Abstract

Sixty-four CD-1 female mice were assigned to onez of four water treatment groups: Control (distilled, deionized water) (C); Fluoride (50 ppm F as NaF) (F); Aluminum (100 ppm Al as AlCl3) (Al); and Al & F (50 ppm F & 100 ppm Al) (AlF). One-half of the animals in each group were mated. The study was terminated on the 5th days after parturition. Pregnancy and lactation (P & L) reduced tibia Al more than 50% in the C, F, and Al groups, and 34% in the AlF group. In contrast, brain Al increased 168% in the F group, and 260% to 350% in the remaining three groups. P & L decreased tibia calcium (Ca) between 10% and 20% in all four groups, whereas the kidney Ca reduction ranged from 21% to 24%. However, heart Ca increased a minimum of 11% in the F group and a maximum of 169% in the AlF group. A maximum reduction of tibia zinc by pregnancy was obtained in the AlF group, reflecting the lowest fetal zinc in the group. The study demonstrated that pregnancy and lactation may increase the need of Al, Ca, and zinc in the vital organs such as brain,heart and fetus. These extra requirements may be fulfilled at the expense of the bones and less active organs such as kidneys. The study suggests that Al may be essential during pregnancy and lactation for increased cell proliferation.

• Related Studies :

  • New data for the validation of the mean daily maximum permissible concentration of hydrogen fluoride in atmospheric air

    1.  Round-the-clock exposure to hydrogen fluoride concentrations of 0.10 and 0.03 mg/m3 causes inhibition in the central nervous system, decreases the activity of a number of enzymes, impairs the phosphorus-calcium metabolism, and causes the accumulation of fluorine in the body and damage to the internal organs and bone tissue. 2.  A

  • Fluoride in Drinking Water: A Scientific Review of EPA’s Standards.

    Excerpts: Summary Under the Safe Drinking Water Act, the U.S. Environmental Protection Agency (EPA) is required to establish exposure standards for contaminants in public drinking-water systems that might cause any adverse effects on human health. These standards include the maximum contaminant level goal (MCLG), the maximum contaminant level (MCL), and the secondary

  • Systematic impacts of fluoride exposure on the metabolomics of rats.

    Highlights The risk of chronic endemic fluorosis exists in many countries and regions. Comprehensive metabolomic analysis was used to study the effects of fluoride. Multivariate statistics were used to detect metabolite profile changes. Fluoride exposure caused amino acid, fatty acid, and energy metabolism disorders. Fluoride exposure caused oxidative stress,

  • A fatality due to ingestion of hydrofluoric acid.

    We report a fatal case of hydrofluoric acid (HF) ingestion with suicidal intent. Quantitation using an ion-selective electrode for fluoride in fresh bile, gastric contents, kidney, liver, skeletal muscle, urine, and vitreous humor yielded 6.5, 39.0, 10.0, 6.0, 4.5, 5.0, and 4.5 ppm, respectively. In addition to the unfixed specimens,

  • Medical aspects of excessive fluoride in a water supply

    A 10-year study of 116 persons in Bartlett and 121 in Cameron, Tex., was conducted to determine if prolonged exposure to fluoride in the water supply of Bartlett had produced detectable physiological effects. Bartlett's water contained about 8 p.p.m. F until 1952, when an experimental defluoridation unit was installed, reducing the

• Related FAN Content :

  • Fluoride Affects Learning & Memory in Animals

    An association between elevated fluoride exposure and reduced intelligence has now been observed in 65 IQ studies. Although a link between fluoride and intelligence might initially seem surprising or random, it is actually consistent with a large body of animal research. This animal research includes the following 45 studies (out

  • NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects

    The NRC's analysis on fluoride and the brain.

  • Skeletal Fluorosis: The Misdiagnosis Problem

    It is a virtual certainty that there are individuals in the general population unknowingly suffering from some form of skeletal fluorosis as a result of a doctor's failure to consider fluoride as a cause of their symptoms. Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a consistent feature of these reports is that fluorosis patients--even those with crippling skeletal fluorosis--are misdiagnosed for years by multiple teams of doctors who routinely fail to consider fluoride as a possible cause of their disease.

  • "Pre-Skeletal" Fluorosis

    As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.

  • Fluoride's Direct Effects on Brain: Animal Studies

    The possibility that fluoride ingestion may impair intelligence and other indices of neurological function is supported by a vast body of animal research, including over 40 studies that have investigated fluoride's effects on brain quality in animals. As discussed by the National Research Council, the studies have consistently demonstrated that fluoride, at widely varying concentrations, is toxic to the brain.