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Results for “FLUORIDE POISONING”

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At least 973 records · Page 54Linked to original sources
PubMed2002

Burns caused by dilute hydrofluoric acid in the bleach.

Two male cleaning workers aged 62 (patient 1) and 28-(patient 2) presented with red, swollen, aching hands and fingers. At the first interview, the fingers of the right hand of both patients were swollen from the proximal interphalangeal joint to the tip of the finger. The fingers were red and intensely painful. The bleach that both patients used contained 9.5% hydrofluoric acid, and therefore we diagnosed their symptoms as those of burns caused by this agent. We subcutaneously injected 8.5% calcium gluconate into the affected fingers and dressed them with gauze soaked in cooled 0.025% benzethonium chloride. The patients did not use gloves at work, neither of them knew that the cleaning fluid contained dilute hydrofluoric acid, and they were unaware of the danger of this agent. They had not received proper education about the care and handling of poisons and deleterious substances such as hydrofluoric acid. The doctors who had examined the patients in the emergency ward overlooked the possibility of hydrofluoric acid burns, although they suspected chemical burns and confirmed the trade name of the cleaning agent. In addition, although the patients presented with intense pain, no white areas of coagulation and blistering, or surrounding erythemas, which are characteristic symptoms of such burns, were evident. The component of the cleaning agent was described on the container label in very small print. Had the words "poison" and "hydrogen fluoride" been printed in large characters, the examining doctors in the emergency ward would probably not have overlooked the presence of hydrofluoric acid, and the patients would perhaps have been more careful when using it. Hydrofluoric acid can be easily obtained by anyone through the Internet, although general consumers could not obtain industrial quantities. Therefore, the number of burn patients who are not familiar with hydrofluoric acid may increase in the future.

Adult↗
PubMed1991

[Drug poisoning in children in Vojvodina].

Epidemiological characteristics of acute drug poisoning in children were investigated over a period of two years (1988-1989). The total number of poisonings was 450. Among causes of poisoning psychopharmaca, especially benzodiazepine, came first (33.3%). They were followed by drugs affecting the nervous system (9.1%), usually by analgoantipyretics, and by drugs affecting the cardiovascular system (7.8%). In 10.6% of the cases poisoning was due to two or more drugs. In 12.3% of the poisonings drug was unknown. Sodium fluoride was the most frequent single cause of acute poisoning. The average age of the poisoned children was 5.1 years. Poisoning with drugs was more frequent among girls than among boys (55:45%). In more than half poisoning accidents there was no one present when poisoning occurred. A major number of poisonings were an attention-getting gesture or a suicidal attempt. There were 11 cases of repeated poisoning with the same drug.

Adolescent↗
PubMed1980

The spectrum of radiographic bone changes in children with fluorosis.

Painful, crippling deformities in Tanzanian children from an area of endemic fluorosis are reported. Excessive fluoride ingestion in pregnant women may possibly poison and alter enzyme and hormonal systems in the fetus causing disturbances to osteoid formation and mineralization. Knock-knees, bowlegs, and saber shins develop when walking begins. Combinations of osteomalacia, osteoporosis, and osteosclerosis result in a spectrum of bone changes from an early age. Male hormones, and dietary and genetic deficiencies may aggravate individual response of actively growing bones. Some radiographic changes suggestive of rickets, hyperparathyroidism and thalassemia were observed.

Adolescent↗
PubMed2004

Effect of fluoride intoxication on lipidperoxidation and antioxidant status in experimental rats.

Fluoride is a potent enzyme poison. Thirty ground water samples from Vellore District, Tamil Nadu, India were analysed for fluoride content and it was revealed that the fluoride content of 24 samples were over and above the permissible limits. In the present study, the experimental rats were orally treated with 25 ppm of fluoride/rat/day for 8 and 16 weeks, respectively, and the levels of lipid peroxidation and antioxidant enzymes were studied to evaluate fluoride intoxication. An increase in the level of lipid peroxides along with a concomitant decrease in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and reduced glutathione content were observed in fluoride administered groups of rats. The altered antioxidant status may be attributed to the increased generation of free radicals.

