Local water supply: a risk to dialysis units?
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OBJECTIVE: To detect, diagnose and treat for endemic fluorosis earlier. METHODS: Six kinds of indices, such as environmental fluoride level, were collected from the population in epidemic and non-epidemic areas of endemic fluorosis with a 1:1 paired-match design. A discriminant analysis model was established by multivariate analysis. Levels of fluoride in environment and biological materials were determined by fluoride electrode method. Living condition of the subjects were measured and interviewed. Function of skeletons and joints was measured. Biochemical and enzyme indices were measured with reagent kits and gel electrophoresis. Other indices were measured by interview. All data collected were analyzed by SAS and MDAS computer software. RESULTS: There was significant overall difference between four kinds of discriminant functions, with an overall agreement of 85.78% (83.33% to 98.86%), based on resubstitution with sampled data. Posterior probabilities for new classification of sampled data automatically and randomly produced from a computer were 86.39% to 99.99%. CONCLUSION: The discriminant functions mentioned above, except for the third one with a too small sample size, can be used in early discrimination of endemic fluorosis caused by exposure to coal burning, or in evaluation for the effectiveness of pharmaceutical therapy, with a power of 95%.
OBJECTIVE: To study the effects of excess fluoride on bone turnover under conditions of diet containing different amount of calcium. METHODS: The experiment was performed on rats raised on a balanced diet with adequate calcium or a monotonous diet with low calcium and given amount of fluoride in their drinking water (F, 100 mg/L) for 2 months or 1 year. RESULTS: Osteomalacia, osteoporosis and accelerated bone turnover were observed with elevated serum alkaline phosphatase (ALP), osteocalcin (BGP) and parathyroid hormone (PTH) in rats fed on low calcium diet and fluoridized water for 2 months. In the rats fed on adequate calcium diet and fluoridized water for 2 months, only slightly increased osteoblastic activity was found while the average width of trabecular bone was increased with elevated serum ALP activity in rats raised on the same diet and water for 1 year. CONCLUSIONS: The basic effect of excess fluoride on bone is the causation of a high bone turnover state which can also be induced to a milder extent by low calcium diet itself. Therefore, the formation of a high bone turnover state is the pathogenetic basis for low dietary calcium intake to exacerbate the severity of skeletal fluorosis.
An experimental study was undertaken to observe effects of fluoride ingestion on lung tissue. The study was conducted on 15 albino rabbits of either sex and experimental fluorosis was induced by daily oral administration of sodium fluoride (NaF) solution. Rabbits were divided into three groups according to the quantity of fluoride ingestion: Group A: rabbits fed with 10 mg/kg/day NaF, Group B: 20 mg/kg/day NaF; and Group C: controls. After six months, the rabbits were sacrificed and their lung tissue was submitted for histopathological examination and fluoride content estimation. On gross examination, pale areas on the surface and dark brown congested areas on cut-section of lungs were seen in rabbits of groups A and B. Histopathological changes of alveolar haemorrhage, congestion, edema fluid, necrosis of alveolar epithelium, distortion of alveolar architecture and desquamation of epithelium of respiratory tract with damage to tracheal cartilage were observed in these groups. These changes were more marked in group B rabbits. Fluoride content of lung tissue homogenate was significantly higher in groups A and B (mean 1.206 ppm and 1.978 ppm respectively) as compared to control (0.1585 ppm). It was concluded that prolonged fluoride ingestion damages pulmonary tissues of rabbits. To the best of our knowledge, effect of chronic fluoride ingestion on lungs has not been reported in the literature, therefore, we had undertaken this study to analyse the effect of chronic fluoride ingestion on lungs.
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Neurological manifestations of skeletal fluorosis have been attributed to compressive radiculomyelopathy. Experimental fluorosis has shown evidence of myopathic changes. Data on human muscle pathology is very scanty. This study included 22 patients with established osteofluorosis. 16 of them showed only EMG changes of neurogenic muscle disease. Histochemistry and histopathology of muscle biopsies showed features of muscle atrophy, evidenced by 'type I' atrophy and 'type I' grouping. No myopathic changes were observed. It may be concluded that the primary changes are related to the nerve, with muscle being affected secondarily. There was no evidence of any primary muscle pathology due to fluorosis.
Having analyzed a total amount of all systems, the authors specified the most important genetic markers predisposing to chronic flour intoxication: the patients demonstrated higher frequency of ACP1*A and PGM1*1-alleles, phenotypes of acid phosphatase AA, of phosphoglucomutase 1+1+ and 2+2+, of dry cerumen consistence--d. The results could help to improve criteria of occupational selection and to specify practical recommendations on prophylaxis of chronic fluor intoxication.
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Skeletal fluorosis typically manifests as a diffuse increase in bone density, whereas avascular necrosis of the epiphyses and diaphyseal marrow are the main skeletal manifestations of sickle cell disease. The diagnostic and therapeutic challenges raised when both disorders are present are illustrated by two cases in Senegalese patients from an area characterized by high fluoride contents in the water and soil. Both had SS sickle cell disease. Skeletal fluorosis was diagnosed during evaluation for avascular necrosis in one patient and in the wake of septic arthritis in the other. Femoral head necrosis is difficult to identify in a patient with skeletal fluorosis. The bone lesions due to sickle cell disease and those due to fluorosis can mimic other bone diseases, most notably metastases. The combination of sickle cell disease and fluorosis results in significant medullary canal narrowing due to cortical thickening and to accumulation of necrotic bone. When performing hip replacement surgery, careful reaming of the medullary canal may reduce the risk of iatrogenic femoral fracture and inappropriate stem placement.
