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PubMedDate not supplied

Water fluoridation: time to reexamine the issue.

Water fluoridation was instituted as a public health measure more than 50 years ago to help limit dental caries. However, with the advent of fluoridated dentifrices, fluoridated infant formulas, and commercially prepared beverages with fluoridated water, the incidence of dental fluorosis is increasing. Health care professionals need to understand the history of water fluoridation, examine the benefits and complications of fluoride, and, if need be, take an informed political stance on an issue that is affecting large numbers among our pediatric population.

Child, Preschool↗
PubMed1997

[Influence of experimental fluorosis on phospholipid content and fatty acid composition in rat brain].

OBJECTIVE: To investigate the pathogenesis of brain damage by fluoride intoxication, phospholipid content, and fatty acid composition in rat brain with fluorosis were annlysed. METHODS: Wistar rats were fed with NaF in various amounts and time periods to produce the animal model with chronic fluorosis. Phospholipid content and fatty acids composition were analysed using high performance liquid chromatography and gas chromatography, respectively. RESULTS: All animals fed with high amount of fluoride suffered from chronic fluorosis. The total brain phospholipid content was lower in the rat treated with fluoride, which mainly influenced phosphatidylethanolamine, phosphatidylcholin, and phosphatidylserine. No modifications were detected in fatty acid and aldehyde compositions of individual phospholipid classes. CONCLUSION: The metabolism of brain phospholipid might be interfered by fluoride accumulated in brain tissue, which is related with the degeneration of neuron. The changes of brain phospholipid could be involved in the pathogenesis of chronic fluorosis.

Animals↗
PubMed1997

[Changes of coenzyme Q content in brain tissues of rats with fluorosis].

Animal models with pathological damage caused by chronic fluorosis to a different extent were duplicated in Wistar rats by feeding them with 66.3 mg/L and 221 mg/L fluorine-containing water for three, five and seven months, respectively. Cholesterol, dolichol and coenzyme Q in animal brain tissues were determined by high performance liquid chromatography. Results showed that no significant difference of cholesterol and dolichol contents in brian tissues between rats with fluorosis and normal controls were detected. Coenzyme Q content of brain tissue in rats fed with fluorine-containing water decreased at early stage of fluorosis, but increased significantly at late stage. It is speculated that changes in content of coenzyme Q could correlate with changes in free radical levels induced by fluorine.

Animals↗
PubMed2003

Amiodarone attenuates fluoride-induced hyperkalemia in vitro.

UNLABELLED: Poisoning by hydrofluoric acid or fluoride salts results in hypocalcemia, hypomagnesemia, and hyperkalemia with subsequent cardiac dysrhythmias. In previous studies, quinidine attenuated fluoride-induced hyperkalemia in vitro, and enhanced survival in animals. Like quinidine, amiodarone is a potassium channel blocker, although amiodarone is more familiar to clinicians due to its recent inclusion in advanced cardiac life support (ACLS) protocols. OBJECTIVES: This in-vitro study of human erythrocytes was designed to determine whether amiodarone could attenuate fluoride-induced hyperkalemia. METHODS: Six healthy volunteers each donated 60 mL of blood on three occasions. Each specimen was divided into 12 tubes, incubated at 37 degrees C, and oxygenated with room air. An aqueous sodium fluoride (F(-)) solution was added to tubes 1-9. Incremental amounts of quinidine were added to tubes 1-4 (Q(1)-Q(4)) to attain calculated concentrations of 0.73 microg/mL, 1.45 microg/mL, 2.9 microg/mL, and 5.8 microg/mL, respectively. Incremental amounts of amiodarone were added to tubes 5-8 (A(1)-A(4)) to attain calculated concentrations of 0.38 microg/mL, 0.75 microg/mL, 1.5 microg/mL, and 3.0 microg/mL, respectively. Tubes 9-12 were controls for each of F(-), amiodarone, quinidine alone, and no additive, respectively. Extracellular potassium concentration ([K(+)]) was followed, and an objective endpoint was defined as the rise in potassium concentration at 6 hours. RESULTS: Fluoride produced a significant change in [K(+)] by 6 hours in all samples. Quinidine produced a J-shaped curve in its ability to attenuate the rise in [K(+)], with only one concentration, Q(3), demonstrating significance versus tube 9 (control). Amiodarone also demonstrated a J-shaped dose-response effect, with statistical significance at A(1), A(2), and A(3) versus tube 9 (control). There was no significant difference among the effective concentrations (Q(3), A(1), A(2), and A(3)) of both drugs. CONCLUSIONS: In this in-vitro model using human blood, amiodarone and quinidine both attenuated F(-)-induced hyperkalemia. Further study is indicated to determine whether amiodarone enhances survival in F(-)-poisoned animals.

