythmias, and respiratory failure. Treatment of this poisoning, including peritoneal dialysis, is discussed. The kinetics of fluoride distribution as measured in this patient suggest a rapid binding of ingested fluoride to bone, followed by gradual release and excretion. Peritoneal dialysis resulted in no significant fluoride removal.

Calcium Hydroxide↗
PubMedDate not supplied

Outbreak of acute fluoride poisoning caused by a fluoride overfeed, Mississippi, 1993.

OBJECTIVE: To determine the extent and confirm the cause of an August 1993 outbreak of acute fluoride poisoning in a small Mississippi community, thought to result from excess fluoride in the public water supply. METHODS: State health department investigators interviewed patrons of a restaurant where the outbreak first became manifest and obtained blood and urine samples for measurement of fluoride levels. State health department staff conducted a random sample telephone survey of community households. Public health environmentalists obtained water and ice samples from the restaurant and tap water samples from a household close to one of the town's water treatment plant for analysis. Health department investigators and town water department officials inspected the fluoridation system at the town's main water treatment plant. RESULTS: Thirty-four of 62 restaurant patrons reported acute gastrointestinal illness over a 24-hour period. Twenty of 61 households that used the community water supply reported one or more residents with acute gastrointestinal illness over a four-day period, compared with 3 of 13 households that did not use the community water supply. Restaurant water and ice samples contained more than 40 milligrams of fluoride per liter (mg/L), more than 20 times the recommended limit, and a tap water sample from a house located near the main treatment plant contained 200 mg/l of fluoride. An investigation determined that a faulty feed pump at one of the town's two treatment plants had allowed saturated fluoride solution to siphon from the saturator tank into the ground reservoir and that a large bolus of this overfluoridated water had been pumped accidentally into the town system. CONCLUSIONS: Correct installation and regular inspection and maintenance of fluoridation systems are needed to prevent such incidents.

Adolescent↗
PubMed1984

Acute fluoride poisoning after ingestion of sodium fluoride tablets.

Between 1978 and 1983, at least 20 children with fluoride poisoning were admitted to two major children's hospitals in Brisbane. Data on telephone calls received by Poisons Information Centres in Australia about fluoride toxicity show that Brisbane, the water supply of which is not fluoridated, received approximately twice as many calls per head of population as were received in Sydney and Melbourne. Concern is also expressed at the standard of packaging of fluoride tablets currently marketed in Australia. A treatment plan for cases of acute fluoride poisoning after oral ingestion is presented.

Acute Disease↗
PubMedDate not supplied

[Effect of glutamine, thymidine and orotate on the nucleic acid content in the cell nuclei of the regenerating liver in sodium fluoride poisoning].

Sodium fluoride inhibits an increase of nucleic acids in the cells nuclei of the rat liver after a partial resection of this organ. Introduction of thymidine to the animals poisoned with sodium fluoride, contrary to glutamine and orotate, causes a sharp decrease in the amount of nuclei in 1 mg of tissue and normalization of the nucleic acid content in them. Changes in the mitotic activity may be connected with a disturbance in the normal ratio of the nucleic acids synthesis precursors.

Animals↗
PubMed2001

Calcium neutralizes fluoride bioavailability in a lethal model of fluoride poisoning.

OBJECTIVES: Acute systemic fluoride poisoning can result in systemic hypocalcemia, cardiac dysrhythmias, and cardiovascular collapse. Topical and intraarterial therapy with calcium or magnesium salts reduces dermal injury from fluoride burns. The mechanism of these therapies is to bind and inactivate the fluoride ion. The purpose of this study is to evaluate the effect of calcium and magnesium to decrease the bioavailability of fluoride in a lethal model of fluoride poisoning. METHODS: In preliminary studies, we determined that fluoride 3.6 mM/kg intraperitoneally in the form of sodium fluoride was uniformly and rapidly fatal in a mouse model. Using this fluoride dose, we performed a controlled, randomized, blinded study of low- and high-dose calcium chloride (1.8 and 3.6 mM/kg intraperitoneally, respectively) and magnesium sulfate (3.6 mM/kg intraperitoneally) to decrease the bioavailability of the fluoride ion. After injection with sodium fluoride, animals were immediately treated with injections of sodium chloride (control), calcium chloride (low- or high-dose), or magnesium sulfate. The major outcome was 6-hour survival using a Cox Proportional Hazard model. RESULTS: All untreated animals died within 60 minutes. Using a Cox Proportional Hazard model, each 1.8 mM/kg dose of calcium chloride administered reduced the risk of death by 33%. Magnesium sulfate treatment was not associated with a hazard reduction. CONCLUSION: Calcium chloride administered simultaneously with sodium fluoride reduces the bioavailability of fluoride poisoning in a mouse model. The equivalent dose of magnesium sulfate does not significantly decrease fluoride bioavailability.

