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PubMed1997

Significant coincidental findings at autopsy in accidental childhood death.

Three cases of unexpected childhood death are presented in which significant potentially life-threatening lesions were identified that were considered coincidental to the cause of death. Two children died of accidental asphyxia and one died of potassium fluoride poisoning. Abnormalities identified at autopsy included established myocarditis (two cases) and cardiac rhabdomyomas (one case). In one case a previously unsuspected abnormal familial karyotype was found. These cases emphasize the value of complete autopsy investigations in all types of sudden childhood death, even when the cause of death appears obvious; they also demonstrate that potentially lethal organic disease may be asymptomatic in childhood and unrelated to death.

Asphyxia↗
PubMed1988

Fluoride-induced hyperkalemia: the role of Ca2+-dependent K+ channels.

Acute fluoride poisoning is associated with sudden cardiac death by an unknown mechanism. Because F- binds to Ca2+ to cause marked hypocalcemia, lowered serum Ca2+ concentrations have been thought to be a major underlying factor in the ventricular irritability of F(-)-toxic patients. However, correction of the hypocalcemia does not prevent sudden death. Paradoxically, while decreasing extracellular Ca2+ levels, in vitro studies have shown F- increases intracellular Ca2+, which is thought to trigger Ca2+-dependent K+ channels and produce a K+ efflux. The K+ efflux may be important clinically, as patients with F- overdose can exhibit hyperkalemia shortly before cardiovascular collapse. In erythrocyte suspensions, we found that propranolol, which increases the sensitivity of the Ca2+-dependent K+ channels, exacerbates the efflux, and quinidine, which blocks the channel, prevents the efflux. In six dogs, 35 mg/kg of sodium fluoride given intravenously produced intractable ventricular fibrillation within 140 minutes. Four dogs given 200 mg of quinidine sulfate with the sodium fluoride developed no ventricular arrhythmias. The data indicate that F--induced hyperkalemia is important in sudden cardiac death following acute fluoride toxicity and that this hyperkalemia is mediated by Ca2+-dependent K+ channels.

Animals↗
PubMed1986

Exposure to fluoride in the chemical industry.

Industries that use fluoride-containing materials are usually aware of their toxicity and adopt adequate medical measures. It has been found that workers in factories who have not been considered as subjected to fluorine hazard and therefore have not been controlled had significantly elevated urinary fluoride levels. Most workers in a medically controlled fertilizer plant had normal urinary levels. Maintenance workers were found to have higher values, up to 12 mg/liter.

Agriculture↗
PubMed1992

Serum fluoride as an indicator of occupational hydrofluoric acid exposure.

To define the relationship between ionic fluoride concentration in the serum of workers and the amount of hydrofluoric acid (HF) in the work environment, pre-and postshift serum and urine samples of 142 HF workers and 270 unexposed workers were examined. The maximum and minimum concentrations of HF in the air in each workshop varied from the mean by less than 30%. The preexposure levels of serum and urinary fluoride in HF workers were higher (P < 0.001) than the control values. This suggests that fluoride excretion from the body continues for at least 12h. The postshift serum and urinary fluoride concentrations of these workers were significantly higher (P < 0.001) than the preshift concentrations. A good correlation (r = 0.64) was obtained between postshift serum fluoride and postshift urine fluoride. There was a linear relationship between mean serum fluoride concentration and HF concentration in the workshop. A mean fluoride concentration of 82.3 micrograms/l with a lower fiducial limit (95%, P = 0.05) of 57.9 micrograms/l was estimated to correspond to an atmospheric HF concentration of 3 ppm. This is the maximum allowable environmental concentration recommended by the Japanese Association of Industrial Health, and it is also the threshold limit value suggested by the American Conference of Governmental Industrial Hygienists. The results demonstrate that exposure to HF can be monitored by determining the serum fluoride concentration.

Adolescent↗
PubMed1975

Calcium-potassium-stimulated net potassium efflux from human erythrocyte ghosts.