Animals↗
PubMed2003

Fluoride toxicity to aquatic organisms: a review.

Published data on the toxicity of fluoride (F-) to algae, aquatic plants, invertebrates and fishes are reviewed. Aquatic organisms living in soft waters may be more adversely affected by fluoride pollution than those living in hard or seawaters because the bioavailability of fluoride ions is reduced with increasing water hardness. Fluoride can either inhibit or enhance the population growth of algae, depending upon fluoride concentration, exposure time and algal species. Aquatic plants seem to be effective in removing fluoride from contaminated water under laboratory and field conditions. In aquatic animals, fluoride tends to be accumulated in the exoskeleton of invertebrates and in the bone tissue of fishes. The toxic action of fluoride resides in the fact that fluoride ions act as enzymatic poisons, inhibiting enzyme activity and, ultimately, interrupting metabolic processes such as glycolysis and synthesis of proteins. Fluoride toxicity to aquatic invertebrates and fishes increases with increasing fluoride concentration, exposure time and water temperature, and decreases with increasing intraspecific body size and water content of calcium and chloride. Freshwater invertebrates and fishes, especially net-spinning caddisfly larvae and upstream-migrating adult salmons, appear to be more sensitive to fluoride toxicity than estuarine and marine animals. Because, in soft waters with low ionic content, a fluoride concentration as low as 0.5 mg F-/l can adversely affect invertebrates and fishes, safe levels below this fluoride/l concentration are recommended in order to protect freshwater animals from fluoride pollution.

Animals↗
PubMed1995

Fatal hydrofluoric acid ingestion: a suicide case report.

Numerous reports of poisonings due to various fluoride salts and also to hydrofluoric acid have appeared in the literature. Hydrofluoric acid, which is recognized as a strong acid, is expected to cause severe burns following acute exposure. This case is reported because the expected burns were not observed, but the laboratory analysis (a blood fluoride concentration of 13 mg/L) supported the ruling of death due to ingestion of hydrofluoric acid.

Administration, Oral↗
PubMed1971

Relationship between internal Na + -K + and the accumulation of 14 C-5-hydroxytryptamine by rat platelets.

1. 5-Hydroxytryptamine (5-HT) transport has been investigated in rat blood platelets poisoned with dinitrophenol-sodium fluoride or ouabain.2. The inhibition of transport produced by different concentrations of the metabolic inhibitors has been correlated with changes in the internal Na(+) and K(+) concentrations of the platelets.3. Platelets poisoned in a high K(+) medium maintained a high internal K(+) concentration in the absence of cellular metabolism. When transferred to Krebs solutions containing different concentrations of Na(+) they accumulated 5-HT by a process that was related to the magnitudes of the internal and external Na(+) concentrations.4. The results are consistent with the hypothesis that the spontaneous movement of ions through the platelet membrane is capable of providing, at least in part, the energy requirements for 5-HT transport.

Animals↗
PubMedDate not supplied

Acute fluoride toxicity. Pathophysiology and management.

Acute intoxication with inorganic fluoride disrupts numerous physiological systems. As a potent acid it acts corrosively on the skin and mucous membranes, producing severe burns. As the most electronegative element it tightly binds many cations essential to homeostasis, producing, for example, profound hypocalcaemia and resultant inhibition of normal blood coagulation. As a metabolic poison it stimulates some enzymes, such as adenylate cyclase, and severely inhibits others, such as Na(+)-K(+)-ATPase and the enzymes of carbohydrate metabolism. Death can result from these processes and also from a delayed, explosive hyperkalaemia. Therapy of acute poisoning is aimed first, at preventing the absorption of fluoride by incorporating it into insoluble fluoride compounds; secondly, at enhancing fluoride tolerance by maintaining normal blood pH and electrolytes, and aggressive general support of the toxic patient; and thirdly, at manipulating renal excretion or removing fluoride with dialysis and haemoperfusion. If the poisoned patient can be supported for 24 hours, the prognosis improves markedly, although delayed toxicity can occur.