Animals↗
PubMed1975

Chronic fluoride poisoning in sheep.

Chronic fluoride poisoning in sheep and cattle was diagnosed on a farm in the Vredenburg district, Cape Province, and confirmed by laboratory analysis. The source of the poisoning was pastures contaminated with rock phosphate dust containing 2,1 to 3,3% of fluoride emitted from a fertilizer factory. Tabulated analyses of blood, liver, bone, pasture and water are given.

Animals↗
PubMed1994

Acute fluoride poisoning from a public water system.

BACKGROUND: Acute fluoride poisoning produces a clinical syndrome characterized by nausea, vomiting, diarrhea, abdominal pain, and paresthesias. In May 1992, excess fluoride in one of two public water systems serving a village in Alaska caused an outbreak of acute fluoride poisoning. METHODS: We surveyed residents, measured their urinary fluoride concentrations, and analyzed their serum-chemistry profiles. A case of fluoride poisoning was defined as an illness consisting of nausea, vomiting, diarrhea, abdominal pain, or numbness or tingling of the face or extremities that began between May 21 and 23. RESULTS: Among 47 residents studied who drank water obtained on May 21, 22, or 23 from the implicated well, 43 (91 percent) had an illness that met the case definition, as compared with only 6 of 21 residents (29 percent) who drank water obtained from the implicated well at other times and 2 of 94 residents (2 percent) served by the other water system. We estimated that 296 people were poisoned; 1 person died. Four to five days after the outbreak, 10 of the 25 case patients who were tested, but none of the 15 control subjects, had elevated urinary fluoride concentrations. The case patients had elevated serum fluoride concentrations and other abnormalities consistent with fluoride poisoning, such as elevated serum lactate dehydrogenase and aspartate aminotransferase concentrations. The fluoride concentration of a water sample from the implicated well was 150 mg per liter, and that of a sample from the other system was 1.1 mg per liter. Failure to monitor and respond appropriately to elevated fluoride concentrations, an unreliable control system, and a mechanism that allowed fluoride concentrate to enter the well led to this outbreak. CONCLUSIONS: Inspection of public water systems and monitoring of fluoride concentrations are needed to prevent outbreaks of fluoride poisoning.

Adolescent↗
PubMed1989

[Fluoride poisoning: mechanism, symptoms and treatment].

The use of fluorides in doses recommended by the International Dental Association is totally safe. Fluoride toxicity occurs only when these doses are exceeded. The human organism is capable of metabolizing fluoride when administered in low doses. Toxic doses though can cause signs and symptoms which vary from simple gastric disturbances to serious health problems or even death. The least fluoride dose which can cause signs and symptoms of fluoride poisoning is called possibly toxic dose. In the present paper the amount of 5 mgF-/kg is considered as the probably toxic dose of fluoride. In the case of accidental ingestion of a fluoride overdose the dentist should be also to calculate the amount of fluoride ingested. A simple method of calculating the amount of fluoride swallowed is presented in this paper. In addition the emergency treatment for fluoride overdoses is discussed. The danger of acute fluoride poisoning has increased lately, especially for children, due to the variety, pleasant taste smell and colour of fluoride products. Dentists should be able to estimate the toxic potential of fluoride in case of accidental poisoning and advise appropriate treatment.

Drug Overdose↗
PubMed1982

Acute fluoride poisoning associated with an on-site fluoridator in a Vermont elementary school.

On August 30 1980, an outbreak of minor illnesses consisting of nausea and vomiting affected 22 individuals attending a farmers market at a school. Illness was associated with the consumption of beverages made from school water (Xc2 = 65.6, p less than .0001); analysis of the water showed high levels of fluoride (1,041 mg/l). The most likely source of the contamination was the school fluoridator, which had accidentally been left on continuous operation.

Adolescent↗
PubMed1991

[The clinical features of 160 cases of acute sodium silicon fluoride poisoning].