In the presence of 8 mM external Ca++, the K+ permeability of human red cell ghosts increases provided K+ is also present in the medium. This increase does not represent K+/K+ exchange but a stimulation of net K+ efflux. The stimulation is half-maximal at 0.7 +/- 0.15 mM (n=5). At concentrations above 4.0 mM, external K+ inhibits net K+ efflux. Similar stimulatory and inhibitory effects of external K were also observed in intact cells after exposure to Pb++ or to Ca++ in the presence of fluoride, iodoacetate plus adenosine, or propranolol, suggesting that a common K+ -activated K+ -specific transfer system may be involved under all of these various circumstances. Internal K+ also stimulates net K+ efflux from ghosts, but it is uncertain whether internal K+ is an absolute requirement for the K+ permeability increase. In contrast to external Na+ which slightly stimulates K+ efflux, internal Na+ inhibits. The inhibition by internal Na+ is abolished by sufficiently high concentrations of external K+, showing that K+ binding to the outer membrane surface and Na+ binding to the internal surface are mutually interdependent. In red cell ghosts the Ca++ -K+ -stimulated net K+ efflux increases with increasing pH until a plateau is reached between pH 7.2 and 8.0. In fluoride-poisoned intact cells, the Ca++-K+ stimulated flux passes through a maximum around pH 6.8. Neither internal nor external Mg++ interferes with the combined effects of Ca++ and K+. Similarly, external EDTA has no influence at concentrations which are far lower than the Ca++ concentration required to produce a maximal response. In contrast, low concentrations of internal EDTA prevent the permeability change.

Biological Transport↗
PubMed1986

[Principles of decisional analysis applied to the screening for occupational diseases: the example of occupational fluorosis].

In this paper, two oral presentations are combined. The first described the broad aspects of decision analysis and the second mentioned those medical data which need to be gathered in order to apply the model to industrial fluorosis. For this purpose, biological and medical observations were collected, both from workers of the aluminium industry and from controls. The five successive steps for building up a decision tree are then demonstrated, the aim of which being to evaluate the fitness of a screening strategy. A computer programme has been developed which may be applied both to occupational or non occupational diseases. Referring to industrial fluorosis, the computerized decision tree showed that screening with preshift urinary fluor, clinical and radiological signs, plus bone fluor rate is required, as soon as the risk corresponds to a 7% prevalence of the disease.

Aluminum↗
PubMed2003

Bone mineral density of the spine and femur in early postmenopausal Turkish women with endemic skeletal fluorosis.

The aim of this prospective, comparative study was to investigate the bone mineral density (BMD) changes in a group of early postmenopausal Turkish women with endemic skeletal fluorosis and to study effects of endemic fluorosis on BMD. Bone mineral density of L2-L4 vertebra, femur neck, femur trochanter, and Ward's triangle were measured in 45 female patients with endemic skeletal fluorosis and 41 age-matched controls by dual X-ray absorbtiometry (DXA). The BMD of L2-L4 vertebra and Ward's triangle were higher in the endemic fluorosis group than in the control group (P < 0.001). Patients with endemic fluorosis had higher femur neck and femur trochanter BMDs than did controls (P < 0.01 and P < 0.05, respectively). There was a positive correlation between serum fluoride content and BMD at the spine (r = 0.345, P = 0.001), femoral neck (r = 0.274, P = 0.011), Ward's triangle (r = 0.295, P = 0.006), and trochanter (r = 0.217, P = 0.045). In conclusion, higher bone mineral density levels were seen in early postmenopausal women with endemic skeletal fluorosis. BMD measurement is a tool in the diagnosis and management of this preventable crippling disease.

Absorptiometry, Photon↗
PubMed2004

Tooth quality in dental fluorosis genetic and environmental factors.