Amiodarone↗
PubMed1997

Acute fluoride toxicity from ingesting home-use dental products in children, birth to 6 years of age.

OBJECTIVE: This paper analyzes reports to the American Association of Poison Control Centers (AAPCC) of suspected overingestion of fluoride by children younger than 6 years of age between 1989 and 1994, and estimates the probably toxic amounts of various home-use fluoride products in children younger than 6 years of age. METHODS: Annual incidence rates of reported fluoride exposures attributed to dietary supplements, toothpaste, and rinses were calculated. Probably toxic amounts of each product were calculated using the frequently cited dose of 5 mg/kg. RESULTS: Children younger than 6 years of age accounted for more than 80 percent of reports of suspected overingestion. While the outcomes were generally not serious, several hundred children were treated at health care facilities each year. A 10 kg child who ingests 50 mg fluoride (10.1 g 1.1% NaF gel; 32.7 g 0.63% SnF2 gel; 33.3 g 1,500 ppm F toothpaste; 50 g 1,000 ppm F toothpaste; and 221 mL 0.05% NaF rinse) will have ingested a probably toxic dose. CONCLUSIONS: Overingestion of fluoride products in the home is preventable. Dentists and other health care providers should educate parents and child care providers about the importance of keeping fluoride products out of reach of children. Manufacturers should be encouraged by the ADA and the FDA to use child-resistant packaging for all fluoride products intended for use in the home.

Acute Disease↗
PubMed1982

Accidental ingestion of NaF tablets by children--report of a poison control center and one case.

Accidental ingestion by children of NaF tablets for caries prophylaxis is a frequent event. However, our own experience from the Poison Information Centre in Vienna and reports from other centers show that these accidents usually do not present a serious risk. The mechanism of fluoride toxicity and symptoms of poisoning are briefly reviewed. The case of a boy who died after ingesting 16 mg fluoride/kg, but whose cause of death is not certain beyond doubt, is discussed.

Child, Preschool↗
PubMed1979

Inorganic and organic fluoride concentrations in tissues after the oral administration of sodium monofluoroacetate (Compound 1080) to rats.

Male rats were used to study the inorganic (ionic) and organic fluoride concentrations in plasma, liver, kidneys and stomach content after oral doses of 0, 2.2, 3.5, 4.0, 5.0 and 7.0 mg sodium monofluoroacetate (SMFA, Compound 1080)/kg body weight. Tissue and plasma ionic fluoride concentrations were observed to be higher in all rats given SMFA as compared to rats in the control group. This observation suggests in vivo defluorination of SMFA. Homogenates of liver obtained from SMFA poisoned rats showed significant increases in ionic fluoride concentration during a 6-day storage period at +4 degrees C, with the total fluoride concentration (ionic and organic) remaining constant. The average percentages of distribution of SMFA (organic fluoride) in plasma, liver, and kidneys were 7.05, 5.07 and 1.68, respectively. Plasma and tissue SMFA concentrations were generally lower than the corresponding stomach fluid SMFA concentrations for all dosage groups. Lethal concentration of SMFA in the liquid stomach content was in the range 84.9--189 micrograms/ml, corresponding to total (ionic and organic) fluoride concentrations in the range of 16.1--36 micrograms/ml.