160 cases of acute sodium silicon fluoride poisoning due to accidental intake are reported in this paper. Owing to the great amount of the chemical taken, the onset was abrupt and the digestive symptoms were prominent and severe. Twelve cases had acute gastritis or acute ulceration as shown by gastroscopy. The cardiovascular findings were notable. Ninety-six cases had abnormal electro-cardiographic findings. Abnormal heart rhythm and S-T segment changes were the main findings. These changes were positively correlated with the toxin amount of fluoride. Two cases died from sudden arrest of heart beat. Lung, kidney, liver, and brain functions were also impaired. The authors suggested diagnostic criteria and control procedures.

Adolescent↗
PubMed1981

Fluoride poisoning and the effect on collagen biosynthesis of osseus and non-osseus tissues of rabbit.

Fluoride poisoning is known to cause a debilitating condition clinically referred to as Fluorisis. The present investigation on the experimental animal model has been carried out to collect information on the precise nature of fluoride action, with special reference to collagen biosynthesis. Rabbits subjected to Fluoride poisoning for varying time intervals were administered with carbon labelled proline. Both osseus and non-osseus tissues were analyzed to measure the rate of incorporation of labelled proline, and index for collagen biosynthesis. Part I of the article is dealing with 14C proline uptake by Hydrolyzed collagen (obtained by centrifugation at 5000 x g) and residual protein of tissues viz: Bone, Tendon, Muscle, Kidney cortex, Skin, Lung, Pinna and Trachea. Part II of the article is dealing with 14C proline uptake by different fraction of collagen Viz: collagenase digested fraction and separated by centrifugation at 9000 x g; native collagen fibril, acid soluble collagen, alkali soluble collagen and non-collagenous protein. The results obtained in Part I, suggest that in Fluoride poisoning collagen biosynthesis has been greatly impaired both in osseus and non-osseus tissues. This has been further confirmed by the results obtained in Part II of the investigation.

Animals↗
PubMed1990

Aortic calcification in chronic fluoride poisoning: biochemical and electronmicroscopic evidence.

Fluoride is known to cause ectopic calcification. The biochemical mechanism(s) involved in the initiation of calcification is not understood and the accompanying ultrastructural changes remain to be elucidated. Therefore, certain relevant parameters have been investigated in the aorta of rabbits administered fluoride, 10 mg NaF/kg body wt, every 24 hr for 17 and 24 months. The significant findings are: (i) degeneration of smooth muscle fibers in the tunica media of the aorta, (ii) presence of electron-dense granules in the mitochondria and on the inner surface of the plasma membrane of smooth muscle cells, (iii) presence of matrix vesicles with electron-dense deposits, (iv) enhanced calcium content and the Ca/P ratio, and (v) increased total glycosaminoglycan (GAG) content with reduced dermatan sulfate. The presence of electron-dense granules in the mitochondria, on the plasma membrane and matrix vesicles is suggestive of the process of calcification. The enhanced calcium content as well as the Ca/P ratio supports the view that the aorta is undergoing mineralization. The total GAG is enhanced, possibly due to an increase in the content of GAGs other than isomers of chondroitin. The observation that conveys an important message is that the dermatan sulfate normally known to exist in high concentrations in soft tissues begins to decrease as the process of calcification sets in. This perhaps would hold true and may serve as an index in the process of ectopic calcification.

Administration, Oral↗
PubMed1980

Fatality due to acute systemic fluoride poisoning following a hydrofluoric acid skin burn.

Reports indicate that death due to hydrofluoric acid exposure is usually the result of inhalation of vapor causing pulmonary edema and fluoride poisoning. Absorption via the skin route of fluoride ion sufficient to cause serious systemic problems and even death has rarely been reported. A fatality resulting from a severe facial burn, which produced acute systemic fluoride poisoning with profound hypocalcemia and hypomagnesemia, is presented. The importance of proper personal protective equipment as well as the immediate initiation of first aid and appropriate medical measures, including the monitoring and replacement of serum calcium and magnesium, are emphasized.

Acute Disease↗
PubMed1980

Acute fluoride poisoning in a New Mexico elementary school.

Thirty-four persons became ill with acute fluoride poisoning shortly after drinking water in an elementary school in Los Lunas, NM. The water supply of the school was supplemented with a concentrated sodium fluoride solution designed to raise fluoride levels in drinking water to 1 to 5 ppm. Two water samples taken after the incident was reported showed elevated fluoride levels of 375 and 93.5 ppm. Malfunction of a relay switch controlling dilution of the fluoride solution produced toxic fluoride levels in the water. The symptoms of all patients were mild and generally of short duration, with two thirds of patients reporting complete resolution within 24 hours. The bitter, salty taste of the water deterred consumption of large amounts and prevented serious intoxication.

Acute Disease↗