The autosomal dominant variety of craniometaphyseal dysplasia was diagnosed in 8 members of three generations of a White family living in the Cape Province and in Natal. Radiographic investigations of these individuals permitted assessment of the spectrum of involvement and of the age relationship of the abnormalities. Characteristic radiographic features included cranial hyperostosis and sclerosis, in association with metaphyseal splaying. Diagnostic precision in this order permits accurate prognostication and rational genetic counseling.
The learning-memory behavior was tested in mice on a Y-maze after drinking different concentration of sodium fluoride. The impairment on the structure of Gray 1 synaptic interface in the CA3 area of mice hippocampus were quantitatively analyzed by electron microscopy and computer image processing appliance. The main results are as follows: the learning ability of mice drinking high concentration of fluoride presented remarkable deterioration, the thickness of post-synaptic density (PSD) was decreased, and the width of synaptic cleft was remarkably increased. The results suggested that the impairment on the learning capability induced by fluorosis may be closely related with the pathological changes of synaptic structure in the brain of mice.
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Lipid peroxidation and antioxidative defence system in blood, liver and heart tissues, nitric oxide metabolites content in brain tissue of rats under binary action of small-doses of ionizing radiation and fluoride intoxication treated by amaranth oil and interval hypoxic training have been studied. Complex using of amaranth oil and interval hypoxic training result in increase both enzymatic, as nonezymatic links of antioxidant defence in all investigated tissues. It was revealed also enhance of NO system metabolites content in brain gomogenate. In this conditions lipid peroxidation processes in liver and heart tissues normalize comparison with essential increase level LPO under binary action influence. On the basis of obtained results LPO metabolites content we can suppossed that complex using of amaranth oil and interval hypoxic training result in increase of organism adaptative possibility. This complex can be using for binary action of ionizing radiation and fluoride intoxication correction.
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To investigate health impact of brick-tea type fluorosis in adults, the total daily fluorine intake, environment fluorine level were determined, the average urinary fluorine content assay and bone X-ray examination were conducted, the clinical manifestations were observed in the brick-tea type bone fluorosis epidemiological study conducted in Naqu County, Tibet at September, 2001. One hundred and eleven adults aged at 30-78 year-old were enrolled. It was found that the fluorine level of drinking water in Naqu County was 0.10 +/- 0.03 mg/L, but the brick-tea water processed foods-zamba and buttered tea had fluorine content of 4.52 +/- 0.74 mg/kg and 3.21 +/- 0.65 mg/kg respectively. The adult daily fluorine intake reached 11.99 mg, among which 99% is originated from the brick-tea containing foods. Positive detection rate of fluorosis osteopathy was 89% and the X-ray film confirmed that the diagnosis rate was 83%. Degenerative arthropathy and ossification of the interosteal membrane, calcification of the tendon were the characteristics that indicated by both the positive signs and reogenological examination. The prevalence of osteosclerosis type (bone matrix increased) was 74%. It is suggested that there were even more severe health impact compared with those in the water type and coal combustion type fluorosis.
OBJECTIVE: To investigate the effects of excessive intake of fluoride on the expression of type II collagen gene and types and morphological change of collagen fiber in the bone tissues of rats. METHODS: A rat model with fluorosis was established by adding 221 mg/L of sodium fluoride (NaF) to drinking water for the rats for 15 days, 30 days and two months, respectively. Type II collagen alpha1 (II) cDNA probe was prepared, and cDNA-mRNA in-situ hybridization was employed to detect change in expression of type II collagen mRNA in the bone tissues of rats with excessive intake of fluoride (221 mg/L NaF). Picrosirius-polarization method was used to observe types of collagen and morphology of collagen fiber in the bone tissues. RESULTS: Chondroblasts were found in the femur and other bone tissues of the rats after exposure to fluoride. cDNA-mRNA in-situ hybridization showed that expression of type II collagen gene could be observed in the cytoplasm of chondrocytic lacuna and chondrified bone tissues. mRNA in collagen of chondrocytes of the rib cartilage reached the peak level 15 days after exposure to fluoride, and decreased gradually one month and two months after exposure. Polychromatic type II collagen, breakage of collagen fiber, disorder array and reduced content of type II collagen could be found in the bone tissues with picrosirius-polarization method. CONCLUSIONS: Excessive intake of fluoride could lead to changes in types and structure of collagen (cross-linkage) of bone tissues, which caused expression of type II collagen gene in the chondrified bone tissues and enhanced its expression in the rib cartilage tissues.
The phenotype frequency distributions of several classical blood genetic markers and dermatoglyphic characters were analyzed in workers of Siberian aluminum plants who had occupational fluorosis. Comparison with healthy workers revealed significant differences in frequencies of several markers. Phenotypes B (AB0), D (Rh), MN (MN), P1 (P), Le a (Lewis), Gc 2-1, Cx (on both hands), Th/I+ (on the left hand), C3, and C4 (HLA) were associated with higher risk of occupational fluorosis.