Animals↗
PubMed1995

Nucleotide Levels Do Not Critically Determine Survival of Maize Root Tips Acclimated to a Low-Oxygen Environment.

We tested the hypothesis that ATP levels and energy charge determine the resistance of maize (Zea mays) root tips to anoxia. We focused on root tips of whole maize seedlings that had been acclimated to low O2 by exposure to an atmosphere of 3% (v/v) O2 in N2. Acclimated anoxic root tips characteristically have higher ATP levels and energy charge and survive longer under anoxia than nonacclimated tips. We poisoned intact, acclimated root tips with either fluoride or mannose, causing decreases in ATP and energy charge to values similar to or, in most cases, below those found in nonacclimated anoxic tips. With the exception of the highest fluoride concentration used, the poisoned, acclimated tips remained much more tolerant of anoxia than nonacclimated root tips. We conclude that high ATP and energy charge are not components critical for the survival of acclimated root tips during anoxia. The reduced nucleotide status in poisoned, acclimated root tips had little effect on cytoplasmic pH regulation during anoxia. This result indicates that in anoxic, acclimated root tips either cytoplasmic pH regulation is not dominated by ATP-dependent processes or these processes can continue in vivo largely independently of any changes in ATP levels in the physiological range. The role of glycolytic flux in survival under anoxia is discussed.

Journal Article↗
PubMed1995

[Epidemiological studies on endemic fluorosis and arsenism in Xinjiang].

Epidemiological and clinical studies on the water of 102 wells containing high-level fluoride and arsenic and a population of 50,760 drinking the water in Kuitun Area, Xinjiang were conducted. Results indicated fluoride and arsenic contents in the well water were associated with geochemical environment, and drinking the water containing high-level fluoride and arsenic for a long-term was the cause of fluorosis and arsenism. Also, diagnostic criteria and major clinical manifestations for fluorosis and arsenism were put forward in the paper. Relationship between fluoride and arsenic contents in the well water and prevalence of fluorosis and arsenism in local residents was analyzed. It suggested fluorosis and arsenism was a systematic disorder and further studies on its potential hazard were merited.

Adolescent↗
PubMed2003

Hydrofluoric acid-induced burns and life-threatening systemic poisoning--favorable outcome after hemodialysis.

BACKGROUND: Skin contact with hydrofluoric acid (HF) may cause serious burns and life-threatening systemic poisoning. The use of hemodialysis in fluoride intoxication after severe dermal exposure to HF has been recommended but not reported. CASE REPORT: A 46-year-old previously healthy man had 7% of his body surface exposed to 71% HE Despite prompt management, with subsequent normalization of the serum electrolytes, recurrent ventricular fibrillation occurred. On clinical suspicion of fluoride-induced cardiotoxicity, acute hemodialysis was performed. The circulatory status stabilized and the patient fully recovered. High fluoride levels in the urine and serum were confirmed by the laboratory. DISCUSSION: There is no ultimate proof that the favorable outcome in this case was significantly attributable to the dialysis. However, most reported exposures of this magnitude have resulted in fatal poisoning. As our patient had normal serum electrolytes and no hypoxia or acidosis at the time of his arrhythmias, it was decided that all efforts should be focused on removing fluoride from his blood. The rationale for performing hemodialysis for this purpose is clear, even though such intervention is more obviously indicated in patients with renal failure. CONCLUSION: Hemodialysis may be an effective and potentially lifesaving additional treatment for severe exposure to HF when standard management has proven insufficient.

Accidents, Occupational↗
PubMed1989

[Clinical picture and treatment of acute thallium poisoning].