Animals↗
PubMed1995

[Acute neuroleptic poisoning].

According to the record of the Poison Control Centre in Zagreb, drugs most frequently implicated in poisoning episodes were benzodiazepines, neuroleptics, anticonvulsants including barbiturates, fluorides and antidepressants, which comprised more than 40% of all drug poisonings. More than 90% of neuroleptic poisonings were symptomatic on admission, 19% were comatose, 45% were drowsy, in 15% extrapyramidal symptoms were present, and only 9% were without symptoms. Severe poisonings in adults were almost all due to suicidal ingestion, while in children low to moderate doses of different neuroleptics caused severe poisoning in 13 cases, with coma, convulsions and most often with acute dystonic reactions. In 30 cases of neuroleptic ingestion more than one drug was involved. The usual combinations were with other neuroleptic or psychoactive drugs such as benzodiazepines, biperiden, carbamazepin and antidepressants. Therapeutic measures were gastric emptying in 32% of cases, biperiden when dystonia was present but only after consultation with the Centre and with 12-14 hours delay, and supportive treatment in all symptomatic patients.

Adult↗
PubMed2004

[Fluorine as a factor in premature aging].

The use of fluorine compounds in various areas of medicine, particularly in dentistry, as well as in agriculture and industry became very popular in the second half of the 20th century. Fluorine owed this widespread acceptance to observations that its compounds stimulate ossification processes and reduce the prevalence of caries. Unfortunately, growing expectations overshadowed the truth regarding interactions of fluoride on the molecular level. The fact was often ignored that fluoride is toxic, even though laboratory data stood for a careful approach to the benefits of usage. Excessive exposure to fluoride may lead to acute poisoning, hyperemia, cerebral edema, and degeneration of the liver and kidneys. Acute intoxication through the airways produces coughing, choking, and chills, followed by fever and pulmonary edema. Concentrated solutions of fluorine compounds produce difficult to heal necrotic lesions. In spite of these dramatic symptoms, acute intoxications are relatively rare; the more common finding is chronic intoxication attributable to the universal presence of fluorine compounds in the environment. The first noticeable signs of excessive exposure to fluoride in contaminated water, air, and food products include discolorations of the enamel. Dental fluorosis during tooth growth and loss of dentition in adulthood are two consequences of chronic intoxication with fluorine compounds. Abnormalities in mineralization processes affect by and large the osteoarticular system and are associated with changes in the density and structure of the bone presenting as irregular mineralization of the osteoid. Fluorine compounds also act on the organic part of supporting tissues, including collagen and other proteins, and on cells of the connective tissue. These interactions reduce the content of collagen proteins, modify the structure and regularity of collagen fibers, and induce mineralization of collagen. Interactions with cells produce transient activation of osteoblasts, stimulate fibroblasts to produce collagenase, and trigger toxic reactions in osteocytes and chondrocytes of trabecular bone. Growing deformations of the skeleton reduce mobility and result in permanent crippling of the patient. Fluoride increases the mass of non-collagen proteins such as proteoglycans and glucosaminoglycans, accelerating skin aging even though protein biosynthesis is generally suppressed. The final outcome includes progressive vascular lesions and disorders of energy metabolism in muscles. In conclusions, the use of fluoride, particularly by dentists and pediatricians, must be controlled and adapted to individual needs. It is worth remembering that fluoride: is the cause of disability due to bone deformations and abnormalities in the musculoskeletal system; reduces the incidence of caries but do not protect against tooth loss; exerts an adverse effect of metabolic processes in the skin; accelerates calcification of vessels and thus reduces their elasticity; inhibits bioenergetic reactions, in particular oxidative phosphorylation, reducing physical activity of muscles. These findings suggest that fluorine may be yet another factor in accelerated aging and revive the dispute started more than two and half thousand years ago whether aging is a physiologic or pathologic process. The understanding of factors modifying the process of aging is the basis for preventive measures aimed at extending life and maintaining full psychosocial activity.

Aging↗