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Iodate exposure

The induction period of the reaction may be curtailed 2 by (1) the presence of an excess of iodic acid, (2) an increase in the concentrations of the reactants, (3) the addition of a trace of arsenic acid, (4) the addition of a mineral acid and (5) exposure to sunlight. On the other hand, the period may be prolonged by the addition of mercuric chloride or by violent shaking. The proportion of the iodine liberated increases with the arsenious acid concentration and passes through a maximum. The iodine appears on the surface of the solution even though the latter may be covered with benzene (or occasionally it appears at a nucleus on the glass). The reduction of periodate to iodate by means of arsenite is a bimolecular reaction and is of the first order with respect to both components.3 At 25° C. it proceeds according to the velocity equation... [Pg.146]

In the reaction of oxalic acid with iodate, the oxidising species are molecular iodine and hypoiodous acid (principally the latter). The induction period observed in the reaction is due to build-up of the oxidising species it is shortened by exposure to light or by the presence of metal ions. As soon as the iodine concentration is appreciable, the reaction rate accelerates rapidly on account of the sequence of reactions... [Pg.488]

L. J. M. Daguerre s photographic process (silver plate sensitized by exposure to iodine vapour) Introduction of (light sensitive) AgBr into photography Iodine (as iodate) found in Chilean saltpetre by A. A. Hayes... [Pg.790]

SODIUM RHODANIDE (540-72-7) NaSCN Exposure to light causes slow decomposition, forming cyanide, sulfur oxides, and nitrous vapors. Violent reaction, possibly explosion, with strong oxidizers, organic peroxides, nitric acid. Incompatible with acids, bases, chlorates, anunonia, amines, amides, alcohols, glycols, caprolactam, nitrates, peroxides and hydroperoxides, potassium chlorate, potassium iodate, silver nitrate, sodium chlorate. Contact with sulfuric acid forms toxic carbonyl sulfide gas. Forms explosive mixture with sodium nitrate. Thermal decomposition releases oxides of sulfur and nitrogen. [Pg.965]

This review demonstrates the tremendous advantages of modern analytical technology for the detection of iodate and perchlorate in aqueous samples, in addition to providing a brief overview on these two species. The measurement of iodate and perchlorate simultaneously, and at nanogram per liter sensitivity, provides great advantage to risk assessors who must balance exposure of these oxy-hahdes and also helps in the evaluation of the differences between potable water and bottled water. [Pg.292]

Potassium Iodate KIO3 K+ + lOy IO3 Is rapidly taken up from gut. Immediately reduced to Iodide (P) and used as such by thyroid cells for the synthesis of hormone Stable under air, exposure to humidity and light. Used to Iodize salt... [Pg.910]

In conclusion, iodine from iodate is available to the thyroid, whether given per os, injected intravenously, or added to the incubation medium of thyroid sfices. However, it is most likely that iodate is reduced to iodide and reaches the thyroid gland in this form. The potent nonenzymatic reduction mechanisms in whole blood, in many tissues, in flour and in other food will greatly diminish general tissue exposure to iodate, but an exact risk assessment should be based on future toxico- and pharmacokinetic studies. [Pg.912]

Blood iodine levels were elevated at subtoxic doses of iodine, indicating adequate exposure. Iodine toxicity manifested itself as reduced performance. Since iron supplementation prevented it, this toxicity may have resulted from an apparent interference of iodate or iodine, respectively, with iron uptake or utiftzation. NOELs for pigs were observed at 400 parts per million (ppm) calcium iodate added to hog mash calves were more susceptible with a NOEL of only 25 ppm. The toxic signs were attributed either to iron deficiency or to general iodine toxicity. [Pg.913]

Despite these reservations, we may conclude that the maximal exposure to 34pg/kg/day of iodate through the use of iodized salt should present no risk for functional or structural lesions. This dose is lower than the peroral NOEL for reproductive toxicology of iodine itself (2-3 mg/kg/day) by a factor of 100, the usual safety factor for establishing acceptable daily intakes (ADI) (Beckmann and Brent, 1984). Ocular toxicity, in particular, is most unlikely to occur since repeated oral exposures to 100 mg/ kg in dogs have failed to induce retinal damage (Webster et ai, 1966). Contrary to Pahuja et, however, we... [Pg.916]

Formal studies of reproductive toxicity of iodates are also lacking. In view of the toxic effects of excessive doses of iodine on the fetus and the unlikely exposure of the fetal system to iodate for the metabolic (toxicokinetic) reasons outlined above, there appears to be no need for additional studies. [Pg.916]


See other pages where Iodate exposure is mentioned: [Pg.506]    [Pg.202]    [Pg.360]    [Pg.407]    [Pg.608]    [Pg.608]    [Pg.608]    [Pg.611]    [Pg.318]    [Pg.682]    [Pg.289]    [Pg.141]    [Pg.300]    [Pg.202]    [Pg.360]    [Pg.407]    [Pg.608]    [Pg.608]    [Pg.1897]    [Pg.959]    [Pg.967]    [Pg.1215]    [Pg.287]    [Pg.880]    [Pg.909]    [Pg.911]    [Pg.911]    [Pg.913]    [Pg.913]    [Pg.913]    [Pg.914]    [Pg.915]    [Pg.915]    [Pg.916]    [Pg.426]   
See also in sourсe #XX -- [ Pg.911 ]




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