Dental fluorosis (DF) affects the appearance and structure of tooth enamel and can occur following ingestion of excess fluoride during critical periods of amelogenesis. This tooth malformation may, depending on its severity, influence enamel and dentin microhardness and dentin mineralization. Poor correlation between tooth fluoride (F) concentration and DF severity was shown in some studies, but even when a correlation was present, tooth fluoride concentration explained very little of DF severity. This fact calls into question the generally accepted hypothesis that the main factor responsible for DF severity is tooth fluoride concentration. It has been shown previously that genetic factors (susceptibility to DF) play an important role in DF severity although DF severity relates to individual susceptibility to fluoride exposure (genetics), tooth fluoride concentration relates to fluoride ingestion (environmental). The objective of this study was to investigate the correlation between tooth fluoride concentration, DF severity, and tooth mechanical and materials properties. Three strains of mice (previously shown to have different susceptibility to DF) at weaning were treated with four different levels of F in their water (0, 25, 50, and 100 ppm) for 6 weeks. Mice teeth were tested for fluoride by instrumental neutron activation analysis (INAA), DF severity determined by quantitative light-induced fluorescence [QLF], and tooth quality (enamel and dentin microhardness and dentin mineralization). Tooth fluoride concentration (environment factor) correlated positively with DF severity (QLF) (rs=0.608), fluoride treatment group (rs=0.952). However, tooth fluoride concentration correlated negatively with enamel microhardness (rs=-0.587), dentin microhardness (rs=-0.268) and dentin mineralization (rs=-0.245). Dental fluorosis (genetic factor) severity (QLF) correlated positively with fluoride treatment (rs=0.608) and tooth fluoride concentration (rs=0.583). DF severity correlated negatively with enamel microhardness (rs=-0.564) and dentin microhardness (rs=-0.356). Genetic factors (DF severity) and the environmental factor (fluoride concentration in tooth structure) have similar influence on tooth biomechanical properties, whereas only the environmental factor has an influence on tooth material property (mineralization).

Administration, Oral↗
PubMed2005

Severe bone deformities in young children from vitamin D deficiency and fluorosis in Bihar-India.

A case-control study was undertaken to understand the etiopathology of the bone deformities among young children in a fluoride-affected village of the Bihar State. Two villages were selected: one village with high fluoride in drinking water (7.9 +/- 4.15 ppm), and the other village with normal levels of fluoride (0.6 +/- 0.31 ppm) as the control village. The source of drinking water was bore wells in both the villages. Two hundred and forty subjects from 54 households (HHs) of the high-fluoride village (HFV) and 1443 subjects from 197 HHs of the control village were selected for the study. Dental mottling (DM) was observed in 50% and skeletal deformities of various forms were observed in 20% of the total population of HFV, whereas, in the control village, DM was 6% and skeletal deformities were absent. The prevalence of both, DM and skeletal deformities was high in the younger age group of 1.5 to 14 years. Genu valgum, genu varum, bowing of tibia, saber shin, and widening of the lower ends of long bones at the wrist were the typical skeletal deformities observed among affected children in the HFV. X-rays of the children with deformities revealed varying degrees of bending of bones and enlargement of epiphyseal ends of metaphyses with fraying of bone and ligamental calcification. A survey indicated significantly low calcium and high phosphorus intake among the population of the HFV as compared to that of the control village, possibly resulting from low intake of milk and high intake of potatoes, respectively. The mean urinary fluoride level was significantly higher in the children of the HPV, both with and without deformities, as compared to that of the control village. The mean serum 25 OHD3 (25 Hydroxy Vitamin D) and calcium levels were significantly lower and alkaline phosphatase activity was significantly higher among the children with deformities as compared to those without deformities from the HFV and the control village. Serum intact parathyroid hormone (IPTH) levels were high in children both with and without deformities in the HFV as compared to those in the control village. No significant differences were observed in the concentration of serum and urinary creatinine, and Cu, and Mg levels between the HFV and the control village. It can be concluded that some of the children from the HFV manifested severe bone deformities (rickets), which were confirmed by the existence of low serum calcium and vitamin D levels.

Adolescent↗