Cobalt is absorbed though the lungs, gastrointestinal tract, and skin. Since it is a component of the vitamin B12 (cyanocobalamin), it is distributed to most tissues of the body. It is transported in the blood, often bound to albumin, with the highest levels being found in the liver and kidney. Cobalt is excreted mainly in the urine and faeces. (L29)
IDENTIFICATION AND USE: Cobalt fluoride forms rose-red crystals or powder. It is used as a catalyst for organic reactions, and as a fluorinating agent. HUMAN EXPOSURE AND TOXICITY: Initial symptoms from ingestion include salivation, nausea, abdominal pain, vomiting, and diarrhea and are secondary to the local action of fluoride on the intestinal mucosa. Systemic symptoms are varied and severe: increased irritability of the central nervous system consistent with the Ca2+ binding effect of fluoride and the resulting hypocalcemia; hypotension, presumably owing to central vasomotor depression as well as direct cardiotoxicity; and stimulation and then depression of respiration. Death can result from respiratory paralysis or cardiac failure. ANIMAL STUDIES: The liver, heart and kidneys of rats given acute exposure to cobalt fluoride were examined microscopically. Hyperemia, hemorrhage and cytoplasmic changes were noted, while the kidney glomeruli were rich in cells and basal membranes were thickened. Cells of the proximal tubules were swollen and showed vacuolization and degeneration. In the hearts of some rats proliferative and edematous interstitial tissue and swollen muscle fibers were observed and focal degeneration, vacuolization and necrosis associated with disappearance of the cross striations were noted. Chronic manifestations of excess fluoride in cattle are dental fluorosis and osteofluorosis.
Cobalt is believed to exhibit its toxicity through a oxidant-based and free radical-based processes. It produces oxygen radicals and may be oxidized to ionic cobalt, causing increased lipid peroxidation, DNA damage, and inducing certain enzymes that lead to cell apoptosis. Cobalt has also been shown to block inorganic calcium channels, possibly impairing neurotransmission. Cobalt can also chelate lipoic acids, impairing oxidation of pyruvate or fatty acids. In addition, cobalt may inhibit DNA repair by interacting with zinc finger DNA repair proteins, and has also been shown to inhibit heme synthesis and glucose metabolism. Cobalt may activate specific helper T-lymphocyte cells and interact directly with immunologic proteins, such as antibodies (IgA and IgE) or Fc receptors, resulting in immunosensitization. (L29)
There is inadequate evidence for the carcinogenicity of cobalt and cobalt compounds in humans. There is sufficient evidence for the carcinogenicity of cobalt metal powder in experimental animals. There is limited evidence for the carcinogenicity of metal alloys containing cobalt, chromium and molybdenum in experimental animals. ... Overall Evaluation: Cobalt and cobalt compounds are possibly carcinogenic to humans (Group 2B). /Cobalt and cobalt compounds/
... Most of the absorption takes place in the intestine. The degree of fluoride absorption correlates with its water solubility ... A second route of absorption is through the lungs ... Fluoride is distributed widely in organs and tissues but is concentrated in bone and teeth, and the skeletal burden is related to intake and age. ... The kidneys are the major site of fluoride. Small amounts of fluoride also appear in sweat, milk, and intestinal secretions; in a very hot environment, sweat can account for nearly 50% of the total fluoride excretion. /Fluorides/
...Experiments demonstrated that storage of fluoride in bones occurs as result of repeated exposures to concentrations that are but slightly, if at all, irritant. /Fluoride/
Following ingestion, soluble fluorides are rapidly absorbed from the gastrointestinal tract at least to the extent of 97%. Absorbed fluoride is distributed throughout the tissues of the body by the blood. Fluoride concentrations in soft tissues fall to pre-exposure levels within a few hours of exposure. Fluoride exchange with hydroxyl radicals of hydroxyapatite (the inorganic constituent of bone) to form fluorohydroxyapatite. Fluoride that is not retained is excreted rapidly in urine. In adults under steady state intake conditions, the urinary concentration of fluoride tends to approximate the concentration of fluoride in the drinking water. This reflects the decreasing retention of fluoride (primarily in bone) with increasing age. Under certain conditions perspiration may be an important route of fluoride excretion. The concentration of fluoride retained in bones and teeth is a function of both the concentration of fluoride intake and the duration of exposure. Periods of excessive fluoride exposure will result in increased retention in the bone. However, when the excessive exposure is eliminated, the bone fluoride concentration will decrease to a concentration that is again reflective of intake. /Fluoride/
Exposure to aqueous solution of cobaltous fluoride reduced wettability & free surface energy of org layers of tooth enamel & dentine from humans or whales in vitro. It is possible that effect on wettability may contribute to anticaries effect.