The authors report results of treatment of 16 patients whose disease was caused by premeditated poisoning with thallium fluoride. The first signs of the disease appeared in 5 patients 30-38 hours and in the remaining 2-4 days after ingestion of poisoned food and were manifested by dyspepsia, leg pain. Then neurological symptoms of polyneuritis and encephalomyelitis prevailed. Within 1-3 weeks alopecia, xeroderma, herpetic phenomena appeared. Most patients showed disorders of the psycho-emotional sphere (intoxication encephalopathies of anxiety-paranoia type). Severe grades of thallitoxicosis were marked by involvement of the myocardium, liver and kidneys. Excretion of the nucleus is slow: with the urine (45%), with feces (55%). For correct diagnosis and for solution medical forensic problems examination of the content of thallium in the blood, urine, feces and hair is of importance. Treatment tactics are described in detail.

Acute Disease↗
PubMed1991

Fluoride ingestion in children: a review of 87 cases.

All cases of fluoride ingestion in children younger than 12 years old reported to the Rocky Mountain Poison Center between January 1 and December 31, 1986, were retrospectively reviewed. Eighty-seven cases were identified. Eighty-four cases involved accidental ingestion of dental fluoride products in the home (tablets, drops, rinses) in children 8 months to 6 years old. Two older children (8 and 9 years old) became symptomatic after fluoride treatment by a dentist. A 13-month-old child died after ingesting an unknown amount of sodium fluoride insecticide, the only insecticide exposure in our series. Postmortem total serum calcium value was 4.8 mg/dL (normal 8.8 to 10.3). No other patients had serious symptoms or sequelae. Twenty-six (30%) of 87 became symptomatic, with gastrointestinal symptoms (nausea, vomiting, diarrhea, abdominal pain) in 25 patients and drowsiness in 1. Only 3 patients became symptomatic later than 1 hour after ingestion. Analysis of data from 70 cases with sufficient information revealed that as the amount of fluoride ingested increased, the percentage of patients with symptoms increased. Not including the fatal case, 6 patients had serum calcium levels measured, and all were normal. Children who ingested up to 8.4 mg/kg of elemental fluoride in dental products had mild and self-limited symptoms, mostly gastrointestinal.

Accidents↗
PubMed2000

In vitro effects of sodium fluoride and sodium dichromate on dynamic properties of human erythrocyte membrane.

Sodium fluoride (NaF) and sodium dichromate (Na2Cr2O7) are two different toxic compounds which are used as a dental caries prophylactic and as an oxidising agent in various industrial areas, respectively. However, accidental fluoride and chromate poisoning is not a rare occurrence, even death may result from cardiac or respiratory failure. In the present work, alterations produced by NaF, Na2Cr2O7 and temperature changes in the molecular dynamics of the human erythrocyte membrane were studied, in vitro, by the spin-labelling ESR technique. Human intact erythrocyte cells spin labelled with 5- and 16-doxyl stearic acids (5-DSA and 16-DSA) and treated with 40 microM NaF and 5 microM Na2Cr2O7 at 37 degrees C were used to quantify membrane fluidity. This was performed by measuring the changes in the order parameter (S), correlation time (tau) and phase transition temperature using recorded electron spin resonance (ESR) spectra. Experimental results show that 5 microM Na2Cr2O7 and 40 microM NaF do not produce any significant effects on the order parameter of 5-DSA spin label while they cause appreciable changes in the correlation time of the same label. As for 16-DSA, while Na2Cr2O7 does not produce any measurable effect on the order parameter of this label, NaF does in a certain extent. Although weak, the effects of both compounds on the correlation time of 16-DSA are found to be well above the experimental error limits. Change in temperature was observed to alter significantly S and tau parameters which show biphasic character in the temperature range of 5-50 degrees C. Activation energies of the hydrocarbon chains above and below transition temperatures were also determined for untreated and NaF or Na2Cr2O7 treated erythrocyte cells and the effect of NaF and Na2Cr2O7 on these energies and transition temperatures were discussed.

Chromates↗